subject:(carcinogenesis)

1. Khare, Shikha. Chemopreventive action of purified herbal agents in animal models of carcinogenesis.

Degree: 2005, Jamia Hamdard University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/37388

newline Advisors/Committee Members: Athar, Mohammad.

Subjects/Keywords: carcinogenesis

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APA (6^th Edition):

Khare, S. (2005). Chemopreventive action of purified herbal agents in animal models of carcinogenesis. (Thesis). Jamia Hamdard University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/37388

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):

Khare, Shikha. “Chemopreventive action of purified herbal agents in animal models of carcinogenesis.” 2005. Thesis, Jamia Hamdard University. Accessed April 21, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/37388.

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

MLA Handbook (7^th Edition):

Khare, Shikha. “Chemopreventive action of purified herbal agents in animal models of carcinogenesis.” 2005. Web. 21 Apr 2021.

Vancouver:

Khare S. Chemopreventive action of purified herbal agents in animal models of carcinogenesis. [Internet] [Thesis]. Jamia Hamdard University; 2005. [cited 2021 Apr 21]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/37388.

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

Council of Science Editors:

Khare S. Chemopreventive action of purified herbal agents in animal models of carcinogenesis. [Thesis]. Jamia Hamdard University; 2005. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/37388

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

Oregon State University

2. Orner, Gayle A. Dehydroepiandrosterone carcinogenesis and tumor modulating effects in trout.

Degree: PhD, Toxicology, 1995, Oregon State University

URL: http://hdl.handle.net/1957/34877

Subjects/Keywords: Carcinogenesis

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APA (6^th Edition):

Orner, G. A. (1995). Dehydroepiandrosterone carcinogenesis and tumor modulating effects in trout. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/34877

Chicago Manual of Style (16^th Edition):

Orner, Gayle A. “Dehydroepiandrosterone carcinogenesis and tumor modulating effects in trout.” 1995. Doctoral Dissertation, Oregon State University. Accessed April 21, 2021. http://hdl.handle.net/1957/34877.

MLA Handbook (7^th Edition):

Orner, Gayle A. “Dehydroepiandrosterone carcinogenesis and tumor modulating effects in trout.” 1995. Web. 21 Apr 2021.

Vancouver:

Orner GA. Dehydroepiandrosterone carcinogenesis and tumor modulating effects in trout. [Internet] [Doctoral dissertation]. Oregon State University; 1995. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/1957/34877.

Council of Science Editors:

Orner GA. Dehydroepiandrosterone carcinogenesis and tumor modulating effects in trout. [Doctoral Dissertation]. Oregon State University; 1995. Available from: http://hdl.handle.net/1957/34877

Michigan State University

3. Mugera, G. M. (Gerald Munene). Cycad toxicosis and related carcinogenesis in animals.

Degree: PhD, Department of Pathology, 1965, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:35146

Subjects/Keywords: Carcinogenesis

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APA (6^th Edition):

Mugera, G. M. (. M. (1965). Cycad toxicosis and related carcinogenesis in animals. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:35146

Chicago Manual of Style (16^th Edition):

Mugera, G M (Gerald Munene). “Cycad toxicosis and related carcinogenesis in animals.” 1965. Doctoral Dissertation, Michigan State University. Accessed April 21, 2021. http://etd.lib.msu.edu/islandora/object/etd:35146.

MLA Handbook (7^th Edition):

Mugera, G M (Gerald Munene). “Cycad toxicosis and related carcinogenesis in animals.” 1965. Web. 21 Apr 2021.

Vancouver:

Mugera GM(M. Cycad toxicosis and related carcinogenesis in animals. [Internet] [Doctoral dissertation]. Michigan State University; 1965. [cited 2021 Apr 21]. Available from: http://etd.lib.msu.edu/islandora/object/etd:35146.

Council of Science Editors:

Mugera GM(M. Cycad toxicosis and related carcinogenesis in animals. [Doctoral Dissertation]. Michigan State University; 1965. Available from: http://etd.lib.msu.edu/islandora/object/etd:35146

Hong Kong University of Science and Technology

4. Yang, Lei. Understanding the role of RGS20 in tumorigenesis and metastasis.

Degree: 2012, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-63087 ; https://doi.org/10.14711/thesis-b1190240 ; http://repository.ust.hk/ir/bitstream/1783.1-63087/1/th_redirect.html

► RGS (regulator of G protein signaling) proteins serve as negative regulators of G protein signaling. Since the discovery of the first RGS protein, more than… (more)

Subjects/Keywords: G proteins ; Carcinogenesis

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APA (6^th Edition):

Yang, L. (2012). Understanding the role of RGS20 in tumorigenesis and metastasis. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-63087 ; https://doi.org/10.14711/thesis-b1190240 ; http://repository.ust.hk/ir/bitstream/1783.1-63087/1/th_redirect.html

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):

Yang, Lei. “Understanding the role of RGS20 in tumorigenesis and metastasis.” 2012. Thesis, Hong Kong University of Science and Technology. Accessed April 21, 2021. http://repository.ust.hk/ir/Record/1783.1-63087 ; https://doi.org/10.14711/thesis-b1190240 ; http://repository.ust.hk/ir/bitstream/1783.1-63087/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Yang, Lei. “Understanding the role of RGS20 in tumorigenesis and metastasis.” 2012. Web. 21 Apr 2021.

Vancouver:

Yang L. Understanding the role of RGS20 in tumorigenesis and metastasis. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2012. [cited 2021 Apr 21]. Available from: http://repository.ust.hk/ir/Record/1783.1-63087 ; https://doi.org/10.14711/thesis-b1190240 ; http://repository.ust.hk/ir/bitstream/1783.1-63087/1/th_redirect.html.

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

Council of Science Editors:

Yang L. Understanding the role of RGS20 in tumorigenesis and metastasis. [Thesis]. Hong Kong University of Science and Technology; 2012. Available from: http://repository.ust.hk/ir/Record/1783.1-63087 ; https://doi.org/10.14711/thesis-b1190240 ; http://repository.ust.hk/ir/bitstream/1783.1-63087/1/th_redirect.html

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

NSYSU

5. Huang, Jian-yuan. Investigation of the Homeobox (HOX) gene expression in human gastric carcinogenesis.

Degree: Master, Institute of Biomedical Sciences, 2009, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0623109-181128

► In the past study, we used a human gastric stem cell clone, KMU-GI2, isolated from endoscopically biopsied gastric mucosa. As we maintained this KMU-GI2 cell… (more)

Subjects/Keywords: HOX; Homeobox; gastric carcinogenesis

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APA (6^th Edition):

Huang, J. (2009). Investigation of the Homeobox (HOX) gene expression in human gastric carcinogenesis. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0623109-181128

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):

Huang, Jian-yuan. “Investigation of the Homeobox (HOX) gene expression in human gastric carcinogenesis.” 2009. Thesis, NSYSU. Accessed April 21, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0623109-181128.

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

MLA Handbook (7^th Edition):

Huang, Jian-yuan. “Investigation of the Homeobox (HOX) gene expression in human gastric carcinogenesis.” 2009. Web. 21 Apr 2021.

Vancouver:

Huang J. Investigation of the Homeobox (HOX) gene expression in human gastric carcinogenesis. [Internet] [Thesis]. NSYSU; 2009. [cited 2021 Apr 21]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0623109-181128.

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

Council of Science Editors:

Huang J. Investigation of the Homeobox (HOX) gene expression in human gastric carcinogenesis. [Thesis]. NSYSU; 2009. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0623109-181128

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

Cape Peninsula University of Technology

6. Petrova, Antoinette. Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms .

Degree: 2009, Cape Peninsula University of Technology

URL: http://etd.cput.ac.za/handle/20.500.11838/1487

► This thesis provides the first scientific evidence of the photoprotective properties of rooibos and honeybush herbal tea extracts and to some extent, two major honeybush… (more)

▼ This thesis provides the first scientific evidence of the photoprotective properties of rooibos and honeybush herbal tea extracts and to some extent, two major honeybush polyphenols, hesperidin and mangiferin. These properties were demonstrated using in vivo models by: Providing evidence for the inhibition of tumour promotion by ultraviolet B (UVB) radiation in a two-stage skin carcinogenesis mouse model. Topical application of polyphenol-rich extracts of rooibos and honeybush prior to UVB tumour promotion of 7,12-dimethylbenz[a]anthracene (DMBA)-initiated mouse skin, inhibited the formation of tumours. The rooibos and honeybush extracts decreased the incidence and volume of the tumours. Topical application of hesperidin and mangiferin were less effective than the honeybush extracts as only the tumour volume was decreased, but not the incidence. Providing evidence for the inhibition of photodamage of the skin by UVB exposure in a mouse model. Topical application of polyphenolic rich extracts of honeybush prior to UVB irradiation of mouse skin reduced erythema, peeling, oedema and hyperplasia. The depletion of antioxidant enzymes catalase and superoxide dismutase (SOD) was prevented. The extracts protected the skin from oxidative and direct DNA damage, and reduced lipid peroxidation. The induction of cyclooxygenase-2 (COX-2) and ornithine decarboxylase (ODC) was also reduced. Topical application of the polyphenols hesperidin and mangiferin showed reduced protective effects compared to the extracts. Suggesting the possible mechanisms by which honeybush and the polyphenols protect against photocarcinogenesis such as reducing tumour promotion, inflammation and oxidative stress. Suggesting the benefits of including honeybush and rooibos as cosmeceuticals in skin care products and sunscreens as part of the strategy for preventing skin cancer. Discussing the recommendations for further study such as investigating more specific chemopreventive activities of these two South African herbal teas and their polyphenols, dose response studies and clinical evaluations.

Subjects/Keywords: rooibos; honeybush; carcinogenesis; mouse model

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APA (6^th Edition):

Petrova, A. (2009). Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms . (Thesis). Cape Peninsula University of Technology. Retrieved from http://etd.cput.ac.za/handle/20.500.11838/1487

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):

Petrova, Antoinette. “Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms .” 2009. Thesis, Cape Peninsula University of Technology. Accessed April 21, 2021. http://etd.cput.ac.za/handle/20.500.11838/1487.

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

MLA Handbook (7^th Edition):

Petrova, Antoinette. “Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms .” 2009. Web. 21 Apr 2021.

Vancouver:

Petrova A. Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms . [Internet] [Thesis]. Cape Peninsula University of Technology; 2009. [cited 2021 Apr 21]. Available from: http://etd.cput.ac.za/handle/20.500.11838/1487.

