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Endometrial Cancer Patients (endometrial + cancer_patient)
Selected AbstractsHereditary nonpolyposis colorectal cancer in endometrial cancer patientsINTERNATIONAL JOURNAL OF CANCER, Issue 5 2008Sang Nam Yoon Abstract Endometrial cancer is the second most common cancer in hereditary nonpolyposis colorectal cancer (HNPCC). It has often been overlooked to explore the possibility of HNPCC in endometrial cancer patients. Our study was to investigate how many HNPCC patients existed among endometrial cancer patients. Among patients who underwent hysterectomy for endometrial cancer at Seoul National University Hospital from 1996 to 2004, 113 patients were included, whose family history and clinical data could be obtained and tumor specimens were available for microsatellite instability (MSI) testing and immunohistochemical (IHC) staining of MLH1, MSH2 and MSH6 proteins. There were 4 (3.5%) clinical HNPCC patients fulfilling the Amsterdam criteria II, and 2 (2/4, 50%) of them carried MSH2 germline mutations. There were also 8 (7.1%) suspected HNPCC (s-HNPCC) patients fulfilling the revised criteria for s-HNPCC, and one (1/8, 12.5%) of them revealed MLH1 germline mutation. In 101 patients, who were not clinical HNPCC or s-HNPCC, 11 patients showed both MSI-high and loss of expression of MLH1, MSH2 or MSH6 proteins, and 2 (2/11, 18.2%) of them showed MSH6 germline mutations. In 113 patients with endometrial cancer, we could find 5 (4.4%) HNPCC patients with MMR germline mutation and 2 (1.8%) clinical HNPCC patients without identified MMR gene mutation. Family history was critical in detecting 3 HNPCC patients with MMR germline mutation, and MSI testing with IHC staining for MLH1, MSH2 and MSH6 proteins was needed in the diagnosis of 2 HNPCC patients who were not clinical HNPCC or s-HNPCC, especially for MSH6 germline mutation. © 2007 Wiley-Liss, Inc. [source] CYP1A1, SULT1A1, and SULT1E1 polymorphisms are risk factors for endometrial cancer susceptibilityCANCER, Issue 9 2008Hiroshi Hirata MD Abstract BACKGROUND. In estrogen biosynthetic pathways, many enzymes are important for metabolism, detoxification, and bioavailability. Polymorphisms in these genes may have an effect on the enzymes' function. For example, higher expression and activation of biosynthetic enzymes and lower expression and activation of conjugation enzymes may lead to high toxicity or carcinogenesis. The authors hypothesized that single nucleotide polymorphisms (single nucleotide polymorphisms) of CYP1A1, CYP1A2, CYP1B1, CYP17, SULT1A1, SULT1E1, and SHBG genes may be risk factors for endometrial cancer. METHODS. DNA samples from 150 cases of endometrial cancer and healthy controls (n = 165) were analyzed by polymerase chain reaction,restriction fragment length polymorphism (PCR-RFLP) to determine the genotypic frequency of 13 different polymorphic loci on the CYP1A1 (m1, m2, m3, m4), CYP1A2 1F, CYP1B1 codon432, COMT codon158, CYP17, SULT1A1 (Arg213His, 14A/G, 85C/T in the 3, flanking region), SULT1E1-64G/A promoter region, and SHBG genes. Genotyping was validated by direct DNA sequencing. The authors also investigated the relation between expression of CYP1A1 in endometrial cancer tissues and genotypes of CYP1A1 m1. RESULTS. A decreased frequency of TC + CC genotype of the CYP1A1 m1 (T/C) polymorphism was observed in endometrial cancer patients compared with controls (OR = 0.42; 95% CI, 0.27,0.69). The T-A haplotype of CYP1A1 m1 and m2 was increased in endometrial cancer patients (P = .017). The frequency of CYP1A1 m1 T/C + C/C was higher in a high CYP1A1 expression group (P = .009). The authors also found that individuals carrying the variants of SULT1A1 codon213 and 2 single nucleotide polymorphisms in the 3, flanking region (14A/G and 85C/T) had an increased risk for endometrial cancer. The frequencies of G-A-C and A-G-T haplotypes of these 3 variants were higher in endometrial cancer patients (P < .0001; P = .0002). In addition, the frequency of combined genotypes (SULT1A1 213 GA + AA and CYP1A1 m1 TT) was higher in endometrial cancer patients. (OR, 4.58; 