Microsatellite Instability in Type I Endometrial Carcinoma
Author Information
Author(s): Choi Yoo Duk, Choi Jin, Kim Jo Heon, Lee Ji Shin, Lee Jae Hyuk, Choi Chan, Choi Ho Sun, Lee Min Cheol, Park Chang Soo, Juhng Sang Woo, Nam Jong Hee
Primary Institution: Chonnam National University Medical School
Hypothesis
This study aimed to investigate the prevalence of EMAST in type I endometrial carcinoma and its correlation with mismatch repair genes or p53.
Conclusion
About 38.5% of type I endometrial carcinomas exhibited EMAST, which was rarely associated with alterations in hMSH2 or hMLH1.
Supporting Evidence
- 20.5% of tumors showed high microsatellite instability (MSI-H).
- 38.5% of tumors exhibited elevated microsatellite alterations at selected tetranucleotide repeats (EMAST).
- 87.5% of MSI-H tumors had loss of hMSH2 or hMLH1 expression.
Takeaway
In a study of 39 patients with a type of uterine cancer, about 4 out of 10 had a specific genetic change called EMAST, which is not often linked to certain gene problems.
Methodology
The study examined 39 cases of type I endometrial carcinoma using PCR for microsatellite markers and immunohistochemistry for protein expression.
Limitations
The study's sample was not evenly distributed across FIGO stages, which may affect the results.
Participant Demographics
Patients aged 30 to 68 years, with a mean age of 53.4 years.
Statistical Information
P-Value
0.010
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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