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

Council of Science Editors:

Petrova A. Modulation of ultrviolet light induced skin carcinogenesis by extracts of Rooibos and Honeybush using a mouse model:elucidating possible protective mechanisms . [Thesis]. Cape Peninsula University of Technology; 2009. Available from: http://etd.cput.ac.za/handle/20.500.11838/1487

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

7. Papanagnou, Panagiota. Διερεύνηση του μηχανισμού δράσης των ογκοκατασταλτικών πρωτεϊνών p21WAF1/CIP1 και ARF.

Degree: 2014, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/41756

►

P21WAF1/CIP1 is a universal cyclin-dependent kinase inhibitor and plays a crucial role in the DNA damage response (DDR) pathway. P21WAF1/CIP1 is a multifunctional molecule whose… (more)

▼

P21WAF1/CIP1 is a universal cyclin-dependent kinase inhibitor and plays a crucial role in the DNA damage response (DDR) pathway. P21WAF1/CIP1 is a multifunctional molecule whose role in carcinogenesis as a tumor-suppressor is being disputed. In this study, there was used the doxycycline inducible cell system Saos2-p21WAF1/CIP1 Τet ON and there was conducted a gel-free iTRAQ proteomic analysis at three different time points, i.e. 12, 48 and 96 hrs after the induction of p21WAF1/CIP1in order to investigate the effects of the long-term expression of p21WAF1/CIP1 in a p53 null background. Proteomics combined with bioinformatics indicated that the proteins which are mostly affected by p21WAF1/CIP1 are those associated with DNA replication (up-regulation) and mitotis-associated ones (down-regulation). Given that deregulation of the mitotic machinery along with disturbed control of genome replication have been linked to the triggering of genomic instability, the results pay credit to the notion that p21WAF1/CIP1 exhibits a “vicious” pro-tumorigenic facet.On the other hand, ΑRF (alternative reading frame) is also a tumor-suppressive protein, being assigned with multiple intracellular duties. Recently, there was demonstrated an interrelation among the DDR kinase ATM and ARF. Here, there were applied a series of molecular and in situ techniques as well as bioinformatics in order to identify a possible interplay among ARF and the ATM-related kinase ATR or even among ARF and the DDR component MKK7. Further, there were analyzed xenografts in mice in order to characterize the anti-angiogenic activity of ARF when ATM is suppressed. The resulting data indicate that ARF participates in a perplexed network of signaling relationships within the DDR landscape and that ATM suppression may be harnessed as a novel anti-angiogenic strategy in p53-deficient tumors.

Η p21WAF1/CIP1 είναι ένας «καθολικός» αναστολέας των κυκλινο-εξαρτώμενων κινασών και παίζει κρίσιμο ρόλο στο μονοπάτι της απόκρισης στην βλάβη του DNA (DDR). Η p21WAF1/CIP1 είναι ένα πολυλειτουργικό μόριο ενώ στην καρκινογένεση ο αρχικός της χαρακτηρισμός της ως ογκοκατασταλτικής πρωτεΐνης να αμφισβητείται. Στην παρούσα έρευνα χρησιμοποιήθηκε ένα επαγώγιμο κυτταρικό σύστημα, το Saos2-p21WAF1/CIP1 Τet ON, και διενεργήθηκε ελεύθερη-γέλης πρωτεωμική ανάλυση iTRAQ σε 3 διαφορετικά χρονικά σημεία μετά την επαγωγή της p21WAF1/CIP1, δηλ. στις 12, 48 και 96 ώρες, με σκοπό να αποσαφηνιστούν οι ογκογενετικές ιδιότητες της p21WAF1/CIP1 που πιθανό να σκιαγραφούνται καλύτερα όταν η έκφραση της p21WAF1/CIP1 είναι παρατεταμένη και απουσιάζει η ογκοκατασταλτική πρωτεΐνη p53. Η πρωτεωμική ανάλυση ακολουθούμενη από αναλύσεις δεδομένων με την βοήθεια βιοπληροφορικής έδειξε πως ανάμεσα στις περισσότερο επηρεαζόμενες πρωτεΐνες που υφίστανται αυξορρύθμιση και μειορρύθμιση από την p21WAF1/CIP1 είναι εκείνες που συμμετέχουν στην αντιγραφή του DNA και την μίτωση, αντίστοιχα. Δεδομένου ότι η απορρύθμιση της αντιγραφικής αλλά και της μιτωτικής μηχανής έχουν συνδεθεί με την πυροδότηση της γενωμικής…

Subjects/Keywords: Καρκινογένεση; Carcinogenesis; P21WAF1/Cip1; ARF

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APA (6^th Edition):

Papanagnou, P. (2014). Διερεύνηση του μηχανισμού δράσης των ογκοκατασταλτικών πρωτεϊνών p21WAF1/CIP1 και ARF. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/41756

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):

Papanagnou, Panagiota. “Διερεύνηση του μηχανισμού δράσης των ογκοκατασταλτικών πρωτεϊνών p21WAF1/CIP1 και ARF.” 2014. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed April 21, 2021. http://hdl.handle.net/10442/hedi/41756.

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

MLA Handbook (7^th Edition):

Papanagnou, Panagiota. “Διερεύνηση του μηχανισμού δράσης των ογκοκατασταλτικών πρωτεϊνών p21WAF1/CIP1 και ARF.” 2014. Web. 21 Apr 2021.

Vancouver:

Papanagnou P. Διερεύνηση του μηχανισμού δράσης των ογκοκατασταλτικών πρωτεϊνών p21WAF1/CIP1 και ARF. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/10442/hedi/41756.

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

Council of Science Editors:

Papanagnou P. Διερεύνηση του μηχανισμού δράσης των ογκοκατασταλτικών πρωτεϊνών p21WAF1/CIP1 και ARF. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. Available from: http://hdl.handle.net/10442/hedi/41756

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

8. Nayeem Bilal. Biochemical studies on the effects of chronic unpredictable stress on nitrosamine induced carcinogenesis; -.

Degree: Biochemistry, 2013, Aligarh Muslim University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/12844

None

Bibliography given

Advisors/Committee Members: Naheed Banu.

Subjects/Keywords: biochemistry; Carcinogenesis

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APA (6^th Edition):

Bilal, N. (2013). Biochemical studies on the effects of chronic unpredictable stress on nitrosamine induced carcinogenesis; -. (Thesis). Aligarh Muslim University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/12844

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):

Bilal, Nayeem. “Biochemical studies on the effects of chronic unpredictable stress on nitrosamine induced carcinogenesis; -.” 2013. Thesis, Aligarh Muslim University. Accessed April 21, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/12844.

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

MLA Handbook (7^th Edition):

Bilal, Nayeem. “Biochemical studies on the effects of chronic unpredictable stress on nitrosamine induced carcinogenesis; -.” 2013. Web. 21 Apr 2021.

Vancouver:

Bilal N. Biochemical studies on the effects of chronic unpredictable stress on nitrosamine induced carcinogenesis; -. [Internet] [Thesis]. Aligarh Muslim University; 2013. [cited 2021 Apr 21]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/12844.

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

Council of Science Editors:

Bilal N. Biochemical studies on the effects of chronic unpredictable stress on nitrosamine induced carcinogenesis; -. [Thesis]. Aligarh Muslim University; 2013. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/12844

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

9. Nida Suhail. Biochemical studies on the effect of stress on DMBA -TPA induced carcinogenesis; -.

Degree: Biochemistry, 2013, Aligarh Muslim University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/12846

►

Cancer is one of the leading causes of death in most well developed countries. It has been established that multiple stepwise alterations of the original… (more)

Subjects/Keywords: biochemistry; Carcinogenesis; Chemoprevention; Stress

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APA (6^th Edition):

Suhail, N. (2013). Biochemical studies on the effect of stress on DMBA -TPA induced carcinogenesis; -. (Thesis). Aligarh Muslim University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/12846

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):

Suhail, Nida. “Biochemical studies on the effect of stress on DMBA -TPA induced carcinogenesis; -.” 2013. Thesis, Aligarh Muslim University. Accessed April 21, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/12846.

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

MLA Handbook (7^th Edition):

Suhail, Nida. “Biochemical studies on the effect of stress on DMBA -TPA induced carcinogenesis; -.” 2013. Web. 21 Apr 2021.

Vancouver:

Suhail N. Biochemical studies on the effect of stress on DMBA -TPA induced carcinogenesis; -. [Internet] [Thesis]. Aligarh Muslim University; 2013. [cited 2021 Apr 21]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/12846.

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

Council of Science Editors:

Suhail N. Biochemical studies on the effect of stress on DMBA -TPA induced carcinogenesis; -. [Thesis]. Aligarh Muslim University; 2013. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/12846

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

University of Texas Southwestern Medical Center

10. Lee, Eunmyong. The Role of Autophagy in Early Development and Tumor Suppression Using a Zebrafish Model System.

Degree: 2013, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/1738

► Autophagy is an evolutionarily conserved lysosomal degradation pathway which involves the sequestration of cytoplasmic components into a double membraned structure called the autophagosome. By using… (more)

Subjects/Keywords: Autophagy; Carcinogenesis; Morphogenesis; Zebrafish

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APA (6^th Edition):

Lee, E. (2013). The Role of Autophagy in Early Development and Tumor Suppression Using a Zebrafish Model System. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1738

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):

Lee, Eunmyong. “The Role of Autophagy in Early Development and Tumor Suppression Using a Zebrafish Model System.” 2013. Thesis, University of Texas Southwestern Medical Center. Accessed April 21, 2021. http://hdl.handle.net/2152.5/1738.

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

MLA Handbook (7^th Edition):

Lee, Eunmyong. “The Role of Autophagy in Early Development and Tumor Suppression Using a Zebrafish Model System.” 2013. Web. 21 Apr 2021.

Vancouver:

Lee E. The Role of Autophagy in Early Development and Tumor Suppression Using a Zebrafish Model System. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2013. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/2152.5/1738.

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

Council of Science Editors:

Lee E. The Role of Autophagy in Early Development and Tumor Suppression Using a Zebrafish Model System. [Thesis]. University of Texas Southwestern Medical Center; 2013. Available from: http://hdl.handle.net/2152.5/1738

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

University of Delaware

11. Viswanathan, Vignesh. MicroRNAs in normal and malignant colon stem cells and their possible role in stem cell origin of colon cancer.

