Merkel cell carcinoma in an HIV-1-infected man.
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Carcinoma, Merkel Cell↗
Biomedical subjects
Radhika Gade-Andavolu
Publications and source records attributed to Radhika Gade-Andavolu.
Leptomeningeal carcinomatosis in a patient with metastatic prostate cancer: case report and literature review.
BACKGROUND: Leptomeningeal metastasis is discovered at autopsy in approximately 5% of patients with systemic cancer. Until recently with the introduction of magnetic resonance imaging (MRI), premorbid diagnosis was extremely difficult. In particular, initial spinal fluid cytology is diagnostic in less than 50% of autopsy-verified patients, although repeated spinal fluid examinations may increase the yield significantly. Leptomeningeal metastasis in metastatic prostate cancer has been reported in only 14 patients previously. CASE DESCRIPTION: We recently studied such a patient and were able to establish a correct diagnosis based solely on the MRI and the presence of an elevated cerebrospinal fluid (CSF) prostate-specific antigen (PSA). Only 3 previous patients with leptomeningeal prostate metastasis have undergone CSF PSA evaluations. CONCLUSION: We believe that, in such patients, the combination of MRI and CSF studies can overcome the lack of sensitivity of CSF cytology.
Aged↗
RANTES: a genetic risk marker for multiple sclerosis.
UNLABELLED: Regulated upon activation, normal T-cell expressed and secreted (RANTES) is a beta-chemokine and has been detected in brain lesions of multiple sclerosis (MS) patients. Considering its potential role in MS, we screened two functional polymorphisms in the proximal promoter region of the RANTES in MS patients versus controls. METHODS: We examined 140 postmortem brain samples from subjects with a primary diagnosis of MS, and peripheral blood samples from 216 control subjects. The RANTES-28C/G and -403G/A promoter polymorphisms were examined. All subjects were non-Hispanic Caucasians. RESULTS: MS cases differed from controls showing a significant association with the 403G/A polymorphism (odds ratio, 2.359, [1.465-3.799]; P=0.0001), but not the -28C/G (P=NS) polymorphism. There was a significant association of the -28G allele with both early onset (P=0.031) and longer survival (P=0.006). CONCLUSION: There is a significant but complex association of the RANTES gene with MS.
Adult↗
A multigene test for the risk of sporadic breast carcinoma.
BACKGROUND: Although the identification of the BRCA1 and BRCA2 genes have been of great interest, these genes account for less than 5% of all breast carcinoma cases. The remaining cases are sporadic. Reanalysis of a large twin study suggested that genetic factors may play a significant role in sporadic breast and other carcinomas. Sporadic breast carcinoma is polygenically inherited. Multiple genes are likely to have an additive effect, each gene accounting for a fraction of the variance. One factor that may have an impact on the development of hormonally responsive breast tumors is the duration of exposure of the breast to estrogen. Therefore, one of the demographic risk factors for breast carcinoma is an early age of onset of menarche. The current study was based on the hypothesis that genes that play a role in demographic risk factors may be breast carcinoma risk genes in their own right. The authors hypothesized that six genes relevant to the timing of the onset of menarche and related risk factors might be candidate genes for breast carcinoma. These were the leptin gene (LEP), the leptin receptor gene (LEPR), the catechol-0-methyltransferase gene (COMT), the dopamine D(2) receptor gene (DRD2), the estrogen 1 receptor gene (ESR1), and the androgen receptor gene (AR). METHODS: The authors examined 67 women with postmenopausal sporadic breast carcinoma and 145 gender and race-matched controls. RESULTS: Five of these genes accounted for a significant percent of the variance (r(2)) of breast carcinoma. The following r(2) and P values were calculated: LEP: 0.073, P < or = 0.0001; LEPR: 0.064, P < or = 0.0002; COMT: 0.073, P < or = 0.0001; AR: 0.040, P < or = 0.0035; and DRD2: 0.018, P < or = 0.05. When evaluated in a multivariate regression analysis, they accounted collectively for 24% of the variance of breast carcinoma (P < or = 0.0001). These genes accounted for 40% of the variance (P < or = 0.00001) in a subset of age-matched cases. Individual gene scores were added to form a breast carcinoma risk score (BCRS) that ranged from 0 to 17. When the BCRS was evaluated in a receiver operator characteristic plot, the area under the curve was 0.80 for the full set and 0.869 for the age-matched set. The relative breast carcinoma risk for the different BCRS scores ranged from 0.10 to 11.9. CONCLUSIONS: These results demonstrate a potentially powerful method of evaluating the additive effect of multiple breast carcinoma risk genes to form a potentially clinically useful assessment of women's risk for sporadic breast carcinoma.
Adult↗
Molecular interactions of leptin and prostate cancer.
BACKGROUND: Epidemiological studies have found obesity to be a risk factor for prostate cancer. Our prior independent studies in women have reported a strong relationship between variants of OB (leptin) gene, body mass index, and age at menarche and sporadic breast cancer. The current study investigates an association between genetic variants of the human obesity gene, serum leptin levels, and body mass index in subjects with prostate carcinoma and in age- and gender-matched normal subjects. METHODS: Blood samples from 69 patients with prostate cancer and 137 age-matched control subjects were collected. Serum leptin level was investigated by radioimmunoassay, and body mass index was calculated. Allele sizes were determined via standard polymerase chain reaction. Statistical analysis was performed using SPSS10.0 computer software. RESULTS: There was a strong association with significantly elevated serum leptin levels, high body mass index, and higher frequency of LEPR longer alleles in patients with prostate cancer than in control subjects. By contrast, a modest but not significant increase in the frequency of LEP short alleles was found in patients with prostate cancer as compared with control subjects. Analysis within groups 1 (low leptin level and low body mass index) and 2 (other) showed a significant association only in group 2, with high frequency of OB gene variants (LEPR long alleles and LEP short alleles) in patients with prostate cancer but not in control subjects. CONCLUSIONS: These results represent the first report of a significant association between specific leptin gene alleles, serum leptin levels, and body mass index in subjects with prostate cancer. Consistent with prior reports, we also report a significantly elevated serum leptin level in patients with prostate cancer, suggesting a strong link with obesity as an increased risk factor.
Alleles↗
Association of CCR5 delta32 deletion with early death in multiple sclerosis.
PURPOSE: The interaction between chemokines and their receptors is extremely important in controlling T cell migration into sites of CNS inflammation. Because trafficking of inflammatory T cells into the central nervous system (CNS) is a key player in the pathogenesis of multiple sclerosis (MS), we investigated the possible association of CCR5 delta32 deletion in this disorder. METHODS: DNA isolated from postmortem brain tissue samples of 132 patients with MS and from blood tissue samples of 163 gender and ethnicity-matched healthy controls was used to screen for the CCR5 delta32 deletion allele. RESULTS: An increased frequency of 32-bp deletion allele was found to be associated with early death (P = 0.00005) and with a progressive reduction in the years of survival (onset to death). The death hazard ratio of CCR5 with deletion versus no deletion was 2.12, suggesting that MS patients with the 32-bp deletion have twice the mortality rate of patients with the normal genotype. This effect was more significant in females (hazard ratio 3.58). CONCLUSION: A strong association of the CCR5delta32 deletion with early death could serve as a prognostic marker for MS.
Alleles↗