Identifying aggressive forms of endometrioid-type endometrial cancer: new insights into molecular subtyping

Abstract

Summary Clinical heterogeneity represents a great challenge for cancer therapeutics. Molecular classification of patients into different subtypes based on genetic or epigenetic characteristics has the potential to revolutionize the clinical care and mechanistic understanding of a wide spectrum of cancers, including endometrial carcinoma, the most common gynecological cancer affecting women.

Failure to recognize preoperatively high-risk endometrial carcinoma is associated with a poor outcome

“…Our retrospective study, indirectly confirms the very recent understanding that better molecular characterization of ECs is required to preoperatively indicate the most appropriate surgical or medical treatment [15]. In our setting, two-thirds of cases that were preoperatively misdiagnosed (68.6%) were upgraded to EEC G3 by definitive pathology.…”

“…Furthermore, over the last 2 years, some groups [11][12][13][14][15] have investigated the prognostic value of different molecular alterations involved in endometrial carcinogenesis. They have demonstrated that the genomic features of ECs allow for reclassification, which may help in choosing the surgical and adjuvant treatment for women with aggressive tumors.…”

The most important questions in cancer research and clinical oncology—Question 2–5. Obesity-related cancers: more questions than answers

“…One study showed that obesity and physical inactivity were associated with a higher risk of CTNNB1-negative colorectal cancer [ 52 ]. This is consistent with findings in studies of the classical endometrioid endometrial cancer in obese women, which are usually negative [ 53 ]. A recent study analyzing The Cancer Genome Atlas (TCGA) data concluded that gene expression in endometrial cancer is related to BMI [ 54 ].…”

Advances in the drug therapies of acute myeloid leukemia (except acute promyelocytic leukemia)

“…Sapacitabine (Medical Isotopes, USA) is another novel oral cytosine nucleoside analog, which can break the DNA strands causing apoptosis. 21 , 22 Kantarjian et al tested the efficacy and toxicity of sapacitabine in a randomized Phase II study. They treated the patients starting with a dose of 200 mg twice a day for 7 days, followed by 300 mg twice a day for 7 days and then 400 mg twice a day for 7 days.…”