Degree: PhD, University of Delaware, Department of Department Biological Sciences, 2014, University of Delaware

URL: http://udspace.udel.edu/handle/19716/16788

► The role of miRNAs in colon cancer development pertaining specifically to the stem cell origin of cancer is yet to be elucidated. We hypothesized that… (more)

▼ The role of miRNAs in colon cancer development pertaining specifically to the stem cell origin of cancer is yet to be elucidated. We hypothesized that perturbation of miR expression levels contributes to changes in target gene belonging to self-renewal pathways, which initiate colon tumorigenesis. Our miR profiling studies to identify miRs that regulate colon cancer stem cells (CSCs) were broadly divided in two parts. In one study we profiled the normal crypt bottom subsection that is enriched in stem cells and identified miR23b to be one of the miRs to have a significant differential expression. MiR23b has already been identified as having a role in renal, prostate, bladder, breast and colon cancers involving cell migration, invasion and apoptosis. Recently, a role for miR23b in ovarian CSCs and response to chemotherapy has also been elucidated. Consequently, I postulated that miR23b regulates colon CSCs. My results showed that miR23b is overexpressed in the ALDEFLUOR high sub-population of HT29 and SW480 colon cancer cells. It was shown to control the colon CSC phenotype and significantly affects proliferation, cell cycle, self-renewal, EMT, invasion and chemoresistance to the anti-cancer drug 5- FU. I validated that the colon CSC marker LGR5 is a target of miR23b, showing its role in modulating Wnt signaling. MiR23b also influences the transcription of multiple gene targets such as ATF2 and AKT2, which were identified by our extensive RNA SEQ analysis. The other aspect of the study was to identify miRs, which are differentially expressed in the CSCs as compared to the normal SCs from fresh patient samples. Normal and tumor tissue were initially screened for the expression of multiple putative CSC markers (ALDH1, LRIG1, CD166, ABCG2, BMI1, Telomerase) with an aim to decide which markers should be used alone or in combination to isolate SCs. My results indicated for the first time that SC markers ALDH1, LRIG1 and CD166 do not co-stain cells in tumors suggesting a co-existence of subpopulations of CSCs in tumor. MiR profiling identified miRs such as miR200c, miR92a, miR20a and miR93 that had a significant differential expression in ALDEFLUOR high tumor cells as compared to ALDEFLUOR high normal cells. MiR92a was also significantly upregulated in ALDEFLUOR high cells of colon cancer cell lines HT29 and regulated its proliferation. Future studies have to be done on the other newly recognized candidate miRs that show differential expression in primary tumor SCs. Understanding the role of miRs in CSCs could contribute to identification of new targets for therapeutic intervention. Advisors/Committee Members: Boman, BruceGalileo, Deni S..

Subjects/Keywords: RNA.; Colon (Anatomy) – Cancer.; Carcinogenesis

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APA (6^th Edition):

Viswanathan, V. (2014). MicroRNAs in normal and malignant colon stem cells and their possible role in stem cell origin of colon cancer. (Doctoral Dissertation). University of Delaware. Retrieved from http://udspace.udel.edu/handle/19716/16788

Chicago Manual of Style (16^th Edition):

Viswanathan, Vignesh. “MicroRNAs in normal and malignant colon stem cells and their possible role in stem cell origin of colon cancer.” 2014. Doctoral Dissertation, University of Delaware. Accessed April 21, 2021. http://udspace.udel.edu/handle/19716/16788.

MLA Handbook (7^th Edition):

Viswanathan, Vignesh. “MicroRNAs in normal and malignant colon stem cells and their possible role in stem cell origin of colon cancer.” 2014. Web. 21 Apr 2021.

Vancouver:

Viswanathan V. MicroRNAs in normal and malignant colon stem cells and their possible role in stem cell origin of colon cancer. [Internet] [Doctoral dissertation]. University of Delaware; 2014. [cited 2021 Apr 21]. Available from: http://udspace.udel.edu/handle/19716/16788.

Council of Science Editors:

Viswanathan V. MicroRNAs in normal and malignant colon stem cells and their possible role in stem cell origin of colon cancer. [Doctoral Dissertation]. University of Delaware; 2014. Available from: http://udspace.udel.edu/handle/19716/16788

Columbia University

12. Henckels, Eric Patrick. Regulation of Matrix Metallopeptidase-1 in Breast Cancer Metastasis.

Degree: 2013, Columbia University

URL: https://doi.org/10.7916/D8TT4Z9W

► Matrix Metallopeptidase 1 (MMP-1) expression has repeatedly been correlated to tumorigenesis and metastasis. Yet, MMP-1 regulation in a metastatic context remains largely unknown. Here we… (more)

Subjects/Keywords: Oncology; Metastasis; Carcinogenesis; Breast – Cancer

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APA (6^th Edition):

Henckels, E. P. (2013). Regulation of Matrix Metallopeptidase-1 in Breast Cancer Metastasis. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8TT4Z9W

Chicago Manual of Style (16^th Edition):

Henckels, Eric Patrick. “Regulation of Matrix Metallopeptidase-1 in Breast Cancer Metastasis.” 2013. Doctoral Dissertation, Columbia University. Accessed April 21, 2021. https://doi.org/10.7916/D8TT4Z9W.

MLA Handbook (7^th Edition):

Henckels, Eric Patrick. “Regulation of Matrix Metallopeptidase-1 in Breast Cancer Metastasis.” 2013. Web. 21 Apr 2021.

Vancouver:

Henckels EP. Regulation of Matrix Metallopeptidase-1 in Breast Cancer Metastasis. [Internet] [Doctoral dissertation]. Columbia University; 2013. [cited 2021 Apr 21]. Available from: https://doi.org/10.7916/D8TT4Z9W.

Council of Science Editors:

Henckels EP. Regulation of Matrix Metallopeptidase-1 in Breast Cancer Metastasis. [Doctoral Dissertation]. Columbia University; 2013. Available from: https://doi.org/10.7916/D8TT4Z9W

University of Southern California

13. Shahin, Sophia Allaf. Ascorbate and dehydroascorbate enhance the cytotoxicity and morphological transformation of C3H/10T½ C1 8 mouse embryo cells induced by soluble chromium (VI) compounds.

Degree: MS, Experimental and Molecular Pathology, 2014, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/385505/rec/923

► Hexavalent chromium [Cr(VI)]‐containing compounds are human carcinogens. They cause cancers in the respiratory system when inhaled, and stomach, kidney/other internal cancers when ingested. Soluble and… (more)

▼ Hexavalent chromium [Cr(VI)]‐containing compounds are human carcinogens. They cause cancers in the respiratory system when inhaled, and stomach, kidney/other internal cancers when ingested. Soluble and insoluble hexavalent chromium [Cr(VI)] compounds induce base substitution, deletion, addition, and frameshift mutations. Cr(VI) compounds also induce DNA‐DNA cross links and DNA‐protein cross-links in mammalian cells. ❧ In this thesis, we examined the ability of the soluble chromium compounds, sodium chromate (Na₂CrO₄), calcium chromate (CaCrO₄) and potassium dichromate (K₂Cr₂O₇), to induce cytotoxicity and morphological transformation in cultured C3H/10T½ Cl 8 (10T1/2) mouse embryo cells. We tested the hypothesis that the intracellular reductants, ascorbate and dehydroascorbate, can reduce Cr(VI), to Cr(V), Cr(IV), and Cr(III) intracellularly, making Cr(VI) a strong cytotoxin in mammalian cells. Ascorbate is present in serum at concentrations in the mM range under physiological conditions in humans, but is only present in the μM range in mouse embryo cells grown in BME cell culture medium plus 10% fetal calf serum. ❧ We hypothesized that the relatively weak responses for induction of morphological transformation of mammalian cells by Cr(VI) compounds in culture (dose‐dependent but weak induction of foci by lead chromate, and no induction of foci by calcium chromate, potassium dichromate , and sodium chromate) is due to the small amounts of ascorbate in cultures of mammalian cells that are insufficient to reduce Cr(VI) to Cr(V), Cr(IV), and Cr(III). Therefore, we investigated the cytotoxic effects of ascorbate on 10T½ mouse embryo cells, and the effects of the highest non‐cytotoxic concentrations of ascorbate on Cr(VI)‐induced cytotoxicity in 10T½ cells, using reduction in plating efficiency as our cytotoxicity assay. Cell survival data showed that ascorbate exerted significant cytotoxic effects at concentrations of 0.00625 mM and higher on 10T½ mouse embryo cells. Furthermore, when 10T½ cells were treated with both Cr(VI) and ascorbate, ascorbate played dual roles. It served as a pro‐oxidant (enhancer of the cytotoxicity of chromate) at concentrations up to 0.1 mM, and as an anti‐oxidant (reducer of the cytotoxicity of chromate) at concentrations of 0.25 mM and higher. This information is important for our ongoing and future experiments, where we designed a protocol to incorporate ascorbate into our assays assessing the cytotoxicity and cell transforming activity of Cr(VI) compounds. At concentrations of 0.1 mM and lower, ascorbate enhanced the cell transforming ability of Cr(VI) compounds to induce morphological transformation. Advisors/Committee Members: Landolph, Joseph R., Jr. (Committee Chair).

Subjects/Keywords: chemical; chromium; physical carcinogenesis

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APA (6^th Edition):

Shahin, S. A. (2014). Ascorbate and dehydroascorbate enhance the cytotoxicity and morphological transformation of C3H/10T½ C1 8 mouse embryo cells induced by soluble chromium (VI) compounds. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/385505/rec/923

Chicago Manual of Style (16^th Edition):

Shahin, Sophia Allaf. “Ascorbate and dehydroascorbate enhance the cytotoxicity and morphological transformation of C3H/10T½ C1 8 mouse embryo cells induced by soluble chromium (VI) compounds.” 2014. Masters Thesis, University of Southern California. Accessed April 21, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/385505/rec/923.

MLA Handbook (7^th Edition):

Shahin, Sophia Allaf. “Ascorbate and dehydroascorbate enhance the cytotoxicity and morphological transformation of C3H/10T½ C1 8 mouse embryo cells induced by soluble chromium (VI) compounds.” 2014. Web. 21 Apr 2021.

Vancouver:

Shahin SA. Ascorbate and dehydroascorbate enhance the cytotoxicity and morphological transformation of C3H/10T½ C1 8 mouse embryo cells induced by soluble chromium (VI) compounds. [Internet] [Masters thesis]. University of Southern California; 2014. [cited 2021 Apr 21]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/385505/rec/923.

Council of Science Editors:

Shahin SA. Ascorbate and dehydroascorbate enhance the cytotoxicity and morphological transformation of C3H/10T½ C1 8 mouse embryo cells induced by soluble chromium (VI) compounds. [Masters Thesis]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/385505/rec/923

University of Hong Kong

14. Hu, Xiaobin. The role of Uhrf1 in development and tumorigenesis.

Degree: 2014, University of Hong Kong

URL: http://hdl.handle.net/10722/225205

Subjects/Keywords: Ubiquitin; Carcinogenesis

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APA (6^th Edition):

Hu, X. (2014). The role of Uhrf1 in development and tumorigenesis. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/225205

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):

Hu, Xiaobin. “The role of Uhrf1 in development and tumorigenesis.” 2014. Thesis, University of Hong Kong. Accessed April 21, 2021. http://hdl.handle.net/10722/225205.

