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PubMedDate not supplied

[Initiation of the mouse sarcoma virus oncogene v-K-ras during the chemical treatment of proto-oncogene C-ras].

On the basis of the results obtained in the laboratories of Weinberg, Barbacid et al. describing the responsibility of one or another mutation in one of coding triplets of the ras family gene both for chemical and viral cancerogenesis, we draw the conclusion that it is impossible to distinguish these two causes of cancer appearance. It is shown that the cause of mice viral sarcoma v-K ras development from the cellular protooncogene C-ras may consist in the chemical reaction of one of coding triplet nucleotides with cancerogenic substance.

Animals↗
PubMed1997

Molecular modeling of c-erbB2 receptor dimerization: coiled-coil structure of wild and oncogenic transmembrane domains--stabilization by interhelical hydrogen bonds in the oncogenic form.

Dimerization models of c-erbB2 transmembrane domains (Leu651-Ile675) are studied by molecular mechanics and molecular dynamics simulations. Both wild and Glu mutated transmembrane helices exhibit the same relative orientation for favorable associations and dimerize preferentially in left-handed coiled-coil structures. The mutation point 659 belongs to the interfacing residues, and in the transforming domain, symmetric hydrogen bonds between Glu carboxylic groups stabilize the dimeric structure. The same helix packing found for the wild dimers, except side-chain-side-chain hydrogen bonds, suggests that the transmembrane domains dimerize according to similar process. Structural and energetical characterization of the models are presented.

Amino Acid Sequence↗
PubMed2006

Seroprevalence atlas of infections with oncogenic and non-oncogenic human papillomaviruses in Finland in the 1980s and 1990s.

Vaccines against high-risk (hr) human papillomaviruses (HPVs) causing cervical cancer may soon be licensed. Thus, nature of HPV epidemics needs to be studied now. Random sampling for studies on HPV epidemiology was done from all 230,998 women belonging to the population-based Finnish Maternity Cohort and having a minimum of 2 pregnancies between 1983 and 1994. First pregnancy serum specimens were retrieved for 7,805 subjects, and were analyzed for antibodies to HPV6/11, 16 and 18 with standard ELISAs. HPV16 seroprevalence almost doubled from the 1980s to the 1990s, and the epidemic spread to new areas in 23-31 year olds, i.e. the bulk of pregnant female population in the southwest part of the country. The HPV16 epidemic in the 14-22 year olds in 1983-1988 (1961-1974 birth cohorts) and in the 23-31 year olds in 1989-1994 (1958-1971 birth cohorts) overlapped with strong clustering of HPV16 and HPV18 infections in the latter (odds ratio 8.0, 95% confidence interval 6.6-9.7). Similar clustering of HPV16 and HPV6/11 infections was not found. The epidemic and the clustering may be due to high transmission probability of the hrHPV types and increase in sexual activity of the index birth cohorts.

Adolescent↗