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Biomedical subjects

Robert M Wenham

Publications and source records attributed to Robert M Wenham.

10 recordsLinked to original sources
PubMed2006

Sexual health in women treated for cervical cancer: characteristics and correlates.

OBJECTIVE: A large proportion of women with a history of cervical cancer experience sexual problems as a result of treatment. The present study examined whether differences in sexual health between cervical cancer survivors and women with no history of cervical cancer could be explained by selected demographic, clinical, and psychosocial and physical factors. METHODS: Women treated between 1 and 5 years previously for stage 0 to II cervical cancer and age- and education-matched women with no history of cancer undergoing routine cervical cancer screening were recruited to participate. All participants had a partner with whom they had ever been sexually active. Women completed measures of sexual health, vaginal changes, partner relationship quality, perceived physical appearance, and sexual self-concept. RESULTS: Cervical cancer survivors reported significantly (p<.05) less sexual interest, more sexual dysfunction, and lower sexual satisfaction. The most consistent predictors of sexual health after treatment among survivors were time since diagnosis, receipt of radiotherapy, partner relations, and perceived physical appearance, as well as vaginal changes. These variables accounted for about 50% of the variance in sexual health outcomes. CONCLUSION: The findings suggest that efforts to improve sexual health in women with a history of cervical cancer must move beyond the direct effects of cancer treatment on vaginal anatomy and physiology. Sexual rehabilitation interventions should consider partner relationships, perceived physical appearance, and women's attitudes toward themselves as sexual beings, in addition to vaginal changes. Future research should use prospective longitudinal research designs incorporating appropriate comparison groups to further explore this issue.

Adult↗
PubMed2005

IGF1 (CA)19 repeat and IGFBP3 -202 A/C genotypes and the risk of prostate cancer in Black and White men.

We investigated the relationship between the insulin-like growth factor-1 (IGF1) cytosine-adenine repeat (CA)(19) polymorphism located upstream of the gene's transcription start site, the insulin-like growth factor binding protein-3 (IGFBP3) -202 A/C promoter region polymorphism, and prostate cancer risk in Black and White men. Study subjects were U.S. veterans ages 41 to 75 years identified at the Durham Veterans Administration Medical Center over a 2.5-year period. Controls (n = 93) were frequency matched to cases (n = 100) based on race (Black or White) and age. Multivariable unconditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI) for the associations between the polymorphisms and prostate cancer risk. For Blacks and Whites combined, an inverse association between prostate cancer and being homozygous for the most common IGF1 repeat allele, (CA)(19), (adjusted OR, 0.3; 95% CI, 0.1-0.7) was observed. Similar associations were noted for both Blacks (OR, 0.2; 95% CI, 0.0-0.8) and Whites (OR, 0.4; 95% CI, 0.1-1.6) separately. No statistically significant associations between the IGFBP3 C allele and prostate cancer were noted for Blacks (adjusted OR, 2.3; 95% CI, 0.8-6.2) or Whites (OR, 1.0; 95% CI, 0.3-3.1). The prevalence of the homozygous IGF1 (CA)(19) genotype was much lower in Black controls (21%) than White controls (46%), which may, in part, explain the increased prostate cancer incidence in Black versus White men. Further research is needed to confirm these findings.

Adult↗
PubMed2004

Progesterone receptor promoter +331A polymorphism is associated with a reduced risk of endometrioid and clear cell ovarian cancers.