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

MLA Handbook (7^th Edition):

Hu, Xiaobin. “The role of Uhrf1 in development and tumorigenesis.” 2014. Web. 21 Apr 2021.

Vancouver:

Hu X. The role of Uhrf1 in development and tumorigenesis. [Internet] [Thesis]. University of Hong Kong; 2014. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/10722/225205.

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

Council of Science Editors:

Hu X. The role of Uhrf1 in development and tumorigenesis. [Thesis]. University of Hong Kong; 2014. Available from: http://hdl.handle.net/10722/225205

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

University of Limerick

15. Hayes, Christopher J. The utilisation of microfluidic qPCR technology for the identification of novel cancer biomarkers.

Degree: 2017, University of Limerick

URL: http://hdl.handle.net/10344/6556

►

peer-reviewed

Cancer is a major cause of death worldwide causing 1 in 6 deaths globally with approximately 14 million new cases and 8.8 million cancer… (more)

▼

peer-reviewed

Cancer is a major cause of death worldwide causing 1 in 6 deaths globally with approximately 14 million new cases and 8.8 million cancer related deaths in 2015. This figure is expected to increase to 21.7 million cases and 13 million deaths by 2030. In Ireland, an average of 30,000 new cases of cancer are diagnosed each year. The number is also expected to rise to over 40,000 per year by 2020. A key focus to reverse this trend is the identification of new prognostic markers and therapeutic targets that can be used to predict the incidence or outcome of the disease. These targets can also be used to screen populations to identify symptomatic patients, identify differential diagnosis and for the clinical staging of cancer. The quest for a better understanding of the carcinogenesis process has led to impressive growth in the field of large-scale and high-throughput biology which has become a driving force behind the emergence of new technologies. Large scale gene expression profiling is an essential tool for many biological and medical investigations. Higher throughputs and increased levels of specificity coupled with reduced volumes of samples and reagents is a dominant factor. . The development and application of a microfluidic platform to analyse biological samples at a rate of approximately one thousand data points per hour is demonstrated in this thesis. Utilisation of such a platform gives an advantage over many traditional systems and allows for the manipulation of smaller quantities to achieve corresponding biological outcomes. This thesis investigates the application of microfluidic gene expression profiling to identify biomarkers in colorectal and breast carcinoma, envisioning that future validation tests using a microfluidic platform could produce an expression assay to aid the stratification of the disease. The focus is on candidate genetic targets that are regulating extracellular matrices production which are central components of a tumour’s microenvironment, possessing key roles for tumour formation, growth and potential metastatic spread. In two genetic studies of colorectal and breast cancer malignancies, a number of genes from the extracellular matrix family emerge as being statistically differentially expressed. Correlations of the genes with the histopathological parameters along with heterogeneity of the tumours are investigated also. Genetic targets identified could potentially serve as molecular markers in screening, diagnosis and treatment strategies for the individualised care of patients in the future.

Advisors/Committee Members: Dalton, Tara, Kiely, Patrick A..

Subjects/Keywords: cancer; Ireland; carcinogenesis; biomarkers; genetic

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APA (6^th Edition):

Hayes, C. J. (2017). The utilisation of microfluidic qPCR technology for the identification of novel cancer biomarkers. (Thesis). University of Limerick. Retrieved from http://hdl.handle.net/10344/6556

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):

Hayes, Christopher J. “The utilisation of microfluidic qPCR technology for the identification of novel cancer biomarkers.” 2017. Thesis, University of Limerick. Accessed April 21, 2021. http://hdl.handle.net/10344/6556.

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

MLA Handbook (7^th Edition):

Hayes, Christopher J. “The utilisation of microfluidic qPCR technology for the identification of novel cancer biomarkers.” 2017. Web. 21 Apr 2021.

Vancouver:

Hayes CJ. The utilisation of microfluidic qPCR technology for the identification of novel cancer biomarkers. [Internet] [Thesis]. University of Limerick; 2017. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/10344/6556.

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

Council of Science Editors:

Hayes CJ. The utilisation of microfluidic qPCR technology for the identification of novel cancer biomarkers. [Thesis]. University of Limerick; 2017. Available from: http://hdl.handle.net/10344/6556

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

University of British Columbia

16. Hanham, Ann Frances. The clastogenic activity of phenolic oxidation products.

Degree: PhD, Zoology, 1983, University of British Columbia

URL: http://hdl.handle.net/2429/24298

► Several epidemiological studies .have demonstrated the importance of diet in the development of gastro-intestinal carcinomas in man. This study examines the role of plant phenolics,… (more)

▼ Several epidemiological studies .have demonstrated the importance of diet in the development of gastro-intestinal carcinomas in man. This study examines the role of plant phenolics, major components of the human diet. Employing a CHO cell test system, it was observed that phenolics with at least two hydroxyl groups in the ortho position, relative to each other were particularly clastogenic. This activity was abolished by the addition of S9, a rat liver microsomal preparation. The clastogenic activity of these compounds was found to increase with time, alkaline pH, and the presence of transition metals. It was therefore deduced that the source of activity might be an oxidative by-product. High' pressure liquid chromatography was used to separate out these oxidative products. No activity was found to reside in any of the separated components or combinations of components. Further study therefore centred on oxidative products not retained by chromatography and on those labile to this.process. Under oxidative conditions, the presence of hydrogen peroxide was detected. Levels measured were sufficient to explain the clastogenic activity of completely oxidized solutions of phenolic acids. Addition of the enzyme, catalase, appeared to abolish all activity of completely oxidized solutions. Hydrogen peroxide could not, however, account for the genotoxic effects measured in freshly prepared solutions. The presence of superoxide was detected in actively oxidizing solutions of plant phenolics. Its production appeared to be pH-dependent. Addition of superoxide dismutase increased the clastogenic activity of compounds tested, presumably by converting superoxide to peroxide, a more stable oxidative by-product. Addition of tyrosinase, a monophenol oxidase, also increased the clastogenic activity of freshly prepared solutions. Since this enzyme catalyzes the oxidation of several phenolics without subsequent generation of peroxide, it was deduced that phenolic free radicals must also be present which could be at least partially responsible for the enhanced biological activity. Electron spin resonance proved this was the case. Using electron spin resonance, the primary oxidative products were characterized both at high pH and by enzymatic activation. The results obtained agree with those published in the literature. Several reports in the literature have suggested that phenolics may also act as free radical scavengers. The importance of plant phenolics in diet may therefore depend on the oxidative conditions of the system to be tested. Under oxidative conditions, free radicals appear to be generated, which are capable of causing mutations and chromosomal rearrangements. Phenolic oxidation products may therefore play a role as initiators and promotors of carcinogenesis. However, under alternate conditions, phenolics may also act to scavenge free radicals, and could therefore be classed as inhibitors of carcinogenesis.

Subjects/Keywords: Phenols; Carcinogenesis

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APA (6^th Edition):

Hanham, A. F. (1983). The clastogenic activity of phenolic oxidation products. (Doctoral Dissertation). University of British Columbia. Retrieved from http://hdl.handle.net/2429/24298

Chicago Manual of Style (16^th Edition):

Hanham, Ann Frances. “The clastogenic activity of phenolic oxidation products.” 1983. Doctoral Dissertation, University of British Columbia. Accessed April 21, 2021. http://hdl.handle.net/2429/24298.

MLA Handbook (7^th Edition):

Hanham, Ann Frances. “The clastogenic activity of phenolic oxidation products.” 1983. Web. 21 Apr 2021.

Vancouver:

Hanham AF. The clastogenic activity of phenolic oxidation products. [Internet] [Doctoral dissertation]. University of British Columbia; 1983. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/2429/24298.

Council of Science Editors:

Hanham AF. The clastogenic activity of phenolic oxidation products. [Doctoral Dissertation]. University of British Columbia; 1983. Available from: http://hdl.handle.net/2429/24298

University of New South Wales

17. Kalyuga , Maria. Exploration of the role of the ETS transcription factor ESE2 in breast cancer.

Degree: Clinical School - St Vincent's Hospital, 2011, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/51251 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9903/SOURCE02?view=true

► Thesis abstract: Breast cancer represents a leading cancer-related diagnosis of Australian women, with treatments ultimately still ineffective for many patients. Investigating the mechanisms behind normal… (more)

▼ Thesis abstract: Breast cancer represents a leading cancer-related diagnosis of Australian women, with treatments ultimately still ineffective for many patients. Investigating the mechanisms behind normal breast development is a means to identify processes involved in carcinogenesis, as they are frequently corrupted to facilitate tumour initiation and progression. The PRL signaling pathway is vital for the function of the mammary tissue during pregnancy and lactation. The mouse ELF5 and its human counterpart, ESE2, were identified as downstream targets of this pathway and have subsequently been characterised as crucial players in mammary gland development. In addition, limited evidence has pointed to the possibility of this protein being involved in human breast carcinogenesis, although a direct link remains pending. The current body of work was aimed at exploring the role of the human ESE2 in breast cancer. This was achieved through the use of a range of large and small-scale in vitro techniques to, firstly, attempt to identify potential ESE2 binding partners. Secondly, a model of inducible, stable ESE2 downregulation was employed to establish the function of ESE2 in the T47D breast cancer cell line, in the context of progesterone signaling, which is an important mediator of normal and aberrant mammary gland behaviour. It was determined that inhibiting a progestin-mediated ESE2 increase led to the augmentation of the previously characterised anti-proliferative effects of this hormone. An equivalent overexpression model was generated and characterised in detail. Negative effects of ESE2 on cell proliferation and adhesion were identified and were accompanied by changes at the level of apoptosis, gene transcription activity and other molecular changes. The data gathered is the first study to directly examine the role of ESE2 in human breast cancer. Advisors/Committee Members: Ormandy, Christopher , Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW.

Subjects/Keywords: Breast cancer; Human breast carcinogenesis

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APA (6^th Edition):

Kalyuga , M. (2011). Exploration of the role of the ETS transcription factor ESE2 in breast cancer. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/51251 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9903/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Kalyuga , Maria. “Exploration of the role of the ETS transcription factor ESE2 in breast cancer.” 2011. Doctoral Dissertation, University of New South Wales. Accessed April 21, 2021. http://handle.unsw.edu.au/1959.4/51251 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9903/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Kalyuga , Maria. “Exploration of the role of the ETS transcription factor ESE2 in breast cancer.” 2011. Web. 21 Apr 2021.

Vancouver:

Kalyuga M. Exploration of the role of the ETS transcription factor ESE2 in breast cancer. [Internet] [Doctoral dissertation]. University of New South Wales; 2011. [cited 2021 Apr 21]. Available from: http://handle.unsw.edu.au/1959.4/51251 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9903/SOURCE02?view=true.

