Mismatch repair and clinical response to immune checkpoint inhibitors in endometrial cancer.
Yoland AntillDaniel D BuchananClare L ScottPublished in: Cancer (2021)
Endometrial cancer is common, and a subset recurs and requires additional treatment. Some of these are recognized as being susceptible to immune therapies and are said to have mismatch repair deficiency (dMMR). However, this clinical trial highlights which cases are more likely to respond well: those containing mutations in genes known as Lynch genes and also some with mutations in POLE/POLD1 ("ultra-hypermutation" genes). In contrast, the majority of dMMR endometrial cancers have silencing or DNA methylation of one of these genes, MLH1, and do not seem to be as responsive to single-agent immune therapy. The availability of combination therapies may be important to consider for these women.
Keyphrases
- endometrial cancer
- genome wide
- dna methylation
- clinical trial
- genome wide identification
- bioinformatics analysis
- magnetic resonance
- high resolution
- randomized controlled trial
- genome wide analysis
- polycystic ovary syndrome
- mesenchymal stem cells
- pregnant women
- magnetic resonance imaging
- transcription factor
- adipose tissue
- metabolic syndrome
- open label
- replacement therapy
- phase iii
- chemotherapy induced