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PubMed1988

Differential expression of cellular oncogenes during rat liver development.

The expression of a number of proto-oncogenes (myc, erb B, Ha-ras, bas, rel, mos, sis, myb, ki-ras, fms, src and fos) was studied in developing rat liver. Northern blot hybridization shows that cellular counterpart of erb B, Ha-ras, and fos oncogenes were in an early stage of liver development, and the expressions of these proto-oncogenes gradually decreased as the liver developed, while c-myc transcript was found only in the rat fetal liver. The transcripts of these oncogenes were found in high level in Morris hepatoma 7777. Bas proto-oncogene was found in high expression at early stages of rat liver development but was not in hepatoma 7777. The expression of other proto-oncogenes studied (src, fm, rel, mos, sis, myb and ki-ras) did not change significantly during liver development and was almost the same in hepatoma and normal adult liver. Southern blot analysis demonstrates that gene amplification and apparent gene rearrangement were not responsible for the change in expression of erb B, Ha-ras, myc and fos proto-oncogenes. Our study gives further evidence that erb B, myc, Ha-ras and fos proto-oncogenes are involved in the control of cell growth and in the process of rat hepatocarcinogenesis.

Aging↗
PubMed2003

Expression of oncogenes depends on biotin in human small cell lung cancer cells NCI-H69.

Oncogenes play important roles in cell proliferation and biotin status correlates with gene expression and proliferation rates in human cells. In this study we determined whether biotin supply affects biotin homeostasis, expression of oncogenes, and proliferation rates in NCI-H69 small cell lung cancer cells. NCI-H69 cells were cultured in media containing deficient (0.025 nmol/L), physiologic (0.25 nmol/L), or pharmacologic (10 nmol/L) concentrations of biotin for 3 weeks. Biotin concentrations in culture media correlated negatively with biotin transport rates, suggesting that cells responded to marginal biotin supply with increased expression of biotin transporters. Increased biotin uptake was not sufficient to prevent depletion of intracellular biotin in cells cultured in biotin-deficient medium, as judged by decreased activity of biotin-dependent propionyl-CoA carboxylase and decreased biotinylation of histones. The expression of oncogenes N-myc, c-myb, N-ras, and raf correlated with biotin supply in media: oncogene expression increased by up to 20% in cells cultured in pharmacologic medium compared to physiologic controls; oncogene expression decreased by up to 47% in cells cultured in deficient medium. This observation is consistent with a role for biotin in oncogene-dependent metabolic pathways. Cellular uptake of thymidine (marker for proliferation) was not affected by biotin supply, suggesting that effects of biotin-dependent expression of oncogenes on the growth of tumor cells are quantitatively minor. The clinical significance of effects of biotin supply on expression of oncogenes remains to be elaborated.

Biological Transport↗
PubMed1983

Characterization of a human colon/lung carcinoma oncogene.

DNA sequences capable of inducing oncogenic transformation of NIH3T3 mouse cells are found in a number of human tumour cell lines. When DNAs of these cell lines are applied to monolayer cultures of the mouse fibroblasts, foci of transformed cells are observed 2-3 weeks later. DNA from cells of such primary foci can be used in turn to induce foci in a second cycle of gene transfer. The human DNA sequences responsible for transformation have been called oncogenes, the best characterized of which is closely related to the Harvey murine sarcoma virus oncogene. Here we present a characterization of an oncogene which we found originally to be present in DNA of the SW480 colon carcinoma cell line. We indicate its structural outlines and demonstrate, in extension of reported results, its presence in an activated form in the genome of several types of human tumour cell lines as well as in biopsy tissue from an adenocarcinoma of the large bowel. We identify this tumour oncogene with c-Ki-ras2, one of two known members of the Kirsten ras family of human proto-oncogenes, extending a series of recent reports which have demonstrated homologies between human oncogenes and those of Harvey and Kirsten murine sarcoma viruses. The c-Ki-ras2 oncogene of several tumour cell lines is shown to be amplified.

Colonic Neoplasms↗
PubMedDate not supplied

Homologous cell-derived oncogenes in avian carcinoma virus MH2 and murine sarcoma virus 3611.

