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  • 1.
    Bharadwaj, Mausumi
    et al.
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), NOIDA, India.
    Hussain, Showket
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), NOIDA, India.
    Tripathi, Richa
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), NOIDA, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Mehrotra, Ravi
    Division of Cytopathology, Institute of Cytology & Preventive Oncology (ICMR), NOIDA, India.
    Human Papillomavirus (HPV): Diagnosis and Treatment2014Inngår i: Animal Biotechnology: Models in Discovery and Translation / [ed] Ashish Verma & Anchal Singh, Elsevier, 2014, s. 95-120Kapittel i bok, del av antologi (Fagfellevurdert)
  • 2.
    Hussain, Showket
    et al.
    Institute of Cytology & Preventive Oncology (ICMR), Noida, Uttar Pradesh, India.
    M., Yuvaraj
    Institute of Cytology & Preventive Oncology (ICMR), Noida, Uttar Pradesh, India.
    Thakur, Nisha
    Institute of Cytology & Preventive Oncology (ICMR), Noida, Uttar Pradesh, India.
    Salam, Irfana
    Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Singh, Neha
    Panjab University, Chandigarh, India.
    Mir, Mohammad Muzaffar
    Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Bhat, Mohammad Akbar
    Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Siddiqi, Mushtaq A.
    Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Das, Bhudev C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi, India.
    Bharadwaj, Mausumi
    Institute of Cytology & Preventive Oncology (ICMR), Noida, Uttar Pradesh, India.
    Association of cyclin D1 gene polymorphisms with risk of esophageal squamous cell carcinoma in Kashmir Valley: a high risk area2011Inngår i: Molecular Carcinogenesis, ISSN 0899-1987, E-ISSN 1098-2744, Vol. 50, nr 7, s. 487-98Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Investigation of potential association of SNPs (G870A, rs9344; G1722C, rs678653) of cyclin D1 gene (CCND1) with susceptibility to esophageal squamous cell carcinoma (ESCC) in Kashmir valley (India). The study included 302 subjects comprising 151 ESCC cases and 151 controls. PCR-RFLP and direct sequencing were employed for genotyping. The G870A polymorphism, the individuals carrying GA + AA genotype was having 2.80-fold increased risk for development of ESCC (OR 2.8, 95% CI = 1.77-4.4; P = 0.0001) compared to GG genotype. Further a significantly higher risk was observed in individuals who consume >3 cups per day of salted tea (OR = 5.1; 95% CI = 1.6-16.7; P = 0.0016) and had smoking habits (OR = 6.3; 95% CI = 2.9-13.9; P = 0.0005). We also demonstrate for the first time in CCND1 1722 locus, the CC genotype was strongly associated with increased risk of developing ESCC (OR = 2.58; 95% CI = 1.61-4.15; P = 0.0001). In addition, the frequency of polymorphic C allele was also found to be higher in cases (OR = 1.92; 95% CI = 1.37-2.69; P = 0.0002). There appears to be an influence of CCND1 G870A/G1772C genotypes on genetic susceptibility to ESCC.

  • 3.
    Hussain, Showket
    et al.
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Salam, Irfana
    Department of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Bandil, Kapil
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Yuvaraj, M
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Akbar Bhat, Mohammad
    Department of Cardiovascular Thoracic Surgery, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Muzaffar Mir, Mohammad
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Siddiqi, Mushtaq A.
    Department of Cardiovascular Thoracic Surgery, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Jammu and Kashmir, India.
    Sobti, Ranbir C.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics & Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Das, Bhudev C.
    Dr. B.R. Ambedkar Centre for Biomedical Research (ACBR) University of Delhi (North Campus), Delhi, India.
    Methylation-mediated gene silencing of suppressor of cytokine signaling-1 (SOCS-1) gene in esophageal squamous cell carcinoma patients of Kashmir valley2011Inngår i: Journal of Receptor and Signal Transduction Research, ISSN 1079-9893, E-ISSN 1532-4281, Vol. 31, nr 2, s. 147-56Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    CONTEXT: Esophageal squamous cell carcinoma (ESCC) is a leading cause of cancer-related deaths in Jammu and Kashmir. The negative regulation of tumor suppressor gene leading to change in signaling pathway is one of the major mechanisms responsible for tumorigenic transformation.

