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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amplification of L-myc oncogene was noticed in a malignant meningioma originating from the right sphenoidal wing of a 54-year-old female. The patient underwent three surgical resections plus radiotherapy over a period of 11 years and then the growth rate of the tumor became much greater with a severely invasive appearance. Using Southern blot hybridization, L-myc amplification was examined on the specimen resected at the fourth operation. As a result, approximately five-fold amplification was confirmed, which has not been previously reported except for that in a small cell carcinoma of the lung. This result may suggest that L-myc amplification is responsible to some extent for the malignant transformation in this meningioma.
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PMID:[Amplification of L-myc oncogene in malignant meningioma. Case report]. 172 40

Oncogenic activation of myc genes in human cancer involves deregulated expression of myc proteins with no major structural alterations. Here two independent small cell lung carcinoma (SCLC) cell lines were found to express similar novel proteins antigenically related to L-myc. cDNAs corresponding to these proteins were cloned and shown to encode chimeric polypeptides with amino-terminal sequences from a novel gene named rlf joined to the L-myc protein. Although the chimeric mRNAs were shown to be identical, they result from distinct DNA rearrangements. The L-myc fusion protein may represent another activation mechanism of the myc proto-oncogenes.
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PMID:A fusion protein formed by L-myc and a novel gene in SCLC. 185 Oct 85

One hundred forty-two foci of small cell lung carcinoma (SCLC) from 47 patients were examined for amplification of myc family oncogenes (c-myc, N-myc, and L-myc), by dot blot hybridization using formalin-fixed and paraffin-embedded materials which were resected surgically or obtained at autopsy. Some selected patients were also examined by in situ hybridization. Amplification of myc family genes was detected in 11 patients (23.4%) (c-myc in one, N-myc in five, and L-myc in five). Two of the 11 patients (one with N-myc and one with L-myc) had heterogenously amplified clones. In the patient with N-myc amplification, amplification was detected in metastatic tumors in the pancreas, lung, and pleura, but not in the liver and lymph node metastases. In the primary tumor, areas with and without N-myc amplification were seen. In the patient with L-myc amplification, although amplification was not detected in the surgically resected primary lesion, mediastinal lymph node metastatic lesions obtained at autopsy showed L-myc gene amplification. These two cases, together with previously reported evidence, suggest that myc gene amplification plays an important role in malignant progression, rather than development, of SCLC. In Stage III and IV groups, patients with over ten-fold myc gene amplification were suggested to survive for a shorter time than patients without such amplification (P = 0.06).
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PMID:Heterogenous amplification of myc family oncogenes in small cell lung carcinoma. 217 44

The interactions of cytogenetic and molecular genetic changes in the pathogenesis and progression of lung cancer are complex. To the practicing pathologist, certain of these changes may prove useful as diagnostic or prognostic markers and may help in selecting patients for particular types of therapy. Changes such as 3p14-23 deletions, c-myc amplification, and L-myc RFLPs have already been reported to predict aggressive behavior in lung cancer. Future studies will clarify the application of these changes to the clinical care and treatment of patients with carcinoma of the lung.
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PMID:The cytogenetics and molecular genetics of lung cancer. Implications for pathologists. 220 63

The myc family of cellular oncogenes contains three known members. The N-myc and c-myc genes have 5'-noncoding exons, strikingly homologous coding regions, and display similar oncogenic potential in an in vitro transformation assay. The L-myc gene is less well characterized, but shows homology to N-myc and c-myc (ref. 6; also see below). c-myc is expressed in most dividing cells, and deregulated expression of this gene has been implicated in the development of many classes of tumours. In contrast, expression of N-myc has been found only in a restricted set of tumours, most of which show neural characteristics; these include human neuroblastoma, retinoblastoma and small cell lung carcinoma (SCLC). L-myc expression has so far been found only in SCLC. Activated N-myc and L-myc expression has been implicated in oncogenesis; for example, although N-myc expression has been found in all neuroblastomas tested, activated (greatly increased) N-myc expression, resulting from gene amplification, is correlated with progression of the tumour. We now report that high-level expression of N- and L-myc is very restricted with respect to tissue and stage in the developing mouse, while that of c-myc is more generalized. Furthermore, we demonstrate that N-myc is not simply a neuroectoderm-specific gene; both N- and L-myc seem to be involved in the early stages of multiple differentiation pathways. Our findings suggest that differential myc gene expression has a role in mammalian development and that the normal expression patterns of these genes generally predict the types of tumours in which they are expressed or activated.
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PMID:Differential expression of myc family genes during murine development. 241 62

The L-myc, N-myc and c-myc genes are members of the myc oncogene family. In particular, L-myc is novel, and amplification of L-myc is still unknown except in small cell lung carcinoma. We examined L-myc amplification in 30 human neuroblastomas using Southern blot hybridization, and found that the L-myc gene was amplified approximately 5-fold in GOTO, a human neuroblastoma cell line. The N-myc gene was also amplified approximately 60-fold and furthermore, over-expression of L-myc and N-myc genes was observed in this cell line. In this report, we describe the coamplification of the myc gene family in the GOTO neuroblastoma cell line.
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PMID:Coamplification of the L-myc and N-myc oncogenes in a neuroblastoma cell line. 250 Dec 44