Council of Science Editors:

Kalyuga M. Exploration of the role of the ETS transcription factor ESE2 in breast cancer. [Doctoral Dissertation]. University of New South Wales; 2011. Available from: http://handle.unsw.edu.au/1959.4/51251 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9903/SOURCE02?view=true

Michigan State University

18. Baranyi, Bonnie Lynn. Factors involved in target specificity of the hepatocarcinogen N-2-acetylaminofluorene with regard to cell type and location within the genome.

Degree: PhD, Department of Pharmacology and Toxicology, 1982, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:34585

Subjects/Keywords: Carcinogens; Carcinogenesis

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APA (6^th Edition):

Baranyi, B. L. (1982). Factors involved in target specificity of the hepatocarcinogen N-2-acetylaminofluorene with regard to cell type and location within the genome. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:34585

Chicago Manual of Style (16^th Edition):

Baranyi, Bonnie Lynn. “Factors involved in target specificity of the hepatocarcinogen N-2-acetylaminofluorene with regard to cell type and location within the genome.” 1982. Doctoral Dissertation, Michigan State University. Accessed April 21, 2021. http://etd.lib.msu.edu/islandora/object/etd:34585.

MLA Handbook (7^th Edition):

Baranyi, Bonnie Lynn. “Factors involved in target specificity of the hepatocarcinogen N-2-acetylaminofluorene with regard to cell type and location within the genome.” 1982. Web. 21 Apr 2021.

Vancouver:

Baranyi BL. Factors involved in target specificity of the hepatocarcinogen N-2-acetylaminofluorene with regard to cell type and location within the genome. [Internet] [Doctoral dissertation]. Michigan State University; 1982. [cited 2021 Apr 21]. Available from: http://etd.lib.msu.edu/islandora/object/etd:34585.

Council of Science Editors:

Baranyi BL. Factors involved in target specificity of the hepatocarcinogen N-2-acetylaminofluorene with regard to cell type and location within the genome. [Doctoral Dissertation]. Michigan State University; 1982. Available from: http://etd.lib.msu.edu/islandora/object/etd:34585

Rutgers University

19. Zhao, Yuhan, 1985-. The role of P53 signaling pathway in aging and cancer.

Degree: PhD, Pharmacology, Cellular and Molecular, 2018, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/59291/

► Part I: p53 codon 72 SNP and aging p53 has dual functions on longevity. p53 plays a crucial role in tumor suppression to prevent early… (more)

▼ Part I: p53 codon 72 SNP and aging p53 has dual functions on longevity. p53 plays a crucial role in tumor suppression to prevent early death due to cancer. However, constitutively increased p53 activity accelerates the decline of stem/progenitor cells’ self-renewal function, which leads to accelerated aging and a reduced lifespan. In humans, the role of p53 in aging and longevity has not been well established. As a haploinsufficient gene, p53 is under the tight regulation in cells. Attenuation of p53 function (even with only 2-fold change) contributes greatly to tumorigenesis. p53 codon 72 single nucleotide polymorphism (SNP) is a naturally occurring common SNP with a nucleotide change, which results in either an arginine (R72) or a proline (P72) at codon 72. p53 codon 72 SNPs can influence the activity of p53. The P72 allele is weaker than the R72 allele in inducing apoptosis and suppressing cellular transformation. However, it is unclear whether the change of p53 activity in humans by the functional SNP could impact longevity. A perspective cohort study with an aging human population showed that P72 allele is associated with longer survival despite its increased risk for cancer development (van Heemst et al., 2005). These findings strongly suggest that p53 activity is reversely associated with aging, and functional SNPs in the p53 pathway could impact upon the lifespan in humans. In this study, we employed a mouse model system with knock-in of the human p53 gene (Hupki) carrying either R72 or P72 SNP to investigate the impact of p53 codon 72 SNP upon longevity and its underlying mechanism. Mice with p53 P72 allele showed weaker transcriptional activity than the R72 allele toward a subset of p53 target genes, suggesting that these mice retain the function of p53 codon 72 SNP in humans. We found that although mice with p53 P72 have increased cancer risk compared to mice with p53 R72, those mice with p53 P72 who escaped tumor development have longer lifespans compared to mice with p53 R72 that do not develop tumors. Mice with p53 P72 displayed a delayed aging process compared to mice with p53 R72, including less reduced bone density, less decreased dermal thickness and better wound healing ability. We further compared the effects of p53 codon 72 SNPs on stem cell population and function as a possible mechanism that contributes to their differences in longevity. Compared to mice with p53 R72, mice with p53 P72 allele have a smaller number of long-term stem/progenitor cells and better self-renewal function during the aging process. Consistent results were observed when long-term stem cell’s ability of engraftment and repopulation was evaluated by bone marrow transplantation assay. Taken together, results from this study demonstrate that p53 codon 72 SNP has a direct impact on aging and longevity in vivo in mouse models, and strongly support the role of p53 in the regulation of stem/progenitor cells’ function and longevity. Part II: Mechanism of mutant p53 accumulation and gain-of-function (GOF) in tumors p53 is the most… Advisors/Committee Members: Feng, Zhaohui (chair), Hu, Wenwei (internal member), Carpizo, Darren (internal member), Zong, Wei-Xing (outside member), School of Graduate Studies.

Subjects/Keywords: Aging; Carcinogenesis; p53 protein

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APA (6^th Edition):

Zhao, Yuhan, 1. (2018). The role of P53 signaling pathway in aging and cancer. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/59291/

Chicago Manual of Style (16^th Edition):

Zhao, Yuhan, 1985-. “The role of P53 signaling pathway in aging and cancer.” 2018. Doctoral Dissertation, Rutgers University. Accessed April 21, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/59291/.

MLA Handbook (7^th Edition):

Zhao, Yuhan, 1985-. “The role of P53 signaling pathway in aging and cancer.” 2018. Web. 21 Apr 2021.

Vancouver:

Zhao, Yuhan 1. The role of P53 signaling pathway in aging and cancer. [Internet] [Doctoral dissertation]. Rutgers University; 2018. [cited 2021 Apr 21]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/59291/.

Council of Science Editors:

Zhao, Yuhan 1. The role of P53 signaling pathway in aging and cancer. [Doctoral Dissertation]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/59291/

University of Arizona

20. JAFFE, DEBORAH RUTH. MOUSE SKIN TUMOR INITIATION BY IONIZING RADIATION AND THE DETECTION OF DOMINANT TRANSFORMING GENE(S).

Degree: 1987, University of Arizona

URL: http://hdl.handle.net/10150/184146

► The initiating potential of a range of 4 MeV X-rays was studied using the mouse skin two-stage model of carcinogenesis. A single dose of radiation… (more)

▼ The initiating potential of a range of 4 MeV X-rays was studied using the mouse skin two-stage model of carcinogenesis. A single dose of radiation was followed by promotion with 12-O-tetradecanoyl phorbol-13-acetate (TPA). The effect of TPA on tumor incidence when applied as a single dose 24 hours prior to irradiation was examined. Studies were also designed to investigate the effect of promotion duration on tumor incidence. Animals were promoted with TPA for 10 or 60 weeks. Evidence presented here indicates that ionizing radiation can act as an initiator in this model system. All animals that were promoted with TPA for the same duration had a similar incidence of papillomas (pap) regardless of radiation or TPA pretreatment. However, squamous cell carcinomas (scc) arose only in animals that were initiated with ionizing radiation followed by TPA promotion. Increasing the promotion duration enhanced the incidence of scc at the lower initiation dose. TPA pretreatment at the higher irradiation dose resulted in an overall decrease in tumor incidence. At the lower dose of radiation, TPA pretreatment resulted in an increase in the incidence of scc. The incidence of basal cell carcinomas (bcc) was dose dependent and appeared to be independent of TPA promotion. Although ionizing radiation acts as a weak initiator in mouse skin, the conversion of pap to scc was higher than that reported for chemical initiators. To test this further animals were initiated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) followed by biweekly promotion with TPA. After 20 weeks of promotion, the animals were treated with either acetone, TPA or 8 fractions of 1 MeV electrons. Data indicate that the dose and fractionation protocol used in this study enhanced the progression of pre-existing pap. To examine the role of oncogene activation in radiation induced mouse skin tumors, DNA from various tumors (pap, bcc, scc) were examined for the presence of dominant transforming activity by the NIH3T3 and Rat-2 focus assays. Dominant transforming activity was observed in all tumor types but not in normal or treated epidermis or corresponding liver. The transformed phenotype was further confirmed by growth in soft agar and tumorigenicity in Nude mice. Southern blot hybridization to ras (Ha, Ki, N), raf, neu, erbB and β-lym indicate that these genes are not responsible for the observed transforming activity. These data suggest that the oncogenic sequences activated in these tumors are unique. The work presented here also provides evidence for novel c-myc transcripts and corresponding genomic rearrangements in a few of the tumors studied. Advisors/Committee Members: Bowden, G. Tim (committeemember), Gerner, Eugene W. (committeemember), Duffy, John J. (committeemember), Gandolfi, A. Jay (committeemember), Sipes, I. Glenn (committeemember).

Subjects/Keywords: Radiation carcinogenesis.; Ionizing radiation.; Carcinogenesis.

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APA (6^th Edition):

JAFFE, D. R. (1987). MOUSE SKIN TUMOR INITIATION BY IONIZING RADIATION AND THE DETECTION OF DOMINANT TRANSFORMING GENE(S). (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/184146

Chicago Manual of Style (16^th Edition):

JAFFE, DEBORAH RUTH. “MOUSE SKIN TUMOR INITIATION BY IONIZING RADIATION AND THE DETECTION OF DOMINANT TRANSFORMING GENE(S). ” 1987. Doctoral Dissertation, University of Arizona. Accessed April 21, 2021. http://hdl.handle.net/10150/184146.

MLA Handbook (7^th Edition):

JAFFE, DEBORAH RUTH. “MOUSE SKIN TUMOR INITIATION BY IONIZING RADIATION AND THE DETECTION OF DOMINANT TRANSFORMING GENE(S). ” 1987. Web. 21 Apr 2021.

Vancouver:

JAFFE DR. MOUSE SKIN TUMOR INITIATION BY IONIZING RADIATION AND THE DETECTION OF DOMINANT TRANSFORMING GENE(S). [Internet] [Doctoral dissertation]. University of Arizona; 1987. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/10150/184146.

