subject:(Adult T cell leukemia)

1. Takachi, Takayuki. Human T-cell leukemia virus type 1 Tax oncoprotein represses the expression of the BCL11B tumor suppressor in T-cells : ヒトT細胞白血病ウイルス１型の癌蛋白Taxは癌抑制遺伝子BCL11Bの発現を抑制する.

Degree: 博士（医学）, 2015, Niigata University / 新潟大学

URL: http://hdl.handle.net/10191/35559

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学位の種類: 博士（医学）. 報告番号: 甲第4067号. 学位記番号: 新大院博（医）甲第656号. 学位授与年月日: 平成27年9月24日

Cancer Science. 2015, 106(4), 461-465.

Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of… (more)

Subjects/Keywords: Adult T cell leukemia; BCL11B; HBZ; HTLV-1; Tax

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Takachi, T. (2015). Human T-cell leukemia virus type 1 Tax oncoprotein represses the expression of the BCL11B tumor suppressor in T-cells : ヒトT細胞白血病ウイルス１型の癌蛋白Taxは癌抑制遺伝子BCL11Bの発現を抑制する. (Thesis). Niigata University / 新潟大学. Retrieved from http://hdl.handle.net/10191/35559

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Takachi, Takayuki. “Human T-cell leukemia virus type 1 Tax oncoprotein represses the expression of the BCL11B tumor suppressor in T-cells : ヒトT細胞白血病ウイルス１型の癌蛋白Taxは癌抑制遺伝子BCL11Bの発現を抑制する.” 2015. Thesis, Niigata University / 新潟大学. Accessed March 05, 2021. http://hdl.handle.net/10191/35559.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Takachi, Takayuki. “Human T-cell leukemia virus type 1 Tax oncoprotein represses the expression of the BCL11B tumor suppressor in T-cells : ヒトT細胞白血病ウイルス１型の癌蛋白Taxは癌抑制遺伝子BCL11Bの発現を抑制する.” 2015. Web. 05 Mar 2021.

Vancouver:

Takachi T. Human T-cell leukemia virus type 1 Tax oncoprotein represses the expression of the BCL11B tumor suppressor in T-cells : ヒトT細胞白血病ウイルス１型の癌蛋白Taxは癌抑制遺伝子BCL11Bの発現を抑制する. [Internet] [Thesis]. Niigata University / 新潟大学; 2015. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10191/35559.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Takachi T. Human T-cell leukemia virus type 1 Tax oncoprotein represses the expression of the BCL11B tumor suppressor in T-cells : ヒトT細胞白血病ウイルス１型の癌蛋白Taxは癌抑制遺伝子BCL11Bの発現を抑制する. [Thesis]. Niigata University / 新潟大学; 2015. Available from: http://hdl.handle.net/10191/35559

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

2. 牧山, 純也. Treatment outcome of elderly patients with aggressive adult T cell leukemia-lymphoma: Nagasaki University Hospital experience : 長崎大学病院における高齢者成人T細胞白血病・リンパ腫 (ATL) の治療成績.

Degree: 博士(医学), 2014, Nagasaki University / 長崎大学

URL: http://hdl.handle.net/10069/35926

► VCAP (vincristine, cyclophosphamide, doxorubicin, and prednisone)-AMP (doxorubicin, ranimustine, and prednisone)-VECP (vindesine, etoposide, carboplatin, and prednisone) is a standard regimen for aggressive adult T cell leukemia-lymphoma… (more)

Subjects/Keywords: Adult T cell leukemia-lymphoma (ATL); Chemotherapy; Elderly patients

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

牧山, �. (2014). Treatment outcome of elderly patients with aggressive adult T cell leukemia-lymphoma: Nagasaki University Hospital experience : 長崎大学病院における高齢者成人T細胞白血病・リンパ腫 (ATL) の治療成績. (Thesis). Nagasaki University / 長崎大学. Retrieved from http://hdl.handle.net/10069/35926

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

牧山, 純也. “Treatment outcome of elderly patients with aggressive adult T cell leukemia-lymphoma: Nagasaki University Hospital experience : 長崎大学病院における高齢者成人T細胞白血病・リンパ腫 (ATL) の治療成績.” 2014. Thesis, Nagasaki University / 長崎大学. Accessed March 05, 2021. http://hdl.handle.net/10069/35926.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

牧山, 純也. “Treatment outcome of elderly patients with aggressive adult T cell leukemia-lymphoma: Nagasaki University Hospital experience : 長崎大学病院における高齢者成人T細胞白血病・リンパ腫 (ATL) の治療成績.” 2014. Web. 05 Mar 2021.

Vancouver:

牧山 �. Treatment outcome of elderly patients with aggressive adult T cell leukemia-lymphoma: Nagasaki University Hospital experience : 長崎大学病院における高齢者成人T細胞白血病・リンパ腫 (ATL) の治療成績. [Internet] [Thesis]. Nagasaki University / 長崎大学; 2014. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10069/35926.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

牧山 �. Treatment outcome of elderly patients with aggressive adult T cell leukemia-lymphoma: Nagasaki University Hospital experience : 長崎大学病院における高齢者成人T細胞白血病・リンパ腫 (ATL) の治療成績. [Thesis]. Nagasaki University / 長崎大学; 2014. Available from: http://hdl.handle.net/10069/35926

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

3. Kohart, Nicole Ann, Kohart. Models, Mechanisms, and Treatment of Adult T-cell Leukemia/Lymphoma Bone Metastasis.

Degree: PhD, Comparative and Veterinary Medicine, 2017, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1503248777003095

► Adult T-cell Leukemia/Lymphoma (ATL) is a rapidly fatal hematological malignancy that develops in a subset of Human T-cell Leukemia Virus Type 1 (HTLV-1) carriers after… (more)

▼ Adult T-cell Leukemia/Lymphoma (ATL) is a rapidly fatal hematological malignancy that develops in a subset of Human T-cell Leukemia Virus Type 1 (HTLV-1) carriers after a 20-40 year latency. ATL has a unique relationship to bone characterized by aggressive bone invasion, long latency in the marrow, osteolytic bone metastasis, and hypercalcemia of malignancy. ATL bone metastasis and paraneoplastic syndromes cause substantial patient morbidity and a poor prognosis of less than a year. Novel therapeutic approaches for ATL are imperative to improve patient quality of life and prognosis. Therapies targeting both tumor and the bone microenvironment have been investigated in other bone tropic tumors but largely remain unstudied in ATL bone metastasis. This is due to the lack of understanding the mechanisms of the ATL tumor-bone communication and the paucity of appropriate animal models to study this focus of the disease. Several animal models exist to study the pathogenesis of HTLV-1 and ATL; however, models to recapitulate and describe the intimate tumor-bone interaction have not been well described. In this study, we developed and characterized novel xenograft mouse models of ATL bone metastasis. We introduced primary and in vitro HTLV-1 transformed cell lines into the tibias of immunosuppressed mice. Mice developed aggressive bone tumors and distant metastasis within 4 weeks. Tumor-bone phenotypes of xenograft mice ranged from minimal bone changes, mixed osteolytic/osteoblastic lesions, to marked osteolytic phenotypes similar to what is seen in clinical patients. The RVATL xenograft model with the greatest degree of tumor-associated osteolysis had significantly higher mRNA expression of parathyroid hormone-related protein (PTHrP), suggesting a significant paracrine role for PTHrP in ATL bone metastasis. Knockdown of PTHrP in an ATL cell line significantly decreased tumor growth and associated osteolysis in vivo. These models mimic key aspects of ATL in bone and will be useful for preclinical and pathogenesis studies of ATL bone metastasis. Elevated levels of bone acting factors PTHrP, interleukin-6 (IL-6), and macrophage inflammatory protein-1a (MIP-1a) are found in serum of patients with ATL. Studies have defined an endocrine role for these factors to act on osteoclasts at distant sites to promote widespread bone resorption and hypercalcemia; however, the paracrine role they play in the ATL-bone communication remains elusive. We investigated the paracrine role of osteolytic factors PTHrP, MIP-1a, and autotaxin in bone lymphoma through overexpressing each in a leukemic T-cell line, Jurkat that does not normally express these factors. PTHrP overexpression resulted in marked pathologic osteolysis in vivo and significant bone loss in ex vivo calvarial assays. These findings showed a sufficient and significant paracrine role for PTHrP in pathologic osteolysis in T-cell lymphoma bone metastasis. In addition, this report describes a novel tool that will be useful to dissect the critical factors in bone lymphoma that are…

Subjects/Keywords: Comparative; Pathology; Adult T cell Leukemia Lymphoma; bone metastasis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kohart, Nicole Ann, K. (2017). Models, Mechanisms, and Treatment of Adult T-cell Leukemia/Lymphoma Bone Metastasis. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1503248777003095

Chicago Manual of Style (16^th Edition):

Kohart, Nicole Ann, Kohart. “Models, Mechanisms, and Treatment of Adult T-cell Leukemia/Lymphoma Bone Metastasis.” 2017. Doctoral Dissertation, The Ohio State University. Accessed March 05, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1503248777003095.

MLA Handbook (7^th Edition):

Kohart, Nicole Ann, Kohart. “Models, Mechanisms, and Treatment of Adult T-cell Leukemia/Lymphoma Bone Metastasis.” 2017. Web. 05 Mar 2021.

Vancouver:

Kohart, Nicole Ann K. Models, Mechanisms, and Treatment of Adult T-cell Leukemia/Lymphoma Bone Metastasis. [Internet] [Doctoral dissertation]. The Ohio State University; 2017. [cited 2021 Mar 05]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1503248777003095.

Council of Science Editors:

Kohart, Nicole Ann K. Models, Mechanisms, and Treatment of Adult T-cell Leukemia/Lymphoma Bone Metastasis. [Doctoral Dissertation]. The Ohio State University; 2017. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1503248777003095

Vanderbilt University

4. Elliott, Natalina Elizabeth. The role of activating mutations in the FERM domain of janus kinase 3 in the development of adult t-cell leukemia/lymphoma.

Degree: PhD, Cancer Biology, 2013, Vanderbilt University

URL: http://hdl.handle.net/1803/10404

► Adult T-cell leukemia/lymphoma (ATLL) is an incurable peripheral T-cell malignancy where most patients succumb within the first year of diagnosis. Development of ATLL requires human… (more)

▼ Adult T-cell leukemia/lymphoma (ATLL) is an incurable peripheral T-cell malignancy where most patients succumb within the first year of diagnosis. Development of ATLL requires human T-cell lymphotrophic virus type 1 (HTLV-I) retroviral infection followed by accumulation of somatic mutations and changes in gene expression. The discovery of genes and pathways involved in the initiation of ATLL may provide novel therapeutic targets for treatment of this fatal disease. Since the IL-2 signaling pathway plays an important role in ATLL development, mutational analysis of IL-2 signaling pathway components should yield a better understanding of disease progression and outcome. Janus kinase 3 (JAK3), a nonreceptor tyrosine kinase is a key kinase upstream in the IL-2 signaling pathway. Activating somatic mutations in JAK3 have been described in leukemias and lymphomas including acute megakaryoblastic leukemia and natural killer/T-cell lymphoma. Three mutations in the regulatory FERM domain of JAK3 were identified in four of the thirty-six ATLL patients screened and no mutations were found in the twenty-four screened ethnically matched controls. These somatic, missense mutations occurred in the amino terminal regulatory FERM domain. JAK3 FERM domain may play an autoregulatory role by inhibiting kinase activity in the absence of IL-2. In cell culture assays all three FERM domain mutations induce gain of function in JAK3 and can be inhibited with a JAK specific kinase inhibitor, tofacitinib. One of the JAK3 FERM domain mutations (E183G) was characterized in vivo and found to be oncogenic in cooperation with the loss of cell cycle regulatory proteins p16(INK4a) and p14(ARF). These findings emphasize the importance of JAK3 activation in ATLL development and offer a novel therapeutic target for this incurable disease. Advisors/Committee Members: Utpal Davé MD (committee member), Scott Hiebert PhD (committee member), William Pao MD PhD (committee member), Stephen Brandt MD (Committee Chair).

