Homogeneously staining chromosomal regions contain amplified copies of an abundantly expressed cellular oncogene (c-myc) in malignant neuroendocrine cells from a human colon carcinoma.

Alitalo, Kari; Schwab, Manfred; Lin, C. C.; Varmus, Harold; Bishop, J. Michael

doi:10.1073/pnas.80.6.1707

Cited by 639 publications

(245 citation statements)

References 37 publications

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“…Amplification of the c-Myc gene has been found in several types of human tumors, including lung, breast, and colon carcinomas. 39,40 In summary, we identified the role of XB130 in tumor growth by promoting cell proliferation and survival in thyroid cancer cells. Microarray data suggest that XB130 has profound effects on the expression of genes related to cell proliferation and survival.…”

Section: Discussionmentioning

confidence: 87%

XB130, a Novel Adaptor Protein, Promotes Thyroid Tumor Growth

Shiozaki

Lodyga

Bai

et al. 2011

The American Journal of Pathology

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Adaptor proteins with multimodular structures can participate in the regulation of various cellular functions. We have cloned a novel adaptor protein, XB130, which binds the p85␣ subunit of phosphatidyl inositol 3-kinase and subsequently mediates signaling through RET/ PTC in TPC-1 thyroid cancer cells. In the present study, we sought to determine the role of XB130 in the tumorigenesis in vivo and in related molecular mechanisms. In WRO thyroid cancer cells, knockdown of XB130 using small interfering RNA inhibited G 1 -S phase progression, induced spontaneous apoptosis, and enhanced intrinsic and extrinsic apoptotic stimulus-induced cell death. Growth of tumors in nude mice formed from XB130 shRNA stably transfected WRO cells were significantly reduced, with decreased cell proliferation and increased apoptosis. Microarray analysis identified 246 genes significantly changed in XB130 shRNA transfected cells. Among them, 57 genes are related to cell proliferation or survival, including many transcription regulators. Ingenuity Pathway Analysis showed that the topranked disease related to XB130 is cancer, and the top molecular and cellular functions are cellular growth and proliferation and cell cycle. A human thyroid tissue microarray study identified expression of XB130 in normal thyroid tissue as well as in human thyroid carcinomas. These observations suggest that the expression of XB130 in these cancer cells may affect cell proliferation and survival by controlling the expression of multiple genes, especially transcription regulators.

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Section: Discussionmentioning

confidence: 87%

XB130, a Novel Adaptor Protein, Promotes Thyroid Tumor Growth

Shiozaki

Lodyga

Bai

et al. 2011

The American Journal of Pathology

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“…brane (ICN Biomedicals, Costa Mesa, CA) [18] and hybridized sequentially as previously described [8] to the following 32p_ labeled, nick-translated eDNA probes: a 6.6-kb BamHI fragment of a human c-Ha-ras eDNA probe [19]; a 406-bp EcoRIApaI restriction fragment derived from a human TGFa eDNA clone, pTGF-CI [20]; a 6.0-kb EcoRI/HindlII fragment of the human c-myc eDNA probe [21]; and a 770-bp human ~-actin eDNA probe (Oncor, Gaithersburg, MD).…”

Section: Introductionmentioning

confidence: 99%

Transformation of mouse mammary epithelial cells with the Ha‐ras but not with the neu oncogene results in a gene dosage‐dependent increase in transforming growth factor‐α production

et al. 1989

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An enhanced expression of transforming growth factor-a (TGF~) was demonstrated in two clones of NOG-8 mouse mammary epithelial ceils, NOG-8 SR1 and NOG-8 SR2, that have been transformed by a v-Ha-ras oneogene. The amount of TGF~t production in NOG-8 SRI and NOG-8 SR2 ceils was dependent on the level of p21 r'~ expression in these clones, which directly correlated with their cloning efficiency in soft agar. There was also a decrease in the number of epidermal growth factor (EGF) receptors on the NOG-8 SR1 and NOG-8 SR2 ceils that is proportional to the amount of TGFct secreted. These effects were specific for ras because neu-transformed NOG-8 ceils grew in soft agar at a comparable level to NOG-8 SR2 ceils yet did not show any increase in TGF~ production or change in EGF receptor expression.

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“…In breast cancer, the chromosome 8 region where the gene is localized has been identified as one of the three most commonly amplified regions of the genome (Courjal et al, 1997); this region also is commonly amplified in small cell lung carcinoma (Little et al, 1985), leukaemia (Dalla-Farera et al, 1985), and colon carcinoma (Alitalo et al, 1983). C-myc has been considered to be the dominant oncogene in this region, driving the selection of this amplification in cancer.…”

mentioning

confidence: 99%

C-myc amplification in breast cancer: a meta-analysis of its occurrence and prognostic relevance

et al. 2000

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Data from basic research suggests that amplification of the proto-oncogene c-myc is important in breast cancer pathogenesis, but its frequency of amplification and prognostic relevance in human studies have been inconsistent. In an effort to clarify the clinical significance of c-myc amplification in breast cancer, we conducted a comprehensive literature search and a meta-analysis in which 29 studies were evaluated. The weighted average frequency of c-myc amplification in breast tumours was 15.7% (95% CI = 12.5–18.8%), although estimates in individual studies exhibited significant heterogeneity, P < 0.0001. C-myc amplification exhibited significant but weak associations with tumour grade (RR = 1.61), lymph-node metastasis (RR = 1.24), negative progesterone receptor status (RR = 1.27), and postmenopausal status (RR = 0.82). Amplification was significantly associated with risk of relapse and death, with pooled estimates RR = 2.05 (95% CI = 1.51–2.78) and RR = 1.74 (95% CI = 1.27–2.39), respectively. This effect did not appear to be merely a surrogate for other prognostic factors. These results suggest that c-myc amplification is relatively common in breast cancer and may provide independent prognostic information. More rigorous studies with consistent methodology are required to validate this association, and to investigate its potential as a molecular predictor of specific therapy response. © 2000 Cancer Research Campaign http://www.bjcancer.com

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Homogeneously staining chromosomal regions contain amplified copies of an abundantly expressed cellular oncogene (c-myc) in malignant neuroendocrine cells from a human colon carcinoma.

Cited by 639 publications

References 37 publications

XB130, a Novel Adaptor Protein, Promotes Thyroid Tumor Growth

XB130, a Novel Adaptor Protein, Promotes Thyroid Tumor Growth

Transformation of mouse mammary epithelial cells with the Ha‐ras but not with the neu oncogene results in a gene dosage‐dependent increase in transforming growth factor‐α production

C-myc amplification in breast cancer: a meta-analysis of its occurrence and prognostic relevance

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