    OBJECTIVE: In the present study, the role of silencing of suppressor of cytokine signaling-1 (SOCS-1) gene, a negative regulator of JAK/STAT pathway, was analyzed in ESCC.

    METHODS: The expression pattern of SOCS-1 gene was analyzed in esophageal tumor biopsies although normal adjacent tissues that served as controls. Reverse transcriptase polymerase chain reaction (RT-PCR), immunohistochemistry, methylation-specific PCR (MSP), and human papillomavirus (HPV) detection were performed to assess the expression pattern and promoter methylation of SOCS-1 gene including HPV status in a total of 75 surgically resected tissue specimens.

    RESULTS: Compared with the level of SOCS-1 expression in normal tissues, 53% (40/75) of the tumor tissues expressed either undetectable or reduced SOCS-1 expression (>50% loss of expression), which was significantly associated with advanced clinical stage or severe histopathological grade of the disease (P < 0.01). Aberrant promoter methylation of the SOCS-1 gene was found in 45% (34/75) of the esophageal tumor tissues, which was also found to be significantly associated with advanced stage of esophageal carcinoma (P < 0.01). The prevalence of HPV infection was found in 19% of tumor cases, whereas no HPV could be detected in any of the normal adjacent tissues.

    CONCLUSION: Transcriptional inactivation of SOCS-1 gene, primarily due to its promoter hypermethylation although HPV infection, may play an important role in esophageal carcinogenesis in Kashmir.

  • 4.
    Hussain, Showket
    et al.
    ICPO (ICMR), NOIDA, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Salam, Irfana
    Department of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical Sciences, Kashmir, India.
    Bhat, Mohammad A.
    Department of Cardiovascular Thoracic Surgery, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, India.
    Kakkar, Nandita
    Department of Histopathology, PGIMER, Chandigarh, India.
    Mir, Mohammad M.
    Department of Clinical Biochemistry, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, India.
    Siddiqi, Mushtaq A.
    Department of Immunology and Molecular Medicine Sher-I-Kashmir Institute of Medical Sciences, Srinagar, India.
    Basir, Seemi F.
    Department of Biosciences Jamia Millia Islamia, Delhi, India.
    Bharti, Alok C.
    ICPO (ICMR), NOIDA, India.
    Bharadwaj, Mausumi
    ICPO (ICMR), NOIDA, India.
    Das, Bhudev C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi (North Campus), Delhi, India.
    Abstract 2722: Transcription factor NF-kB in esophageal squamous cell carcinoma: Alterations in activity and expression during Human Papillomavirus infection2011Inngår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 71, nr 8 Suppl, artikkel-id Abstract 2722Artikkel i tidsskrift (Fagfellevurdert)
  • 5.
    Singh, Neha
    Högskolan i Skövde, Institutionen för biovetenskap. Högskolan i Skövde, Forskningscentrum för Systembiologi.
    Breakthrough insight into HPV infection as an emerging risk factor in prostate cancer2015Inngår i: Onkologi i Sverige, ISSN 1653-1582, nr 3, s. 76-77Artikkel i tidsskrift (Annet (populærvitenskap, debatt, mm))
  • 6.
    Singh, Neha
    et al.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Kakkar, Nandita
    Department of Urology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Singh, S. K.
    Department of Histopathology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Sobti, Ranbir C.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Overexpression of signal transducer and activator of transcription (STAT-3 and STAT-5) transcription factors and alteration of suppressor of cytokine signaling (SOCS-1) protein in prostate cancer2012Inngår i: Journal of Receptor and Signal Transduction Research, ISSN 1079-9893, E-ISSN 1532-4281, Vol. 32, nr 6, s. 321-7Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Prostate cancer is a leading cause of mortality in men worldwide especially in developing countries like India. The molecular mechanisms of the oncogenic signaling pathway(s) that are involved in prostate carcinogenesis play a crucial role in disease progression and persistence. There is an important role of signal transducer and activator of transcriptions (STATs) particularly STAT-3 and STAT-5 and its negative regulator suppressor of cytokine signaling-1 (SOCS-1).