Subjects/Keywords: adult t-cell leukemia/lymphoma; Leukemia; FERM; JAK3; ATLL; HTLV-1; IL-2; mutation; t-cell

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Elliott, N. E. (2013). The role of activating mutations in the FERM domain of janus kinase 3 in the development of adult t-cell leukemia/lymphoma. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10404

Chicago Manual of Style (16^th Edition):

Elliott, Natalina Elizabeth. “The role of activating mutations in the FERM domain of janus kinase 3 in the development of adult t-cell leukemia/lymphoma.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed March 05, 2021. http://hdl.handle.net/1803/10404.

MLA Handbook (7^th Edition):

Elliott, Natalina Elizabeth. “The role of activating mutations in the FERM domain of janus kinase 3 in the development of adult t-cell leukemia/lymphoma.” 2013. Web. 05 Mar 2021.

Vancouver:

Elliott NE. The role of activating mutations in the FERM domain of janus kinase 3 in the development of adult t-cell leukemia/lymphoma. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1803/10404.

Council of Science Editors:

Elliott NE. The role of activating mutations in the FERM domain of janus kinase 3 in the development of adult t-cell leukemia/lymphoma. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/10404

Kyoto University / 京都大学

5. Nagai, Yuya. T memory stem cells are the hierarchical apex of adult T-cell leukemia. : 記憶型T幹細胞を頂点とした成人T細胞白血病の階層構造の解明.

Degree: 博士(医学), 2015, Kyoto University / 京都大学

URL: http://hdl.handle.net/2433/202670 ; http://dx.doi.org/10.14989/doctor.k19267

新制・課程博士

甲第19267号

医博第4031号

Subjects/Keywords: adult T-cell leukemia; HTLV-1; T memory stem cell; T cell differentiation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nagai, Y. (2015). T memory stem cells are the hierarchical apex of adult T-cell leukemia. : 記憶型T幹細胞を頂点とした成人T細胞白血病の階層構造の解明. (Thesis). Kyoto University / 京都大学. Retrieved from http://hdl.handle.net/2433/202670 ; http://dx.doi.org/10.14989/doctor.k19267

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Nagai, Yuya. “T memory stem cells are the hierarchical apex of adult T-cell leukemia. : 記憶型T幹細胞を頂点とした成人T細胞白血病の階層構造の解明.” 2015. Thesis, Kyoto University / 京都大学. Accessed March 05, 2021. http://hdl.handle.net/2433/202670 ; http://dx.doi.org/10.14989/doctor.k19267.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Nagai, Yuya. “T memory stem cells are the hierarchical apex of adult T-cell leukemia. : 記憶型T幹細胞を頂点とした成人T細胞白血病の階層構造の解明.” 2015. Web. 05 Mar 2021.

Vancouver:

Nagai Y. T memory stem cells are the hierarchical apex of adult T-cell leukemia. : 記憶型T幹細胞を頂点とした成人T細胞白血病の階層構造の解明. [Internet] [Thesis]. Kyoto University / 京都大学; 2015. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2433/202670 ; http://dx.doi.org/10.14989/doctor.k19267.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Nagai Y. T memory stem cells are the hierarchical apex of adult T-cell leukemia. : 記憶型T幹細胞を頂点とした成人T細胞白血病の階層構造の解明. [Thesis]. Kyoto University / 京都大学; 2015. Available from: http://hdl.handle.net/2433/202670 ; http://dx.doi.org/10.14989/doctor.k19267

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

6. Nagai, Yuya. T memory stem cells are the hierarchical apex of adult T-cell leukemia.

Degree: 2015, Kyoto University

URL: http://hdl.handle.net/2433/202670

Subjects/Keywords: adult T-cell leukemia; HTLV-1; T memory stem cell; T cell differentiation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nagai, Y. (2015). T memory stem cells are the hierarchical apex of adult T-cell leukemia. (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/202670

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Nagai, Yuya. “T memory stem cells are the hierarchical apex of adult T-cell leukemia. ” 2015. Thesis, Kyoto University. Accessed March 05, 2021. http://hdl.handle.net/2433/202670.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Nagai, Yuya. “T memory stem cells are the hierarchical apex of adult T-cell leukemia. ” 2015. Web. 05 Mar 2021.

Vancouver:

Nagai Y. T memory stem cells are the hierarchical apex of adult T-cell leukemia. [Internet] [Thesis]. Kyoto University; 2015. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2433/202670.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Nagai Y. T memory stem cells are the hierarchical apex of adult T-cell leukemia. [Thesis]. Kyoto University; 2015. Available from: http://hdl.handle.net/2433/202670

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

7. Tada, Kohei. Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia : 抗HIV薬アバカビルは、TDP1が欠損している成人T細胞白血病を標的とする.

Degree: 博士(医学), 2015, Kyoto University / 京都大学

URL: http://hdl.handle.net/2433/202797 ; http://dx.doi.org/10.14989/doctor.k19363

新制・課程博士

甲第19363号

医博第4040号

Subjects/Keywords: Adult T cell leukemia; Abacavir; TDP1; NRTI; chemotherapy

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tada, K. (2015). Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia : 抗HIV薬アバカビルは、TDP1が欠損している成人T細胞白血病を標的とする. (Thesis). Kyoto University / 京都大学. Retrieved from http://hdl.handle.net/2433/202797 ; http://dx.doi.org/10.14989/doctor.k19363

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tada, Kohei. “Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia : 抗HIV薬アバカビルは、TDP1が欠損している成人T細胞白血病を標的とする.” 2015. Thesis, Kyoto University / 京都大学. Accessed March 05, 2021. http://hdl.handle.net/2433/202797 ; http://dx.doi.org/10.14989/doctor.k19363.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tada, Kohei. “Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia : 抗HIV薬アバカビルは、TDP1が欠損している成人T細胞白血病を標的とする.” 2015. Web. 05 Mar 2021.

Vancouver:

Tada K. Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia : 抗HIV薬アバカビルは、TDP1が欠損している成人T細胞白血病を標的とする. [Internet] [Thesis]. Kyoto University / 京都大学; 2015. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2433/202797 ; http://dx.doi.org/10.14989/doctor.k19363.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tada K. Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia : 抗HIV薬アバカビルは、TDP1が欠損している成人T細胞白血病を標的とする. [Thesis]. Kyoto University / 京都大学; 2015. Available from: http://hdl.handle.net/2433/202797 ; http://dx.doi.org/10.14989/doctor.k19363

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

8. Tada, Kohei. Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia .

Degree: 2015, Kyoto University

URL: http://hdl.handle.net/2433/202797

Subjects/Keywords: Adult T cell leukemia; Abacavir; TDP1; NRTI; chemotherapy

Record Details Similar Records Cite « Share

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tada, K. (2015). Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia . (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/202797

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tada, Kohei. “Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia .” 2015. Thesis, Kyoto University. Accessed March 05, 2021. http://hdl.handle.net/2433/202797.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tada, Kohei. “Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia .” 2015. Web. 05 Mar 2021.

Vancouver:

Tada K. Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia . [Internet] [Thesis]. Kyoto University; 2015. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2433/202797.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tada K. Abacavir, an anti-HIV-1 drug, targets TDP1-deficient adult T cell leukemia . [Thesis]. Kyoto University; 2015. Available from: http://hdl.handle.net/2433/202797

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

9. Macaire, Héloïse. Régulation de l’expression des protéines anti-apoptotiques Bfl-1 et Bcl-xL par les protéines virales Tax et HBZ du virus HTLV-1 et identification de petites molécules anti-Bfl-1 à visée thérapeutique : Regulation of Bfl-1 and Bcl-xL anti-apoptotic protein expression by the HTLV-1 Tax and HBZ proteins and identification of small therapeutic molecules directed against Bfl-1 v.

Degree: Docteur es, Virologie-cancérologie, 2011, Université Claude Bernard – Lyon I

URL: http://www.theses.fr/2011LYO10357

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Le virus humain T lymphotrope de type 1 (HTLV-1) est l’agent étiologique de la leucémie/lymphome T de l’adulte (ATLL) qui se développe après plusieurs décennies… (more)

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Le virus humain T lymphotrope de type 1 (HTLV-1) est l’agent étiologique de la leucémie/lymphome T de l’adulte (ATLL) qui se développe après plusieurs décennies et pour laquelle il n’existe à ce jour pas de traitement efficace. Parmi les protéines virales de HTLV-1, Tax et HBZ jouent un rôle déterminant dans le développement de l’ATLL. Si Tax participe au processus leucémogène dès les étapes précoces, HBZ jouerait plutôt un rôle dans le maintien du phénotype tumoral dans les étapes tardives. Dans ce contexte, là nous nous sommes intéressés à la régulation de l’expression des protéines anti-apoptotiques Bfl-1 et Bcl-xL, par les protéines virales Tax et HBZ. Nous avons montré que Tax induit l’expression des protéines anti-apoptotiques Bfl-1 et Bcl-xL de la famille Bcl-2 via la voie NF-κB, alors que HBZ n’a aucun effet sur leur expression. De plus, Tax coopère avec les facteurs de transcription c-Jun et JunD de la voie AP-1 pour augmenter l’expression de ces gènes anti-apoptotiques. En revanche, HBZ module uniquement la trans-activation de bfl-1 induite par Tax. L’ensemble de nos résultats indique donc que Tax joue un rôle prépondérant dans l’activation de l’expression de Bfl-1 et de Bcl-xL et suggère que Bfl-1 et Bcl-xL sont exprimées au cours des étapes précoces et tardives du développement de l’ATLL. Par une stratégie d’ARN interférence, nous avons ensuite montré que Bfl-1 et/ou Bcl-xL sont impliquées dans la survie de lignées cellulaires T infectées par HTLV-1, suggérant que Bfl-1 et Bcl-xL représentent des cibles thérapeutiques potentielles pour traiter l’ATLL. Actuellement, il existe des petites molécules ciblant les membres anti-apoptotiques de la famille Bcl-2, mais aucune ne cible spécifiquement Bfl-1. En collaboration avec la société IMAXIO, nous avons identifié par deux cribles à haut débit 83 molécules capables d’inhiber l’activité anti-apoptotique de Bfl-1. L’une de ces molécules induit spécifiquement la mort de lignées cellulaires T infectées par HTLV-1 pour lesquelles Bfl-1 représente un gène de survie. Ainsi, ce travail doit permettre à terme de développer de futurs médicaments dirigés contre Bfl-1 et de proposer une nouvelle stratégie thérapeutique ciblée contre l’ATLL

Human T lymphotropic virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATLL) that develops after several decades and for which there is no effective treatment. Among the viral proteins of HTLV-1, Tax and HBZ play a major role in the development of ATLL. If Tax participates in the initiation of leukemogenesis from the early stages, HBZ rather plays a role in maintaining the tumor phenotype in the late stages. The aims of our study were to better understand the regulation of Bfl-1 and Bcl-xL anti-apoptotic protein expression by Tax and HBZ viral proteins, as well as their role in the survival of HTLV-1-infected T-cells to propose new therapeutic strategies. We showed that Tax induces Bfl-1 and Bcl-xL expression via the NF-κB pathway, whereas HBZ has no effect on their expression. Tax also cooperates with…

Advisors/Committee Members: Valentin, Hélène (thesis director).

