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PubMed1991

N-myc and c-myc oncogenes amplification in medulloblastomas. Evidence of particularly aggressive behavior of a tumor with c-myc amplification.

N-myc and c-myc amplification was investigated in 27 medulloblastomas. DNA was extracted from 19 formalin fixed and paraffin embedded tumors and from fresh frozen tumor tissue in 8 other cases. The results showed no evidence of amplification of N-myc oncogene and only 1 case had a 27 fold amplification of c-myc. Cytogenetically, this neoplasm presented numerous double minute chromosomes (DMs). Moreover, it had an unusual rapidly aggressive course with massive cerebrospinal fluid dissemination unresponsive to intrathecal chemotherapy. Our results indicate a low incidence of N-myc and c-myc gene amplification in medulloblastomas, suggesting that the oncogenic mechanism in these neoplasms is not closely related to DNA gene amplification. C-myc amplification, although not frequently observed, may however provide a growth advantage for medulloblastoma cells in vivo, favoring their rapid dissemination. Medulloblastomas with c-myc activation may represent a subgroup of tumors with a more aggressive behavior.

Adolescent↗
PubMed1995

[Correlation between malignancy of gastric cancer and c-myc DNA amplification or overexpression of c-myc protein].

The amplification of c-myc DNA for fresh frozen tissue of 31 gastric adenocarcinomas was examined with dot blot hybridization method. Using the avidin-biotin peroxidase complex method, the expression of c-myc protein was examined immunohistochemically for formalin-fixed paraffin embedded tissue of 51 gastric adenocarcinomas including the same cases for c-myc DNA analysis. c-myc DNA amplification was detected in only 4 cases (12.9%). However, c-myc protein overexpression was recognized in 21 cases (41.2%). Only one of 4 cases showing c-myc DNA amplification indicated overexpression of c-myc protein. There was no statistically significant relation of c-myc protein overexpression with clinicopathological factors (histology, depth of invasion, invasion of the vessels, metastasis, intraabdominal dissemination and histological staging). These results suggest overexpression of c-myc protein could be recognized even in early gastric cancer indicating the relation of this gene product with proliferation of gastric cancer cells, although its role in the progression and metastasis of gastric adenocarcinoma might be minimal.

Adenocarcinoma↗
PubMed1993

Amplification of the c-myc gene in human hepatocellular carcinoma: biologic significance.

To elucidate the prevalence and biologic significance of the c-myc gene in human hepatocellular carcinoma (HCC), DNA samples were taken from the paired tumorous and nontumorous tissues of 77 cases of resected primary HCC and were analyzed by Southern blot hybridization. We demonstrated modest, but significant c-myc amplification (group A) in 28 (36.4%) of the cases: 1.6- to 2.0-fold in 18, 2.1- to 3.0-fold in four, and > 3.0-fold in six. Compared to HCC without c-myc amplification (group B), group A HCC occurred more often in patients < 50 years old (54.5% vs 29.1%, p < 0.02) with serum alpha-fetoprotein (AFP) levels > 320 ng/mL (61.1% vs 14.6%, p < 0.00002). Group A HCC occurred more frequently in patients with hepatitis B virus infection than in those with hepatitis C virus infection (p < 0.03). Group A HCC was more likely to be poorly differentiated (44.8% vs 10.5%, p < 0.004) and associated with intrahepatic portal vein spread (57.1% vs 28.6%, p < 0.02). The c-myc amplification did not correlate with sex or tumor size. For small HCC, group A had a worse one-year survival rate than group B (72.2% vs 90.9%, p < 0.04). These findings suggest that c-myc amplification is not an uncommon event in human hepatocarcinogenesis, occurs more frequently in young patients who have an elevated serum AFP level or HBV infection, and is related to the biologic behavior of HCC.

Adult↗
PubMed1990

myc gene amplification and expression in primary human neuroblastoma.

Although N-myc amplification in neuroblastomas correlates with poor prognosis, not all neuroblastomas which fail to respond to therapy have N-myc amplification. To determine whether other modes of myc gene activation underlie progression of some neuroblastomas, 45 were analyzed for amplification of N-myc, c-myc and L-myc and 26 were studied for transcription of these oncogenes. N-myc amplification was found in 6 of 45 tumors; no tumor had amplification of c-myc or L-myc. Transcription of both N-myc and c-myc occurred in 21 of 26 neuroblastomas. No tumor without N-myc amplification had a level of N-myc expression near that of a tumor or cell line with amplification. One tumor with N-myc amplification was the only specimen with N-myc but not c-myc expression. Five samples had c-myc but not N-myc expression; all had histological features of ganglioneuroma. DNA index did not correlate with myc gene amplification or expression. It is concluded that N-myc and c-myc are commonly expressed in primary untreated neuroblastomas, but in the absence of N-myc amplification, expression of these genes does not appear to correlate with disease progression.