    METHODS: In the present study, the expression and localization of STAT and SOCS-1 proteins in prostate cancer by immunohistochemistry in a total of 150 formalin-fixed, paraffin-embedded human prostate tissues of different grade obtained by radical prostatectomies or transurethral resection.

    RESULTS: A significantly strong STAT-3 expression pattern in 68% (65/95) prostate cancer cases as compared to 12% (5/55) in benign prostatic hyperplasia (BPH) controls (P < 0.001) was observed. Interestingly the SOCS-1 expression was found to be significantly elevated in prostate cancer cases (P < 0.001).

    CONCLUSIONS: The present study demonstrates overexpression of STAT-3 and STAT-5 proteins and a contrasting role of SOCS-1 in prostate cancer. These results suggest a critical association between altered expression of STAT-3 and STAT-5 with SOCS-1 and indicate its potential role as a negative regulator independent of JAK-STAT pathway in tumorigenic transformation of prostate tissue. The results of the present report focuses on the fundamental differences in major oncogenic signaling cascades between benign and malignant form of prostate tissue that plays a crucial role in prostate cancer biology.

  • 7.
    Singh, Neha
    et al.
    Högskolan i Skövde, Institutionen för biovetenskap. Högskolan i Skövde, Forskningscentrum för Systembiologi. Department of Biotechnology, Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), NOIDA, India.
    Kakkar, Nandita
    Department of Histopathology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Singh, Shrawan K.
    Department of Urology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Sobti, Ranbir C.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), NOIDA, India.
    Implication of high risk Human papillomavirus HR-HPV infection in prostate cancer in Indian population- A pioneering case-control analysis2015Inngår i: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 5, artikkel-id 7822Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Prostate cancer is the second most common cancer with sexual history as a consistent risk factor. This is the pioneering study that evaluates the frequency of HPV infection in prostate cancer in India. Ninety five (95) histopathologically confirmed cancer and fifty five (55) BPH from Indian population were analyzed for HPV infection using a pair of consensus sequence primer followed by type specific PCRs for both high-risk and low-risk HPV types. The data demonstrate HPV infection in 41% of prostate tumor biopsies and 20% in BPH. Subsequent PCR- based HPV typing using type - specific primers revealed 32% were infected with HPV type 16 whereas 6% were found to be positive for HPV type 18, while in BPH controls only 5% of the BPH controls were infected with HPV 16 and this difference was highly significant (p = 0.0004). Significant proportion of HPV infected (74%) cases belonged to stage III and IV (p < 0.001) with a high Gleason score ≥8 (p = 0.003). The study represents for the first time the incidence of HPV infection in prostate cancer in Indian population and strengthens the hypothesis that HPV infection could be one of the co factor associated with progression of prostate cancer.