Subjects/Keywords: Virus humain T lymphotrope de type 1 (HTLV-1); Leucémie / lymphome T de l'adulte (ATLL); Tax; HBZ; Bfl-1; Bcl-xL; Apoptose; Cible thérapeutique; Human T-cell leukemia virus type 1; Adult T-cell leukemia / lymphoma (ATLL); Tax; HBZ; Bfl-1; Bcl-xL; Apoptosis; Therapeutic target; 579.2

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Macaire, H. (2011). Régulation de l’expression des protéines anti-apoptotiques Bfl-1 et Bcl-xL par les protéines virales Tax et HBZ du virus HTLV-1 et identification de petites molécules anti-Bfl-1 à visée thérapeutique : Regulation of Bfl-1 and Bcl-xL anti-apoptotic protein expression by the HTLV-1 Tax and HBZ proteins and identification of small therapeutic molecules directed against Bfl-1 v. (Doctoral Dissertation). Université Claude Bernard – Lyon I. Retrieved from http://www.theses.fr/2011LYO10357

Chicago Manual of Style (16^th Edition):

Macaire, Héloïse. “Régulation de l’expression des protéines anti-apoptotiques Bfl-1 et Bcl-xL par les protéines virales Tax et HBZ du virus HTLV-1 et identification de petites molécules anti-Bfl-1 à visée thérapeutique : Regulation of Bfl-1 and Bcl-xL anti-apoptotic protein expression by the HTLV-1 Tax and HBZ proteins and identification of small therapeutic molecules directed against Bfl-1 v.” 2011. Doctoral Dissertation, Université Claude Bernard – Lyon I. Accessed March 05, 2021. http://www.theses.fr/2011LYO10357.

MLA Handbook (7^th Edition):

Macaire, Héloïse. “Régulation de l’expression des protéines anti-apoptotiques Bfl-1 et Bcl-xL par les protéines virales Tax et HBZ du virus HTLV-1 et identification de petites molécules anti-Bfl-1 à visée thérapeutique : Regulation of Bfl-1 and Bcl-xL anti-apoptotic protein expression by the HTLV-1 Tax and HBZ proteins and identification of small therapeutic molecules directed against Bfl-1 v.” 2011. Web. 05 Mar 2021.

Vancouver:

Macaire H. Régulation de l’expression des protéines anti-apoptotiques Bfl-1 et Bcl-xL par les protéines virales Tax et HBZ du virus HTLV-1 et identification de petites molécules anti-Bfl-1 à visée thérapeutique : Regulation of Bfl-1 and Bcl-xL anti-apoptotic protein expression by the HTLV-1 Tax and HBZ proteins and identification of small therapeutic molecules directed against Bfl-1 v. [Internet] [Doctoral dissertation]. Université Claude Bernard – Lyon I; 2011. [cited 2021 Mar 05]. Available from: http://www.theses.fr/2011LYO10357.

Council of Science Editors:

Macaire H. Régulation de l’expression des protéines anti-apoptotiques Bfl-1 et Bcl-xL par les protéines virales Tax et HBZ du virus HTLV-1 et identification de petites molécules anti-Bfl-1 à visée thérapeutique : Regulation of Bfl-1 and Bcl-xL anti-apoptotic protein expression by the HTLV-1 Tax and HBZ proteins and identification of small therapeutic molecules directed against Bfl-1 v. [Doctoral Dissertation]. Université Claude Bernard – Lyon I; 2011. Available from: http://www.theses.fr/2011LYO10357

10. 佐々木, 了政. YM155 suppresses cell proliferation and induces cell death in human adult T-cell leukemia/lymphoma cells : 成人T細胞白血病細胞株においてYM155は抗アポトーシスタンパクの発現を抑制しアポトーシスを誘導する.

Degree: 医学博士, 2016, Iwate Medical University / 岩手医科大学

URL: http://id.nii.ac.jp/1181/00005674/

2015

Subjects/Keywords: YM155; Surviving; STAT3; Mcl-1; Adult T-cell leukemia; YM155; Surviving; STAT3; Mcl-1; Adult T-cell leukemia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

佐々木, �. (2016). YM155 suppresses cell proliferation and induces cell death in human adult T-cell leukemia/lymphoma cells : 成人T細胞白血病細胞株においてYM155は抗アポトーシスタンパクの発現を抑制しアポトーシスを誘導する. (Thesis). Iwate Medical University / 岩手医科大学. Retrieved from http://id.nii.ac.jp/1181/00005674/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

佐々木, 了政. “YM155 suppresses cell proliferation and induces cell death in human adult T-cell leukemia/lymphoma cells : 成人T細胞白血病細胞株においてYM155は抗アポトーシスタンパクの発現を抑制しアポトーシスを誘導する.” 2016. Thesis, Iwate Medical University / 岩手医科大学. Accessed March 05, 2021. http://id.nii.ac.jp/1181/00005674/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

佐々木, 了政. “YM155 suppresses cell proliferation and induces cell death in human adult T-cell leukemia/lymphoma cells : 成人T細胞白血病細胞株においてYM155は抗アポトーシスタンパクの発現を抑制しアポトーシスを誘導する.” 2016. Web. 05 Mar 2021.

Vancouver:

佐々木 �. YM155 suppresses cell proliferation and induces cell death in human adult T-cell leukemia/lymphoma cells : 成人T細胞白血病細胞株においてYM155は抗アポトーシスタンパクの発現を抑制しアポトーシスを誘導する. [Internet] [Thesis]. Iwate Medical University / 岩手医科大学; 2016. [cited 2021 Mar 05]. Available from: http://id.nii.ac.jp/1181/00005674/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

佐々木 �. YM155 suppresses cell proliferation and induces cell death in human adult T-cell leukemia/lymphoma cells : 成人T細胞白血病細胞株においてYM155は抗アポトーシスタンパクの発現を抑制しアポトーシスを誘導する. [Thesis]. Iwate Medical University / 岩手医科大学; 2016. Available from: http://id.nii.ac.jp/1181/00005674/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

11. Pérès, Eléonore. La souris humanisée : modèle d'étude in vivo du processus leucémogène induit par HTLV-1 : The humanized mouse : an in vivo model for the leukemogenic process induced by HTLV-1.

Degree: Docteur es, Sciences de la Vie, 2017, Lyon

URL: http://www.theses.fr/2017LYSEN043

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La leucémie T de l’adulte (ATL), caractérisée par une prolifération dérégulée de lymphocytesT CD4+ activés, se développe chez des individus infectés par le virus T-lymphotropehumain… (more)

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La leucémie T de l’adulte (ATL), caractérisée par une prolifération dérégulée de lymphocytesT CD4+ activés, se développe chez des individus infectés par le virus T-lymphotropehumain (HTLV-1). Une période asymptomatique de plusieurs décennies sépare l’infection del’apparition des symptômes cliniques de l’ATL, rendant complexe la compréhension des étapesinitiales de la leucémogenèse. Le modèle de la souris humanisée dans laquelle est reconstituéun système hémato-lymphoïde humain est pertinent pour étudier ces étapes, depuis l’infectionpar HTLV-1 jusqu’à l’apparition de la lymphoprolifération. Grâce à ce modèle, mes travaux dethèse ont aidé à mieux comprendre deux mécanismes importants. D’abord, le rôle du chimiotactisme dans le contact cellule infectée-cellule non infectée in vivo. En inhibant la sécrétion de leukotriène B4, un chimioattractant, dans des souris humanisées et infectées, la charge proviraleest plus faible que celle des souris témoins et la prolifération des CD4+ activés est égalementréduite, soulignant le rôle du leukotriène B4 dans la primo-infection. Ensuite, j’ai étudié l’implicationdes protéines PDZ dans le processus leucémogène in vivo. En effet, certaines de cesprotéines, dont Scribble, interagissent avec le PBM (PDZ-domain Binding Motif) de la protéinevirale Tax. Des souris humanisées ont été infectées avec un provirus soit sauvage soit muté auniveau du PBM et j’ai montré, dès 5 semaines après infection, que l’interaction de ce domaineavec des protéines PDZ augmente la prolifération des CD4+ activés et perturbe l’expression degènes impliqués dans la prolifération, l’organisation du cytosquelette et des voies de l’apoptose.Ces résultats attestent du rôle du PBM de Tax dans le soutien de la lymphoprolifération in vivo.

Human T-Cell Leukemia Virus 1 (HTLV-1) is the causative agent of Adult T-cell Leukemia(ATL) characterized by a deregulated proliferation of activated CD4+ T cells. An asymptomaticperiod of several decades separates the infection and the onset of the leukemia, complicating thestudy of the initial leukemogenic steps. Humanized mouse models are relevant to study thosesteps as these mice harbor human hemato-lymphoid cells that can be infected by HTLV-1.I used this animal model to better characterized two biological mecanisms during my thesis.First, the role of chemotaxis in infected-non infected cell contact in vivo. Inhibiting the secretionof leukotriene B4, a potent chemoattractant, in HTLV-1-infected humanized mice reduces theproviral load and the proliferation of activated CD4+ T cells. Those results establish the importanceof leukotriene B4 in HTLV-1 primo-infection. Next, I focused on the importance of thePDZ proteins in the leukemogenic process in vivo. The PDZ-domain Binding Motif (PBM) ofthe Tax viral protein interacts with several cellular PDZ proteins including Scribble. I infectedhumanized mice either with a wild-type or a PBM-mutated provirus of HTLV-1. I showed thatinteraction of the Tax PBM with PDZ proteins enhances activated CD4+ T cells proliferationfrom 5 weeks after…

Advisors/Committee Members: Duc Dodon, Madeleine (thesis director).

Subjects/Keywords: HTLV-1; Souris humanisée; Leucémie T de l’adulte; Leucémogenèse; Protéines PDZ; Chimiotactisme; HTLV-1; Humanized mouse; Adult t-cell Leukemia; Leukemogenesis; PDZ proteins; Chimiotaxis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pérès, E. (2017). La souris humanisée : modèle d'étude in vivo du processus leucémogène induit par HTLV-1 : The humanized mouse : an in vivo model for the leukemogenic process induced by HTLV-1. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2017LYSEN043

Chicago Manual of Style (16^th Edition):

Pérès, Eléonore. “La souris humanisée : modèle d'étude in vivo du processus leucémogène induit par HTLV-1 : The humanized mouse : an in vivo model for the leukemogenic process induced by HTLV-1.” 2017. Doctoral Dissertation, Lyon. Accessed March 05, 2021. http://www.theses.fr/2017LYSEN043.

MLA Handbook (7^th Edition):

Pérès, Eléonore. “La souris humanisée : modèle d'étude in vivo du processus leucémogène induit par HTLV-1 : The humanized mouse : an in vivo model for the leukemogenic process induced by HTLV-1.” 2017. Web. 05 Mar 2021.

Vancouver:

Pérès E. La souris humanisée : modèle d'étude in vivo du processus leucémogène induit par HTLV-1 : The humanized mouse : an in vivo model for the leukemogenic process induced by HTLV-1. [Internet] [Doctoral dissertation]. Lyon; 2017. [cited 2021 Mar 05]. Available from: http://www.theses.fr/2017LYSEN043.

Council of Science Editors:

Pérès E. La souris humanisée : modèle d'étude in vivo du processus leucémogène induit par HTLV-1 : The humanized mouse : an in vivo model for the leukemogenic process induced by HTLV-1. [Doctoral Dissertation]. Lyon; 2017. Available from: http://www.theses.fr/2017LYSEN043

Kyoto University / 京都大学

12. Mitagami, Yu. Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice : インターフェロンγはHBZトランスジェニックマウスの炎症とTリンパ腫の発症を促進する.

Degree: 博士(医科学), 2016, Kyoto University / 京都大学

URL: http://hdl.handle.net/2433/215454 ; http://dx.doi.org/10.14989/doctor.k19628

新制・課程博士

甲第19628号

医科博第66号

Subjects/Keywords: human T-cell leukemia virus type 1; adult T-cell leukemia; HTLV-1 bZIP factor; IFN-gamma

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mitagami, Y. (2016). Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice : インターフェロンγはHBZトランスジェニックマウスの炎症とTリンパ腫の発症を促進する. (Thesis). Kyoto University / 京都大学. Retrieved from http://hdl.handle.net/2433/215454 ; http://dx.doi.org/10.14989/doctor.k19628

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mitagami, Yu. “Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice : インターフェロンγはHBZトランスジェニックマウスの炎症とTリンパ腫の発症を促進する.” 2016. Thesis, Kyoto University / 京都大学. Accessed March 05, 2021. http://hdl.handle.net/2433/215454 ; http://dx.doi.org/10.14989/doctor.k19628.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mitagami, Yu. “Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice : インターフェロンγはHBZトランスジェニックマウスの炎症とTリンパ腫の発症を促進する.” 2016. Web. 05 Mar 2021.