Council of Science Editors:

JAFFE DR. MOUSE SKIN TUMOR INITIATION BY IONIZING RADIATION AND THE DETECTION OF DOMINANT TRANSFORMING GENE(S). [Doctoral Dissertation]. University of Arizona; 1987. Available from: http://hdl.handle.net/10150/184146

21. Batazzi, Adriana. Elucidating the role of Keratin 17 in cervical carcinogenesis.

Degree: 2014, Johns Hopkins University

URL: http://jhir.library.jhu.edu/handle/1774.2/37211

► Cervical malignancies develop when viral genes from high-risk strains of the Human Papilloma Virus (HPV) such as HPV type 16 and 18 are expressed in… (more)

▼ Cervical malignancies develop when viral genes from high-risk strains of the Human Papilloma Virus (HPV) such as HPV type 16 and 18 are expressed in the cervical epithelium. Expression of Keratin 17 (K17), an intermediate filament cytoskeletal protein that is robustly upregulated in a variety of epithelial-derived tumors, is positively correlated with the progression of cervical lesions and is considered a reliable prognostic biomarker for cervical cancer. We previously reported that the genetic loss of Krt17 attenuates skin tumorigenesis in a mouse model for spontaneous basaloid tumor formation, correlating with a modulation of T helper 1/ T helper 17 (Th1/Th17) and T helper 2 (Th2) inflammatory cytokine expression, and resulting in dampened recruitment of immune cells to the site of tumor formation. The present study aims to understand the role of K17 in cervical carcinogenesis using the HPV16tg mouse model, which spontaneously forms squamous cell carcinoma-like lesions in cervical epithelia when females are treated with estrogen. We hypothesized that onset and progression of HPV16tg-induced cervical lesions would be delayed in the absence of K17, and that K17’s immunomodulatory role extends to the cervical epithelium. Compared to wildtype controls, HPV16tg/+ mice exhibit robust hyperplasia of cervical epithelia, as well as increased cervical epithelial proliferation and vasculature 3 months after receiving an estrogen implant. All of these trademarks of cancer were found to be attenuated with the genetic loss of Krt17. Whereas several Th1 pro-inflammatory cytokines are upregulated in HPV16tg/+ cervical tissue relative to wildtype control, these are further upregulated in the Krt17 null background, a finding that is consistent with the literature on cervical carcinogenesis, but opposite to what prevails in the ear skin tumors occurring in the same mice. Collectively, these findings support the notion that K17 expression is positively correlated with the progression of tumors and extends the idea that K17 functions as an immune response modulator in both cervical and skin carcinogenesis. The observed differences in inflammatory readouts between ear and cervical epithelia suggest that K17’s impact on signaling pathways and gene expression occurs in a tissue and/or context-dependent manner.

Subjects/Keywords: Cervical Carcinogenesis; Keratin 17; Inflammatory Immune Response

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APA (6^th Edition):

Batazzi, A. (2014). Elucidating the role of Keratin 17 in cervical carcinogenesis. (Thesis). Johns Hopkins University. Retrieved from http://jhir.library.jhu.edu/handle/1774.2/37211

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):

Batazzi, Adriana. “Elucidating the role of Keratin 17 in cervical carcinogenesis.” 2014. Thesis, Johns Hopkins University. Accessed April 21, 2021. http://jhir.library.jhu.edu/handle/1774.2/37211.

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

MLA Handbook (7^th Edition):

Batazzi, Adriana. “Elucidating the role of Keratin 17 in cervical carcinogenesis.” 2014. Web. 21 Apr 2021.

Vancouver:

Batazzi A. Elucidating the role of Keratin 17 in cervical carcinogenesis. [Internet] [Thesis]. Johns Hopkins University; 2014. [cited 2021 Apr 21]. Available from: http://jhir.library.jhu.edu/handle/1774.2/37211.

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

Council of Science Editors:

Batazzi A. Elucidating the role of Keratin 17 in cervical carcinogenesis. [Thesis]. Johns Hopkins University; 2014. Available from: http://jhir.library.jhu.edu/handle/1774.2/37211

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

22. Soni, Bihari Lal. Global protein profiling during rat lingual carcinogenesis and validation of differentiator proteins in human tongue; -.

Degree: Life Science, 2015, INFLIBNET

URL: http://shodhganga.inflibnet.ac.in/handle/10603/49148

None

Bibliography p.110 - 123 Appendix p.124 - 143 and Publication P.144

Advisors/Committee Members: Vaidya, Milind M.

Subjects/Keywords: Carcinogenesis; Global; Protein

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APA (6^th Edition):

Soni, B. L. (2015). Global protein profiling during rat lingual carcinogenesis and validation of differentiator proteins in human tongue; -. (Thesis). INFLIBNET. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/49148

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):

Soni, Bihari Lal. “Global protein profiling during rat lingual carcinogenesis and validation of differentiator proteins in human tongue; -.” 2015. Thesis, INFLIBNET. Accessed April 21, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/49148.

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

MLA Handbook (7^th Edition):

Soni, Bihari Lal. “Global protein profiling during rat lingual carcinogenesis and validation of differentiator proteins in human tongue; -.” 2015. Web. 21 Apr 2021.

Vancouver:

Soni BL. Global protein profiling during rat lingual carcinogenesis and validation of differentiator proteins in human tongue; -. [Internet] [Thesis]. INFLIBNET; 2015. [cited 2021 Apr 21]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/49148.

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

Council of Science Editors:

Soni BL. Global protein profiling during rat lingual carcinogenesis and validation of differentiator proteins in human tongue; -. [Thesis]. INFLIBNET; 2015. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/49148

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

Oregon State University

23. Kelly, Jack D. Oxidative stress and carcinogenesis in trout.

Degree: PhD, Toxicology, 1992, Oregon State University

URL: http://hdl.handle.net/1957/37254

Subjects/Keywords: Carcinogenesis – Animal models

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APA (6^th Edition):

Kelly, J. D. (1992). Oxidative stress and carcinogenesis in trout. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/37254

Chicago Manual of Style (16^th Edition):

Kelly, Jack D. “Oxidative stress and carcinogenesis in trout.” 1992. Doctoral Dissertation, Oregon State University. Accessed April 21, 2021. http://hdl.handle.net/1957/37254.

MLA Handbook (7^th Edition):

Kelly, Jack D. “Oxidative stress and carcinogenesis in trout.” 1992. Web. 21 Apr 2021.

Vancouver:

Kelly JD. Oxidative stress and carcinogenesis in trout. [Internet] [Doctoral dissertation]. Oregon State University; 1992. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/1957/37254.

Council of Science Editors:

Kelly JD. Oxidative stress and carcinogenesis in trout. [Doctoral Dissertation]. Oregon State University; 1992. Available from: http://hdl.handle.net/1957/37254

UCLA

24. Davoren, Michael Joshua. Cancer Risk Reduction Through Active Management of Genotoxicity.

Degree: Molecular Toxicology, 2018, UCLA

URL: http://www.escholarship.org/uc/item/3m12828m

► Cancer is the second leading cause of death in developed countries. Despite advances in both therapies and our understanding of the carcinogenesis process itself, consistently… (more)

▼ Cancer is the second leading cause of death in developed countries. Despite advances in both therapies and our understanding of the carcinogenesis process itself, consistently effective treatments remain elusive for a large number of cancer subtypes. For this reason, the minimization of cancer risk is a high priority subject. At the moment, cancer risk management is generally characterized by abstention rather than active engagement. The importance of avoiding activities associated with carcinogenesis-inducing genotoxicity, such as smoking, is well ingrained in the public consciousness as an anticancer strategy. The development of treatments that positively reduce genotoxicity poses a novel method of protection against general cancer risk, as well as the mitigation of risk from scenarios such as inflammation-inducing infections or genotoxic radiation exposure. The first part of this thesis describes the development of a genotoxicity mitigating compound, Yel002. In yeast and mouse models, Yel002 reduced both genotoxicity and lethality resulting from radiation exposure. Administration of this compound up to 24 hours after an otherwise lethal dose of ionizing radiation reduced radiation-induced hematopoietic depletion and systemic DNA damage markers. Although issues with compound stability made it difficult to use consistently, its development establishes a pipeline for the testing and use of similar compounds.The second part of this thesis work describes the characterization of a Lactobacillus strain, L. johnsonii 456, associated with anti-inflammatory and anti-genotoxic outcomes in mice. Although originally derived from a murine host, the strain survives in both in vivo and in vitro models of the human gut, suggesting that these protective effects could be applicable to humans as well. Importantly, the strain’s ability to inhibit pathogen growth and binding to human gut monolayer cells was demonstrated experimentally. As pathogenic bacteria are a major source of inflammation in the gastrointestinal tract, future probiotic intervention with this strain could result in active intervention strategies to manage local and systemic genotoxicity. The third part of this work is a reprint of the previously published review article, Mouse models for radiation-induced cancers, included with the gracious approval of Mutagenesis. The mouse models described represent important animal models for the testing of active genotoxicity management interventions. Finally, two appendices are included to describe subtle factors that influence the carcinogenesis pathway. Appendix I is a version of the article in submission Glyphosate Based Herbicides and Cancer Risk: A Post IARC Decision Review of Potential Mechanisms, Policy, and Avenues of Research, describing the heavily debated carcinogenic potential of the pesticide glyphosate and how it might exert effects through the microbiome. Appendix II is a reprint of the article BALR-6 regulates cell growth and cell survival in B-lymphoblastic leukemia, and elucidates a novel lncRNA-based…

Subjects/Keywords: Toxicology; Microbiology; Carcinogenesis; Genotoxicity; Inflammation; Microbiome; Radiation

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APA (6^th Edition):

Davoren, M. J. (2018). Cancer Risk Reduction Through Active Management of Genotoxicity. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/3m12828m

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):

Davoren, Michael Joshua. “Cancer Risk Reduction Through Active Management of Genotoxicity.” 2018. Thesis, UCLA. Accessed April 21, 2021. http://www.escholarship.org/uc/item/3m12828m.

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

MLA Handbook (7^th Edition):

Davoren, Michael Joshua. “Cancer Risk Reduction Through Active Management of Genotoxicity.” 2018. Web. 21 Apr 2021.

Vancouver:

Davoren MJ. Cancer Risk Reduction Through Active Management of Genotoxicity. [Internet] [Thesis]. UCLA; 2018. [cited 2021 Apr 21]. Available from: http://www.escholarship.org/uc/item/3m12828m.

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

Council of Science Editors:

Davoren MJ. Cancer Risk Reduction Through Active Management of Genotoxicity. [Thesis]. UCLA; 2018. Available from: http://www.escholarship.org/uc/item/3m12828m

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

Columbia University

25. Chiu, Hua-Sheng. Aberrantly Expressed CeRNAs Account for Missing Genomic Variability of Cancer Genes via MicroRNA-Mediated Interactions.

