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  • 1.
    Sobti, R. C.
    et al.
    Department of Biotechnology, Panjab University, Chandigarh 160014, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh 160014, India.
    Hussain, Showket
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Suri, Vanita
    Department of Obstetrics and Gynaecology, Post Graduate Institute of Medical Education and Research, Chandigarh 160014, India.
    Bharti, A. C.
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Das, B. C.
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), Noida, India / Ambedkar Centre for Biomedical Research, Delhi University, Delhi, India.
    Overexpression of STAT3 in HPV-mediated cervical cancer in a north Indian population2009In: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 330, no 1-2, p. 193-9Article in journal (Refereed)
    Abstract [en]

    The constitutively activated STAT family members, particularly STAT3, have been shown to possess transforming properties, and are strongly correlated with tumor development and progression. STAT3 transmits signals from many cytokines and growth factors to target genes in the nucleus through the Jak/Stat signaling pathway. HPV is the main etiological factor in the development of cervical cancer. In the current study, the expression of STAT3 was analyzed in various stages of HPV-mediated cervical carcinogenesis. Tissue biopsies from 100 patients with cervical cancer of different stages and normal tissues from patients undergoing hysterectomy were selected for studying the HPV status and STAT3 expression. HPV status of each corresponding biopsy was analyzed by PCR and typing. The mRNA expression was analyzed by reverse-transcriptase polymerase chain reaction (RT-PCR). HPV infection was detected in majority of cases: 75% (9/12) in precancer, 85% (34/40) stage I & II, and 95% (36/38) in stage III & IV of cervical cancer cases by L1 PCR. Further sub typing revealed HPV16 in 100% (9/9) of L1 positives in precancerous & 90% (63/70) in different stages of cancer. Significant level of STAT3 mRNA expression was predominantly found in cervical cancer cases as compared to normal controls (P = 0.001). We also found a significant correlation of STAT3 expression in cases infected with HPV (P = 0.001). Our results indicate a potentially interactive effect between HPV 16/18 and transcriptional activation of STAT3 gene in cervical carcinogenesis. To our knowledge, this is the first such study to be reported from India. Further investigations are needed to determine the influence of STAT3 expression on cervical carcinogenesis and its possible interaction with HPV infection status.

  • 2.
    Sobti, Ranbir Chander
    et al.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Askari, Marjan
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Nikbakht, Mohsen
    Department of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Sharma, Suresh C.
    Department of Radiotherapy and Oncology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Abitew, Abayneh Munshea
    Department of Zoology, Punjab University, Chandigarh, India.
    Genetic variants of EGFR (142285G>A) and ESR1 (2014G>A) gene polymorphisms and risk of breast cancer2012In: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 369, no 1-2, p. 217-25Article in journal (Refereed)
    Abstract [en]

    Breast cancer is one of the most common cancers in women worldwide. The estrogen receptor alpha (ESR1) and epidermal growth factor receptor (EGFR) have been known to play a vital role in development and progression of breast cancer. The aim of the present study was to determine the relationship, if any, between genetic polymorphism in (ESR1) 2014G>A (T594T) and (EGFR) 142285G>A (R521K) with risk of breast cancer and the prognosis in a heterogeneous North Indian population that is known for its diverse ethnicity. A case-control study in a total of 300 individuals comprising of 150 breast cancer patients and 150 normal controls was performed. PCR-RFLP was employed for genotyping. The G/A heterozygous genotype EGFR R521K, was slightly higher in cases (56.7 %) than in controls (48.3 %) (P = 0.20). The results indicated that EGFR polymorphism does not show any significant association with breast cancer in this population. On the other hand, the mutant A/A genotype ESR1 codon 594, showed a 6.4-folds risk for breast cancer and this association was highly significant (P = 0.00) as compared to wild GG genotype, the heterozygous G/A genotype also showed a significant association with disease (P = 0.00, OR = 2.03). In addition, the frequency of A allele was also higher in cases (36 %) than in controls (19 %) and a highly significant difference was observed with wild G allele (63.3 % in cases and 6.6 % in controls). This clearly indicates that there appears to be an influence of ESR1 codon 594 genotypes on genetic susceptibility to breast cancer. Further a significantly higher risk was observed in individuals who had diabetes {OR = 3.04 (1.68-5.50), P = 0.00} and females with ESR polymorphism in pre-menopause patients that had undergone menopause above the age of 50 years {OR = 3.58 (1.86-6.90), P < 0.05}. The different ethnic backgrounds and geographical locations have complimented the present genotypic analysis and have highlighted the influence of ethnicity, race and geographic location in genetic predisposition to breast cancer.