Vancouver:

Mitagami Y. Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice : インターフェロンγはHBZトランスジェニックマウスの炎症とTリンパ腫の発症を促進する. [Internet] [Thesis]. Kyoto University / 京都大学; 2016. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2433/215454 ; http://dx.doi.org/10.14989/doctor.k19628.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mitagami Y. Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice : インターフェロンγはHBZトランスジェニックマウスの炎症とTリンパ腫の発症を促進する. [Thesis]. Kyoto University / 京都大学; 2016. Available from: http://hdl.handle.net/2433/215454 ; http://dx.doi.org/10.14989/doctor.k19628

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

13. Mitagami, Yu. Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice .

Degree: 2016, Kyoto University

URL: http://hdl.handle.net/2433/215454

Subjects/Keywords: human T-cell leukemia virus type 1; adult T-cell leukemia; HTLV-1 bZIP factor; IFN-gamma

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mitagami, Y. (2016). Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice . (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/215454

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mitagami, Yu. “Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice .” 2016. Thesis, Kyoto University. Accessed March 05, 2021. http://hdl.handle.net/2433/215454.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mitagami, Yu. “Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice .” 2016. Web. 05 Mar 2021.

Vancouver:

Mitagami Y. Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice . [Internet] [Thesis]. Kyoto University; 2016. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2433/215454.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mitagami Y. Interferon-γ promotes inflammation and development of T-cell lymphoma in HTLV-1 bZIP factor transgenic mice . [Thesis]. Kyoto University; 2016. Available from: http://hdl.handle.net/2433/215454

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

14. Cheminant, Morgane. Rôle des récepteurs NK dans les lymphoproliférations T matures. Exemple des leucémies/lymphomes T de l'adulte associés à l'HTLV-1 et des lymphoproliférations T intestinales primitives : Role of NK Receptors in Peripheral T-cell Lymphoma. Example of Adult T-cell Leukemia/Lymphoma and Primary Gastro-intestinal T-cell Lymphoproliferative Disease.

Degree: Docteur es, Sciences de la vie et de la santé, 2018, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2018SACLS301

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Les lymphomes T périphériques (PTCLs) sont des entités hétérogènes dont la classification a récemment été révisée. Plus de 25 entités de lymphomes T ou NK… (more)

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Les lymphomes T périphériques (PTCLs) sont des entités hétérogènes dont la classification a récemment été révisée. Plus de 25 entités de lymphomes T ou NK matures sont ainsi classées selon leur présentation clinico-biologique et leur origine cellulaire présumée, justifiant l’étude approfondie de leur phénotype. Des récepteurs NK (NKRs) ont été mis en évidence dans certains lymphomes cutanés. En outre, un lymphome intra-épithélial intestinal, appelé maladie coeliaque réfractaire de type II (MCRII), dérive d’un lymphocyte caractérisé par des marqueurs T et NK. Ces constatations nous ont amenés à évaluer l’expression de NKRs sur un panel représentatif de PTCLs, constitué en particulier de PTCLs primitifs intestinaux et de leucémies/lymphomes T de l’adulte associés à l’HTLV-1 (ATL). Dans l’ATL, nous montrons que KIR3DL2 est exprimé par les cellules tumorales des formes aigües. Le virus HTLV-1 et la méthylation de son promoteur jouent un rôle dans l’expression de KIR3DL2. Enfin, un anticorps monoclonal dirigé contre KIR3DL2, IPH4102, est capable de tuer spécifiquement les cellules primaires d’ATL KIR3DL2 ex vivo par un mécanisme dépendant d’effecteurs NK autologues. Dans les lymphoproliférations T intestinales primitives, nous montrons que NKp46 est un nouveau biomarqueur pour leur diagnostic et leur stratification thérapeutique. En effet, NKp46 est exprimé sur les cellules anormales de la MCRII, et sur les lymphomes T primitifs intestinaux agressifs, mais pas sur les indolents et les MC non compliquées. Enfin, les cellules primaires exprimant NKp46 sont sensibles ex vivo à la cytotoxicité induite par un anticorps monoclonal dirigé contre NKp46 et couplé à une toxine.Ces résultats nous ont permis de discuter l’origine cellulaire de ces lymphomes et le rôle de ces NKRs dans la lymphomagénèse. Dans une optique translationnelle, l’expression des NKRs peut aider au diagnostic de ces entités parfois difficiles à individualiser, et enfin constituer une cible thérapeutique intéressante.

Peripheral T-cell lymphoma (PTCLs) are heterogeneous entities whose classification has recently been revised. More than 25 entities are thus classified according to their clinico-biological presentation and their presumed cellular origin, justifying the in-depth study of their phenotype. NK receptors (NKRs) have been demonstrated in some cutaneous lymphomas. In addition, a less known intestinal lymphoma, called type II refractory celiac disease (RCDII), arises from an intraepithelial lymphocyte characterized by T and NK markers. These findings led us to evaluate the expression of NKRs on a representative panel of PTCLs, focusing on primary gastrointestinal (GI) T-cell lymphoproliferative diseases (T-LPD) and HTLV-1 associated adult T leukemia/lymphoma (ATL).In ATL, we show that KIR3DL2 expression is mainly associated with acute-type ATL. HTLV-1 has a preferential tropism for KIR3DL2+ lymphocytes and may play a role in KIR3DL2 expression induction, combined with the hypomethylation status of KIR3DL2 promoter. The benefit of targeting KIR3DL2 by…

Advisors/Committee Members: Hermine, Olivier (thesis director).

Subjects/Keywords: Récepteurs NK; Leucémies/lymphomes T de l'adulte associés à l'HLTV-1; Kir3dl2; NKp46; Lymphoproliferations T intestinales primitives; Maladie coeliaque réfractaire; NK receptors; Adult T-Cell Leukemia/Lymphoma; Kir3dl2; NKp46; Primary Gastro-Intestinal T-Cell Lymphoproliferative Disease; Refractory Celiac Disease

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cheminant, M. (2018). Rôle des récepteurs NK dans les lymphoproliférations T matures. Exemple des leucémies/lymphomes T de l'adulte associés à l'HTLV-1 et des lymphoproliférations T intestinales primitives : Role of NK Receptors in Peripheral T-cell Lymphoma. Example of Adult T-cell Leukemia/Lymphoma and Primary Gastro-intestinal T-cell Lymphoproliferative Disease. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2018SACLS301

Chicago Manual of Style (16^th Edition):

Cheminant, Morgane. “Rôle des récepteurs NK dans les lymphoproliférations T matures. Exemple des leucémies/lymphomes T de l'adulte associés à l'HTLV-1 et des lymphoproliférations T intestinales primitives : Role of NK Receptors in Peripheral T-cell Lymphoma. Example of Adult T-cell Leukemia/Lymphoma and Primary Gastro-intestinal T-cell Lymphoproliferative Disease.” 2018. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed March 05, 2021. http://www.theses.fr/2018SACLS301.

MLA Handbook (7^th Edition):

Cheminant, Morgane. “Rôle des récepteurs NK dans les lymphoproliférations T matures. Exemple des leucémies/lymphomes T de l'adulte associés à l'HTLV-1 et des lymphoproliférations T intestinales primitives : Role of NK Receptors in Peripheral T-cell Lymphoma. Example of Adult T-cell Leukemia/Lymphoma and Primary Gastro-intestinal T-cell Lymphoproliferative Disease.” 2018. Web. 05 Mar 2021.

Vancouver:

Cheminant M. Rôle des récepteurs NK dans les lymphoproliférations T matures. Exemple des leucémies/lymphomes T de l'adulte associés à l'HTLV-1 et des lymphoproliférations T intestinales primitives : Role of NK Receptors in Peripheral T-cell Lymphoma. Example of Adult T-cell Leukemia/Lymphoma and Primary Gastro-intestinal T-cell Lymphoproliferative Disease. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2018. [cited 2021 Mar 05]. Available from: http://www.theses.fr/2018SACLS301.

Council of Science Editors:

Cheminant M. Rôle des récepteurs NK dans les lymphoproliférations T matures. Exemple des leucémies/lymphomes T de l'adulte associés à l'HTLV-1 et des lymphoproliférations T intestinales primitives : Role of NK Receptors in Peripheral T-cell Lymphoma. Example of Adult T-cell Leukemia/Lymphoma and Primary Gastro-intestinal T-cell Lymphoproliferative Disease. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2018. Available from: http://www.theses.fr/2018SACLS301

Kyoto University / 京都大学

15. Tanaka, Azusa. HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization : HTLV-1 bZIP Factorは転写因子FoxO3aの機能および局在に影響を及ぼしアポトーシスを阻害する.

Degree: 博士(医科学), 2014, Kyoto University / 京都大学

URL: http://hdl.handle.net/2433/185199 ; http://dx.doi.org/10.14989/doctor.k17979

新制・課程博士

甲第17979号

医科博第48号

Subjects/Keywords: HTLV-1 bZIP Factor; Apoptosis; FoxO3a; Adult T-cell leukemia

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tanaka, A. (2014). HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization : HTLV-1 bZIP Factorは転写因子FoxO3aの機能および局在に影響を及ぼしアポトーシスを阻害する. (Thesis). Kyoto University / 京都大学. Retrieved from http://hdl.handle.net/2433/185199 ; http://dx.doi.org/10.14989/doctor.k17979

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tanaka, Azusa. “HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization : HTLV-1 bZIP Factorは転写因子FoxO3aの機能および局在に影響を及ぼしアポトーシスを阻害する.” 2014. Thesis, Kyoto University / 京都大学. Accessed March 05, 2021. http://hdl.handle.net/2433/185199 ; http://dx.doi.org/10.14989/doctor.k17979.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tanaka, Azusa. “HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization : HTLV-1 bZIP Factorは転写因子FoxO3aの機能および局在に影響を及ぼしアポトーシスを阻害する.” 2014. Web. 05 Mar 2021.

Vancouver:

Tanaka A. HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization : HTLV-1 bZIP Factorは転写因子FoxO3aの機能および局在に影響を及ぼしアポトーシスを阻害する. [Internet] [Thesis]. Kyoto University / 京都大学; 2014. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2433/185199 ; http://dx.doi.org/10.14989/doctor.k17979.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tanaka A. HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization : HTLV-1 bZIP Factorは転写因子FoxO3aの機能および局在に影響を及ぼしアポトーシスを阻害する. [Thesis]. Kyoto University / 京都大学; 2014. Available from: http://hdl.handle.net/2433/185199 ; http://dx.doi.org/10.14989/doctor.k17979

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

16. 国廣, 真里枝. Heat Shock Enhances the Expression of the Human T Cell Leukemia Virus Type-I (HTLV-I) Trans-Activator (Tax) Antigen in Human HTLV-I Infected Primary and Cultured T Cells : ヒートショックは、ヒトT細胞白血病ウイルスI型（HTLV-1）感染者由来の初代培養と継代培養されたT細胞のTax抗原発現を促進する.

