Comprehensive Profiling of EGFR/HER Receptors for Personalized Treatment of Gynecologic Cancers

Abstract

The primary gynecologic cancers include cancers of the endometrium, ovary, and cervix. Worldwide, cervical cancer is the most common gynecologic cancer, whereas endometrial cancer is the most common in the US. Ovarian cancer is the fifth most deadly cancer in women, with 5-year survival rates for advanced disease at only 27%. As such, there is an urgent need for reliable screening tools and novel targeted therapeutic regimens for these malignancies. The EGFR/HER family of receptors has been associated with the development and progression of many solid tumors. Despite clear roles for these receptors in other cancers, the expression of HER family members in gynecologic cancers and their relationship with disease stage, grade, and response to treatment remain controversial. In this review, we describe the existing evidence for the use of HER family members as diagnostic and prognostic indicators as well as their potential as therapeutic targets in gynecologic cancers.

Differential expression of egfr-1, mmp-3, and mmp-9 in spontaneous abortions, induced abortions, and tubal pregnancies

“…Wright et al found that the expression of α 1 and α 6 -adhesion molecules which are essential for invasion or interaction with the extracellular matrix were decreased in the extravillous trophoblastic cell line by blocking epidermal growth factor receptor (EGFR/HER1) activation (21). In contrast, EGFR is overexpressed in approximately 50% of endometrial tumors and is significantly associated with decreased survival in patients with Type II endometrial cancer (22,23).…”

Expression and clinical role of chemoresponse-associated genes in ovarian serous carcinoma

“…Epidermal growth factor receptor (EGFR) has been extensively studied in OC, but its prognostic role and its relevance as therapeutic target remain controversial [32].…”

EGFR (Epidermal Growth Factor Receptor)

“…Endometrial cancer: Samples taken from 28 woman with endometrial cancer showed three different mutations in separate patients. L688F and E690K were in exon 18 and K754E in exon 19, which is in contrast to others responsive to lapatinib treatment (Leslie et al, 2013;Reyes et al, 2014) Colorectal cancer: EGFR mutation status of 13 patients among 35 male and 23 female patients at different stages of colorectal cancer showed exon 20 mutation but not exons 18,19 and 21 mutations (Oh et al, 2011). S492R EGFR ectodomain mutation also increases the mutation rate and mABCH12 was suggested to prevent the effect of mutated EGFR (Dong et al, 2019).…”