Managing menopausal symptoms after gynecological cancer

Obstetricians & Gynecologists, Family Physicians Learning Objectives: After participating in this activity, physicians should be better able to select appropriate candidates with endometrial cancer for fertility-sparing treatment. Educate patients with endometrial cancer regarding the risks and benefits of standard of care therapy and conservative therapy and screen appropriate patients for Lynch syndrome.

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“…24 Hormone replacement can be considered after weighing the potential and proven benefits with the theoretical risk of increased recurrence. 102 …”

Section: Discussionmentioning

confidence: 97%

Fertility-Sparing Management of Endometrial Adenocarcinoma

Dorais

Dodson

Calvert

et al. 2011

Obstetrical &Amp; Gynecological Survey

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“…(44) One small prospective clinical trial of ERT administered to ovarian cancer patients suggested that ERT was associated with prolonged survival. However, the study failed to stratify the patients by tumor ER expression either at enrollment or at time of recurrence.…”

Section: Discussionmentioning

confidence: 99%

Tissue-Specific Pathways for Estrogen Regulation of Ovarian Cancer Growth and Metastasis

et al. 2010

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Menopausal estrogen (E2) replacement therapy increases the risk of estrogen receptor (ER)-positive epithelial ovarian cancers (EOC). Whether E2 is tumorigenic or promotes expansion of undiagnosed pre-existing disease is unknown. To determine E2 effects on tumor promotion, we developed an intraperitoneal mouse xenograft model using ZsGreen fluorescent ER− 2008 and ER+ PEO4 human EOC cells. Tumor growth was quantified by in vivo fluorescent imaging. In ER+ tumors, E2 significantly increased size, induced progesterone receptors, and promoted lymph node metastasis, confirming that ER are functional and foster aggressiveness. Laser captured human EOC cells from ER− and ER+ xenografted tumors were profiled for expression of E2-regulated genes. Three classes of E-regulated EOC genes were defined, but less than 10% were shared with E-regulated breast cancer genes. Since breast cancer selective ER modulators (SERMs) are therapeutically ineffective in EOC, we suggest that our EOC-specific E-regulated genes can assist pharmacologic discovery of ovarian targeted SERM.

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“…Водночас тривалий прийом КОК підвищує ризик розвитку раку шийки матки. Результа-ти новітніх експериментальних досліджень демонструють участь естрогенів у розвитку даного виду раку [76].…”

Section: менеджмент менопаузи в жінок із онкологічною патологіею в анunclassified