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Tumor Dormancy, Quiescence, and Senescence, Volume 2 - Aging, Cancer, and Noncancer Pathologies (Paperback, Softcover reprint of the original 1st ed. 2014)
Loot Price: R4,316
Discovery Miles 43 160
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Tumor Dormancy, Quiescence, and Senescence, Volume 2 - Aging, Cancer, and Noncancer Pathologies (Paperback, Softcover reprint of the original 1st ed. 2014)
Series: Tumor Dormancy and Cellular Quiescence and Senescence, 2
Expected to ship within 10 - 15 working days
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In this second volume in the series exploring Tumor Dormancy,
Quiescence, and Cellular Senescence, discussion is focused on the
role of tumor dormancy in diseases such as breast cancer,
melanoma, prostate cancer, liver cancer and lung cancer. M. A.
Hayat, the series editor, writes in the preface that little is
known of factors regulating the transition of residual cancer into
a dormant state or the subsequent reinitiation of growth. A
majority of us, he says, have in situ tumors that may remain
dormant or may progress into a lethal form of cancer; the former
are prevented from recruiting their own blood supply. Section I
covers Molecular Mechanisms, with chapters on the role of NAE
inhibitor MLN4924; oncogene-induced senescence; the role played by
mitogen-activated protein kinase in the induction of cellular
senescence; mechanisms of premature cell senescence and other
topics. Section II examines Tumor and Cancer, discussing defects in
chromatin structure and diseases; the role of fibrosis in tumor
progression and the dormant to proliferative switch; the function
of ING proteins in cancer and senescence and more. The final
section is devoted to Stem Cells and Cancer Stem Cells, featuring
chapters showing that senescent-derived pluripotent stem cells are
able to redifferentiate into fully rejuvenated cells; that the
transcription factor Gata2 regulates quiescence in haematopoietic
stem and progenitor cells; and discussing dormancy and recurrence
of cancer stem cells in bone. The contributors point out that the
quiescent state regulates hematopoietic stem cells and muscle stem
cells, and detail the role of kinase in the mediation of reversible
quiescent state in a subset of ovarian, pancreatic, and colon
cancers. Molecular mechanisms underlying stress-induced cellular
senescence and accumulation of reactive oxygen species and
induction of premature senescence are also presented. Discussion
includes the important role of microRNAs in oxidative
stress-induced apoptosis and senescence and the effect of microRNA
as a modulator of cell proliferation in lung cancer. The book
includes an explanation of the suppression of cellular senescence
in glioblastoma brain tumor. Taking a broad and varied perspective,
this volume was written by 70 contributors representing
11Â countries.
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