Degree: 博士(医学), 2017, University of the Ryukyus / 琉球大学

URL: http://hdl.handle.net/20.500.12000/36646

Subjects/Keywords: HTLV-I; Tax; heat shock; adult T cell leukemia (ATL)

1 more image…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

国廣, �. (2017). Heat Shock Enhances the Expression of the Human T Cell Leukemia Virus Type-I (HTLV-I) Trans-Activator (Tax) Antigen in Human HTLV-I Infected Primary and Cultured T Cells : ヒートショックは、ヒトT細胞白血病ウイルスI型（HTLV-1）感染者由来の初代培養と継代培養されたT細胞のTax抗原発現を促進する. (Thesis). University of the Ryukyus / 琉球大学. Retrieved from http://hdl.handle.net/20.500.12000/36646

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

国廣, 真里枝. “Heat Shock Enhances the Expression of the Human T Cell Leukemia Virus Type-I (HTLV-I) Trans-Activator (Tax) Antigen in Human HTLV-I Infected Primary and Cultured T Cells : ヒートショックは、ヒトT細胞白血病ウイルスI型（HTLV-1）感染者由来の初代培養と継代培養されたT細胞のTax抗原発現を促進する.” 2017. Thesis, University of the Ryukyus / 琉球大学. Accessed March 05, 2021. http://hdl.handle.net/20.500.12000/36646.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

国廣, 真里枝. “Heat Shock Enhances the Expression of the Human T Cell Leukemia Virus Type-I (HTLV-I) Trans-Activator (Tax) Antigen in Human HTLV-I Infected Primary and Cultured T Cells : ヒートショックは、ヒトT細胞白血病ウイルスI型（HTLV-1）感染者由来の初代培養と継代培養されたT細胞のTax抗原発現を促進する.” 2017. Web. 05 Mar 2021.

Vancouver:

国廣 �. Heat Shock Enhances the Expression of the Human T Cell Leukemia Virus Type-I (HTLV-I) Trans-Activator (Tax) Antigen in Human HTLV-I Infected Primary and Cultured T Cells : ヒートショックは、ヒトT細胞白血病ウイルスI型（HTLV-1）感染者由来の初代培養と継代培養されたT細胞のTax抗原発現を促進する. [Internet] [Thesis]. University of the Ryukyus / 琉球大学; 2017. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/20.500.12000/36646.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

国廣 �. Heat Shock Enhances the Expression of the Human T Cell Leukemia Virus Type-I (HTLV-I) Trans-Activator (Tax) Antigen in Human HTLV-I Infected Primary and Cultured T Cells : ヒートショックは、ヒトT細胞白血病ウイルスI型（HTLV-1）感染者由来の初代培養と継代培養されたT細胞のTax抗原発現を促進する. [Thesis]. University of the Ryukyus / 琉球大学; 2017. Available from: http://hdl.handle.net/20.500.12000/36646

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Kyoto University

17. Tanaka, Azusa. HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization .

Degree: 2014, Kyoto University

URL: http://hdl.handle.net/2433/185199

Subjects/Keywords: HTLV-1 bZIP Factor; Apoptosis; FoxO3a; Adult T-cell leukemia

Record Details Similar Records Cite « Share

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tanaka, A. (2014). HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization . (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/185199

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tanaka, Azusa. “HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization .” 2014. Thesis, Kyoto University. Accessed March 05, 2021. http://hdl.handle.net/2433/185199.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tanaka, Azusa. “HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization .” 2014. Web. 05 Mar 2021.

Vancouver:

Tanaka A. HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization . [Internet] [Thesis]. Kyoto University; 2014. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2433/185199.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tanaka A. HTLV-1 bZIP Factor Suppresses Apoptosis by Attenuating the Function of FoxO3a and Altering its Localization . [Thesis]. Kyoto University; 2014. Available from: http://hdl.handle.net/2433/185199

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

18. Kawata, Takahito. Dual inhibition of the mTORC1 and mTORC2 signaling pathways is a promising therapeutic target for Adult T-cell Leukemia .

Degree: 2018, Kyoto University

URL: http://hdl.handle.net/2433/232109

Subjects/Keywords: adult t cell leukemia; Akt; mTORC; TOR Serinr-Threonine Kinases; HTLV-1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kawata, T. (2018). Dual inhibition of the mTORC1 and mTORC2 signaling pathways is a promising therapeutic target for Adult T-cell Leukemia . (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/232109

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kawata, Takahito. “Dual inhibition of the mTORC1 and mTORC2 signaling pathways is a promising therapeutic target for Adult T-cell Leukemia .” 2018. Thesis, Kyoto University. Accessed March 05, 2021. http://hdl.handle.net/2433/232109.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kawata, Takahito. “Dual inhibition of the mTORC1 and mTORC2 signaling pathways is a promising therapeutic target for Adult T-cell Leukemia .” 2018. Web. 05 Mar 2021.

Vancouver:

Kawata T. Dual inhibition of the mTORC1 and mTORC2 signaling pathways is a promising therapeutic target for Adult T-cell Leukemia . [Internet] [Thesis]. Kyoto University; 2018. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2433/232109.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kawata T. Dual inhibition of the mTORC1 and mTORC2 signaling pathways is a promising therapeutic target for Adult T-cell Leukemia . [Thesis]. Kyoto University; 2018. Available from: http://hdl.handle.net/2433/232109

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

19. Mohamed, Mahgoub Mohamed Ahmed Mohamed. Sporadic on/off switching of HTLV-1 Tax expression is crucial to maintain the whole population of virus-induced leukemic cells .

Degree: 2018, Kyoto University

URL: http://hdl.handle.net/2433/232139

Subjects/Keywords: HTLV-1; Tax; HBZ; adult T-cell leukemia-lymphoma; computational simulation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mohamed, M. M. A. M. (2018). Sporadic on/off switching of HTLV-1 Tax expression is crucial to maintain the whole population of virus-induced leukemic cells . (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/232139

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mohamed, Mahgoub Mohamed Ahmed Mohamed. “Sporadic on/off switching of HTLV-1 Tax expression is crucial to maintain the whole population of virus-induced leukemic cells .” 2018. Thesis, Kyoto University. Accessed March 05, 2021. http://hdl.handle.net/2433/232139.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mohamed, Mahgoub Mohamed Ahmed Mohamed. “Sporadic on/off switching of HTLV-1 Tax expression is crucial to maintain the whole population of virus-induced leukemic cells .” 2018. Web. 05 Mar 2021.

Vancouver:

Mohamed MMAM. Sporadic on/off switching of HTLV-1 Tax expression is crucial to maintain the whole population of virus-induced leukemic cells . [Internet] [Thesis]. Kyoto University; 2018. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2433/232139.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mohamed MMAM. Sporadic on/off switching of HTLV-1 Tax expression is crucial to maintain the whole population of virus-induced leukemic cells . [Thesis]. Kyoto University; 2018. Available from: http://hdl.handle.net/2433/232139

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

20. Meireles, Ana Luísa Langanke Pedroso. Quantificação de células endoteliais circulantes em portadores assintomáticos do vírus linfotrópico humano de células T do tipo 1 (HTLV1) por citometria de fluxo.

Degree: Mestrado, Distúrbios do Crescimento Celular, Hemodinâmicos e da Hemostasia, 2009, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5167/tde-09062009-170516/ ;

►

Células endoteliais provenientes da medula óssea (MO) participam da fisiopatologia de várias doenças que possuem dano vascular como fator em comum. Apesar de consideradas evento… (more)

▼

Células endoteliais provenientes da medula óssea (MO) participam da fisiopatologia de várias doenças que possuem dano vascular como fator em comum. Apesar de consideradas evento raro, encontram-se em quantidade aumentada na circulação periférica de pacientes oncológicos. Evidências sugerem que células endoteliais progenitoras (CEPs) contribuem para a angiogênese tumoral. Com esta descoberta, CEPs e células endoteliais maduras (CEMs) vêm sendo estudadas como potenciais alvos terapêuticos com o uso de drogas anti-angiogênicas. Portadores do vírus linfotrópico humano de células T do tipo 1 (HTLV1) têm possibilidade de desenvolver doenças causadas pelo vírus com elevada taxa de mortalidade, com destaque para a Leucemia/Linfoma de células T do Adulto (ATL). O tratamento para a forma sintomática da doença permanece desapontador. Este foi um estudo transversal desenvolvido com o objetivo de quantificar células endoteliais circulantes no sangue de portadores assintomáticos do HTLV1 em comparação a indivíduos saudáveis, por citometria de fluxo. Foram estudados 30 indivíduos portadores do vírus HTLV1, pareados por idade e sexo com o grupo controle. Três pacientes tiveram o diagnóstico de ATL sendo retirados da pesquisa. Foi utilizada como critério de inclusão a sorologia para HTLV1+, e negativa para as demais doenças transmissíveis por transfusão. Em nosso estudo os valores de CEPs encontrados foram maiores na população portadora assintomática (mediana: 0,8288 células / mm 3 ) em relação à população controle (mediana: 0,4905 células / mm 3 ; p = 0,035). Não houve diferença estatística entre a quantificação de CEMs e células endoteliais ativadas entre os portadores assintomáticos e o grupo controle saudável. Nossos achados sugerem que exista atividade angiogênica mesmo na ausência de transformação neoplásica, e que o valor de CEPs pode ser utilizado como marcador de atividade de doença e aplicado para monitorar a eficácia antitumoral da terapia antiangiogênica

Endothelial cells originated from the bone marrow (BM) take part in the physiopathology of several diseases which have vascular damage as a common factor. In spite of being a rare event, they are found in augmented quantity in the peripheral circulation of cancer patients. Evidence indicates that bone marrow-derived endothelial progenitor cells (CEPs) can contribute to tumor angiogenesis. Upon such a finding, circulating CEPs and mature endothelial cells (CEMs) have been researched as potential therapeutic targets and antiangiogenic drugs can be an option in anti-tumor therapy. Human T Cell Lymphotropic Virus Type 1 (HTLV1) carriers may develop diseases caused by the virus with high mortality rate, especially adult T-cell leukemia/lymphoma (ATL). The treatment for the symptomatic form of the disease remains disappointing. This cross-sectional study aimed at quantifying circulating endothelial cells in the blood of HTLV1 asymptomatic carriers in comparison to healthy individuals by flow cytometry. A sample of 30 individuals, HTLV1 carriers, age and sex paired, has been…

Advisors/Committee Members: Pereira, Juliana.

Subjects/Keywords: Células endoteliais; Citometria de fluxo; Endothelial cells; Flow cytometry; Human T-lymphotropic virus 1; Leucemia-linfoma de células T do adulto; Leukemia-lymphoma adult T-cell; Neovascularização patológica; Neovascularization pathologic; Virus linfotrópico de células T humanas tipo 1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Meireles, A. L. L. P. (2009). Quantificação de células endoteliais circulantes em portadores assintomáticos do vírus linfotrópico humano de células T do tipo 1 (HTLV1) por citometria de fluxo. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5167/tde-09062009-170516/ ;

Chicago Manual of Style (16^th Edition):

Meireles, Ana Luísa Langanke Pedroso. “Quantificação de células endoteliais circulantes em portadores assintomáticos do vírus linfotrópico humano de células T do tipo 1 (HTLV1) por citometria de fluxo.” 2009. Masters Thesis, University of São Paulo. Accessed March 05, 2021. http://www.teses.usp.br/teses/disponiveis/5/5167/tde-09062009-170516/ ;.

MLA Handbook (7^th Edition):

Meireles, Ana Luísa Langanke Pedroso. “Quantificação de células endoteliais circulantes em portadores assintomáticos do vírus linfotrópico humano de células T do tipo 1 (HTLV1) por citometria de fluxo.” 2009. Web. 05 Mar 2021.

Vancouver:

Meireles ALLP. Quantificação de células endoteliais circulantes em portadores assintomáticos do vírus linfotrópico humano de células T do tipo 1 (HTLV1) por citometria de fluxo. [Internet] [Masters thesis]. University of São Paulo; 2009. [cited 2021 Mar 05]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5167/tde-09062009-170516/ ;.