OBJECTIVE: The progestagenic milieu of pregnancy and oral contraceptive use is protective against epithelial ovarian cancer. A functional single nucleotide polymorphism in the promoter of the progesterone receptor (+331A) alters the relative abundance of the A and B isoforms and has been associated with an increased risk of endometrial and breast cancer. In this study, we sought to determine whether this polymorphism affects ovarian cancer risk. METHODS: The +331G/A polymorphism was genotyped in a population-based, case-control study from North Carolina that included 942 Caucasian subjects (438 cases, 504 controls) and in a confirmatory group from Australia (535 cases, 298 controls). Logistic regression analysis was used to calculate age-adjusted odds ratios (OR). RESULTS: There was a suggestion of a protective effect of the +331A allele (AA or GA) against ovarian cancer in the North Carolina study [OR, 0.72; 95% confidence interval (95% CI), 0.47-1.10]. Examination of genotype frequencies by histologic type revealed that this was due to a decreased risk of endometrioid and clear cell cancers (OR, 0.30; 95% CI, 0.09-0.97). Similarly, in the Australian study, there was a nonsignificant decrease in the risk of ovarian cancer among those with the +331A allele (OR, 0.83; 95% CI, 0.51-1.35) that was strongest in the endometrioid/clear cell group (OR, 0.60; 95% CI, 0.24-1.44). In the combined U.S.-Australian data that included 174 endometrioid/clear cell cases (166 invasive, 8 borderline), the +331A allele was significantly associated with protection against this subset of ovarian cancers (OR, 0.46; 95% CI, 0.23-0.92). Preliminary evidence of a protective effect of the +331A allele against endometriosis was also noted in control subjects (OR, 0.19; 95% CI, 0.03-1.38). CONCLUSIONS: These findings suggest that the +331G/A progesterone receptor promoter polymorphism may modify the molecular epidemiologic pathway that encompasses both the development of endometriosis and its subsequent transformation into endometrioid/clear cell ovarian cancer.

Adenocarcinoma, Clear Cell↗
PubMed2003

Polymorphisms in BRCA1 and BRCA2 and risk of epithelial ovarian cancer.

PURPOSE: Because inherited BRCA1 or BRCA2 mutations strikingly increase ovarian cancer risk, polymorphisms in these genes could represent low penetrance susceptibility alleles. Previous studies of the BRCA2 N372H polymorphism suggested that HH homozygotes have a modestly increased risk of both breast and ovarian cancer. We have examined whether BRCA2 N372H or common amino acid-changing polymorphisms in BRCA1 predispose to ovarian cancer. EXPERIMENTAL DESIGN: A population-based, case control study of ovarian cancer was performed in North Carolina. Cases included 312 women with ovarian cancer (76% invasive and 24% borderline) and 401 age- and race-matched controls. Blood DNA from subjects was genotyped for BRCA2 N372H and BRCA1 Q356R and P871L. RESULTS: There was no association between BRCA2 N372H and risk of borderline or invasive epithelial ovarian cancer. The overall odds ratio (OR) for HH homozygotes was 0.8 [95% confidence interval (CI) = 0.4-1.5] and was similar in all subsets, including invasive serous cases. In addition, neither the BRCA1 Q356R (OR = 0.9, 95% CI 0.5-1.4) nor P871L (OR = 0.9, 95% CI 0.6-1.9) polymorphisms were associated with ovarian cancer risk. There was a significant racial difference in allele frequencies of the P871L polymorphism (P = 0.64 in Caucasians, L = 0.76 in African-Americans, P < 0.0001). CONCLUSIONS: In this population-based, case control study, common amino acid changing BRCA1 and 2 polymorphisms were not found to affect the risk of developing ovarian cancer.

Adenocarcinoma, Clear Cell↗
PubMed2003

Matrix metalloproteinase-1 gene promoter polymorphism and risk of ovarian cancer.

OBJECTIVE: It has been suggested that the 2G allele of a guanine insertion-deletion promoter polymorphism in the promoter of the matrix metalloproteinase-1 (MMP1) gene may increase susceptibility to ovarian cancer. The 2G allele also has been associated with increased MMP1 expression. We investigated the relationship between the MMP1 polymorphism and ovarian cancer risk in a large population-based, case-control study. METHODS: The MMP1 promoter polymorphism was examined in white blood cell DNA from 311 cases and 387 age- and race-matched controls using a radiolabeled polymerase chain reaction assay. In addition, genotyping of the MMP1 polymorphism performed in 42 advanced-stage invasive serous ovarian cancers was compared to their mean relative MMP1 expression from Affymetrix microarrays. RESULTS: The 2G allele frequency did not differ significantly between cases (0.49) and controls (0.48), and the distribution of genotypes was in Hardy-Weinberg equilibrium. Using 1G homozygotes as the reference group, neither 2G homozygotes (odds ratio 1.1, 95% confidence interval 0.7-1.7) nor heterozygotes plus 2G homozygotes (odds ratio 0.9, 95% confidence interval 0.7-1.3) had an increased risk of ovarian cancer. There was also no relationship between MMP1 genotype and histologic grade, histologic type, stage, or tumor behavior (borderline versus invasive). The mean MMP1 expression was twice as high in 2G homozygotes relative to 1G homozygotes, but this difference was not statistically significant. CONCLUSION: The reported association between the MMP1 promoter polymorphism and ovarian cancer risk was not supported by our data. There was a suggestion that the 2G allele may be associated with higher MMP1 expression, and this finding is worthy of further investigation.

