By Alwin Krämer, Harald Löffler
This e-book provides an updated and thorough assessment of melanoma of unknown basic, encompassing issues starting from epidemiology, tumor biology, and prognostic elements via to the newest diagnostic and healing advances. All facets of administration are coated, together with radiological, nuclear medication, and pathological prognosis, site-specific cures, platinum-based mix chemotherapy, radiotherapy, and novel certain remedies. transparent suggestions is available on prognosis of the tissue of foundation through gene expression and micro-RNA analyses and its healing implications. unique instructions also are supplied at the id of subsets of sufferers with a extra favorable diagnosis, in whom particular therapy deals the opportunity of long term survival or perhaps remedy. Readers will locate melanoma of Unknown fundamental to be an awesome resource of essentially orientated details that would help in supply of the very best take care of sufferers with this tough diagnosis.
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Additional info for Cancer of Unknown Primary
Time trends in survival from cancer of unknown primary: small steps forward. Eur J Cancer. 2013;49(10):2403–10. PubMed Epub 2013/03/23. Eng. 29. Hemminki K, Riihimaki M, Sundquist K, Hemminki A. Site-specific survival rates for cancer of unknown primary according to location of metastases. Int J Cancer. 2013;133(1):182–9. PubMed Epub 2012/12/13. Eng. 30. Hemminki K, Bevier M, Sundquist J, Hemminki A. Site-specific cancer deaths in cancer of unknown primary diagnosed with lymph node metastasis may reveal hidden primaries.
2014;135(10):2475–81. 25. Pukkala E, Martinsen JI, Lynge E, Gunnarsdottir HK, Sparen P, Tryggvadottir L, et al. Occupation and cancer – follow-up of 15 million people in five Nordic countries. Acta Oncol. 2009;48:646–790. PubMed Epub 2009/11/21. Eng. 26. Hemminki K, Sundquist J, Brandt A. Do discordant cancers share familial susceptibility? Eur J Cancer. 2012;48:1200–7. PubMed Epub 2011/10/29. Eng. 27. Blaszyk H, Hartmann A, Bjornsson J. Cancer of unknown primary: clinicopathologic correlations.
This angiogenic incompetence may be overcome at metastatic sites either because the specific environment supports growth of tumor clones without angiogenesis or because of additional genetic alterations occurring after metastatic spread . Support for this hypothesis came from mouse models showing that non-angiogenic tumor cell lines produce only dormant cancers when injected into mice, while their spontaneous switch toward faster-growing cancers is associated with activation of angiogenesis, as demonstrated by gene expression profiling and examination of specific regulators both on the mRNA and protein level [46–48].