Council of Science Editors:

Meireles ALLP. Quantificação de células endoteliais circulantes em portadores assintomáticos do vírus linfotrópico humano de células T do tipo 1 (HTLV1) por citometria de fluxo. [Masters Thesis]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/5/5167/tde-09062009-170516/ ;

University of Iowa

21. Vrieze, Katherine Elna. Using mouse models to investigate the genetics of T-cell acute lymphocytic leukemia.

Degree: PhD, Molecular and Cellular Biology, 2011, University of Iowa

URL: https://ir.uiowa.edu/etd/2785

► T-cell acute lymphocytic leukemia (T-ALL) affects approximately 1,500 people per year in the United States, many of them children. The overall survival rate of… (more)

Subjects/Keywords: ETP-ALL; NOTCH1; T-ALL; T-cell Acute Lymphocytic Leukemia; Cell Biology

Record Details Similar Records Cite « Share

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Vrieze, K. E. (2011). Using mouse models to investigate the genetics of T-cell acute lymphocytic leukemia. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/2785

Chicago Manual of Style (16^th Edition):

Vrieze, Katherine Elna. “Using mouse models to investigate the genetics of T-cell acute lymphocytic leukemia.” 2011. Doctoral Dissertation, University of Iowa. Accessed March 05, 2021. https://ir.uiowa.edu/etd/2785.

MLA Handbook (7^th Edition):

Vrieze, Katherine Elna. “Using mouse models to investigate the genetics of T-cell acute lymphocytic leukemia.” 2011. Web. 05 Mar 2021.

Vancouver:

Vrieze KE. Using mouse models to investigate the genetics of T-cell acute lymphocytic leukemia. [Internet] [Doctoral dissertation]. University of Iowa; 2011. [cited 2021 Mar 05]. Available from: https://ir.uiowa.edu/etd/2785.

Council of Science Editors:

Vrieze KE. Using mouse models to investigate the genetics of T-cell acute lymphocytic leukemia. [Doctoral Dissertation]. University of Iowa; 2011. Available from: https://ir.uiowa.edu/etd/2785

University of Toronto

22. Suliman, Sara. Functions of Notch1, Notch3, and Fringe Glycosyltransferases during Thymocyte β-Selection and T-cell Leukemogenesis.

Degree: 2013, University of Toronto

URL: http://hdl.handle.net/1807/68967

►

T-cells play critical roles in the immune system, from fighting infection and tissue remodeling to anti-tumor immunity. Notch1 (N1) signaling is a conserved signaling pathway… (more)

▼

T-cells play critical roles in the immune system, from fighting infection and tissue remodeling to anti-tumor immunity. Notch1 (N1) signaling is a conserved signaling pathway that is required for T-cell specification and commitment of multi-potent progenitors. Subsequently, N1 co-operates with pre-T-cell receptor (pre-TCR) signaling to induce self-renewal of TCRβ+ CD4/CD8 double negative (DN) progenitors. This “β-selection” process produces large numbers of CD4/CD8 double positive (DP) progenitors whose survival is N1-independent. Thus, N1 signaling plays key roles at several stages of intrathymic T-cell development. However, excessive N1 activation causes T-cell lymphoblastic leukemia/lymphoma (T-LL). Hence, the goal of my thesis was to elucidate how N1 signaling is regulated during thymocyte β-selection. There are four mammalian N receptors (N1-4), activated by ligands of the related Delta-like (DL1 and DL4), and Serrate/Jagged (Jag1 and Jag2) families. Fringe glycosyltransferases modify N receptors, enhancing activation by DL ligands and inhibiting activation by Jag1. My thesis goals were to elucidate: 1) the role of N3 downstream on N1 in thymocyte β-selection and T-cell leukemogenesis; 2) how Fringe glycosyltransferases modulate N1 sensitivity to DL vs Jag family ligands during β-selection; and 3) the global impact of ectopic N1 activation on T-cell development. In Chapter 3, I examined the role of N3 in thymocyte β-selection and N1 induced T-LL using N3–deficient mice, and showed that N3 is dispensable for both processes. In Chapter 4, I demonstrated that Lfng and Mfng have distinct functions in modulating N activation by DL1 and DL4 versus Jag1 during β-selection. Unexpectedly, Jag2-induced β-selection was uniquely insensitive to both Lfng and Mfng. Finally, in Chapter 5, I generated a new mouse model to ectopically activate N1 signaling in TCRβ+ DN progenitors, and used it to demonstrate that N1 signaling impacts thymocyte self-renewal during β-selection in vivo. As expected, ectopic N1 signaling in DP thymocytes altered CD4/CD8 lineage commitment and caused T-LL. However, ectopic N1 activation also prevented development of certain innate-like T-cells and caused T-cell lymphopenia, and eventually lead to auto-immune-like pathologies. Collectively, my findings expanded our understanding of N regulation in β-selection, and revealed unexpected effects of aberrant N1 activation in these stages.

PhD

Advisors/Committee Members: Guidos, Cynthia, Immunology.

Subjects/Keywords: Notch Signaling; T-Cell Development; Leukemia; Thymus; 0982

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Suliman, S. (2013). Functions of Notch1, Notch3, and Fringe Glycosyltransferases during Thymocyte β-Selection and T-cell Leukemogenesis. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/68967

Chicago Manual of Style (16^th Edition):

Suliman, Sara. “Functions of Notch1, Notch3, and Fringe Glycosyltransferases during Thymocyte β-Selection and T-cell Leukemogenesis.” 2013. Doctoral Dissertation, University of Toronto. Accessed March 05, 2021. http://hdl.handle.net/1807/68967.

MLA Handbook (7^th Edition):

Suliman, Sara. “Functions of Notch1, Notch3, and Fringe Glycosyltransferases during Thymocyte β-Selection and T-cell Leukemogenesis.” 2013. Web. 05 Mar 2021.

Vancouver:

Suliman S. Functions of Notch1, Notch3, and Fringe Glycosyltransferases during Thymocyte β-Selection and T-cell Leukemogenesis. [Internet] [Doctoral dissertation]. University of Toronto; 2013. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1807/68967.

Council of Science Editors:

Suliman S. Functions of Notch1, Notch3, and Fringe Glycosyltransferases during Thymocyte β-Selection and T-cell Leukemogenesis. [Doctoral Dissertation]. University of Toronto; 2013. Available from: http://hdl.handle.net/1807/68967

23. 정, 현주. Effect of Tissue Transglutaminase on Steroid Resistance in T-Cell Acute Lymphoblastic Leukemia.

Degree: 2020, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/19265 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000030197

►

AIM: To improve survival in patients with glucocorticoid-resistant T-cell acute lymphoblastic leukemia (T-ALL), it is critical to develop new therapeutic strategies to overcome steroid resistance.… (more)

Subjects/Keywords: Tissue transglutaminase; steroid resistance; T-cell acute lymphoblastic leukemia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

정, �. (2020). Effect of Tissue Transglutaminase on Steroid Resistance in T-Cell Acute Lymphoblastic Leukemia. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/19265 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000030197

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

정, 현주. “Effect of Tissue Transglutaminase on Steroid Resistance in T-Cell Acute Lymphoblastic Leukemia.” 2020. Thesis, Ajou University. Accessed March 05, 2021. http://repository.ajou.ac.kr/handle/201003/19265 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000030197.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

정, 현주. “Effect of Tissue Transglutaminase on Steroid Resistance in T-Cell Acute Lymphoblastic Leukemia.” 2020. Web. 05 Mar 2021.

Vancouver:

정 �. Effect of Tissue Transglutaminase on Steroid Resistance in T-Cell Acute Lymphoblastic Leukemia. [Internet] [Thesis]. Ajou University; 2020. [cited 2021 Mar 05]. Available from: http://repository.ajou.ac.kr/handle/201003/19265 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000030197.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

정 �. Effect of Tissue Transglutaminase on Steroid Resistance in T-Cell Acute Lymphoblastic Leukemia. [Thesis]. Ajou University; 2020. Available from: http://repository.ajou.ac.kr/handle/201003/19265 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000030197

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cincinnati

24. Phelan, James D., B.S. Transcriptional Control of Normal Lymphopoiesis and T-cell Neoplasia by Growth Factor Independent 1.

Degree: PhD, Medicine: Immunology, 2012, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1337351444

► Hematopoietic development is a tightly controlled process in which environmental cues promote or restrict the proliferation and differentiation of bone marrow derived cells. These signals… (more)

Subjects/Keywords: Biology; Gfi1; Notch; Leukemia; Hematopoiesis; T cell; p53

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APA (6^th Edition):

Phelan, James D., B. S. (2012). Transcriptional Control of Normal Lymphopoiesis and T-cell Neoplasia by Growth Factor Independent 1. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1337351444

Chicago Manual of Style (16^th Edition):

Phelan, James D., B S. “Transcriptional Control of Normal Lymphopoiesis and T-cell Neoplasia by Growth Factor Independent 1.” 2012. Doctoral Dissertation, University of Cincinnati. Accessed March 05, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1337351444.

MLA Handbook (7^th Edition):

Phelan, James D., B S. “Transcriptional Control of Normal Lymphopoiesis and T-cell Neoplasia by Growth Factor Independent 1.” 2012. Web. 05 Mar 2021.

Vancouver:

Phelan, James D. BS. Transcriptional Control of Normal Lymphopoiesis and T-cell Neoplasia by Growth Factor Independent 1. [Internet] [Doctoral dissertation]. University of Cincinnati; 2012. [cited 2021 Mar 05]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1337351444.

Council of Science Editors:

Phelan, James D. BS. Transcriptional Control of Normal Lymphopoiesis and T-cell Neoplasia by Growth Factor Independent 1. [Doctoral Dissertation]. University of Cincinnati; 2012. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1337351444

Johannes Gutenberg Universität Mainz

25. Albrecht, Jana. In vitro characterization of human AML-reactive CTL clones generated from the naive subset of healthy donors and adoptive transfer into leukemia-engrafted NSG mice.

Degree: 2012, Johannes Gutenberg Universität Mainz

URL: http://ubm.opus.hbz-nrw.de/volltexte/2013/3368/

►

Acute myeloid leukemia (AML) is a very aggressive cancer of the hematopoietic system. Chemotherapy and immunotherapeutical approaches including hematopoietic stem cell transplantation (HSCT) and donor… (more)

▼

Acute myeloid leukemia (AML) is a very aggressive cancer of the hematopoietic system. Chemotherapy and immunotherapeutical approaches including hematopoietic stem cell transplantation (HSCT) and donor lymphocyte infusion (DLI) are the only curative options available. The beneficial graft-versus-leukemia (GVL) effect of cellular immunotherapy is mostly mediated by donor-derived CD8+ T lymphocytes that recognize minor histocompatibility antigens (mHags) and leukemia-associated antigens (LAAs) presented on the surface of AML blasts (Falkenburg et al. 2008; Kolb 2008). A main complication is graft-versus-host disease (GVHD) that can be induced when cytotoxic T lymphocytes (CTLs) recognize broadly expressed antigens. To reduce the risk of GVHD, specific allogeneic T-cell therapy inducing selective GVL responses could be an option (Barrett & Le Blanc 2010; Parmar et al. 2011; Smits et al. 2011). This requires efficient in vitro strategies to generate AML-reactive T cells with an early differentiation phenotype as well as vigorous effector functions and humanized mouse models to analyze the anti-leukemic potential of adoptively transferred T cells in vivo. In this study, AML-reactive CTL clones and oligoclonal T-cell lines could be reliably generated from the naive subset of healthy HLA-class I-identical donors by stimulation with primary AML blasts in mini-mixed-lymphocyte / leukemia cultures (MLLCs) in eight different patient / donor pairs. These CTLs were promising candidates for cellular immunotherapy because of their relatively early differentiation phenotype and strong proliferative and lytic capabilities. The addition of the common γ-chain cytokine IL-21 to the stimulation protocol enabled more precursors to develop into potent leukemia-reactive CTLs, presumably by its beneficial effects on cell survival and antigen-specific proliferation during the first weeks of cultures. It also strengthened the early-stage phenotype. Three long-term cultured CTLs exemplarily transferred into leukemia-engrafted immunodeficient NSG mice mediated a significant reduction of the leukemic burden after a single transfusion. These results demonstrate that CTL clones with reactivity to patient-derived AML blasts can be isolated from the naive compartment of healthy donors and show potent anti-leukemic effects in vivo. The herein described allo-MLLC approach with in vitro “programmed” naive CTL precursors independent of a HSCT setting is a valuable alternative to the conventional method of isolating in vivo primed donor CTLs out of patients after transplantation (Kloosterboer et al. 2004; Warren et al. 2010). This would make leukemia-reactive CTLs already available at the time point of HSCT, when residual leukemia disease is minimal and the chances for complete leukemia eradication are high. Furthermore, leukemia-reactive CTLs effectively expanded by this in vitro protocol can be used as screening populations to identify novel candidate LAAs and mHags for antigen-specific immunotherapy.

