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Tartu University

1. Balikova, Anna. Studies on the functions of tumor-associated mucin-like leukosialin (CD43) in human cancer cells .

Degree: 2012, Tartu University

Kasvajates on rakud kaotanud kontrolli jagunemise üle, paljunedes valel ajal ja vales kohas sõltumata välistest signaalidest. Kasvajarakkude piiramatu jagunemine on tingitud kasvu ja ellujäämist soodustavate valkude ehk onkovalkude aktivatsioonist ning samaaegsest rakusurma reguleerivate valkude ehk tuumorsupressorite inaktivatsioonist. Kasvajaseoseliste valkude hulk kasvab pidevalt, kuid normaalse raku transformeerumine kasvajarakuks toimub tänu muutustele peamistes signaaliülekande radades, mis vastutavad raku surma ja kasvu eest. Seega on kasvajaseoseliste valkude identifitseerimine ja nende funktsioonide uurimine keskse tähtsusega vähivastaste ravistrateegiate väljatöötamisel. Käesolevas töös uuriti potentsiaalse onkovalgu leukosialiini (CD43) funktsioone inimese kasvajarakkudes. CD43 peeti pikka aega ainult vererakkudele omaseks pinnamolekuliks, kuid järjest enam vihjeid koguneb selle kohta, et CD43 võiks käituda soodustava faktorina mitte-verepäritolu kasvajate tekkes. Mitmed tööd on kirjeldanud kõrget CD43 taset erinevates kasvajarakuliinides ja -kudedes, sealhulgas käärsoolekasvajates. Samas ei ole CD43 leitud normaalsetest soolerakkudest. Samuti on näidatud CD43 seost erinevate signaaliradade komponentidega, mis rakkude elulemust või paljunemist mõjutavad. Antud töö tulemused viitavad, et koostöös tuntud onkovalgu β-kateniiniga soodustab CD43 rakkude ellujäämist ja kasvu. Paljude kasvajate üheks peamiseks tekkepõhjuseks on häired β-kateniini funktsioneerimises, mille tulemusena käivitab β-kateniin rakkude jagunemist stimuleerivate geenide avaldumist. Rakkudes, kus tuumorsupressorite rada on rikutud, võib suurenenud CD43 hulk β-kateniini signaaliraja kaudu viia rakkude kontrollimatu paljunemiseni, mis on aluseks kasvaja moodustumisele. Samas, CD43 ja β-kateniinist lähtuvad liigsed kasvusignaalid kutsuvad rakus esile surmaprotsessi, mis on peamine mehhanism kasvaja tekke takistamisel. Lisaks sellele vähendavad tuumorsupressorid omakorda CD43 hulka rakus. Kokkuvõttes näitavad töö tulemused uusimaid aspekte seoses CD43 võimega rakukasvu soodustada ning seeläbi kasvajat tekitada, ning varem kirjeldamata tagasisidet CD43 ja tuumorsupressorite talitluse vahel, mis võiks olla olulise tähtsusega kasvajate tekke vältimisel.

Subjects/Keywords: Cancer is a complex disease where cells proliferate uncontrollably and spread into different parts of the body. Unlimited division of cancer cells occurs due to activation of proteins that promote cell growth, i.e. oncoproteins, and simultaneous inactivation of proteins that regulate cell death, i.e. tumorsuppressors. Although the number of ascertained cancer-associated proteins continues to grow rapidly, the transformation of a normal cell into a tumor cell depends on changes in several key signaling pathways that regulate cell proliferation and death. Identification of tumor-associated proteins and studying their function might be applied to the elaboration of novel therapeutic strategies. In this work the functions of a potential oncoprotein leukosialin (CD43) were studied in human cancer cells. CD43 has long been regarded as a molecule present exclusively on the surface of blood cells. However, there is a growing body of evidence suggesting that CD43 might play a role in tumor development. Several studies demonstrate high level of CD43 in human solid tumor cells, including colorectal tumors, but it was not detectable in normal colon cells. Moreover, CD43 has been shown to interact with proteins that influence cell survival or proliferation. The results of the present research imply that CD43 in cooperation with the well known oncoprotein β-catenin facilitates cell growth and survival. It is believed that disorders in the functioning of β-catenin frequently lead to the formation of various types of cancer, especially colorectal cancers, since deregulated β-catenin triggers production of proteins that stimulate cell division. In cells with impaired tumorsuppressors, the increased amount of CD43, via β-catenin signaling, might cause uncontrollable proliferation of cells and initiate a tumor. However, excessive growth signals emanating from CD43 and β-catenin actuate the process of cell death, which is the main protective mechanism against tumors. Furthermore, the tumorsuppressors, in turn, decrease the level of CD43 protein. In summary, this work presents new aspects on the ability of CD43 to enhance cell growth and thereby promote tumor formation. Also, a previously undescribed negative feedback loop is proposed between CD43 and tumorsuppressors that might be important in preventing the disease.; tumor cells growth; tumor markers; molecular aspects; proteins; kasvajarakkude kasv; valgud; kasvaja markerid; molekulaaraspektid

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

APA (6th Edition):

Balikova, A. (2012). Studies on the functions of tumor-associated mucin-like leukosialin (CD43) in human cancer cells . (Thesis). Tartu University. Retrieved from http://hdl.handle.net/10062/25631

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

Chicago Manual of Style (16th Edition):

Balikova, Anna. “Studies on the functions of tumor-associated mucin-like leukosialin (CD43) in human cancer cells .” 2012. Thesis, Tartu University. Accessed September 19, 2019. http://hdl.handle.net/10062/25631.

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

MLA Handbook (7th Edition):

Balikova, Anna. “Studies on the functions of tumor-associated mucin-like leukosialin (CD43) in human cancer cells .” 2012. Web. 19 Sep 2019.

Vancouver:

Balikova A. Studies on the functions of tumor-associated mucin-like leukosialin (CD43) in human cancer cells . [Internet] [Thesis]. Tartu University; 2012. [cited 2019 Sep 19]. Available from: http://hdl.handle.net/10062/25631.

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

Council of Science Editors:

Balikova A. Studies on the functions of tumor-associated mucin-like leukosialin (CD43) in human cancer cells . [Thesis]. Tartu University; 2012. Available from: http://hdl.handle.net/10062/25631

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

.