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C Theillet

Publications and source records attributed to C Theillet.

79 records · Page 5Linked to original sources
PubMed1986

Genetic alteration of the c-myc protooncogene (MYC) in human primary breast carcinomas.

We have studied the genomic organization of the c-myc locus (MYC) from 121 human primary breast carcinomas. Two types of alterations were observed: (i) the c-myc protooncogene appeared to be amplified 2- to 15-fold in 38 (32%) of the carcinoma DNAs and (ii) a non-germ-line c-myc-related fragment of variable size was detected in 5 primary breast carcinoma DNAs. With three exceptions, all the tumors containing a genetic alteration of the c-myc locus were invasive ductal carcinomas. A significant correlation (P less than 0.02) was observed between patients more than 50 years old and the presence of a genetically altered c-myc. Enhanced levels of c-myc RNA were observed in 10 of 14 breast carcinomas examined. The c-myc gene was genetically altered in 6 of these 10 tumors. The frequency with which the c-myc gene is altered and its correlation with age suggest that it may play a role in the development of breast carcinomas.

Adenofibroma↗
PubMed1986

High frequency of rare alleles of the human c-Ha-ras-1 proto-oncogene in breast cancer patients.

The c-Ha-ras-1 locus in 104 breast cancer patients and 56 unaffected individuals was examined for allelic restriction fragment-length polymorphism. Four common and 16 rare alleles were detected in the combined populations. The distribution of common and rare alleles differed significantly between the two populations. The common restriction fragments represented 91% of the allele pool in the unaffected population. In breast cancer patients, these common alleles represented only 59% of the allele pool (P less than .001). More specifically, the frequency of two of the common fragments, the 6.5- and 8.0-kilobase alleles, was significantly diminished in the breast cancer population (P less than .001 and P less than .02, respectively). The frequency of rare c-Ha-ras-1 alleles and hence genotypes composed of two rare alleles was increased in the breast cancer population (P less than .001). One of the rare alleles had a significant (P less than .05) association with these breast cancer patients. These results suggest that genotype analysis of the c-Ha-ras-1 locus, in combination with other clinical parameters, may be of prognostic value in assessing the potential for cancer.

Adult↗
PubMed1986

Loss of a c-H-ras-1 allele and aggressive human primary breast carcinomas.

The human H-ras protooncogene was shown to be expressed in 16 of 22 invasive ductal carcinomas of the breast. The K- and N-ras protooncogenes were either not expressed or expressed at low levels. No amplification or rearrangement of the three ras genes was detected among the 104 breast carcinoma DNAs tested. These results indicate that the overexpression of H-ras in human breast tumors is not correlated with alteration of the protooncogene. In addition, we did not find any point mutation at the codon 12 of the H-ras or K-ras protooncogenes in 32 and 64, respectively, tumor DNAs examined. However, in tumor DNAs from 14 of 51 patients, heterozygous for H-ras-1 related BamHI restriction fragments, one allele was lost. This allele loss did not alter ras Mr 21,000 protein expression. Correlation with clinicopathological data showed, however, that the loss of one H-ras-1 allele in breast carcinoma DNAs is significantly linked to histological Grade III tumors, the lack of estrogen and/or progesterone receptors, and the subsequent occurrence of distal metastasis. Our results thus indicate that the loss of one H-ras-1 allele correlates with the most aggressive primary carcinomas of the breast.

Aged↗
PubMed1985

Presence of an allelic EcoRI restriction fragment of the c-mos locus in leukocyte and tumor cell DNAs of breast cancer patients.

Structure of the human c-mos protooncogene in DNAs from breast tumors, leukemic cells, and lymphocytes from normal individuals was analyzed by restriction enzyme digestion and Southern blot. In 6 of 75 breast tumor DNAs, we found an EcoRI 5-kilobase extra band hybridizing with a human c-mos probe containing all of the sequences homologous to v-mos oncogene. This band was also found in lymphocyte DNA from 3 of these patients, indicating a restriction fragment length polymorphism. This polymorphism was not found in a series of 69 lymphocyte DNAs from the unaffected population. Moreover, 1 of 73 leukemic cell DNAs exhibited the 5-kilobase band. These results indicate that this rare polymorphism is significantly more frequently found in patients with breast cancer than in the rest of the population (P less than 0.05, by a chi 2 test with Yates correction.

Alleles↗
PubMedDate not supplied

[Oncogenes, anti-oncogenes and their alterations in human tumors].

This review summarizes the discovery of oncogenes which are the activated versions of normal cellular protooncogenes which serve essential functions in the control of cell proliferation and differentiation. Their activation disrupts the normal control mechanism which rests on the subtle balance between their effects and those of anti-oncogenes or tumor suppressor genes. One may reasonably hope that defining a complete profile of alterations of both these types of essential genes in the tumor or in the clinically healthy individual will be invaluable to assess prognosis or genetic predisposition, respectively.

Animals↗
PubMedDate not supplied

Concurrent abnormal expression of erbB-2, myc and ras genes is associated with poor outcome of ovarian cancer patients.

Epithelial ovarian cancer probably occurs due to activation of several different combinations of genes, which produce cancers that vary biologically and clinically. We tested this hypothesis in 100 consecutive ovarian carcinomas by molecular biology techniques at the DNA and protein levels in three genes (erbB-2, myc, ras), which are frequently altered in this tumor system. Abnormally high expression of erbB-2 gene encoded p185 protein was observed in 31% of the samples, while erbB-2 gene amplification was detected by Southern analysis in 8%. ErbB-2 abnormal gene expression did not significantly affect the clinical outcome of patients, conferring a marginal worsening of survival. In 25 out of 96 (26%) tumor samples there was myc amplification. Higher levels of the ras-encoded p21 protein than in normal ovaries and benign ovarian tumors were found in 45% of the samples. Simultaneous overexpression of p185 and p21 was associated with shorter disease free (p = 0.02) and overall survival (p = 0.04) at significance levels notably higher than those observed for these oncoproteins singly. In addition, survival of patients with myc amplification and high p185/p21 coexpression was significantly worse (p < 0.05) than that of patients with normal levels. Our data suggest that concurrent abnormal gene expression may act synergistically to endow ovarian tumor cells with a highly aggressive phenotype. Evaluation of these genes may be helpful in the biological characterization of ovarian cancer and in defining individual patient prognosis.

Adult↗