The L-myc gene is the third member of the myc family of proto-oncogenes. Amplification and elevated expression of the L-myc gene has been detected in a subset of small cell lung carcinoma (SCLC) cell lines. The biological properties and functions of the L-myc gene and its product have not yet been elucidated. Monoclonal antibodies against two myc homology boxes were used to characterize the L-myc gene product. These antibodies react with two groups of polypeptides of apparent masses of 60, 61 and 66 kd (the long forms), and 34 and 37 kd (the short forms) in SCLC cells expressing L-myc transcripts. The long form L-myc proteins are associated with the nuclear fraction of the cells. The short form L-myc proteins are present in the cytoplasmic fraction, though diffusion of the short forms from the nucleus during cell fractionation cannot be ruled out. The half-life of the long form polypeptides is approximately 45-90 min. The short form polypeptides have a half-life of approximately 120-180 min. The L-myc protein is not detectable in the mitotic cells, suggesting that the L-myc protein expression is tightly regulated during the cell cycle.
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PMID:The human L-myc gene is expressed as two forms of protein in small cell lung carcinoma cell lines: detection by monoclonal antibodies specific to two myc homology box sequences. 254 55

The possible existence of amplification or rearrangement of protooncogenes was examined in more than 100 surgical specimens of human lung carcinoma. Protooncogenes were amplified in 28% of the carcinomas. About 90% of the amplified genes were of the myc, ras, or erbB family. Of the myc family genes, myc was amplified in 14 of 137 tumors and L-myc in four of 108 tumors, but N-myc was not amplified. A high frequency of amplification of myc was observed in squamous cell carcinomas (seven of 37) and of L-myc in small cell carcinomas (two of six). Of the ras family genes, K-ras-2 was amplified in six of the 137 tumors and N-ras in two of the 137 tumors, but no amplification of H-ras-1 was detected. Seven of the eight cases of amplified ras genes were in advanced pathological stages. Of the erbB family genes, erbB-1 (epidermal growth factor receptor) was amplified in 10 of 114 tumors and erbB-2 (HER-2/neu) in one of 51 tumors. Amplifications of the myc, ras, and erbB family genes might be one of the crucial DNA abnormalities involved in the development of human lung carcinomas.
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PMID:Amplification of protooncogenes in surgical specimens of human lung carcinomas. 257 14

Merkel cell carcinoma is a rapidly proliferating neoplasm of neuroectodermal origin presenting in skin. Karyotypes obtained in direct preparations of three Merkel cell carcinomas were analyzed and compared with six other tumors which were reported in the literature. Of the nine tumors studied so far, eight (89 per cent) showed structural abnormalities of chromosome 1. These abnormalities were in the form of trisomy for chromosome 1q22----ter. Furthermore, it was also observed that the breaks of these rearrangements on chromosome 1 occurred at the bands to which c-oncogenes N-ras (p31), L-myc (p32), c-src (p36), c-ski (q22-22), and the beta-subunit of the nerve growth factor (NGF) (p22) were localized. In addition to structural changes, five out of the nine tumors (55.5 per cent) were trisomic for chromosome 1. Merkel cell tumors are often confused with small cell carcinoma of lung or peripheral neuroepithelioma. The cytogenetic abnormalities such as rearrangement of chromosome 3p and t(11;22)(q23;q12) which characterize lung carcinoma and peripheral neuroepithelioma, respectively, were not seen in any of the nine Merkel cell tumors studied. Thus it appears that rearrangement of chromosome 1 was non-randomly associated with Merkel cell carcinoma. It is of interest to note that genes involved in neuronal development and or differentiation have been mapped to the bands at which breaks occurred in these tumors. The significance of these changes is briefly discussed.
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PMID:Non random cytogenetic changes characterize Merkel cell carcinoma. 276 51

Nine cell lines established from various malignant tissues of patients with small cell lung carcinoma (SCLC) were examined for chromosomal abnormalities and myc gene amplification. Cytogenetic studies revealed that all cell lines were aneuploid, often with a bimodal distribution with modal concentrations in the hypodiploid and hypertriploid range. With respect to chromosome #3, deletions of 3p were confined to six of nine SCLC "classic" lines. The region of overlap of the observed 3p deletions lies within 3p21-3p24 which is in agreement with previous assignments. Six of the nine lines tested with c-, N-, and L-myc probes showed an increase of between ten- and 100 fold in myc gene copy number. Coamplification of two or more of these genes was not observed in any cell line. Five of the six lines with myc gene amplification had cytogenetic markers of gene amplification either in the form of homogeneously staining regions (HSR) or double minutes (DM). Our results confirm that cytogenetically visible deletions of 3p are often present in cell lines established from patients with SCLC, and that mutually exclusive c-, L-, or N-myc gene amplification is also a common event in SCLC cell lines.
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PMID:Cytogenetic abnormalities in human small cell lung carcinoma: cell lines characterized for myc gene amplification. 283 10


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