Retroviral oncogenes (v-onc) are derived from cellular genes (c-onc) which are highly conserved among different species. Retrovirus-transduced oncogenes are most commonly associated with the induction of haematopoietic tumours and sarcomas. The avian retrovirus Mill Hill no. 2 (MH2) was isolated from a spontaneous ovarian tumour of a chicken and is distinguished by the predominant induction of liver and kidney carcinomas in fowl. MH2 also induces transformation of fibroblasts, macrophages and epithelial cells in culture. The genome of MH2 contains two unrelated and independently expressed cell-derived oncogenes, v-mil and v-myc. Three other viral isolates among avian acute transforming retroviruses contain the v-myc oncogene, but only MH2 contains both v-myc and v-mil. Hence, some of the pathogenic specificities of MH2 may be due to the simultaneous expression of two oncogenes. The murine sarcoma virus 3611 (3611-MSV) isolated from a mouse carrying lung carcinoma and peritoneal tumours, induces fibrosarcomas in newborn mice and the transformation of fibroblasts and epithelial cells in culture. The oncogenic properties of 3611-MSV are due to the presence in its genome of a cell-derived oncogene termed v-raf. We report here that the two independently transduced oncogenes v-mil and v-raf are closely related and that they were apparently derived from homologous cellular genes of avian and mammalian species.

Animals↗
PubMed2005

Is oncogene addiction angiogenesis-dependent?

Does an activated oncogene that initiates tumor growth need to remain activated to maintain the cancer phenotype? This question has been answered affirmatively by experiments in which doxycycline-regulated oncogene activation induces growth of large tumors that regress completely upon oncogene inactivation--a phenomenon called oncogene addiction. We assemble here the evidence that oncogene addiction is angiogenesis-dependent. Although activated oncogenes increase tumor cell proliferation and decrease their apoptosis, these activities are not sufficient to expand tumor mass beyond a microscopic size. Oncogenes must also induce tumor angiogenesis for expansion of tumor mass. We propose experiments to validate the "endothelial centric" hypothesis of oncogene addiction.

Animals↗
PubMed1983

Multi-step genetic regulation of oncogene expression in fish hereditary melanoma.

Melanoma occurring spontaneously in Xiphophorus fish hybrids is a model system in which involvement of cellular oncogenes and multi-step regulation of their expression have been identified by classical genetics. The macromelanophore gene in platyfish (Xiphophorus maculatus) is a sex-linked codominant gene which determines the black spot patterns of macromelanophores in the skin. The macromelanophore locus includes a cellular oncogene which potentially induces neoplasms of the pigment cells. Expression of the oncogene is regulated by a multi-step genetic process and brings about a characteristic phenotype associated with pigment cell differentiation at each step. The multi-step genetic regulation of oncogene expression can be recognized by interspecific hybridization of the platyfish with swordtails (Xiphophorus helleri) which have not developed the macromelanophore gene. When platyfish are hybridized with swordtails, the F1 offspring carrying this gene develop a preneoplastic state. When the F1 offspring are back-crossed to swordtails, the backcross offspring develop a heritable form of melanoma with a characteristic inheritance pattern. This heritable form of melanoma occurs at an early age and has a well differentiated character. Thus, the first and second steps of oncogene expression bring about a preneoplastic state in the F1 offspring and a heritable form of melanoma in the backcross offspring, respectively. These steps may be due to progressive substitution of platyfish chromosomes with swordtail chromosomes in germ line cells, resulting in a progressive reduction of the dosage of regulatory genes in the platyfish genome. The third step of oncogene expression brings about a sporadic form of melanoma in the hybrid offspring bearing the preneoplastic state and heritable form of melanoma spontaneously or through induction by carcinogens. This form of melanoma has a poorly differentiated character. The incidence of this form is considerably enhanced by aging in adult life, thus exhibiting age-specific incidence. It is likely that this step is due to mutational events in regulatory genes, which occur in somatic cells following chromosome substitution in germ line cells by hybridization. The albino gene enhances the malignancy of the two forms of melanoma and the incidence of the sporadic form of melanoma, possibly by suppressing the differentiation of transformed pigment cells. These facts and speculations are summarized in Fig. 6. The molecular identification of oncogenes in this melanoma system and their transfer into the swordtail eggs may provide a useful means for studying oncogene expression during development, growth, and aging of animals.

Age Factors↗
PubMed1987

Expression of oncogenes in human tumours with special reference to the head and neck region.

