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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Estrogen contributes to the onset, persistence, and malignant progression of cervical cancer in a human papillomavirus-transgenic mouse model
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Estrogen contributes to the onset, persistence, and malignant progression of cervical cancer in a human papillomavirus-transgenic mouse model

机译：在人乳头瘤病毒转基因小鼠模型中，雌激素有助于宫颈癌的发作，持续和恶性进展

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摘要

Cervical cancer is a leading cause of death by cancer among women worldwide. High-risk human papillomaviruses (HPVs) are the major etiological agents for cervical cancer, but other factors likely contribute to cervical cancer, because these cancers commonly arise decades after initial exposure to HPV. Estrogen is thought to be one such cofactor; however, its temporal requirements in human cervical cancer are not known. Here we evaluate the temporal requirements of estrogen in cervical carcinogenesis in a mouse model for HPV-associated cervical cancer. Tumors arising in HPV16 transgenic mice treated with estrogen for 9 months were greatly increased in their size compared with tumors developing after 6 months of estrogen treatment. HPV16 transgenic mice treated 6 months with estrogen followed by 3 months without exogenous estrogen had significantly fewer tumors and the tumors were smaller and less aggressive than those arising in mice treated the full 9 months. Importantly, cervical cancers that arose in the mice treated the first 6 of 9 months with estrogen must have regressed, based upon the reduced incidence of cancers in these mice compared with those treated for 6 months with estrogen, then immediately analyzed. We conclude that estrogen plays a critical role not only in the genesis of cervical cancer but also in its persistence and continued development in this mouse model. These findings raise the clinically relevant possibility that, if human cervical cancer has a similar dependence on estrogen for continued tumor growth, then antiestrogen therapy may be effective in the treatment of cervical cancer.
机译：宫颈癌是全世界女性死于癌症的主要原因。高危型人乳头瘤病毒（HPV）是宫颈癌的主要病因，但其他因素也可能导致宫颈癌，因为这些癌症通常是在初次接触HPV后数十年发生的。雌激素被认为是这样一种辅助因子。然而，其在人类宫颈癌中的时间要求尚不清楚。在这里，我们评估在HPV相关宫颈癌的小鼠模型中宫颈癌发生过程中雌激素的时间需求。与用雌激素治疗6个月后发展成的肿瘤相比，用雌激素治疗9个月的HPV16转基因小鼠中产生的肿瘤的大小大大增加。与在整整9个月中治疗的小鼠相比，用雌激素治疗6个月，然后在没有外源雌激素的情况下进行3个月治疗的HPV16转基因小鼠的肿瘤明显更少，并且肿瘤更小且侵袭性更小。重要的是，与使用雌激素治疗6个月的小鼠相比，用雌激素治疗9个月的前6个月的小鼠患上宫颈癌的几率要低，因此必须逆转宫颈癌。我们得出的结论是，雌激素不仅在子宫颈癌的发生中起着关键作用，而且在其持久性和在该小鼠模型中的持续发展中也起着至关重要的作用。这些发现增加了临床相关的可能性，即如果人类子宫颈癌对雌激素具有相似的持续肿瘤生长依赖性，那么抗雌激素疗法可能有效治疗子宫颈癌。

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