Adolescent↗
PubMed1993

int-2 amplification in breast cancer: association with decreased survival and relationship to amplification of c-erbB-2 and c-myc.

Amplification of the int-2 oncogene was measured in a series of breast tumours and related to amplification of the c-myc and c-erbB-2 oncogenes, histopathological features and relapse-free and overall survival. int-2 was amplified in 11%, c-myc in 20% and c-erbB-2 in 27% of the tumours assessed. int-2 amplification was associated with large tumour size (p < 0.05) and reduced relapse-free (p < 0.05) and overall (p < 0.0005) survival. c-myc amplification was associated with poor tumour differentiation (p < 0.05) but had no association with prognosis. c-erbB-2 amplification was associated with low levels of expression of oestrogen receptor mRNA (p < 0.05), poor tumour differentiation (p < 0.05) and shortened relapse-free (p < 0.0001) and overall survival (p < 0.0001). This is the first report of an association between amplification of the int-2 oncogene in breast tumours and a significantly increased risk of death from breast cancer, and suggests that int-2 may be useful for identifying breast-cancer patients having a poor prognosis.

Breast Neoplasms↗
PubMed1990

[A study of amplifications of myc gene (c-myc and N-myc) in human ovarian cancer].

Amplifications of myc oncogenes (c-myc, N-myc) were studied by Southern blot hybridization methods in ovarian cancers. Fourteen cases were primary ovarian cancers and one case was metastatic ovarian cancer. Primary and metastatic foci of three primary ovarian cancers were compared. A serous adenocarcinoma had a c-myc gene amplification more than 10 fold without N-myc gene amplification. This case also had an amplification in other c-myc probes with upper and down streams of the second exon. The results suggested that this case had c-myc gene expression. One of these cases had 5 fold amplification of the metastatic focus compared with the primary focus. The amplified c-myc gene did not show relations among clinical courses, prognosis and histologies.

Adult↗
PubMed1997

[N-myc oncogene amplification in tumors of the sympathetic nervous system: preliminary study of methods and clinico-pathologic correlations].

Tumors of the sympathetic nervous system (NT), namely neuroblastoma (NB) and ganglioneuroblastoma (GNB), have a variable clinical course. Prognostic factors include clinical stage, age of the patient, histological grade, and changes at the genomic level, of which amplification of N-myc oncogene is a well recognized phenomenon. The aim of this study was to establish the status of the N-myc oncogene in NT and to compare the results with histopathological grading, with risk groups according to criteria outlined by Joshi et al., and with the clinical stage. To detect the amplification of N-myc oncogene we used differential polymerase chain reaction (D-PCR). Amplified N-myc oncogene was found in 10 out of 31 investigated children with NB (32%). The result of D-PCR could not be interpreted reliably in two patients. Of seven children with GNB the N-myc amplification was found in one case. None of seven children with ganglioneuroma was found to have amplified N-myc oncogene. The tumors with N-myc amplification were histologically poorly differentiated of undifferentiated with a high mitotic activity-8 children were classified as a high risk category; in two we had not enough surgical material to evaluate the histological prognostic factors. The correlation of N-myc status with clinical stage revealed N-myc amplification in two of 9 children classified as clinical stage III, and in eight of 11 children classified as clinical stage IV. The N-myc amplification was not found in any child diagnosed at stage I, II and IV. Five of 10 children with NB and N-myc amplification died of the disease progression. Four children died in the group of 19 children without N-myc amplification. The median of follow-up was 18 months. The patient with GNB and N-myc amplification also died of the disease progression. Although the follow-up period of the investigated group of patients was short, the results showed that the amplification of N-myc oncogene was associated with tumors of patients diagnosed at a late clinical stage (III and IV), and with tumors whose morphology and age were assessed collectively under the term "high risk group".

Child↗
PubMed1992

Amplification of the c-myc oncogene in radiation-induced rat skin tumors as a function of linear energy transfer and dose.

The c-myc oncogene was previously shown to be amplified in large, later-stage carcinomas of the rat skin induced by 0.8-MeV electrons. In a panel of 70 tumors induced by neon ions (45 keV/microns), c-myc amplification was rare, and in contrast to the data for tumors induced by low-linear-energy transfer (LET) (0.3 keV/microns) radiation, showed no correlation with tumor size, growth period, or time, but was associated with radiation dose. The tissue specificity for c-myc amplification seen in tumors induced by electrons was not seen in tumors induced by neon ions. These results suggest that quite distinct molecular mechanisms operate even in late stages of carcinogenesis that depend on the LET of the inducing radiation. Furthermore, the results suggest that c-myc amplification observed in tumors induced by low-LET radiation is not a general property of rat skin carcinomas, but is linked mechanistically to the inducing radiation, even though it is not detectable until many months after exposure and tumor appearance.

Animals↗
PubMed1994

[Amplification of C-myc oncogene in squamous cell carcinoma of the larynx].