Degree: 2014, Columbia University

URL: https://doi.org/10.7916/D8610XBW

► There is growing evidence that RNAs compete for binding and regulation by a finite pool of microRNAs (miRs), thus regulating each other through a competing… (more)

Subjects/Keywords: Carcinogenesis; Oncogenes; Bioinformatics; RNA; Biology – Classification; Genetics

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APA (6^th Edition):

Chiu, H. (2014). Aberrantly Expressed CeRNAs Account for Missing Genomic Variability of Cancer Genes via MicroRNA-Mediated Interactions. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8610XBW

Chicago Manual of Style (16^th Edition):

Chiu, Hua-Sheng. “Aberrantly Expressed CeRNAs Account for Missing Genomic Variability of Cancer Genes via MicroRNA-Mediated Interactions.” 2014. Doctoral Dissertation, Columbia University. Accessed April 21, 2021. https://doi.org/10.7916/D8610XBW.

MLA Handbook (7^th Edition):

Chiu, Hua-Sheng. “Aberrantly Expressed CeRNAs Account for Missing Genomic Variability of Cancer Genes via MicroRNA-Mediated Interactions.” 2014. Web. 21 Apr 2021.

Vancouver:

Chiu H. Aberrantly Expressed CeRNAs Account for Missing Genomic Variability of Cancer Genes via MicroRNA-Mediated Interactions. [Internet] [Doctoral dissertation]. Columbia University; 2014. [cited 2021 Apr 21]. Available from: https://doi.org/10.7916/D8610XBW.

Council of Science Editors:

Chiu H. Aberrantly Expressed CeRNAs Account for Missing Genomic Variability of Cancer Genes via MicroRNA-Mediated Interactions. [Doctoral Dissertation]. Columbia University; 2014. Available from: https://doi.org/10.7916/D8610XBW

Columbia University

26. Rajbhandari, Presha. Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma.

Degree: 2016, Columbia University

URL: https://doi.org/10.7916/D8J67H0X

► Neuroblastoma is a heterogeneous pediatric malignancy originating from the developing sympathetic nervous system, with poor long-term survival for high-risk patients (~40%). About half of advanced… (more)

▼ Neuroblastoma is a heterogeneous pediatric malignancy originating from the developing sympathetic nervous system, with poor long-term survival for high-risk patients (~40%). About half of advanced neuroblastomas harbor high-level amplification of the MYCN gene, and these tumors show few, if any, additional driver lesions. Despite significant increase in the body of knowledge of genetics in neuroblastoma, all the high-risk patients follow similar therapeutic procedures and little advancement has been made on molecular target based therapies. The major challenge is to dissect the complexity and heterogeneity of these tumors to find driver genes and activated pathways that are essential for the survival of these cancer cells. We used an integrated systems biology approach to define the core regulatory machinery responsible for maintenance of an aggressive neuroblastoma phenotypic state. In the first part of the thesis, I will discuss our computational approach to decipher the tumor heterogeneity by subtype classification, followed by identification of master regulator protein modules for three distinct molecular subtypes of high-risk neuroblastomas, which were validated in a large independent cohort of cases. We propose that such modules are responsible for integrating the effect of mutations in upstream pathways and for regulating the genetic programs and pathways necessary for tumor state implementation and maintenance. The second part of the thesis is focused on experimental validation of putative master regulators in the subtype of neuroblastomas associated with MYCN amplification. By using RNAi screening followed by experimental and computational analyses to elucidate the interdependencies between the top master regulators, we identified TEAD4-MYCN positive feedback loop as a major tumor maintenance mechanism in this subtype. While MYCN regulates TEAD4 transcriptionally, TEAD4 regulates MYCN through transcriptional and post-translational mechanisms. Jointly, MYCN and TEAD4 regulate 90% of inferred MR proteins and causally orchestrate 70% of the subtype-specific gene expression signature. TEAD4 gene expression was associated with neuroblastoma patient survival independently of age, tumor stage and MYCN status (P=2.1e-02). In cellular assays, MYCN promoted growth and repressed differentiation, while TEAD4 activated proliferation and DNA damage repair programs, the signature hallmarks of MYCN-amplified neuroblastoma cells. Specifically, TEAD4 was shown to induce MYCN-independent proliferation by transactivating key genes implicated in high-risk neuroblastoma pathogenesis, including cyclin-dependent kinases, cyclins, E2Fs, DNA replication factors, checkpoint kinases and ubiquitin ligases. The critical role of the core master regulator module in controlling tumor cell viability, both in vitro and in vivo, and its clinical relevance as a prognostic factor highlights TEAD4 as a novel and highly effective candidate target for therapeutic intervention. In this thesis, we demonstrate that interrogation of…

Subjects/Keywords: Genetic regulation; Carcinogenesis; Neuroblastoma – Genetic aspects; Oncology

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APA (6^th Edition):

Rajbhandari, P. (2016). Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8J67H0X

Chicago Manual of Style (16^th Edition):

Rajbhandari, Presha. “Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma.” 2016. Doctoral Dissertation, Columbia University. Accessed April 21, 2021. https://doi.org/10.7916/D8J67H0X.

MLA Handbook (7^th Edition):

Rajbhandari, Presha. “Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma.” 2016. Web. 21 Apr 2021.

Vancouver:

Rajbhandari P. Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma. [Internet] [Doctoral dissertation]. Columbia University; 2016. [cited 2021 Apr 21]. Available from: https://doi.org/10.7916/D8J67H0X.

Council of Science Editors:

Rajbhandari P. Systematic elucidation of transcriptional network necessary for initiation and maintenance of high-risk neuroblastoma. [Doctoral Dissertation]. Columbia University; 2016. Available from: https://doi.org/10.7916/D8J67H0X

Boston University

27. Nathan, Ajay Sridhar. Using microRNAs (miRNAs) as therapeutic agents in cancer: targeting the link between the downregulation of miRNAs and oncogenesis.

Degree: MS, Medical Sciences, 2018, Boston University

URL: http://hdl.handle.net/2144/33018

► With the worldwide prevalence of cancer, this disease has constituted a major public health problem for many years without great success in the development of… (more)

▼ With the worldwide prevalence of cancer, this disease has constituted a major public health problem for many years without great success in the development of treatment. This is due in part to the large genetic heterogeneity that exists, even between cancers of the same class. The current standard of care focuses on targeting shared elements such as rapid cell division, yet treatments like chemotherapy have tremendous cytotoxic and off-target adverse effects. Recently, a different link has been discovered that is shared by cancers of diverse types: the disruption in the regulation and expression of microRNAs (miRNAs). miRNAs, produced endogenously from discrete genes that exist for them, have been shown to be master regulators of diverse processes, including growth and division. They serve to downregulate or silence the expression of certain genes at the post-transcriptional level, with each miRNA regulating multiple target messenger RNAs. This provides an important therapeutic potential because the correction in the expression of any one miRNA, especially if it has tumor-suppressive functions, has the ability to inhibit cancer formation, growth, and metastasis by multiple related pathways. The mechanisms by which the expression of miRNA is altered in cancer are reciprocal; that is, the processes that lead to oncogenesis alter the production of miRNA and altered production of miRNA can lead to increased tumorigenicity. In particular, it has been found that miRNA is globally downregulated in most cancers. The downregulation of miRNA can arise incidentally because of chromosomal abnormalities that occur with cancer, or miRNA can be directly repressed through transcriptional control, epigenetic modification, or disruption in the biogenic production process. When miRNAs are downregulated, the condition can contribute to the main hallmarks of cancer: uncontrolled growth, angiogenesis, metastasis, and evasion of anti-growth and apoptotic signals. A therapeutic strategy that has been investigated in numerous preclinical studies is miRNA replacement therapy, and this treatment has been shown to be extremely efficacious with a wide range of candidates and targets in diverse cancer systems. However, these advances have only led to two clinical trials, partly because of the lack of efficacious delivery methods. Nevertheless, with the rapid advances being made in gene therapy to address these shortcomings, a translation of these benefits from the bench-to-bedside is almost certain. Advisors/Committee Members: Spencer, Jean L. (advisor), Offner, Gwynneth D. (advisor).

Subjects/Keywords: Oncology; miRNA; Cancer; Carcinogenesis; Mechanism; Oncogenesis; Therapy

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APA (6^th Edition):

Nathan, A. S. (2018). Using microRNAs (miRNAs) as therapeutic agents in cancer: targeting the link between the downregulation of miRNAs and oncogenesis. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/33018

Chicago Manual of Style (16^th Edition):

Nathan, Ajay Sridhar. “Using microRNAs (miRNAs) as therapeutic agents in cancer: targeting the link between the downregulation of miRNAs and oncogenesis.” 2018. Masters Thesis, Boston University. Accessed April 21, 2021. http://hdl.handle.net/2144/33018.

MLA Handbook (7^th Edition):

Nathan, Ajay Sridhar. “Using microRNAs (miRNAs) as therapeutic agents in cancer: targeting the link between the downregulation of miRNAs and oncogenesis.” 2018. Web. 21 Apr 2021.

Vancouver:

Nathan AS. Using microRNAs (miRNAs) as therapeutic agents in cancer: targeting the link between the downregulation of miRNAs and oncogenesis. [Internet] [Masters thesis]. Boston University; 2018. [cited 2021 Apr 21]. Available from: http://hdl.handle.net/2144/33018.