Adult↗
PubMed2002

Stage IIB-IVB cervical adenocarcinoma: prognostic factors and survival.

OBJECTIVE: The incidence of cervical adenocarcinoma is increasing relative to squamous cell carcinoma and all cervical cancers. Few reports have described the outcome of patients with advanced cervical adenocarcinoma. The purpose of this study was to determine the prognostic factors and survival for patients with stage IIB-IVB disease. METHODS: Institutional Review Board approval was obtained to perform a computerized search of all women diagnosed with cervical adenocarcinoma at our three institutions between 1982 and 2000. Medical records were retrospectively reviewed. Clinical follow-up was obtained from the SGO database and tumor registry and via correspondence with health care providers. Statistical analysis was performed using logistic regression for clinical variables and the log-rank test to compare Kaplan-Meier survival estimates. RESULTS: Eighty-three women with FIGO stage IIB-IVB cervical adenocarcinoma were identified. The median patient age was 53 years (range, 22-88). The median follow-up of 17 (20%) surviving patients was 33 months (range, 6-147); 66 (80%) died during the study interval. Stage IIB disease, young patient age, and grade 1 histology were independent variables having a favorable impact on survival (each P < 0.02). Stage IIB patients (n = 41) were more likely to be alive at 2 (64% vs 8%) and 5 years (30% vs 0%) than women with stage IIIA-IVB disease (n = 42; P < 0.01). CONCLUSIONS: Women diagnosed with advanced stage cervical adenocarcinoma have a poor prognosis. Prospective, multicenter trials of platinum-based chemoradiation or other novel therapies are urgently needed in the treatment of this highly lethal disease.

Adenocarcinoma↗
PubMed2002

Molecular aspects of ovarian cancer.

Ovarian cancer is caused by genetic alterations that disrupt proliferation, apoptosis, senescence and DNA repair. Approximately 10% of ovarian cancers arise in women who have inherited mutations in cancer susceptibility genes (BRCA1 or BRCA2). The ability to perform genetic testing allows identification of women at increased risk who can be offered prophylactic oophorectomy or other interventions aimed at preventing ovarian cancer. The vast majority of ovarian cancers are sporadic, resulting from the accumulation of genetic damage over a lifetime. Several specific genes involved in ovarian carcinogenesis have been identified, including the p53 tumour suppressor gene and HER2/ neu andPIC3KA oncogenes. The recent availability of expression microarrays has facilitated the simultaneous examination of thousands of genes, and this promises to extend further our understanding of the molecular events involved in the development of ovarian cancers. Hopefully, this knowledge can be translated into effective screening, treatment, surveillance, and prevention strategies in the future.

Cell Transformation, Neoplastic↗
PubMed2002

Can Monsel's Transmit Nosocomial Infections? A Microbiological Investigation.

OBJECTIVE.: Our objective was to test whether common nosocomial pathogenic bacteria can be cultured in Monsel's paste, 20% ferric subsulfate, an astringent solution with styptic qualities that causes hemostasis when applied topically to small cuts. MATERIALS AND METHODS.: First, samples of Monsel's paste were collected and plated onto 4 media. Bacterial growth was evaluated at 48 hours. Second, thioglycollate medium was inoculated with a combination of Monsel's paste and actively growing stock bacteria. After 2 days, the samples were subcultured. They were evaluated for growth at 5 days. Next, samples of Monsel's were inoculated with 10Pseudomonas aeruginosa or 10Clostridium perfringens. The samples of inoculated paste were examined at 5-minute intervals thereafter to evaluate bacterial survival. RESULTS.: Neither the open samples of Monsel's solution nor the inoculated samples of Monsel's solution grew bacteria. When the samples inoculated with 10 organisms were examined at timed intervals after inoculation, no bacteria were noted after 5 minutes. CONCLUSIONS.: It is unlikely that nosocomial bacteria could survive exposure to Monsel's solution. Thus, potential contamination of the solution is unlikely, and subsequent transmission of infection is improbable.

Journal Article↗