  • 8.
    Singh, Neha
    et al.
    Högskolan i Skövde, Institutionen för biovetenskap. Högskolan i Skövde, Forskningscentrum för Systembiologi. Department of Biotechnology, Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Oncology, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Sharma, Upma
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Suri, Vanita
    Department of Obstetrics and Gynecology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Nijhawan, Raje
    Department of Cytology & Gynae. Pathology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Sobti, R. C.
    Department of Biotechnology, Panjab University, Chandigarh, India / Vice Chancellor BBA (Central) University, Lucknow, India.
    The protective role of the -1306C>T functional polymorphism in matrix metalloproteinase-2 gene is associated with cervical cancer: implication of human papillomavirus infection2016Inngår i: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 37, nr 4, s. 5295-5303Artikkel i tidsskrift (Fagfellevurdert)
  • 9.
    Singh, Neha
    et al.
    Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Genetics, 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, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics, Institute of Cytology and Preventive Oncology (ICMR), Noida, India.
    Das, B. C.
    Ambedkar Centre for Biomedical Research, Delhi University, New Delhi, India.
    Sobti, R. C.
    Panjab University, Chandigarh, India.
    Abstract 2719: Aberrant expression of transcription factors STAT-3 and STAT-5 and their epigenetic control by SOCS-1 gene: The STAT signaling crosstalk in HPV coupled cervical carcinogenesis2011Inngår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 71, nr 8 Suppl, artikkel-id Abstract 2719Artikkel i tidsskrift (Fagfellevurdert)
  • 10.
    Singh, Neha
    et al.
    Department of Biotechnology, Panjab University, Chandigarh, India / Centre for Stem Cell and Tissue Engineering, Panjab University, Chandigarh, India.
    Sobti, R. C.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Suri, Vanita
    Department of Obstetrics and Gynecology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
    Nijhawan, Raje
    Department of Cytology and Gynae Pathology, PGIMER, Sector-12, Chandigarh, India.
    Sharma, Shweta
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), NOIDA, India.
    Das, B. C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi (North Campus), Delhi, 110 007, INDIA.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), NOIDA, India.
    Hussain, Showket
    Division of Molecular Genetics and Biochemistry, Institute of Cytology and Preventive Oncology (ICMR), NOIDA, India.
    Downregulation of tumor suppressor gene PML in uterine cervical carcinogenesis: impact of human papillomavirus infection (HPV)2013Inngår i: Gynecologic Oncology, ISSN 0090-8258, E-ISSN 1095-6859, Vol. 128, nr 3, s. 420-6Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVES: Cervical cancer is a leading gynecological cancer in Indian women and is caused due to infection with high risk human pappilloma virus (HR-HPV) 16 and 18. It has been well documented that PML (promyelocytic leukemia) enhances viral infectivity and plays a crucial role in antiviral response mechanisms. The aim of the present study was to evaluate the role of PML gene with context to HPV infection in cervical carcinogenesis.

    METHODS: The expression pattern of PML was analyzed by western blotting and immunohistochemistry in a total of 170 fresh surgically resected cervical tissue specimens comprising precancer (n=12), cancer (n=118) and normal controls (n=40) recruited from PGIMER, Chandigarh, India. HPV status was analyzed by L1 consensus PCR followed by type specific PCR for HR-HPV types 16 and 18 and low risk types 6 and 11.

    RESULTS: A significant downregulation of PML protein was observed in the majority of cervical cancer and precancer cases 68% (89/130) compared to normal controls. The loss of expression pattern of PML gene was significantly increased with severity of disease both clinically and pathologically (p<0.001). HPV infection was detected in the majority of cancer cases 96% (113/118) and in 83% (10/12) of precancer lesions whereas no infection could be detected in normal controls. Interestingly, all the 68% (89/130) cervical cancer cases that showed downregulation of PML were HPV infected (p=0.0001).

    CONCLUSION: Taken together, these observations suggest that the downregulation of PML gene and its synergism with HPV infection may play an important role and may serve as a new marker for early diagnosis and therapeutic intervention for cervical carcinogenesis.

  • 11.
    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 population2009Inngår i: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 330, nr 1-2, s. 193-9Artikkel i tidsskrift (Fagfellevurdert)
    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.

  • 12.
    Sobti, R. C.
    et al.
    Department of Biotechnology, Panjab University, Sector-14, Chandigarh, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Sector-14, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), I-7, Sector-39, Noida, India.
    Suri, Vanita
    Department of Gynaecology and Obstetrics, PGIMER, Sector-12, Chandigarh, India.
    Nijhawan, Raje
    Department of Cytology & Gynae Pathology, PGIMER, Sector-12, Chandigarh, India.
    Bharti, A. C.
    Division of Molecular Oncology, Institute of Cytology & Preventive Oncology (ICMR), I-7, Sector-39, Noida, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), I-7, Sector-39, Noida, India.
    Das, B. C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi, (North Campus), Delhi, India.
    Aberrant promoter methylation and loss of suppressor of cytokine signalling-1 gene expression in the development of uterine cervical carcinogenesis2011Inngår i: Cellular Oncology, ISSN 2211-3428, E-ISSN 2211-3436, Vol. 34, nr 6, s. 533-43Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Cervical cancer is a leading cause of cancer related deaths in women worldwide caused due to infection of high-risk human papillomaviruses. As JAK/STAT signalling pathway has been shown to play an important role during carcinogenesis, we studied the role of silencing of Suppressor of Cytokine Signalling-1 (SOCS-1) gene, a negative regulator of JAK/STAT pathway in cervical cancer.

