Download Central Nervous System Metastasis, the Biological Basis and by Diane Palmieri Ph.D. (auth.), Diane Palmieri (eds.) PDF

By Diane Palmieri Ph.D. (auth.), Diane Palmieri (eds.)

This quantity will hide what's recognized in regards to the biology and therapy of CNS metastasis, together with novel chapters reminiscent of the way forward for particular treatments. it is going to start with an outline of the normal historical past and hazard components for CNS metastases that would greatly conceal all melanoma histologies. this may be via three chapters that would disguise the biology. those comprise: molecular biology, discussing what's identified approximately particular genes/proteins all in favour of the method and version platforms to check mind metastasis; the mind microenvironment, concentrating on the way it isn't like the microenvironment of different organs of the physique; and the blood-brain barrier, which incorporates a dialogue of permeability with admire to mind metastases. A bankruptcy on experimental imaging will conceal either the biology of mind metastasis from an imaging standpoint and use of imaging recommendations to review mind metastases. The scientific chapters will speak about treatment plans with separate chapters on surgical procedure, chemotherapy and radiation. moreover, leptomeningeal metastasis should be given its personal bankruptcy. ultimately, caliber of existence matters often is the concluding chapter.

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Extra resources for Central Nervous System Metastasis, the Biological Basis and Clinical Considerations

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Mol Cancer Res 7:1438–1445 36. Xie TX, Huang FJ, Aldape KD et al (2006) Activation of stat3 in human melanoma promotes brain metastasis. Cancer Res 66(6):3188–3196 2 The Molecular Biology of Brain Metastasis 39 37. Slamon D, Clark G, Wong S et al (1987) Human breast cancer: correlation of relapse and survival with amplification of the HER-2/neu oncogene. Science 235:177–182 38. Schechter AL, Stern DF, Vaidyanathan L et al (1984) The neu oncogene: an erb-B-related gene encoding a 185,000-Mr tumour antigen.

To induce signaling, TGFb binds to a heterodimeric complex of two serine/threonine receptors known as TGFRbI and TGFRbII. To date, 7 TGFRbI and 5 TGFRbII receptors have been identified in the human genome [100]. A third receptor, either endoglin or betaglycan, has also been identified and appears to assist in ligand binding. Betaglycan promotes TGFb2 binding to the receptor whereas Endoglin binds 36 S. Woditschka et al. TGFb1 and 2 [100]. Two Endoglin isoforms have been identified – Endoglin Long (L-End) which can bind TGFb and Endoglin Short (S-End) which cannot bind TGFb [100].

Woditschka et al. TGFb1 and 2 [100]. Two Endoglin isoforms have been identified – Endoglin Long (L-End) which can bind TGFb and Endoglin Short (S-End) which cannot bind TGFb [100]. Following ligand binding, the receptors induce phosphorylation of Smad2 and Smad3, which can then heterodimerize with Smad4 and translocate to the nucleus thereby regulating gene expression [101, 102]. TGFb signaling has also been shown to act independently of the Smad proteins and signal through common signaling mediators such as PI3K/AKT, Ras/ERK, and Src [101, 102].

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