Recurrence of cervical cancer and its resistance to progestin therapy in a mouse model

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dc.contributor.authorMehta, Fabiola F.
dc.contributor.authorBaik, Seunghan
dc.contributor.authorChung, Sang-Hyuk
dc.date.accessioned2020-03-10T17:12:00Z
dc.date.available2020-03-10T17:12:00Z
dc.date.issued11/29/2016
dc.description.abstractStudies using K14E6/K14E7 transgenic mice expressing E6 and E7 oncoprotein of human papillomavirus type 16 (HPV16) have demonstrated that estrogen (E2) is required for the genesis and growth of cervical cancer. Our prior study using the same mouse model has showed that progestin drug medroxyprogesterone acetate (MPA) promotes regression of primary cervical cancer. In the present study, we use the same transgenic mouse model to determine whether the cancer recurs after MPA therapy. Cervical cancer recurred even if MPA treatment was continued. Unlike primary cervical cancer, the cancer recurred even in the absence of exogenous E2 when MPA treatment was ceased. Furthermore, recurrent cervical cancer did not fully regress upon MPA treatment. Our results support that MPA fails to completely eliminate primary cervical cancer cells and that remaining cancer cells grow independent of exogenous E2 and are refractory to MPA
dc.identifier.citationCopyright 2016 Oncotarget. Recommended citation: Mehta, F. F., S. Baik, and S. H. Chung. "Recurrence of cervical cancer and its resistance to progestin therapy in a mouse model." Oncotarget 8, no. 2 (2017): 2372-2380. DOI: https://doi.org/10.18632/oncotarget.13676. URL: http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=13676&path[]=43462. Reproduced in accordance with the original publisher’s licensing terms and with permission from the author(s).
dc.identifier.urihttps://hdl.handle.net/10657/5924
dc.language.isoen_US
dc.publisherOncotarget
dc.subjectcervical cancer
dc.subjecthuman papillomavirus
dc.subjectHPV
dc.subjectrecurrence
dc.subjecttherapy resistance
dc.subjectmedroxyprogesterone acetate (MPA)
dc.titleRecurrence of cervical cancer and its resistance to progestin therapy in a mouse model
dc.typeArticle

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