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Alterations of the P16 gene in uterine cervical carcinoma from Indian patients
  1. A. Tripathi (Bhar)*,
  2. S. Banerjee,
  3. A. Roy,
  4. S. Roychowdhury and
  5. C. K. Panda*
  1. * Department of Oncogene Regulation, Chittaranjan National Cancer Institute, Calcutta, India
  2. Department of Human Genetics and Genomics, Indian Institute of Chemical Biology, Calcutta, India
  3. Department of Pathology, Medical College and Hospital, Calcutta, India
  1. Address correspondence and reprint requests to: Dr. C. K. Panda, Department of Oncogene Regulation, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Calcutta-700026, India. Email: ckpanda{at}


In our analysis, alterations in the P16 tumor suppressor gene were seen in 33% (15/46) of sampled uterine cervical lesions. Among the alterations, mutations in P16 were detected in 15% (7/46) of the samples. One mutation occurred at intron 1/exon 2 splice junction. All the other mutations were in exon 2 with three of them as silent mutations. The promoter hypermethylation and homozygous deletion of P16 gene were detected in 6.5% (3/46) and 8.7% (4/46) of the samples respectively. Loss of heterozygosity and microsatellite size alterations at the P16 locus were seen in 17% (8/46) of the samples. HPV16/18 infection was detected in 76% (35/46) of the samples. But no association was found between P16 alterations and HPV infection. Thus, it seems that P16 inactivation may be associated with the development of some uterine cervical carcinoma.

  • allelic alterations (LOH/MA)
  • homozygous deletion
  • human papillomavirus (HPV)
  • hypermethylation
  • mutation
  • P16

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