  • 3.
    Sobti, Ranbir Chander
    et al.
    Department of Biotechnology, Panjab University, 160014 Chandigarh, India.
    Berhane, Nega
    Department of Biotechnology, University of Gondar, Gondar, Ethiopia.
    Melese, Shiferaw
    Department of Mathematics, University of Gondar, Gondar, Ethiopia.
    Mahdi, Salih Abdul
    Department of Biotechnology, Panjab University, 160014 Chandigarh, India.
    Gupta, Libsy
    Department of Biotechnology, Panjab University, 160014 Chandigarh, India.
    Thakur, Hitender
    Department of Biotechnology, Panjab University, 160014 Chandigarh, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, 160014 Chandigarh, India.
    Impact of XPD gene polymorphism on risk of prostate cancer on north Indian population2012In: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 362, no 1-2, p. 263-8Article in journal (Refereed)
    Abstract [en]

    Prostate cancer is the second most diagnosed cancer in men next to skin cancer in the developed world. Risk of disease varies most prominently with age, ethnicity, family history, and diet. Genetic polymorphism of some genes has been implicated in increasing the risk. The XPD (Xeroderma pigmentosum group D) gene codes for a DNA helicase involved in transcription and nucleotide excision repair. The aim of this study is to evaluate the effect of XPD 751 Lys/Gln polymorphism on risk of prostate cancer on north Indian patients. Blood sample from 150 prostate cancer patients, 150 from Prostate Hyper Plasia and equal number of samples from healthy control groups was collected from North India. The polymerase chain reaction and restrictive fragment length polymorphism techniques were implemented. Statistically non-significant increase risk of prostate cancer was observed with patients having Gln/Gln genotype (OR 1.62, 95% CI).

  • 4.
    Sobti, Ranbir Chander
    et al.
    Department of Biotechnology, Panjab University, India.
    Kler, Rupinder
    Department of Biotechnology, Panjab University, India.
    Sharma, Yash Paul
    Department of Cardiology, PGIMER, Chandigarh 160012, India.
    Talwar, Kewal Krishan
    Department of Cardiology, PGIMER, Chandigarh 160012, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, India.
    Risk of obesity and type 2 diabetes with tumor necrosis factor-α 308G/A gene polymorphism in metabolic syndrome and coronary artery disease subjects2012In: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 360, no 1-2, p. 1-7Article in journal (Refereed)
    Abstract [en]

    Tumor Necrosis Factor-alpha (TNF-α) has been implicated in the pathogenesis of insulin resistance and obesity. The increased expression of TNF-α in adipose tissue is known to induce insulin resistance, and a polymorphism at position -308 in the promoter region of TNF-α gene may lead to its increased transcription in adipocytes. The objective of this work was to determine the role of TNFα-308G/A gene polymorphism in metabolic syndrome (MetS) and coronary artery disease (CAD) with obesity and type 2 diabetes mellitus (T2DM). A total of 250 MetS and 224 CAD patients and 214 controls were studied. TNFα-308G/A polymorphism was detected from the whole blood genomic DNA using PCR-amplification refractory mutation system. The 2 × 2 contingency tables and multiple regression analysis were used for determining the association of genotypes with obesity and type 2 diabetes mellitus (T2DM) in MetS and CAD subjects. In CAD subjects with T2DM, the AG genotypes showed a very strong association (P < 0.0001; OR 0.194, 95%CI 0.103-0.365). In CAD subjects with obesity, the AA (P = 0.049; OR 2.449) and AG genotypes showed a strong association (P < 0.0001; OR 0.206). In both males and females, AG genotype and G allele (P < 0.0001) showed a strong association with T2DM. In MetS subjects with T2DM, there was a strong association with AG (P = 0.002; OR 4.483) as well as AA+AG genotypes (P = 0.002; OR 4.255). The AA and AG genotype (P = 0.001; OR 5.497) in males showed a strong 4.6- and 5.4-fold risks, respectively, with obesity. In females, only AG genotype showed a strong 4.5-fold risk with obesity (P = 0.001). In MetS subjects with obesity, the AA genotype (P = 0.043; OR 3.352) as well as AG showed a very strong association (P = 0.001; OR 5.011). The AG genotypes showed a high 3.5-fold risk with T2DM in females (P = 0.011). In CAD subjects, AG genotype showed a protective effect in both obese males and females (P < 0.0001). Heterozygous TNFα-308G/A gene variant may be an important risk factor for MetS with T2DM and obesity in both males and females, but may have a protective role in CAD subjects with obesity and T2DM. A allele may be an important risk factor for MetS and CAD with obesity as well as CAD subjects with T2DM.

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