    METHODS: The expression pattern of SOCS-1 mRNA and protein was analyzed in different stages of cervical tumor biopsies while normal cervical tissues served as controls. RT-PCR, immunohistochemistry and methylation-specific PCR (MSP) were performed to assess the expression pattern and promoter methylation of SOCS-1 gene in a total of 120 fresh surgically resected cervical tissue specimens comprising precancer (n = 12), cancer (n = 78) and normal controls (n = 30).

    RESULTS: Compared with expression of SOCS-1 in normal tissues, 64% of the tumor tissues expressed either undetectable or reduced expression. Aberrant promoter methylation of SOCS-1 was found in 61% of the cervical tumor tissues. SOCS-1 expression and methylation were significantly associated with severity of the disease (p < 0.01).

    CONCLUSION: We demonstrate for the first time the transcriptional inactivation of SOCS-1 gene due to hypermethylation and synergism with HPV infection which may play an important role in cervical carcinoma.

  • 13.
    Sobti, Ranbir C.
    et al.
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Singh, Neha
    Department of Biotechnology, Panjab University, Chandigarh, India.
    Hussain, Showket
    Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Suri, Vanita
    Department of Gynaecology and Obstetrics, PGIMER, Chandigarh, India.
    Bharadwaj, Mausumi
    Division of Molecular Genetics and Biochemistry, Institute of Cytology & Preventive Oncology (ICMR), Noida, India.
    Das, Bhudev C.
    Dr. B.R. Ambedkar Research Centre for Biomedical Research (ACBR), University of Delhi, India.
    Deregulation of STAT-5 isoforms in the development of HPV-mediated cervical carcinogenesis2010Inngår i: Journal of Receptor and Signal Transduction Research, ISSN 1079-9893, E-ISSN 1532-4281, Vol. 30, nr 3, s. 178-188Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Cervical cancer is the second most common cancer and is leading cause of cancer related deaths in women worldwide. High Risk-Human papillomavirus (HPV) types play an important role in cervical carcinogenesis. Considering the important role of signal transducer and activator of transcription-5 (STAT-5), an important member of JAK/STAT family which plays a crucial role in various cancers and HPV as a key mediator in the development of cervical carcinogenesis, the purpose of the current study was to examine the possible relationship between HPV infection and expression of STAT-5 gene isoforms in cervical cancer.

    METHODS: A total of 120 fresh cervical tissue specimens comprising precancer (n = 12), cancer (n = 78) and normal controls (n = 30) were analyzed for HPV infection and expression pattern of STAT-5 mRNA (both isoforms STAT-5a and STAT-5b) and protein in different stages of cervical carcinoma biopsies by reverse-transcriptase-PCR, western blotting and immunohistochemistry.

    RESULTS: A significantly increased expression of STAT-5 was detected in most of the cervical tumors (P < 0.001), whereas it was almost undetectable in normal controls. Also the study of relative contribution of STAT-5 isoforms revealed a higher expression pattern of STAT-5b and was associated with severity of the disease. On the contrary, STAT-5a was found to be significantly downregulated in cervical tumor tissues (P < 0.001). HPV infection was found in 90% of the cervical cancer cases and was significantly associated with STAT-5 overexpression (P = 0.001).

    CONCLUSIONS: We observed for the first time the differential expression pattern of STAT-5 isoforms in cervical cancer and that STAT-5 may play an important role in the progression of HPV-mediated cervical cancer.

  • 14.
    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 cancer2012Inngår i: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 369, nr 1-2, s. 217-25Artikkel i tidsskrift (Fagfellevurdert)
    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.

  • 15.
    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 population2012Inngår i: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 362, nr 1-2, s. 263-8Artikkel i tidsskrift (Fagfellevurdert)
    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).

  • 16.
    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 subjects2012Inngår i: Molecular and Cellular Biochemistry, ISSN 0300-8177, E-ISSN 1573-4919, Vol. 360, nr 1-2, s. 1-7Artikkel i tidsskrift (Fagfellevurdert)
    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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