C-myc amplification in 22 squamous cell carcinomas and 10 normal tissues (control) from the larynx was assessed by dot hybridization technique. Significant amplification of C-myc oncogene was found in malignant tumours as compared with the normal tissues. The extent of amplification also correlated with advanced tumour stages. There was a significant increase in C-myc amplification in TNM stages III and IV when compared with the stages I and II. These data suggested that C-myc oncogene might be activated by gene amplification and it might have a key role in determining the aggressiveness of laryngeal carcinoma.

Carcinoma, Squamous Cell↗
PubMed1994

Investigation of c-myc oncogene amplification in colorectal cancer.

Tumour DNA samples of 20 patients with colorectal carcinoma were tested for c-myc amplification, using a quantitative dot-blot hybridization. Statistical analysis involving clinical and histological parameters like degree of differentiation, Dukes' stage, TNM staging system, age, sex and severity of disease, was applied to estimate the prognostic value of c-myc amplification. The amplification of the investigated oncogene--1.61-fold on the average--was found to significantly correlate with the presence of distant metastasis (corr. coeff.: 0.506, P < 0.05) and the severe course of the disease (corr. coeff.: 0.468, P < 0.05). This result supports the hypothesis that tumour cells with c-myc amplification represent a more malignant and aggressive phenotype. It is also worth noting that both c-myc amplification and formation of distant metastasis are late events in the progression of colorectal cancer, which accounts for the more severe course of the disease.

Adult↗
PubMed1992

c-myc gene amplification in selected node-negative breast cancer patients correlates with high rate of early relapse.

In breast cancers with histologically negative axillary nodes selected for high frequency of recurrence, the amplification of c-myc, erbB-2 and int-2 genes was found to concern, respectively 25% (16/65), 31% (25/81) and 14% (10/70) of tumours. Their relation with tumour progression expressed by relapse-free survival is reported. Using univariate analyses, c-myc amplified tumours showed significant association with early (30-month period after diagnosis) (P = 0.0013) and intermediate (50-month period after diagnosis) (P = 0.0398) risks of recurrence. In contrast, only a trend towards higher relapse was observed in erbB-2 amplified breast cancers with respect to later events (occurring over the first 30-month period). Multivariate analyses indicated that c-myc amplification is an independent prognostic factor stronger than oestrogen receptor status and tumour size to define a high risk subset in node-negative patients selected for high frequency of recurrence.

Adult↗
PubMed1988

Establishment of a peripheral T-cell lymphoma cell line showing amplification of the c-myc oncogene.

A new T-cell lymphoma cell line, designated T34, was established from freshly isolated lymph node tumor cells of a patient with non-Hodgkin's diffuse large cell lymphoma. The T34 cells, as well as the parental lymphoma cells, showed mature helper/inducer immunophenotypes in that they formed spontaneous sheep erythrocyte rosettes and reacted with OKT-3 and OKT-4 monoclonal antibodies. They were negative for OKT-6, OKT-8, terminal deoxynucleotidyl transferase, WT-1, and HLA-DR antigens. Molecular analysis revealed that the T34 cells contained 8- to 16-fold amplified c-myc DNA. The same genetic change was observed in parental lymphoma cells, indicating that the c-myc amplification had occurred in vivo. There was no gross rearrangement of the c-myc DNA. The c-myc gene of the T34 cell line was actively transcribed into normal-sized c-myc mRNA. Cytogenetic analysis showed that both the T34 and the parental lymphoma cells had a near-triploid karyotype with multiple structural chromosome changes. The terminal end of the long arm of chromosome No. 8, the chromosomal locus of single-copy c-myc, was elongated (8q+ chromosome), perhaps reflecting the site of c-myc amplification. These data suggested that amplification of the c-myc oncogene played some role in progression and proliferation of this peripheral T-cell neoplasm.

Aged↗
PubMed1994

Clinicopathologic correlations and short-term prognosis in musculoskeletal sarcoma with c-myc oncogene amplification.

The prognostic significance of c-myc oncogene amplification was investigated in a series of 44 patients with musculoskeletal malignancy. There were 21 bone tumors and 23 soft tissue sarcomas. Amplification of the c-myc oncogene was detected in 11 tumors: 4 bone tumors and 7 soft tissue sarcomas. In 9 of the 11 myc-amplified tumors a high grade of malignancy was revealed histologically. The relative frequency of c-myc amplification was higher in grade IV tumors. After a mean follow-up of 18 months, 6 of 11 patients with c-myc-amplified tumors and 12 of 33 patients with nonamplified tumors either exhibited recurrence or died of tumor disease. Both 3-year estimated overall survival and disease-free survival probability were lower for patients with myc-amplified tumors. Amplification of the c-myc oncogene was associated with poor short-term prognosis. Although gene amplification was encountered sporadically in musculoskeletal sarcomas, the reported data suggest that analysis of c-myc may provide valid information on prognosis.

Adolescent↗