Human EJ bladder carcinoma oncogene is homologue of Harvey sarcoma virus ras gene

Parada, Luis F.; Tabin, Clifford J.; Shih, Chiaho; Weinberg, Robert A.

doi:10.1038/297474a0

Cited by 858 publications

(372 citation statements)

References 34 publications

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“…These studies parallel the discovery of dominant oncogenes, whose transforming ability was discovered by their ability to convert preneoplastic cells with deletions in tumor suppressor genes into fully malignant and angiogenic neoplasms (23)(24)(25)(26). The loss of a nuclear tumor suppressor gene is an early event in the elaborate sequence that leads to tumorigenesis.…”

Section: Discussionmentioning

confidence: 89%

Neuroendocrine Lung Tumors: Grade Correlates with Proliferation but not Angiogenesis

Arbiser

Cohen

et al. 2001

Modern Pathology

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Angiogenesis has been implicated in the progression of human neoplasia from benign precursor to invasive and metastatic phenotypes. The acquisition of dominant oncogenes in preneoplastic cells in vitro and in vivo has been associated with the increased ability of tumor cells to secrete angiogenic mediators and recruit blood vessels. However, in a subset of benign lesions, high levels of angiogenesis have been found before the conversion to invasive and metastatic phenotypes. In many of these benign lesions, dominant oncogenic pathways are activated first; then as malignant potential is acquired, there is a loss of nuclear tumor suppressor genes, such as p53 and p16. We studied neuroendocrine lung tumors (NLT) ranging from typical and atypical carcinoid tumors to large cell neuroendocrine and small cell carcinomas in order to determine whether angiogenesis (as assessed by mean vessel density) and proliferation rates (as assessed by MIB-1 nuclear immunohistochemical staining) correlate with tumor type. We found that increased rates of proliferation, but not angiogenesis, correlate with tumor type. The association of increased proliferation and tumor type may prove to be clinically useful and shed light on the role of sequential oncogenic alterations in NLT.

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Section: Discussionmentioning

confidence: 89%

Neuroendocrine Lung Tumors: Grade Correlates with Proliferation but not Angiogenesis

Arbiser

Cohen

et al. 2001

Modern Pathology

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“…Although a gross chromosomal abnormality was not associated with all the parameters that showed heterogeneity, this does not conflict with the hypothesis that there is a genetic basis for heterogeneity in tumours (Nowell, 1976) as the changes responsible are very likely to be at the molecular level and therefore not detectable by the chromosome banding techniques used in this study. Recent evidence for a molecular change in the DNA being responsible for the onset of neoplasia has been proposed using transfection techniques (Krontiris and Cooper, 1981;Parada et al, 1982;Perucho et al, 1981). Molecular DNA clones-oncogenes-which have been isolated from human bladder and other tumour lines have been shown to transform mouse fibroblast lines (Shih et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

“…enhances tumour production. The oncogene isolated from the EJ bladder line is indistinguishable from its normal allelic counterpart sequence and the activation of such oncogenes in tumour cells may depend on minor structural changes such as point mutations (Parada et al, 1982). Hopefully, molecular hybridisation techniques will enable chromosome mapping of this and other oncogenes and assist our understanding of the structural chromosome anomalies found in the EJ and other tumour cell lines.…”

Section: Discussionmentioning

confidence: 99%

Cellular heterogeneity in a tissue culture cell line derived from a human bladder carcinoma

Hastings¹,

Franks²

1983

Br J Cancer

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Summary To study heterogeneity in a cell line derived from a human bladder carcinoma (EJ), 7 clones were isolated at low passage and examined for differences in culture behaviour, ability to grow in agar and tumorigenicity in nude mice. The parent EJ line had several distinct chromosome populations (both diploid and tetraploid), grew in agar and produced tumours in nude mice. Three of the clones had pseudodiploid modes and 4 had either hypo-or hypertetraploid modes. The 7 clones had 5 marker chromosomes in common but the combination of other marker chromosomes made each clone unique. No Differences were also found in the packing density of the cloned cells and in the cell size. All 7 clones grew in agar but heterogeneity was seen between the clones as shown by widely varying colony-forming efficiencies (0.5-13%). One clone had a high colony-forming ability in agar but failed to produce tumours in nude mice. The other clones were tumorigenic regardless of colony-forming efficiency in agar. Specific chromosome abnormalities were found to be associated with growth in agar and tumorigenicity but not with the growth pattern or the rate of movement of the cloned cells in culture.

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“…In 1982, ras was identified as a human oncogene and activated Ras proteins were shown to be capable of transforming immortalized rodent cells (Der et al, 1982;Parada et al, 1982). However, even at this time, additional cooperating genetic alterations were known to be required for Ras to transform primary cells (Land et al, 1983).…”

Section: History Of Oncogene-induced Senescencementioning

confidence: 99%

Many roads lead to oncogene-induced senescence

2008

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Human EJ bladder carcinoma oncogene is homologue of Harvey sarcoma virus ras gene

Cited by 858 publications

References 34 publications

Neuroendocrine Lung Tumors: Grade Correlates with Proliferation but not Angiogenesis

Neuroendocrine Lung Tumors: Grade Correlates with Proliferation but not Angiogenesis

Cellular heterogeneity in a tissue culture cell line derived from a human bladder carcinoma

Many roads lead to oncogene-induced senescence

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