A major recent advance in cancer research has been in the field of oncogenes. Oncogenes are genes with a proven cancer association and which appear to be particularly implicated in cellular regulation and proliferation. The oncogenic potential of specific cellular genes has now been recognised and this has influenced current thinking concerning the initiation of carcinogenesis. The specific role of an oncogene is still incompletely understood but research with one particular oncogene (ras) has demonstrated that it can be involved in more than one stage of multi-step carcinogenesis. New techniques are being developed and evaluated to determine the expression of specific oncogenes in normal and neoplastic tissues, with a view to using them in future diagnostic immuno-histopathological methods. This review describes the concept of oncogenes and discusses their role in the development of neoplasia. The results of the expression of various oncogenes in human malignancies with special reference to the head and neck regions are discussed. Finally, the future prospects of this research field are examined their and its possible implications in cancer therapy.

Adenoma, Pleomorphic↗
PubMed1987

Control of c-fos and c-myc proto-oncogene induction in rat thyroid cells in culture.

Removal of TSH, insulin, and cortisol from the medium, and decreasing the serum content to 0.2%, abolishes both the proliferate and differentiated state of FRTL-5 rat thyroid cells in culture. In these basal conditions, the individual addition of TSH, insulin, insulin-like growth factor-I (IGF-I), phorbol 12-myristate 13-acetate (TPA), alpha 1-adrenergic agents, or A23187, increase c-myc and/or c-fos proto-oncogene expression. Under the same conditions, only the addition of TSH increased cAMP levels; 8-bromo-cAMP can increase c-myc or c-fos mRNA levels. Pretreatment of cells with phorbol 12,13-dibutyrate, an agent which down regulates the C-kinase, completely inhibits the effect of TPA on proto-oncogene expression but has no affect on the A23187 induced-increase. The sum of these results indicate that at least four separate signal systems independently increase c-myc or c-fos gene expression in FRTL-5 cells cAMP (TSH), C-kinase (TPA), Ca++/phosphoinositide (A23187), and that influenced by insulin/IGF-I. None of the ligands, when individually returned to cells in basal medium (no TSH, insulin, or cortisol and only 0.2% serum), increases cell number; norepinephrine, and A23187 do not increase [3H]thymidine incorporation into DNA under these conditions; and combinations of the ligands can be more than additive in effecting [3H]thymidine incorporation into DNA but are only additive in effecting proto-oncogene expression. Insulin/IGF-I plus TSH or insulin/IGF-I plus norepinephrine can increase both proto-oncogene expression and [3H]thymidine incorporation into DNA to the same extent; however, the former combination can increase cell number whereas the latter cannot. There is therefore no simple correlation between the ability of the above ligands to increase proto-oncogene expression and their ability to increase cell number or induce DNA synthesis. Under conditions where insulin and IGF-I increase proto-oncogene expression but not cell number, they can increase thyroglobulin gene expression. In the presence of TSH, insulin and IGF-I are not additive with each other in their ability to increase thyroglobulin or proto-oncogene gene expression but are additive in their ability to increase cell number. Proto-oncogene expression in FRTL-5 rat thyroid cells, as in other cell systems, may thus be related to functional as well as proliferative responses.

Animals↗
PubMed2005

Detection and characterization of oncogene mutations in preneoplastic and early neoplastic lesions.

Although it has been more than 20 yr since its discovery, the ras family of genes has not yet lost its impact on basic and clinical oncology. These genes remain central to the field of molecular oncology as tools for investigating carcinogenesis and oncogenic signaling, as powerful biomarkers for the identification of those who have or are at high risk of developing cancer, and as oncogene targets for the design and development of new chemotherapeutic drugs. Mutational activation of the K-RAS proto-oncogene is an early event in the development and progression of the colorectal, pancreatic, and lung cancers that are the major causes of cancer death in the world. The presence of point mutational "hot spots" at sites necessary for the activation of this proto-oncogene has led to the development of a number of highly sensitive PCR-based methods that are feasible for the early detection of K-RAS oncogene mutations in the clinical setting. In light of these facts, mutation at the K-RAS oncogene has the potential to serve as a useful biomarker in the early diagnosis and risk assessment of cancers with oncogenic Ras signaling. This chapter describes a highly sensitive method for detecting mutant K-RAS, enriched PCR, and its application to early detection of this oncogene in preneoplastic and early neoplastic lesions of the colon and rectum.

Animals↗
PubMed1997

Hypomethylation of the Xmrk oncogene promoter in melanoma cells of Xiphophorus.

