Institute of Pathology ICMR
Institute of Pathology ICMR
Soni S.,Vardhman Mahavir Medical College and Safdarjung Hospital |
Rath G.,Vardhman Mahavir Medical College and Safdarjung Hospital |
Prasad C.P.,Vardhman Mahavir Medical College and Safdarjung Hospital |
Salhan S.,Vardhman Mahavir Medical College and Safdarjung Hospital |
And 2 more authors.
American Journal of Reproductive Immunology | Year: 2011
Problem Hydatidiform mole (molar pregnancy) is the commonest form of Gestational Trophoblastic Disease, with the risk of undergoing malignant transformation. The molecular pathway leading to pathogenesis and progression of molar pregnancy is barely understood. The study focuses on Fas/FasL system which represents one of the main apoptotic pathways controlling placental morphogenesis. Method of study Placental tissues from 52 patients with complete hydatidiform moles (CHMs) and 55 age-matched controls were examined for Fas and FasL expression using immunohistochemistry, immunofluorescence and Western blotting. The protein expression was also correlated with trophoblast apoptosis (assessed by M30 Cyto DEATH), clinico-pathological parameters and disease progression. Results Immunohistochemistry and immunofluorescence revealed both cytoplasmic and membranous expression of Fas in villous syncytiotrophoblast as well as cytotrophoblast but FasL was confined merely to the cytoplasm of syncytiotrophoblast. Both Fas (cytoplasm and membrane) and FasL were significantly upregulated in syncytiotrophoblast of CHMs (P=0.004, P<0.0001 and P<0.0002 respectively) and showed a positive association between them (P=0.019). However, none of the proteins reveal any correlation with M30 index. The results were revalidated using Western blotting. Conclusion This study demonstrated differential expression of Fas and FasL in CHMs and its implications in the pathogenesis of molar pregnancy has been discussed. © 2010 John Wiley and Sons A/S.
The Gov Of The United States As Represented By The Secretary and Institute Of Pathology Icmr | Date: 2010-11-15
Targeted disruption of the centrin gene leads to attenuation of growth in the Leishmania. Preferred embodiments of the invention provide attenuated strains of Leishmania useful for the preparation of immunogenic preparations including vaccines against a disease caused by infection with a virulent Leishmania strain and as tools for the generation of immunological and diagnostic reagents. Other preferred embodiments provide related immunogenic compositions, methods of generating an immune response, methods for producing a vaccine, and methods of forming attenuated strains of Leishmania.
PubMed | Institute of Pathology ICMR
Type: Journal Article | Journal: DNA and cell biology | Year: 2011
The association of TP53 codon 72 polymorphism with cancer susceptibility remains uncertain and varies with ethnicity. Northeast India represents a geographically, culturally, and ethnically isolated population. The area reports high rate of tobacco usage in a variety of ways of consumption, compared with the rest of Indian population. A total of 411 cancer patients (161 lung, 134 gastric, and 116 oral) and 282 normal controls from the ethnic population were analyzed for p53 codon 72 polymorphism by polymerase chain reaction-restriction fragment length polymorphism. No significant difference in genotypic distribution of p53 between cases and controls was observed. Results suggested betel quid chewing as a major risk factor for all the three cancers (odds ratio [OR]=3.54, confidence interval [CI]=2.01-6.25, p<0.001; OR=1.74, CI=1.04-2.92, p=0.03; and OR=1.85, CI=1.02-3.33, p=0.04 for lung, gastric, and oral cancers, respectively). Tobacco smoking was associated with risk of lung and oral cancers (OR=1.88, CI=1.11-3.19, p=0.01 and OR=1.68, CI=1.00-2.81, p=0.04). Interactions between p53 genotypes and risk factors were analyzed to look for gene-environment interactions. Interaction of smoking and p53 genotype was significant only for oral cancer. Interactions of betel quid with p53 genotypes in lung cancer showed significant increase for all the three genotypes, indicating a major role of betel quid (OR=5.90, CI=1.67-20.81, p=0.006; OR=5.44, CI=1.67-17.75, p=0.005; and OR=5.84, CI=1.70-19.97, p=0.005 for Arg/Arg, Arg/Pro, and Pro/Pro, respectively). In conclusion, high incidence of these cancers in northeast India might be an outcome of risk habits; further, tissue- and carcinogen-specific risk modification by p53 gene is probable.