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We began analyzing https://www.nature.com/articles/onc2009316, but it redirected us to https://www.nature.com/articles/onc2009316. The analysis below is for the second page.

Title[redir]:
The type I insulin-like growth factor receptor regulates cancer metastasis independently of primary tumor growth by promoting invasion and survival | Oncogene
Description:
The type I insulin-like growth factor receptor (IGF1R) regulates multiple aspects of malignancy and is the target of several drugs currently in clinical trials. Although the function of IGF1R in proliferation and survival is well studied, the regulation of metastasis by IGF1R is not as clearly delineated. Previous work showed that disruption of IGF1R signaling by overexpression of a dominant-negative IGF1R inhibited metastasis. To establish a clinically applicable approach to inhibition of metastasis by targeting IGF1R, we examined the effect of an inhibitory antibody against IGF1R, EM164 and its humanized version, AVE1642, on metastasis of cancer cells. EM164 and AVE1642 did not affect primary tumor growth of MDA-435A/LCC6 cells but inhibited metastasis of these cells. Consistent with this inhibition in the formation of metastatic nodules, disruption of IGF1R also resulted in a decreased number of circulating tumor cells in blood of tumor-bearing mice. Disruption of IGF1R with a dominant-negative construct or antibody inhibited invasion across Matrigel in vitro. When tumor cells were directly injected into the circulation through the lateral tail vein of mice, IGF1R disruption also resulted in significant reduction of pulmonary nodules, suggesting that regulation of invasion is not the only function of IGF1R signaling. Further, disruption of IGF1R rendered cells more susceptible to anoikis. Thus, IGF1R regulated metastasis independently of tumor growth. The multiple phenotypes regulated by IGF1R must be considered during development of this therapeutic strategy as inhibition of metastasis independent of inhibition of tumor growth is not easily assessed in phase II clinical trials.

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Keywords {🔍}

cancer, pubmed, article, google, scholar, growth, cas, receptor, insulinlike, metastasis, breast, factor, cells, nature, igfr, cell, res, tumor, antibody, human, yee, access, type, oncogene, sachdev, insulin, zhang, signaling, factori, central, clin, content, invasion, cookies, survival, metastatic, monoclonal, inhibits, tumors, privacy, disruption, inhibition, open, igf, therapy, vivo, irs, biol, research, usa,

Topics {✒️}

nature portfolio permissions reprints privacy policy pi3-kinase/akt pathway brendan melanoma research advertising nature 204 nature 227 nature 436 nature 410 nature social media author information authors isotype-matched control antibody ampk/erk-dependent growth author correspondence mda-435a/lcc6 cells springerlink instant access personal data mda-mb-435 cells bone-seeking clone exhibits preclinical model driven igf-ir kinase data protection permissions nih r01 ca074285 masonic cancer center regulates multiple aspects li sl human cancer cells minn aj human breast cancer recent development breast cancer cells dominant negative mutant chambers af potential cancer therapy circulating tumor cells dominant-negative construct breast cancer metastasis privacy refractory solid tumors single-chain antibodies prostate cancer tumors igf-1rβ/akt article sachdev tumor progression brain-seeking clone national cancer institute growth factor therapy

Questions {❓}

Is cancer a disease of self-seeding?

Schema {🗺️}

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