Melanoma formation in Xiphophorus is caused by the tissue-specific overexpression of the Xmrk oncogene. This gene arose by a non-homologous recombination event between the Xmrk proto-oncogene and an unrelated locus, D, during which the Xmrk transcribed regions were fused to new upstream sequences. Functional analyses of this newly acquired promoter revealed the presence of positive regulatory elements. Since these elements did not activate transcription in a melanoma-specific manner, the methylation state of the Xmrk oncogene promoter in different tissues was analyzed. Digestion with methylation sensitive restriction enzymes followed by PCR amplification demonstrated differential methylation in a melanoma cell line and non-melanoma tissue. The methylation state of single CpG-dinucleotides in genomic DNA from different cell types was investigated by bisulfite genomic sequencing. This analysis revealed a high degree of methylation of the Xmrk oncogene promoter in non-transformed tissues. In contrast, the DNA-region analyzed was completely unmethylated in the melanoma cell line PSM. This effect was oncogene-specific, since the Xmrk proto-oncogene showed CpG-methylation in these cells. Studies with melanoma tissue demonstrated that hypomethylation of the Xmrk oncogene promoter can also be found in DNA from these tumors. This correlation suggests that the methylation status of the promoter might play a role in the overexpression of the Xmrk oncogene in vivo.

Animals↗
PubMed2004

Development of new anti-cancer peptides from conformational energy analysis of the oncogenic ras-p21 protein and its complexes with target proteins.

We have employed a computational approach to design peptides, from known oncogenic proteins, that inhibit tumor growth. This approach has been applied to the ras-p21 protein that becomes oncogenic when single amino acid substitutions occur at critical positions in its polypeptide chain, such as at Gly 12 and Gln 61. In this approach, using two sampling methods, molecular dynamics and the electrostatically driven Monte Carlo (EDMC) method, we have computed the average structures of wild-type and oncogenic forms of ras-p21 alone and bound to a number of its target proteins, such as the ras-binding domain (RBD) of raf, guanine nucleotide exchange protein (GAP) and SOS guanine nucleotide exchange protein (GAP). By superimposing the average structures of the oncogenic forms on those of their wild-type counterparts, we have identified a number of domains that change conformation. These domains are potential effector domains that are involved uniquely in oncogenic ras-p21 signaling. We have therefore synthesized peptides corresponding to these domains and tested them in Xenopus laevis oocytes for their abilities to inhibit oncogenic ras-p21 selectively. Using this approach, we have identified three peptides from ras-p21 and one peptide each from the RBD of raf, GAP and SOS that selectively inhibit oncogenic but not insulin-activated wild-type ras-p21-induced oocyte maturation. We have synthesized the ras-p21 peptides attached to a penetratin leader sequence to enable cell membrane penetration and introduced these peptides into a ras-transformed pancreatic cancer cell line; these peptides, but not an unrelated negative control peptide, cause the cells to undergo complete phenotypic reversion. On the other hand, none of these peptides has any effect on the growth of untransformed pancreatic acinar cells in culture, further suggesting that they may not interfere with normal cell growth. Thus these peptides can be useful agents in the treatment of cancers. We have further used these peptides to demonstrate that oncogenic and wild-type ras-p21 proteins utilize different signal transduction pathways and to identify where these differences occur in cells.

Animals↗
PubMed1991

Transcriptional activation of the melanoma inducing Xmrk oncogene in Xiphophorus.

The melanoma inducing locus of Xiphophorus encodes a tumorigenic version of a novel putative receptor tyrosine kinase (Xmrk). To elucidate the mechanism of oncogenic activation of Xmrk, we compared the structure and expression of two oncogenic loci with the corresponding proto-oncogene. Only minor structural alterations were found to be specific for the oncogenic Xmrk genes. Marked overexpression of the oncogene transcripts in melanoma, which are approximately 1 kb shorter than the proto-oncogene transcript, correlates with the malignancy of the tumors. The tumor transcripts are derived from an alternative transcription start site that is used only in the oncogenic loci. Thus, oncogenic activation of the melanoma inducing Xmrk gene appears primarily to be due to novel transcriptional control and overexpression.

Animals↗
PubMed1989

Oncogene mediated repression of glucocorticoid hormone response elements and glucocorticoid receptor levels.

