In the United States, over 50,000 women get diagnosed with endometrial cancer every year, making it one of the most prevalent gynecologic cancers in the country. Despite the fact that a significant number of these women with low-grade tumors go through surgical procedures and receive adjuvant radiotherapy which cures them, the disease does make a reappearance in a considerable number of women who are unable to survive it. 

The requirement for new treatments that target molecular alterations explicit to high-grade uterine cancers is emphasized by over 8,000 yearly deaths from endometrial cancer. The HER2 (ERBB2) gene is heightened 17%-33% of uterine serous carcinoma, carcinosarcoma, and a subgroup of high-grade endometrioid endometrial tumors according to various corresponding scientific investigations. Due to this, anti-HER2-targeted therapies like lapatinib and trastuzumab were taken by women diagnosed with breast cancer. As opposed to breast cancer, treatment with trastuzumab alone uncovered no reactions in women with repetitive HER2 overexpressing endometrial disease which implies that these cancers might have obtained or natural mechanisms that are resistant to trastuzumab. This article investigates the literature encompassing HER2 in endometrial malignant growth, zeroing in on trastuzumab and other anti-HER2 therapy and resistance procedures distinguished in breast cancer yet relevant to endometrial cancers. 


A combination of treatments that target both HER2 and key oncogenic escape pathways in endometrial disease might be encouraged after getting a clear understanding of resistance pathways.