Akute myeloische Leukämie (AML) ist eine…

Subjects/Keywords: T-Zell-Therapie, Leukämie-reaktive CTL, Präklinisches Leukämie-Mausmodell; T-cell therapy, leukemia-reactive CTL, preclinical leukemia-mousemodel; Life sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Albrecht, J. (2012). In vitro characterization of human AML-reactive CTL clones generated from the naive subset of healthy donors and adoptive transfer into leukemia-engrafted NSG mice. (Doctoral Dissertation). Johannes Gutenberg Universität Mainz. Retrieved from http://ubm.opus.hbz-nrw.de/volltexte/2013/3368/

Chicago Manual of Style (16^th Edition):

Albrecht, Jana. “In vitro characterization of human AML-reactive CTL clones generated from the naive subset of healthy donors and adoptive transfer into leukemia-engrafted NSG mice.” 2012. Doctoral Dissertation, Johannes Gutenberg Universität Mainz. Accessed March 05, 2021. http://ubm.opus.hbz-nrw.de/volltexte/2013/3368/.

MLA Handbook (7^th Edition):

Albrecht, Jana. “In vitro characterization of human AML-reactive CTL clones generated from the naive subset of healthy donors and adoptive transfer into leukemia-engrafted NSG mice.” 2012. Web. 05 Mar 2021.

Vancouver:

Albrecht J. In vitro characterization of human AML-reactive CTL clones generated from the naive subset of healthy donors and adoptive transfer into leukemia-engrafted NSG mice. [Internet] [Doctoral dissertation]. Johannes Gutenberg Universität Mainz; 2012. [cited 2021 Mar 05]. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2013/3368/.

Council of Science Editors:

Albrecht J. In vitro characterization of human AML-reactive CTL clones generated from the naive subset of healthy donors and adoptive transfer into leukemia-engrafted NSG mice. [Doctoral Dissertation]. Johannes Gutenberg Universität Mainz; 2012. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2013/3368/

Universitat Pompeu Fabra

26. Colomer-Lahiguera, Sara, 1981-. The role of CDKN1B-p27kip1 deregulation in the pathogenesis of pediatric T-cell acute lymphoblastic leukemia.

Degree: Departament de Ciències Experimentals i de la Salut, 2015, Universitat Pompeu Fabra

URL: http://hdl.handle.net/10803/523487

► La leucemia linfoblástica aguda de células T (LLA-T) representa el 10 15% de las leucemias pediátricas. La transformación oncogénica de precursores de células T es… (more)

Subjects/Keywords: CDKN1B-p27kip1; T-ALL; Lymphoblastic; MEF2C; SKP2; T-cell; Leukemia; Pediatric; Leucemia; Pediátrica; 616

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APA (6^th Edition):

Colomer-Lahiguera, Sara, 1. (2015). The role of CDKN1B-p27kip1 deregulation in the pathogenesis of pediatric T-cell acute lymphoblastic leukemia. (Thesis). Universitat Pompeu Fabra. Retrieved from http://hdl.handle.net/10803/523487

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Colomer-Lahiguera, Sara, 1981-. “The role of CDKN1B-p27kip1 deregulation in the pathogenesis of pediatric T-cell acute lymphoblastic leukemia.” 2015. Thesis, Universitat Pompeu Fabra. Accessed March 05, 2021. http://hdl.handle.net/10803/523487.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Colomer-Lahiguera, Sara, 1981-. “The role of CDKN1B-p27kip1 deregulation in the pathogenesis of pediatric T-cell acute lymphoblastic leukemia.” 2015. Web. 05 Mar 2021.

Vancouver:

Colomer-Lahiguera, Sara 1. The role of CDKN1B-p27kip1 deregulation in the pathogenesis of pediatric T-cell acute lymphoblastic leukemia. [Internet] [Thesis]. Universitat Pompeu Fabra; 2015. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10803/523487.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Colomer-Lahiguera, Sara 1. The role of CDKN1B-p27kip1 deregulation in the pathogenesis of pediatric T-cell acute lymphoblastic leukemia. [Thesis]. Universitat Pompeu Fabra; 2015. Available from: http://hdl.handle.net/10803/523487

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

27. Calvo, Julien. Etude de l'impact des adipocytes de la moelle osseuse sur le développement et la chimiorésistance des leucémies aigues lymphoblastiques T (LAL-T) : Study of the impact of bone marrow adipocytes on the development and chemoresistance of T cell actue lymphoblastic leukemia (T-ALL).

Degree: Docteur es, Sciences de la vie et de la santé, 2019, Université de Paris (2019-....)

URL: http://www.theses.fr/2019UNIP7114

► Les leucémies aiguës lymphoblastiques T (LAL-T) sont des maladies des progéniteurs T qui surviennent principalement chez l'enfant et le jeune adulte. Des facteurs intrinsèques et… (more)

▼ Les leucémies aiguës lymphoblastiques T (LAL-T) sont des maladies des progéniteurs T qui surviennent principalement chez l'enfant et le jeune adulte. Des facteurs intrinsèques et extrinsèques à la cellule leucémique sont impliqués dans l’initiation et l’expansion leucémique. Les cellules leucémiques infiltrent de nombreux organes dont la Moelle Osseuse (MO) des patients. La MO est composée du tissu hématopoïétique, de cellules stromales, endothéliales, nerveuses et d'adipocytes aussi nommé tissu adipeux médullaire (MAT). Deux types de MAT coexistent, le MAT constitutif, qui concerne les extrémités de certains os et le MAT régulé, qui est généré et s’accroit en réponse à de nombreux stimuli (vieillissement, myéloablation). Chez la souris, les vertèbres thoraciques et caudales contiennent respectivement de la MO pauvre et riche en MAT constitutif. A l’aide du modèle de transplantation in vivo, nous avons observé que les cellules leucémiques de LAL-T humaines et de souris se développent dans les deux territoires médullaires. En revanche, comparées aux cellules leucémiques extraites des vertèbres thoraciques, celles récupérées à partir des vertèbres caudales présentent une expression de marqueurs de surface, un métabolisme global et une progression dans le cycle cellulaire diminuées démontrant un phénotype de dormance. Fonctionnellement, les cellules leucémiques extraites des vertèbres caudales présentent une expansion ex vivo et une propagation in vivo moindre que celles des vertèbres thoraciques. Ces caractéristiques sont le résultat d’une éducation cellulaire indépendante des facteurs intrinsèques puisque les cellules de LAL-T présentent des anomalies génétiques identiques entre les deux territoires médullaires. De plus, cette éducation est un état réversible puisque la transplantation en souris secondaires ou la co-culture à long terme annihile l’ensemble des phénotypes observés dans les vertèbres caudales. Enfin, les cellules leucémiques des vertèbres caudales présentent une résistance intrinsèque plus élevées aux drogues ciblant le cycle cellulaire, i. e. la Vincristine et la Cytarabine mise également en évidence par un protocole in vivo. De façon intéressante, les cellules leucémiques issues du tissu adipeux des gonades ou co-cultivées avec des adipocytes dérivés de cellules stromales partagent les caractéristiques phénotypiques, métaboliques, de progression dans le cycle cellulaire et de chimiorésistance avec les cellules de LAL-T issues des vertèbres caudales. Ces résultats démontrent que les sites de MO orchestrent différemment la propagation des LAL-T et que la MO riche en adipocytes protège les LAL-T des agents utilisés en chimiothérapie. L’analyse transcriptomique préliminaire menée à l’échelon unicellulaire des cellules leucémiques a permis de montrer l’existence d’une population minoritaire dans les vertèbres thoraciques qui partagent une signature transcriptomique commune avec les cellules leucémiques issues des vertèbres caudales. Ces résultats soutiennent l’hypothèse de l’existence d’une niche… Advisors/Committee Members: Pflumio, Françoise (thesis director).

Subjects/Keywords: Leucémies aiguës lymphoblastiques T; Microenvironnement; Adipocytes; Chimiorésistance; T cell acute leukemia; Microenvironment; Adipocytes; Chemoresistance

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Calvo, J. (2019). Etude de l'impact des adipocytes de la moelle osseuse sur le développement et la chimiorésistance des leucémies aigues lymphoblastiques T (LAL-T) : Study of the impact of bone marrow adipocytes on the development and chemoresistance of T cell actue lymphoblastic leukemia (T-ALL). (Doctoral Dissertation). Université de Paris (2019-....). Retrieved from http://www.theses.fr/2019UNIP7114

Chicago Manual of Style (16^th Edition):

Calvo, Julien. “Etude de l'impact des adipocytes de la moelle osseuse sur le développement et la chimiorésistance des leucémies aigues lymphoblastiques T (LAL-T) : Study of the impact of bone marrow adipocytes on the development and chemoresistance of T cell actue lymphoblastic leukemia (T-ALL).” 2019. Doctoral Dissertation, Université de Paris (2019-....). Accessed March 05, 2021. http://www.theses.fr/2019UNIP7114.

MLA Handbook (7^th Edition):

Calvo, Julien. “Etude de l'impact des adipocytes de la moelle osseuse sur le développement et la chimiorésistance des leucémies aigues lymphoblastiques T (LAL-T) : Study of the impact of bone marrow adipocytes on the development and chemoresistance of T cell actue lymphoblastic leukemia (T-ALL).” 2019. Web. 05 Mar 2021.

Vancouver:

Calvo J. Etude de l'impact des adipocytes de la moelle osseuse sur le développement et la chimiorésistance des leucémies aigues lymphoblastiques T (LAL-T) : Study of the impact of bone marrow adipocytes on the development and chemoresistance of T cell actue lymphoblastic leukemia (T-ALL). [Internet] [Doctoral dissertation]. Université de Paris (2019-....); 2019. [cited 2021 Mar 05]. Available from: http://www.theses.fr/2019UNIP7114.

Council of Science Editors:

Calvo J. Etude de l'impact des adipocytes de la moelle osseuse sur le développement et la chimiorésistance des leucémies aigues lymphoblastiques T (LAL-T) : Study of the impact of bone marrow adipocytes on the development and chemoresistance of T cell actue lymphoblastic leukemia (T-ALL). [Doctoral Dissertation]. Université de Paris (2019-....); 2019. Available from: http://www.theses.fr/2019UNIP7114

University of South Florida

28. Dubovsky, Jason A. Epigenetic Modifiers to Augment the Immunogenicity of Chronic Lymphocytic Leukemia.

Degree: 2013, University of South Florida

URL: https://scholarcommons.usf.edu/etd/4623

► Cancer cells employ a litany of immunosuppressive and immunevasive strategies to avoid detection and elimination by the various arms of the innate and adaptive immune… (more)

▼ Cancer cells employ a litany of immunosuppressive and immunevasive strategies to avoid detection and elimination by the various arms of the innate and adaptive immune system. Many hematologic and solid tumors progressively develop a specialized microenvironment which promotes tissue restructuring inflammation while masking the immune signature of the tumor cells themselves. Chronic lymphocytic leukemia, a malignancy of mature B lymphocytes must constantly balance on the precipice of immune recognition. A mature antigen presenting cell themselves, CLL clonal growth is dependent on the very interactions which, if effective, could potentially lead to their demise. To circumvent this, CLL clones set up unique signatures which promote immune recognition yet provide diversionary signals to the remaining immune armament resulting in profound immune dysfunction. While the aforementioned immune dysfunction is widespread, the B cell and T cell repertoire are severely impaired during leukemic progression. The lack of healthy B cells due to displacement by malignant B cells results in the obvious loss of an important antigen presenting cell as well as antibody-based immunity. Additionally, deficient interactions with T cells result in anergy and the preponderance of improperly polarized T lymphocytes which are impotent to eliminate both pathogens and leukemic cells. The result of such severe immune dysfunction is chronic infection and progressive disease which is the primary cause of death in CLL patients. Our research was focused on the premise that alleviating immune dysfunction and providing immunotherapeutic tools will significantly benefit CLL therapy. To this end we developed methods to improve the cellular interaction between CLL cells and T cells a critical step towards improving the antigen presentation capacity of the diseased B cell repertoire. We also identified a therapeutic strategy which can revert the anergic or improperly polarized state of T cells already in circulation allowing those cells to more effectively perform the effector functions necessary to fight pathogenic attack and malignant transformation. Finally, we identified a number of novel targets in CLL which could be used in a vaccinate-induce method to license the elimination of CLL cells by the patient's adaptive immune system. To achieve our goals we utilized a relatively new class of drugs called epigenetic modifiers which specifically alter the chromatin structure resulting in novel genetic signatures which are heritable over cellular generations. The unique properties of these drugs allow for the elicitation of suppressed genetic programs which, when properly controlled, have the potential to reassert healthy lymphocyte functions. Our studies provide a comprehensive therapeutic initiative which, by simultaneously alleviating the major causes of immune dysfunction in addition to facilitating the use of novel active immunotherapeutic strategies could potentially impact clinical therapy for CLL.