We have previously described the inhibition of glucocorticoid-dependent transcription from the mouse mammary tumor virus long terminal repeat promoter by products of the H-ras and v-mos oncogenes. We have studied the effects of conditional oncogenes on expression of glucocorticoid-dependent indicator genes. Expression of the glucocorticoid-dependent transcription of the tyrosine aminotransferase gene was monitored in FTO-2B rat hepatoma cells during Mr 21,000 protein (p21) H-ras induction. A strong transcriptional repression of the tyrosine aminotransferase gene followed p21 H-ras expression. The sequences in a glucocorticoid-dependent promoter which are responsible for the oncogene-mediated repression could be localized to the glucocorticoid response element; a construct in which a 15-base pair glucocorticoid response element was inserted 5' of the thymidine kinase promoter exhibited the oncogene-mediated repression of transcription. We observed a strong repression of glucocorticoid-dependent promoters and promoter constructs not only in the presence of p21 H-ras and p37 v-mos but also with p60 v-src. p57 v-myc, however, had no effect. Oncogene expression is not a sufficient prerequisite for an initial repression of glucocorticoid hormone-dependent gene transcription, since even in the presence of constitutively high levels of oncogene product a transient stimulation of glucocorticoid-dependent gene expression was found. Protein synthesis inhibition experiments revealed that no hormonally induced cellular protein is needed for the oncogene-mediated repression. It seemed reasonable that this phenomenon might reflect oncogene effects on the glucocorticoid receptor. We, therefore, made measurements of the glucocorticoid receptor protein. In the presence of glucocorticoid hormone the receptor translocated rapidly from the cytoplasm to the nucleus. In normal NIH 3T3 cells, after 24-h treatments the nuclear receptor levels had declined to about 50% of those determined at 2 h and in the presence of p21 H-ras they declined to 15%. The levels of cytoplasmic receptor were not affected by p21 H-ras expression.

Animals↗
PubMed1988

[Oncogenes and the origin of leukemia. Acute avian leukemia viruses].

Oncogenes have been intimately associated with the genesis of human neoplasms. A particularly useful system to study the mechanism of tumorigenesis is a small group of avian retroviruses that carry two oncogenes. These viruses causes acute leukemias and can transform hematopoietic cells in vitro. The mechanisms by which viral oncogenes affect the growth control and differentiation of their target cells is now understood in fair detail for two of these virus strains. In the avian erythroblastosis virus AEV, the v-erbB oncogene deregulates the growth control of erythroid precursors, while verbA blocks their terminal differentiation into erythrocytes. Based on the findings that v-erbB oncogene corresponds to a mutated growth factor receptor gene and that v-erbA corresponds to a mutated hormone receptor gene, models have been developed that explain the function of these two oncogenes on a molecular basis. The myelomonocytic leukemia virus MH2 acts by a completely different mechanism. In this case, the v-myc oncogene stimulates the proliferation of macrophage-like cells, while the v-mil gene stimulates them to produce their own growth factor, thus leading to autocrine growth. It will be interesting to determine whether the type of mechanisms of oncogene cooperativity elucidated for acute leukemia viruses are also operative during leukemogenesis in humans.

Alpharetrovirus↗
PubMed1985

The biological role of oncogenes--insights from platelet-derived growth factor: Rhoads Memorial Award lecture.

No one in tumor biology can now be unaware of the overlap between growth factors and oncogenes. Many if not all oncogenes are now perceived as functional components of a mitogenic cascade which is normally controlled by growth factors. Some oncogenes function at the onset of this cascade by directing the synthesis of an automitogenic growth factor. Others function in the interior of the cascade by directing synthesis of a growth factor receptor or a structurally altered receptor derivative. Still other oncogenes appear to be mutated or rearranged homologues of genes the expression of which is normally induced by growth factors. Those of us working with platelet-derived growth factor (PDGF) take particular satisfaction in this new conceptual framework. It is within the molecular biology of PDGF that the overlap between growth factors and oncogenes is illustrated to its fullest and most tangible extent. An oncogene termed c-sis directs synthesis of a functional PDGF subunit. The PDGF receptor protein is in all probability encoded by a member of the src family of oncogenes. Formation of the PDGF:receptor complex stimulates expression of the c-myc and c-fos protooncogenes. My associates and I have devoted the past 10 years to the molecular biology of PDGF. Our studies on the control of the 3T3 cell cycle by PDGF contributed a pair of new jargon terms to the oncology literature--"competence" and "progression." We also had some input into the bottom end of the "oncogene hierarchy" displayed in Chart 1. The effort that we invested paid a pleasant dividend for me when, in the spring of 1984, the American Association for Cancer Research honored me with the Rhoads Memorial Award. What follows is an overview of the PDGF literature which is more anecdotal than comprehensive. My object is to show how the PDGF field moved from the level of whole animal biology, through biochemistry, down to molecular genetics in just 10 years time.

