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From Molecular to Modular Tumor Therapy: - Tumors are Reconstructible Communicatively Evolving Systems (Paperback, 2010 ed.) Loot Price: R5,786
Discovery Miles 57 860
From Molecular to Modular Tumor Therapy: - Tumors are Reconstructible Communicatively Evolving Systems (Paperback, 2010 ed.):...

From Molecular to Modular Tumor Therapy: - Tumors are Reconstructible Communicatively Evolving Systems (Paperback, 2010 ed.)

Albrecht Reichle

Series: The Tumor Microenvironment, 3

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Loot Price R5,786 Discovery Miles 57 860 | Repayment Terms: R542 pm x 12*

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Chronic inflammation is one of the major pathological bases manifesting the development of gastric cancers, hepatitis and hepatocellular carcinoma, cervical cancer, ulcerative colitis and colorectal cancer [1]. Microbial infections, viral infections and autoimmune responses can lead to chronic inflammation-associated cancer formation. Human herpesviruses, such as human cytomegalovirus (HCMV) and Kaposi sarcoma herpesvirus (KSHV) are known to be associated with tumorigenesis and tumor progression. HCMV infection potentiates malignancies of colon cancer and malignant glioma [2,3]. KSHV was initially discovered from Kaposi's sarcoma lesion of an AIDS patient [4]. It was subsequently discovered that KSHV contributed to the pathogenesis of KS, primary effusion lymphoma [5] and lymphoproliferative disorder multicentric Castleman's disease. Emerging evidence shows that herpesvirus infection interferes or inhibits host cell immune defense and maintains a tumor-promoting microenvironment by expressing virulent homologues of host cell proteins that disturb normal cell cycle progression and leads to apoptosis of the host cells. For example, cellular growth and transformation are induced by viral-encoded homologues of cytokines, chemokines or chemokine receptors [6]. The constitutive expression of viral chemokine GPCRs triggers prolonged activation of G protein signaling and eventually becomes the major inputs for chronic leukocyte infiltration and cancer development. GPCRs can serve as proto-oncogenes since overexpression of various wild type GPCRs can transform cells in the presence of their specific ligands. Mutations on GPCRs may result in constitutive signaling and oncogenesis [7]. Naturally occurring mutations in GPCRs have been identified in human tumors [8,9].

General

Imprint: Springer
Country of origin: Netherlands
Series: The Tumor Microenvironment, 3
Release date: November 2012
First published: 2010
Editors: Albrecht Reichle
Dimensions: 235 x 155 x 33mm (L x W x T)
Format: Paperback
Pages: 568
Edition: 2010 ed.
ISBN-13: 978-9400733237
Categories: Books > Medicine > General issues > General
Books > Science & Mathematics > Biology, life sciences > Life sciences: general issues > Evolution
Books > Science & Mathematics > Biology, life sciences > Biochemistry > General
Books > Professional & Technical > Industrial chemistry & manufacturing technologies > Industrial chemistry > Pharmaceutical technology
Books > Medicine > Clinical & internal medicine > Diseases & disorders > Oncology > General
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LSN: 9400733232
Barcode: 9789400733237

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