PMID- 7665253
OWN - NLM
STAT- MEDLINE
DCOM- 19951011
LR  - 20190708
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 64
IP  - 1
DP  - 1995 Feb 20
TI  - Analysis and clinical implications of K-ras gene mutations and infection with 
      human papillomavirus types 16 and 18 in primary adenocarcinoma of the uterine 
      cervix.
PG  - 9-13
AB  - Experimental models indicate that activated ras genes and HPV oncogenic sequences 
      may cooperate in inducing a completely transformed phenotype in epithelial cells. 
      We searched for K-ras gene mutations and HPV type-16 and -18 sequences in 67 
      primary adenocarcinomas of the uterine cervix by analyzing DNAs from 
      formalin-fixed, paraffin-embedded tissue samples. Target sequences were amplified 
      by PCR and analyzed by denaturing gradient gel electrophoresis (DGGE) and 
      sequencing for the detection of K-ras gene mutations and by Southern blotting for 
      the detection of HPV infection. We found 16 mutations in 15 cases; 14 were at 
      codon 12 and 2 at codon 13; 11 were base transitions and 5 were transversions. 
      Mutations were more frequent in mucin-secreting than in non-mucinous tumors. HPV 
      oncogenic sequences were detected in 58 cases with no significant difference 
      between K-ras-mutated and wild-type tumors. HPV oncogenic sequences were also 
      more frequent in mucin-secreting than in non-mucinous tumors. Both molecular 
      events were present simultaneously in 13 out of 58 cases, all of which had 
      histologically grade-2 and grade-3 tumors. Clinico-pathological parameters of the 
      disease and the overall survival, however, were independent of K-ras mutations 
      and of HPV-16 and -18 infection, as shown by univariate and multivariate 
      analysis. In contrast, stage of disease, lymph-node metastases, deep 
      infiltration, clear-cell histology and low grade of differentiation were risk 
      factors for tumor-related death.
FAU - Tenti, P
AU  - Tenti P
AD  - Department of Human Pathology, University of Pavia, Italy.
FAU - Romagnoli, S
AU  - Romagnoli S
FAU - Silini, E
AU  - Silini E
FAU - Pellegata, N S
AU  - Pellegata NS
FAU - Zappatore, R
AU  - Zappatore R
FAU - Spinillo, A
AU  - Spinillo A
FAU - Zara, C
AU  - Zara C
FAU - Ranzani, G N
AU  - Ranzani GN
FAU - Carnevali, L
AU  - Carnevali L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (DNA Primers)
RN  - 0 (DNA, Viral)
RN  - EC 3.6.5.2 (HRAS protein, human)
RN  - EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
SB  - IM
MH  - Adenocarcinoma/*genetics/*virology
MH  - Adult
MH  - Aged
MH  - Base Sequence
MH  - DNA Primers/chemistry
MH  - DNA, Viral/analysis
MH  - Female
MH  - *Genes, ras
MH  - Humans
MH  - Middle Aged
MH  - Molecular Sequence Data
MH  - Papillomaviridae/*genetics
MH  - Papillomavirus Infections/*complications/diagnosis
MH  - Point Mutation
MH  - Proto-Oncogene Proteins p21(ras)/*genetics
MH  - Survival Analysis
MH  - Tumor Virus Infections/*complications/diagnosis
MH  - Uterine Cervical Neoplasms/*genetics/*virology
EDAT- 1995/02/20 00:00
MHDA- 1995/02/20 00:01
CRDT- 1995/02/20 00:00
PHST- 1995/02/20 00:00 [pubmed]
PHST- 1995/02/20 00:01 [medline]
PHST- 1995/02/20 00:00 [entrez]
AID - 10.1002/ijc.2910640104 [doi]
PST - ppublish
SO  - Int J Cancer. 1995 Feb 20;64(1):9-13. doi: 10.1002/ijc.2910640104.