Animals↗
PubMed1987

The involvement of oncogenes and suppressor genes in human neoplasia.

It is clear that there are at least two classes of cancer-related genes. The more characterized of these are the oncogenes, whose activation appears to play a major role in human neoplasia. There are now two families of oncogenes, the myc and ras families, whose cooperation seems capable of transforming normal cells in culture to tumorigenic cells. As such, they appear to form complementation groups with immortalizing and transforming properties, respectively. Moreover, the oncogenes can be subclassified as tyrosine kinases or kinase related, GTP binding proteins, growth factors or growth factor receptors or nuclear proteins. More than 20 viral oncogenes have been identified, for which more than 30 proto-oncogenes or pseudogenes exist in the human genome. Many of these have been cloned, characterized to some extent, and mapped to particular chromosomes or regions of chromosomes. Further, more than 20 additional putative oncogenes or transforming genes have been identified by tumor DNA transfection studies or at sites of integration or translocation for which no viral transforming gene cognates exist. Oncogenes can be activated by increased or unregulated expression, increased copy number (duplication, amplification), or somatic mutation resulting in a protein with increased oncogenic potential. Examples of all of these mechanisms can be found in several specific human cancers or leukemias. The cytogenetic correlate of enhanced expression is a translocation between two chromosomes at specific breakpoints with no net loss of genetic material (e.g., increased c-myc expression resulting from the 8;14 translocation in Burkitt's lymphoma). The phenomenon of increased gene copy number can sometimes be visualized as trisomy or tetrasomy for a particular chromosome but more dramatically as the development of extrachromosomal DMs or as chromosomally integrated HSRs (e.g., the N-myc gene amplification seen in neuroblastoma). Finally, certain somatic mutations can be associated with translocations (e.g., the bcr/abl fusion product created as a result of the 9;22 translocation in chronic myelogenous leukemia), but they are more commonly submicroscopic (as characterized by point mutations in the ras gene family). Evidence is accumulating for a second class of cancer-related genes whose absence or inactivation is associated with tumorigenesis. These genes are associated at the cytogenetic level with chromosomal deletions, in which the breakpoints may be variable, but specific, common regions are consistently deleted.(ABSTRACT TRUNCATED AT 400 WORDS)

Cell Transformation, Neoplastic↗
PubMed1984

Cellular oncogenes, growth factors, and cellular growth control.

In this article we relate the functioning of oncogenes, particularly myc and ras, to current ideas regarding regulation of mammalian cell growth by growth factors. Assuming the genetic basis of transformation to be alterations of several proto-oncogenes, the mechanisms by which transformation could diminish growth control are numerous. The oncogene could interact with a growth factor in several ways. Mutations could alter the quantity of an oncogene's product or its quality through primary structure or covalent modifications such as phosphorylations. Oncogenes could code for a receptor for a growth factor. Various alterations parallel to the above set could then affect growth factor function via receptor changes (including abolished requirement for the factor). Some oncogenes might operate during the chain of intracellular events that must follow growth stimulation. Introduction of such an oncogene (e.g., the coding region for a DNA virus T antigen) would bypass requirements for both growth factors and receptors. Various observations regarding the oncogenes, cell cycle-timed events, and growth factors have been presented in a way we hope will suggest experiments designed to provide a basis for understanding growth regulation at the genetic, biochemical, and cellular levels in normal cells and tumorigenic cells, which have deranged growth regulation.

Cell Cycle↗
PubMed1984

Expression of oncogenes in human leukemias.

Oncogenes of retroviruses are directly related to cancers in animals; however, finding relevant associations with human cancer has been difficult. Studies reported here were designed to assess the extent of protooncogene transcription in human leukemias as compared to normal cells. Low-stringency hybridization of viral oncogene DNAs to cell messenger RNAs was done to determine whether evolutionarily divergent oncogene sequences were increased in leukemic cells. Several oncogenes hybridized at low levels to normal messenger RNAs. Some oncogene transcripts in fresh leukemic cells of 28 patients were present at higher levels than in normal cells. The oncogenes abl, erb, myc, and ras were expressed in all normals tested and a majority of the leukemic cells. However, fes, fps, and src probes hybridized rarely to transcripts in normal cells although more frequently to messenger RNA from leukemic cells. No oncogenes were expressed in specific patterns by cell types. It is concluded that transformation of human hematopoietic cells involves more than one oncogene and may include sequences unrelated to retroviruses.

Animals↗