95% CI, 2.35,8.93). CONCLUSIONS. This is the first report on the combined association of CYP1A1 and SULT gene polymorphisms in endometrial cancer that suggests a decreased single nucleotide polymorphism of CYP1A1 and an increased single nucleotide polymorphism for SULT1A1 and SULT1E1 genes may be risk factors for endometrial cancer in Caucasians. Cancer 2008. © 2008 American Cancer Society. [source] Treatment effects, disease recurrence, and survival in obese women with early endometrial carcinoma,CANCER, Issue 12 2006A Gynecologic Oncology Group study Abstract BACKGROUND. The objective was to examine whether rates of disease recurrence, treatment-related adverse effects, and survival differed between obese or morbidly obese and nonobese patients. METHODS. Data from patients who participated in a randomized trial of surgery with or without adjuvant radiation therapy were retrospectively reviewed. RESULTS. Body mass index (BMI) data were available for 380 patients, of whom 24% were overweight (BMI, 25,29.9), 41% were obese (BMI, 30,39.9), and 12% were morbidly obese (BMI, ,40). BMI did not significantly differ based on age, performance status, histology, tumor grade, myometrial invasion, or lymphovascular-space involvement. BMI > 30 was more common in African Americans (73%) than non-African Americans (50%). Patients with a BMI , 40 compared with BMI < 30 (hazards ratio [HR], 0.42; 95% confidence interval [CI], 0.09,1.84; P = .246) did not have lower recurrence rates. Compared with BMI < 30, there was no significant difference in survival in patients with BMI 30,39.9 (HR, 1.48; 95% CI, 0.82,2.70; P = .196); however, there was evidence for decreased survival in patients with BMI , 40 (HR, 2.77; 95% CI, 1.21,6.36; P = .016). Unadjusted and adjusted BMI hazards ratios for African Americans versus non-African Americans in the current study differed, thus suggesting a confounding effect of BMI on race. Eight (67%) of 12 deaths among 45 morbidly obese patients were from noncancerous causes. For patients who received adjuvant radiation therapy, increased BMI was significantly associated with less gastrointestinal (R, ,0.22; P = .003) and more cutaneous (R, 0.17; P = .019) toxicities. RESULTS. In the current study, obesity was associated with higher mortality from causes other than endometrial cancer but not disease recurrence. Increased BMI was also associated with more cutaneous and less gastrointestinal toxicity in patients who received adjuvant radiation therapy. Future recommendations include lifestyle intervention trials to improve survival in obese endometrial cancer patients. Cancer 2006. © 2006 American Cancer Society. [source] Molecular epidemiological and mutational analysis of DNA mismatch repair (MMR) genes in endometrial cancer patients with HNPCC-associated familial predisposition to cancerCANCER SCIENCE, Issue 9 2008Y. Hirai Recently, a high rate of endometrial cancer has been reported in women with hereditary non-polyposis colorectal cancer (HNPCC), suggesting a relationship between familial endometrial cancers and HNPCC. Familial endometrial cancers constitute only about 0.5% of all endometrial carcinomas and it is essential to examine family histories in detail. A mutational analysis of three DNA mismatch repair (MMR) genes (hMLH1, hMSH2 and hMSH6) in patients with endometrial cancer who meet our criteria for familial predisposition to HNPCC-associated endometrial cancers was performed. Mutations were detected in 18 of the 120 patients (15.0%). Most HNPCC-related endometrial cancers do not meet the New Amsterdam Criteria for HNPCC. These clinical criteria may identify only some HNPCC-associated endometrial cancers. Establishing the correct family history for endometrial cancer patients is important for diagnosing familial endometrial carcinomas. An analysis of MMR genes may be useful for patients with endometrial cancer showing familial aggregation. In addition, gynecologists must be accurately informed, and it is important to perform large-scale, multicenter studies both nationwide and internationally. (Cancer Sci 2008; 99: 1715,1719) [source] | ||||||||||