Subjects/Keywords: Epigenetic; Histone; Leukemia; Lymphocyte; Methylation; T cell; Cell Biology; Immunology and Infectious Disease; Molecular Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dubovsky, J. A. (2013). Epigenetic Modifiers to Augment the Immunogenicity of Chronic Lymphocytic Leukemia. (Thesis). University of South Florida. Retrieved from https://scholarcommons.usf.edu/etd/4623

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dubovsky, Jason A. “Epigenetic Modifiers to Augment the Immunogenicity of Chronic Lymphocytic Leukemia.” 2013. Thesis, University of South Florida. Accessed March 05, 2021. https://scholarcommons.usf.edu/etd/4623.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dubovsky, Jason A. “Epigenetic Modifiers to Augment the Immunogenicity of Chronic Lymphocytic Leukemia.” 2013. Web. 05 Mar 2021.

Vancouver:

Dubovsky JA. Epigenetic Modifiers to Augment the Immunogenicity of Chronic Lymphocytic Leukemia. [Internet] [Thesis]. University of South Florida; 2013. [cited 2021 Mar 05]. Available from: https://scholarcommons.usf.edu/etd/4623.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dubovsky JA. Epigenetic Modifiers to Augment the Immunogenicity of Chronic Lymphocytic Leukemia. [Thesis]. University of South Florida; 2013. Available from: https://scholarcommons.usf.edu/etd/4623

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Helsinki

29. Ilander, Mette. NK-and T-cell function in chronic myeloid leukemia patients treated with interferon-α monotherapy: T-ja NK-solujen toiminta interferoni-α hoidetuilla kroonista myeloista leukemiaa sairastavilla potilailla.

Degree: Agrikultur- och forstvetenskapliga fakulteten, 2011, University of Helsinki

URL: http://hdl.handle.net/10138/28476

► Krooninen myeloinen leukemia (KML) aiheutuu hematopoieettisessa kantasolussa tapahtuvasta kromosomien 9 ja 22 välisestä translokaatiosta. Siinä syntyy Philadelphia kromosomi (Ph) ja itsenäisesti toimiva tyrosiinikinaasi BCR-ABL. BCR-ABL… (more)

▼ Krooninen myeloinen leukemia (KML) aiheutuu hematopoieettisessa kantasolussa tapahtuvasta kromosomien 9 ja 22 välisestä translokaatiosta. Siinä syntyy Philadelphia kromosomi (Ph) ja itsenäisesti toimiva tyrosiinikinaasi BCR-ABL. BCR-ABL häiriinnyttää muun muassa solun lisääntymisen. Tyrosiinikinaasi entsyymien toimintaa estävä hoito kehitettiin 2000-luvun alussa ja se on lisännyt huomattavasti potilaiden elossa pysymistä. Hoitoa ei kuitenkaan pidetä parantavana. Ennen tyrosiinikinaasiestäjien (TKE) aikakautta ensilinjan hoitona käytettiin interferoni-? (IFN-?) hoitoa. Kuitenkin vain pieni osa potilaista hyötyi hoidosta. Osa näistä potilaista pystyi lopettamaan hoidon ilman taudin uusimista. IFN-? hoidon vaikutus ei ole täysin tunnettu, mutta uskotaan, että erot potilaiden immuunipuolustuksissa ovat syynä erilaisille hoitovasteille. Kreutzman, Rohon ym. havaitsivat, että potilailla, jotka ovat kyenneet lopettamaan IFN-? hoidon, on enemmän NK- ja T-soluja verenkierrossa. Heillä on myös ainutlaatuinen klonaalinen T-solu populaatio ja enemmän sytotoksisia CD8+ T-soluja ja vähemmän CD4+ T-soluja. Näiden solujen toiminnallinen merkitys on kuitenkin epäselvä. Tämän maisterintutkielman tavoite oli tutkia T- ja NK-solujen toimintaa IFN-?:lla hoidetuilla KMLpotilailla ja tutkia, ovatko hoidon lopettamaan kyenneiden potilaiden lymfosyytit toiminnallisesti aktiivisempia kuin potilaiden, joita vielä hoidetaan IFN-?:lla. Tutkimme, miten hyvin potilaiden NKsolut tappavat leukeemisia soluja, kuinka aktiivisia solut ovat ja millaisia pintamolekyylejä ne ilmentävät. Lisäksi tutkimme myös miten aktiivisia potilaiden T-solut ovat ja onko niiden sytotoksisuuksissa eroja. Vastoin odotuksia havaitsimme, että IFN-? hoidettujen potilaiden NK-solut eivät tapa leukeemisen solulinjan (K562) soluja terveiden NK-soluja paremmin. Potilailla, joita yhä hoidetaan IFN-?:lla on aktiivisempia T-soluja ja heidän NK-soluillaan on erilaistumaton immuunipuolustusta säätelevä ilmiasu. Sitä vastoin potilaiden, jotka ovat kyenneet lopettamaan IFN-? hoidon, NK-solut ilmentävät kypsän solun pintaproteiineja ja heidän sekä T- että NK-solujen toiminta on uupunutta. Yhteenvetona voidaan todeta, että IFN-? hoito lisää T-solujen aktiivisuutta ja NK-solut saavat immuunipuolustusta säätelevän tehtävän ja niiden määrä lisääntyy. Hoidon loputtua T-solut menettävät aktiivisuutensa sekä NK-solut kypsyvät, menettävät hoidon aiheuttaman ilmiasun ja palaavat KML:lle tyypilliseen anergiaan.

Subjects/Keywords: KML; BCR-ABL; interferon-α; NK-cell; T-cell; NK-solu; T-solu; interferoni-α; chronic myeloid leukemia; Bioteknik; Biotechnology; Biotekniikka

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ilander, M. (2011). NK-and T-cell function in chronic myeloid leukemia patients treated with interferon-α monotherapy: T-ja NK-solujen toiminta interferoni-α hoidetuilla kroonista myeloista leukemiaa sairastavilla potilailla. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/28476

Chicago Manual of Style (16^th Edition):

Ilander, Mette. “NK-and T-cell function in chronic myeloid leukemia patients treated with interferon-α monotherapy: T-ja NK-solujen toiminta interferoni-α hoidetuilla kroonista myeloista leukemiaa sairastavilla potilailla.” 2011. Masters Thesis, University of Helsinki. Accessed March 05, 2021. http://hdl.handle.net/10138/28476.

MLA Handbook (7^th Edition):

Ilander, Mette. “NK-and T-cell function in chronic myeloid leukemia patients treated with interferon-α monotherapy: T-ja NK-solujen toiminta interferoni-α hoidetuilla kroonista myeloista leukemiaa sairastavilla potilailla.” 2011. Web. 05 Mar 2021.

Vancouver:

Ilander M. NK-and T-cell function in chronic myeloid leukemia patients treated with interferon-α monotherapy: T-ja NK-solujen toiminta interferoni-α hoidetuilla kroonista myeloista leukemiaa sairastavilla potilailla. [Internet] [Masters thesis]. University of Helsinki; 2011. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10138/28476.

Council of Science Editors:

Ilander M. NK-and T-cell function in chronic myeloid leukemia patients treated with interferon-α monotherapy: T-ja NK-solujen toiminta interferoni-α hoidetuilla kroonista myeloista leukemiaa sairastavilla potilailla. [Masters Thesis]. University of Helsinki; 2011. Available from: http://hdl.handle.net/10138/28476

University of Toronto

30. Matei, Irina. The Role of ATM in Promoting Normal T cell Development and Preventing T Cell Leukemogenesis.

Degree: 2009, University of Toronto

URL: http://hdl.handle.net/1807/17799

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The immune system recognizes and eliminates an enormous array of pathogens due to the diverse antigen receptor repertoire of T and B lymphocytes. However, the… (more)

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The immune system recognizes and eliminates an enormous array of pathogens due to the diverse antigen receptor repertoire of T and B lymphocytes. However, the development of lymphocytes bearing receptors with unique specificities requires the generation of programmed double strand breaks (DSB) coupled with bursts of proliferation, rendering lymphocytes susceptible to mutations and oncogenic transformation. Thus, mechanisms responsible for monitoring global genomic integrity, such as those coordinated by the ATM (ataxia-telangiectasia mutated) kinase, must be activated during lymphocyte development to limit the oncogenic potential of antigen receptor locus recombination. I show that ATM deficiency compromises TCRα recombination and the post-mitotic survival of T-cell receptor αβ (TCRαβ+) CD4+CD8+ (DP) thymocytes, providing a molecular and developmental basis for the immunodeficiency characteristic of ATM loss. Moreover, I show that in early thymocyte progenitors undergoing TCRβ recombination, ATM loss leads to cell cycle defects and developmental arrest, likely facilitating the acquisition of mutations that contribute to leukemogenesis. Using ATM deficiency as a murine model of T cell precursor acute lymphoblastic leukemia (T-ALL), I demonstrate that IL-7 signaling, a critical survival and proliferation signal during early stages of normal thymocyte development, is also required for leukemic maintenance. Moreover, we show for the first time that in normal and leukemic thymocyte precursors, interleukin 7 receptor (IL-7R) expression and function are controlled by Notch signaling, a key determinant of T cell fate. Collectively, these findings provide insight into the mechanisms by which ATM promotes normal lymphocyte development and protects from neoplastic transformation, while establishing the groundwork for assessing the molecular events that lead to the initiation and stepwise progression of T cell leukemogenesis.

PhD

Advisors/Committee Members: Danska, Jayne, Guidos, Cynthia J., Medical Biophysics.

Subjects/Keywords: ATM; T cell development; T cell leukemia; 0379

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APA (6^th Edition):

Matei, I. (2009). The Role of ATM in Promoting Normal T cell Development and Preventing T Cell Leukemogenesis. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/17799

Chicago Manual of Style (16^th Edition):

Matei, Irina. “The Role of ATM in Promoting Normal T cell Development and Preventing T Cell Leukemogenesis.” 2009. Doctoral Dissertation, University of Toronto. Accessed March 05, 2021. http://hdl.handle.net/1807/17799.

MLA Handbook (7^th Edition):

Matei, Irina. “The Role of ATM in Promoting Normal T cell Development and Preventing T Cell Leukemogenesis.” 2009. Web. 05 Mar 2021.

Vancouver:

Matei I. The Role of ATM in Promoting Normal T cell Development and Preventing T Cell Leukemogenesis. [Internet] [Doctoral dissertation]. University of Toronto; 2009. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1807/17799.

Council of Science Editors:

Matei I. The Role of ATM in Promoting Normal T cell Development and Preventing T Cell Leukemogenesis. [Doctoral Dissertation]. University of Toronto; 2009. Available from: http://hdl.handle.net/1807/17799

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