Council of Science Editors:

Nathan AS. Using microRNAs (miRNAs) as therapeutic agents in cancer: targeting the link between the downregulation of miRNAs and oncogenesis. [Masters Thesis]. Boston University; 2018. Available from: http://hdl.handle.net/2144/33018

University of Surrey

28. Marczylo, Timothy Hywel. Bioactivation of aromatic amines.

Degree: PhD, 1996, University of Surrey

URL: http://epubs.surrey.ac.uk/855902/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336523

► The bioactivation of arylamines was investigated in hepatic microsomal and cytosolic fractions. The bioactivation of 6-aminochrysene to mutagenic intermediates in the Ames test was demonstrated… (more)

▼ The bioactivation of arylamines was investigated in hepatic microsomal and cytosolic fractions. The bioactivation of 6-aminochrysene to mutagenic intermediates in the Ames test was demonstrated for the first time in cytosol from Aroclor 1254-induced rat. Substantial evidence was obtained to demonstrate that this activity was not a consequence of microsomal contamination, including the inhibition of cytosol-mediated bioactivation by the addition of microsomal protein. Investigation of substrate specificity demonstrated that the cytosolic activation of promutagens requires an exocyclic amino group and consequently bioactivation probably involves N-hydroxylation. Extrahepatic cytosol cannot bioactivate either 6AC or 2AA to mutagens and therefore the major site for this activity is the liver. No constitutive hepatic bioactivating activity was demonstrated by rat, mouse, hamster, ferret or pig hepatic cytosol but, moderate bioactivation of 2-aminoanthracene was carried out by human hepatic cytosol. The cytosolic protein responsible for the bioactivation of arylamines was only induced by polychlorinated biphenyls and the best induction was accomplished by highly-substituted planar PCB congeners. However, Aroclor 1254 could not induce cytosol-mediated bioactivation of arylamines in Ah receptor non-responsive (DBA2) mice. Therefore induction of this enzyme system requires the cytosolic Ah receptor Purification of the cytosolic amine oxidase was undertaken with partial success and a protein with an approximate molecular weight of approximately 65. 5kDa was identified as the most likely candidate for the cytosolic enzyme. Microsomes isolated from Aroclor 1254-treated rat could bioactivate arylamines to mutagens in the presence of either NADH or NADPH. In these investigations NADH-dependent bioactivation of IQ and 6-aminochrysene was demonstrated for the first time. Investigation of arylamine bioactivation in the presence of these two cofactors demonstrated sufficient differences to suggest these activities are carried out by different microsomal enzymes. However, both NADPH- and NADH-dependent bioactivation probably involves N-hydroxylation. Two microsomal enzyme systems which may perform this metabolism are the cytochromes P450 and the flavin-monooxygenases. However, the complete oxidation of xenobiotics by cytochrome P450 in the presence of NADH had not been demonstrated previously. In these investigations the cytochrome P450-dependent dealkylation of ethoxy- and methoxy-resorafin were performed in the presence of NADH by Aroclor 1254-induced microsomes. However, there is insufficient evidence to determine whether a cytochrome P450 isoform is responsible for the bioactivation of arylamine but like CYP1 isoforms induction of the microsoe enzyme was regulated by the cytosolic Ah receptor.

Subjects/Keywords: 615.9; Chemical carcinogenesis

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

APA (6^th Edition):

Marczylo, T. H. (1996). Bioactivation of aromatic amines. (Doctoral Dissertation). University of Surrey. Retrieved from http://epubs.surrey.ac.uk/855902/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336523

Chicago Manual of Style (16^th Edition):

Marczylo, Timothy Hywel. “Bioactivation of aromatic amines.” 1996. Doctoral Dissertation, University of Surrey. Accessed April 21, 2021. http://epubs.surrey.ac.uk/855902/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336523.

MLA Handbook (7^th Edition):

Marczylo, Timothy Hywel. “Bioactivation of aromatic amines.” 1996. Web. 21 Apr 2021.

Vancouver:

Marczylo TH. Bioactivation of aromatic amines. [Internet] [Doctoral dissertation]. University of Surrey; 1996. [cited 2021 Apr 21]. Available from: http://epubs.surrey.ac.uk/855902/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336523.

Council of Science Editors:

Marczylo TH. Bioactivation of aromatic amines. [Doctoral Dissertation]. University of Surrey; 1996. Available from: http://epubs.surrey.ac.uk/855902/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336523

University of Glasgow

29. Kerr, Peter Joseph. A study of skin homeostasis and skin tumorigenesis using transgenic mice.

Degree: PhD, 2000, University of Glasgow

URL: http://theses.gla.ac.uk/72204/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366197

► The ability to engineer mice which carry exogenous genes targeted for expression in specific tissues, or have an endogenous gene functionally switched off has allowed… (more)

▼ The ability to engineer mice which carry exogenous genes targeted for expression in specific tissues, or have an endogenous gene functionally switched off has allowed us to examine the role of particular proteins in an in vivo model. This technology, in combination with a well-characterised model of chemically-induced skin carcinogenesis in the mouse, has allowed us to start dissecting the changes that occur during a particular pathway of tumorigenesis. TGFbeta1 has been shown to act as an inhibitor of both normal cellular proliferation and tumour formation. However, it can also accelerate malignant conversion at later stages of carcinogenesis. Previously in this laboratory, mice were generated that overexpressed Tgfbetal in suprabasal layers of skin epidermis under the control of a K10 promoter. These transgenic mice showed an increased proliferation rate in the basal compartment of their epidermis compared to wild-type controls. In this study, it is shown that the change in proliferative index is not dependent on p53, a molecule central to growth control and apoptosis. The K10-Tgfbeta1 mice were crossed on to a Tgfbeta1-null background and the proliferative phenotype of the transgene was examined. An increased basal cell proliferative index was observed whether the background was Tgfbeta1-null or wild-type. TGFbeta1 has been shown to induce apoptosis and a line of transgenic mice overexpressing BCL-2 in the epidermis became available, providing an opportunity to investigate the role of an apoptotic pathway in the skin. These K10-BCL-2 mice were shown to express the transgene at both mRNA and protein levels in suprabasal cells of the epidermis. Normal skin homeostasis, however, was not disrupted by the exogenous BCL-2 and expression of other apoptotic markers was not altered in these mice. Purthermore, K10-5CL-2 mice responded to chemical insult by a skin tumour promoter in the same way as wild-type littermates. K10-Tgfbeta1 mice had demonstrated resistance to papilloma formation during chemical carcinogenesis and tumours on the transgenic mice had also shown a higher rate of malignant conversion in the same experiment. In this study, the effects of epidermally-targeted Tgfbeta1 during tumorigenesis were investigated further by crossing the K10-Tgfbeta1 mice to a tumour-developing K5-RAS transgenic line. Mice carrying both the K5-RAS and K10-Tgfbeta1 transgenes showed no difference in tumour formation compared to those harbouring just the K5-RAS transgene.

Subjects/Keywords: 610; Carcinogenesis; Cancer

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

APA (6^th Edition):

Kerr, P. J. (2000). A study of skin homeostasis and skin tumorigenesis using transgenic mice. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/72204/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366197

Chicago Manual of Style (16^th Edition):

Kerr, Peter Joseph. “A study of skin homeostasis and skin tumorigenesis using transgenic mice.” 2000. Doctoral Dissertation, University of Glasgow. Accessed April 21, 2021. http://theses.gla.ac.uk/72204/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366197.

MLA Handbook (7^th Edition):

Kerr, Peter Joseph. “A study of skin homeostasis and skin tumorigenesis using transgenic mice.” 2000. Web. 21 Apr 2021.

Vancouver:

Kerr PJ. A study of skin homeostasis and skin tumorigenesis using transgenic mice. [Internet] [Doctoral dissertation]. University of Glasgow; 2000. [cited 2021 Apr 21]. Available from: http://theses.gla.ac.uk/72204/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366197.

Council of Science Editors:

Kerr PJ. A study of skin homeostasis and skin tumorigenesis using transgenic mice. [Doctoral Dissertation]. University of Glasgow; 2000. Available from: http://theses.gla.ac.uk/72204/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366197

University of Glasgow

30. Cairney, Margaret. The transformation biology of bovine papillomavirus type 4 in established and primary cells.

Degree: PhD, 1996, University of Glasgow

URL: http://theses.gla.ac.uk/75491/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297054

► Bovine papillomavirus type 4 (BPV-4) induces papillomas in the upper alimentary canal of cattle which can progress to carcinomas in animals feeding on bracken fern.… (more)

▼ Bovine papillomavirus type 4 (BPV-4) induces papillomas in the upper alimentary canal of cattle which can progress to carcinomas in animals feeding on bracken fern. Viral DNA is rarely detected in either naturally occurring or experimentally induced cancers. Similarly, BPV-4 DNA is seldom found in in vitro transformed established cells. These results suggest that presence of BPV-4 is not required for progression to or maintenance of the transformed state. The frequency with which BPV-4 DNA is lost both in vivo and in vitro also suggests that there may be active selection against whole or part of the BPV-4 genome. Several BPV-4-transfected established lines were analysed to examine whether this proposed negative selection was observable at the DNA level. In common with previous in vitro studies, BPV-4 DNA was found to be progressively lost on continued sub-culture. Analysis of cell lines containing BPV-4 DNA showed that there was no overt mutation or rearrangement of viral DNA sequences. The apparent wildtype organisation of viral genes included the E8 open reading frame (ORF). It was originally hypothesised that this viral ORF, which is the second major transforming gene of BPV-4, was an attractive target for negative selection due to the detrimental effect observed on transfecting primary cells with BPV-4 E8 DNA. Previous work also reported amplification and rearrangement of specific host sequences in BPV-4-transformed lines. It was therefore proposed that induction of cellular DNA amplification may be an important aspect of BPV-4 transformation activity. This was investigated in virally-transformed established cells. No BPV-4-mediated DNA amplification was apparent in any of the lines, although involvement of cellular regions of repetitive sequences in manifestation of such amplification may be indicated. The co-factors involved in BPV-4-associated carcinogenesis have been identified as including the mutagens, carcinogens and immunosuppressants present in bracken fern. One of major mutagens present is the flavonoid quercetin. Quercetin has discernible effect on BPV-4 transformation in vitro as it synergises with the virus to fully transform primary bovine fibroblasts (PalF cells). The work described in this thesis confirmed these initial results and extended these findings. Quercetin-treated cells showed a more aggressive transformed morphology than untreated transfectants, whether they had been transfected with whole genome BPV-4 or sub-genomic fragments. However, whereas in non-treated cells the E8 gene was required for anchorage independence, quercetin-treated cells containing the BPV-4 E7 gene alone were found to be capable of anchorage-independent growth. Conversely, and contrary to expectation, quercetin- treated cells transfected with the E8/E7 genes grew very poorly or not at all in semi-solid media. The reasons for the antagonistic action of E8 and quercetin are not yet understood. Independent of quercetin action, results also provided circumstantial evidence that the E8 oncoprotein is responsible for…

Subjects/Keywords: 636.089; Carcinogenesis; Cancer

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

APA (6^th Edition):

Cairney, M. (1996). The transformation biology of bovine papillomavirus type 4 in established and primary cells. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/75491/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297054

Chicago Manual of Style (16^th Edition):

Cairney, Margaret. “The transformation biology of bovine papillomavirus type 4 in established and primary cells.” 1996. Doctoral Dissertation, University of Glasgow. Accessed April 21, 2021. http://theses.gla.ac.uk/75491/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297054.

MLA Handbook (7^th Edition):

Cairney, Margaret. “The transformation biology of bovine papillomavirus type 4 in established and primary cells.” 1996. Web. 21 Apr 2021.

Vancouver:

Cairney M. The transformation biology of bovine papillomavirus type 4 in established and primary cells. [Internet] [Doctoral dissertation]. University of Glasgow; 1996. [cited 2021 Apr 21]. Available from: http://theses.gla.ac.uk/75491/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297054.

Council of Science Editors:

Cairney M. The transformation biology of bovine papillomavirus type 4 in established and primary cells. [Doctoral Dissertation]. University of Glasgow; 1996. Available from: http://theses.gla.ac.uk/75491/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297054

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