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Endometrial Cancer

Endometrial cancer, a tumor originating in the endometrium, is the most common gynaecological tumor in developed countries, and its prevalence is increasing. As the disease is frequently symptomatic at an early stage, endometrial cancer is often diagnosed at stage I. Historically, standard treatment consisted of hysterectomy, bilateral salpingo-oophorectomy, and pelvic lymph node dissection followed by adjuvant therapy tailored based on final histology. Management of endometrial cancer has become more complex during the past 5–10 years for several reasons: changes in histological classification that affect surgical management, adjuvant therapies, and prognosis; changes in the indications and modalities of lymphadenectomy; de-escalation of adjuvant therapy based on data from randomised trials; and discrepancies between the various classifications used to characterize recurrence risk factors.

Clinical, pathologic, and molecular data show that endometrial cancer may be broadly categorized into 2 subgroups. "Type I" carcinomas, or endometrioid endometrial cancers, account for 70% to 80% of endometrial cancers. The majority are low grade, are of endometrioid histology, are commonly driven by excessive estrogen, and are characterized by PTEN loss and mutations in PIK3CA, KRAS, and β-catenin, along with microsatellite instability. Diagnosed early, the prognosis for type I endometrial cancer is favorable, with 5-year survival rates of more than 97% and more than 80% in stage I and stage II, respectively. "Type II" carcinomas, or nonendometrioid endometrial cancers, account for 10% to 20% of endometrial cancers. They are most commonly of serous and clear-cell morphology, are estrogen independent, and are often characterized by genetic alteration in p16, p53, HER2/neu, and E-cadherin. Type II endometrial cancers usually have a poorer prognosis than type I endometrial cancers, and, although less common, account for 44% of endometrial cancer-related deaths.

There is evidence to demonstrate that the most frequently altered molecular pathway in type I endometrial carcinomas is the PI3K/PTEN/AKT pathway, which is dysregulated by oncogenic mutations, PTEN loss of function, and/or overexpression of upstream tyrosine kinase growth factor receptors, leading to uncontrolled cell proliferation and survival. On the other hand, the main pathway alterations in type II endometrial cancers involve the tumor suppressors p53 and/or p16, which cause cell cycle dysregulation and genetic instability. Other features frequently observed in type II cancer are loss of E‑cadherin expression, and the amplification and overexpression of HER2.

In the PI3K/PTEN/AKT pathway, most of the mutations of the catalytic subunit of PI3K, PIK3CA, occur in exon 9 (helical domain) or exon 20 (kinase domain). The type of PIK3CA mutations in endometrial cancers seems to differ according to histological grade; in high-grade endometrioid cancers 67%, of the mutations occur in exon 20 compared with 33% in the low-grade form. Moreover, exon 9 mutations have not been reported in type II cancers, whereas exon 20 mutations have been reported in 21% of type II cases. Amplification of the chromosomal region harboring PIK3CA (3q26) has been reported in 2-14% of type I and in 46% of type II endometrial cancers. PTEN loss of function is the most common genetic alteration in type I endometrial cancers. AKT mutations are very rare in type I and absent in type II, whereas amplification of AKT has yet to be reported.

Currently, increasingly detailed data on the molecular alterations underlying endometrial cancer have been generated and targeted therapies are progressively emerging. Several biological compounds have been moved into phase I and II clinical trials during recent years. Besides, the better characterization of the molecular aberrations of PI3K/PTEN/AKT/mTOR pathway in endometrial cancer has led to the development of novel and more specific compounds against key components of this pathway, providing additional therapeutic avenues. The identification of molecular markers that predict sensitivity to rapalogs and mTORC1 and/or mTORC2 inhibitors will be instrumental for the implementation of these therapeutic strategies.

Creative Biogene, as a leading biotechnology company, is able to offer various endometrial cancer pathway related products including stable cell lines, viral particles and clones for your pathogenesis study and drug discovery projects.


  1. Morice P, et al. Endometrial cancer. The Lancet, 2016, 387(10023): 1094-1108.
  2. Dedes K J, et al. Emerging therapeutic targets in endometrial cancer. Nature Reviews Clinical Oncology, 2011, 8(5):261.
  3. Slomovitz B M, Coleman R L. The PI3K/AKT/mTOR Pathway as a Therapeutic Target in Endometrial Cancer. Clinical Cancer Research, 2012, 18(21):5856-5864.

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