Search PubMed⌕ Search

Biomedical subjects

T G Krontiris

Publications and source records attributed to T G Krontiris.

26 records · Page 2Linked to original sources
PubMed1986

Human restriction fragment length polymorphisms and cancer risk assessment.

The polymorphic restriction fragments of the human Ha-ras locus, produced by the variable tandem repetition (VTR) of a short consensus sequence, fall into three classes based on allelic frequencies. Alleles of the "rare" class (individual frequencies less than 0.5%) have been detected only in white blood cell and tumor DNA of cancer patients. This phenomenon is independent of ethnic origin. No significant association of rare alleles with cancer patients has been demonstrated at an independent tandem repeat locus, VTR4.1. The results suggest that the Ha-ras restriction fragment length polymorphism is useful in cancer risk assessment.

Alleles↗
PubMed1986

Oncogenes.

Many of the genes that are likely participants in the pathogenesis of human neoplasia have been identified. The major classes of events that activate these genes in tumors have also been described. We expect that continuing research on the function of oncogenes will greatly inform our understanding of fundamental growth control processes and, eventually, influence our approaches to treating cancer patients.

Animals↗
PubMed1985

Rearrangement of the gene for the beta chain of the T-cell receptor in T-cell chronic lymphocytic leukemia and related disorders.

Although monoclonal B-cell populations can be identified both by surface-marker analysis and by immunoglobulin-gene rearrangements, this has not been possible with T cells. We have employed cDNA probes that are specific for the entire beta chain of the T-cell receptor, and for its constant and variable regions, to investigate gene rearrangements in T-cell chronic lymphocytic leukemia and related disorders. In three malignant proliferations of helper (T4-positive) T cells, rearrangements of the beta-chain constant-region gene were readily demonstrated. A patient from the Caribbean who had adult T-cell lymphoma and antibody to human T-cell lymphotrophic virus Type I (HTLV-I), a patient with virus-negative chronic lymphocytic leukemia, and a patient with cutaneous T-cell lymphoma (Sézary variant) made up the T4-positive group. Three additional patients with chronic T8 (cytotoxic-suppressor) lymphocytosis and neutropenia were studied; in two; rearrangements were found. In all five patients with constant-region rearrangements, deletions of variable-region restriction fragments were observed as well. The presence of rearrangements of a T-cell receptor gene provides presumptive evidence for the clonal nature of T-cell proliferation and for its neoplastic character.

Adult↗
PubMed1983

The emerging genetics of human cancer.

A rapid and exciting accumulation of data about cellular oncogenes in human tumors has resulted from convergent research on DNA-mediated gene transfer, retroviruses, and tumor cytogenetics. Such work promises to increase our understanding of the genetic events that predispose to, and result in, malignant disease. This knowledge may quickly find clinical application in tumor classification and prediction of risk. Ultimately, therapeutic benefits may be achieved as we begin to explore the mechanisms by which transforming gene products act to defeat the normal regulatory processes of cells.

Cell Transformation, Neoplastic↗
PubMed1982

Transforming genes of human bladder and lung carcinoma cell lines are homologous to the ras genes of Harvey and Kirsten sarcoma viruses.

Blot hybridization analysis indicated that NIH 3T3 mouse bladder transformed by high molecular weight DNAs of a human bladder and a human lung carcinoma cell line contained new sequences homologous, respectively, to the transforming genes of Harvey (rasH) and Kirsten (rasK) sarcoma viruses. The unique ras sequences were present in multiple independent NIH cell lines transformed in both primary and secondary transfection assays and corresponded to ras sequences normally present in human DNAs. The ras gene product was expressed in NIH cells transformed by bladder carcinoma DNAs and in the human bladder carcinoma cell lines at levels 2- to 4-fold greater than the level observed in nontransformed NIH 3T3 cells. These results indicate that the transforming genes of these human tumor cell lines are the cellular homologs of two retroviral transforming genes.

Animals↗
PubMed1981

Transforming activity of human tumor DNAs.

High molecular weight DNAs of 26 human tumors and tumor cell lines were assayed for the presence of transmissible activated transforming genes by transfection of NIH 3T3 mouse cells. DNAs of two bladder carcinoma cell lines induced transformation with high efficiencies (approximately 0.2 transformant per microgram of DNA), whereas DNAs of the other tumors studied lacked detectable transforming activity. These findings suggest that dominant mutations or gene rearrangements can result in the activation of cellular transforming genes in some human tumors.

Animals↗
PubMed1973

Host restriction of Friend leukemia virus. Role of the viral outer coat.

Host restriction of oncogenesis of RNA tumor viruses in vivo is associated with several gene loci. One of these genes, the Fv-1 locus in mice, is expressed in vitro and may be studied in mouse-embryo cultures that are restrictive or permissive for replication of Friend leukemia virus. Two strains of Friend leukemia virus, N-or B-tropic, show reciprocal ability to replicate successfully in either NIH Swiss (N-type) or BALB/c (B-type) cells that differ at the Fv-1 locus. These two strains of virus and two cell lines form a system to measure host restriction in vitro. Measurement of adsorption of Friend leukemia virus to permissive or restrictive cells reveals no difference in rate or total amount of virus bound. Furthermore, studies with virions of vesicular stomatitis virus phenotypically mixed within an envelope containing Friend leukemia virus protein show no differences in penetration or replication of vesicular stomatitis virus. These results strongly suggest that host restriction of Friend leukemia virus is due to an intracellular event in the viral replication cycle.

Animals↗