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From Molecular to Modular Tumor Therapy: - Tumors are Reconstructible Communicatively Evolving Systems (Hardcover, Edition.)
Loot Price: R5,560
Discovery Miles 55 600
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From Molecular to Modular Tumor Therapy: - Tumors are Reconstructible Communicatively Evolving Systems (Hardcover, Edition.)
Series: The Tumor Microenvironment, 3
Expected to ship within 10 - 15 working days
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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].
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