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Tumor Dormancy, Quiescence, and Senescence, Volume 2: Aging, Cancer, and Noncancer Pathologies

ISBN-13: 9789402407662 / Angielski / Miękka / 2016 / 320 str.

M. A. Hayat
Tumor Dormancy, Quiescence, and Senescence, Volume 2: Aging, Cancer, and Noncancer Pathologies Hayat, M. A. 9789402407662 Springer - książkaWidoczna okładka, to zdjęcie poglądowe, a rzeczywista szata graficzna może różnić się od prezentowanej.

Tumor Dormancy, Quiescence, and Senescence, Volume 2: Aging, Cancer, and Noncancer Pathologies

ISBN-13: 9789402407662 / Angielski / Miękka / 2016 / 320 str.

M. A. Hayat
cena 666,07
(netto: 634,35 VAT:  5%)

Najniższa cena z 30 dni: 660,61
Termin realizacji zamówienia:
ok. 30 dni roboczych.

Darmowa dostawa!

This second volume in the series exploring Tumor Dormancy, Quiescence, and Cellular Senescence offers comprehensive discussion of the role of tumor dormancy in diseases including breast cancer, melanoma, prostate cancer, liver cancer and lung cancer.

Kategorie:
Nauka, Medycyna
Kategorie BISAC:
Science > Cytologia
Medical > Oncology - General
Medical > Zdrowie publiczne
Wydawca:
Springer
Seria wydawnicza:
Tumor Dormancy and Cellular Quiescence and Senescence
Język:
Angielski
ISBN-13:
9789402407662
Rok wydania:
2016
Wydanie:
Softcover Repri
Numer serii:
000459764
Ilość stron:
320
Waga:
0.90 kg
Wymiary:
25.4 x 17.8
Oprawa:
Miękka
Wolumenów:
01
Dodatkowe informacje:
Wydanie ilustrowane

Prelims

I.            Molecular Mechanisms

1.       Asymmetric Dimethylarginine Accelerates Cellular Senescence

2.      Membrane-Derived Extracellular Vesicles from Endothelial Progenitor Cells Activate Angiogenesis

3.      Induction of P21-Dependent Senescence: Role of NAE Inhibitor MLN4924  

4.      Regulation of the Novel Senescence Pathway by SKP2 E3 Ligase

5.      Oncogene-Induced Senescence: Role of Mitochondrial Dysfunction

6.      Interleukin- 6 induces Premature Senescence Involving Signal Transducer and Activator of Transcription 3 and Insulin-Like Growth Factor-Binding Protein 5

7.      A Role for the Nuclear Lamina Shape in Cell Senescence and Aging

8.      Upregulation of Alpha-2-Macroglobulin in Replicative Senescence

9.       Elevation of Ceramide in Senescence: Role of Sphingolipid Metabolism

10.  Molecular Signals Underlying Hair Follicle Morphagenesis and Cutaneous Regeneration

11.  Role of Chromatin –Remodeling Factor Jun Dimerization Protein 2 (JDP2) in Cellular Senescence

12.  Induction of Cellular Senescence: Role of Mitogen-Activated Protein Kinase-Interacting Kinase 1

13.  Mechanisms of Premature Cell Senescence

II.            Tumor and Cancer

14.  Nuclear Protein Pirin Negates the Cellular Senescence Barrier Against Cancer Development 

15.  Defects in Chromatin Structure and Diseases

16.  The Role of Fibrosis in Tumor Progression and the Dormant to Proliferative Switch

17.  Diagnosis of Branchial Cyst Carcinoma: Role of Stem Cells and Dormancy

18.  Function of ING Proteins in Cancer and Senescence

19.  Premalignancy and Cellular Senescence

20.  Loss of CDH1 Triggers Premature Senescence in Part Via Activation of Both the RB/E2F1 and the Claspin/CHK1/P53 Tumor Suppressor Pathways

21.  Suppression of Premature Senescence and Promotion of Metastatic Transformation: Role of Reduced TGF-Beta Signaling in Human Cancer Progression

22.  Senescence Escape in Melanoma: Role of Spleen Tyrosine Kinase SYK

23.   Micrometastatic Cancer Cells: Role of Tumor Dormancy in Non-Small Cell Lung Cancer

III. Quiescent CD4+ T Cells Inhibit Multiples Stages of HIV Infection Stem Cells and Cancer Stem Cells

24.  Senescent-Derived Pluripotent Stem Cells are able to Redifferentiate into Fully Rejuvenated Cells

25.  The Transcription Factor Gata2 Regulates Quiescence in Haematopoietic Stem and Progenitor Cells

26.  Dormancy and Recurrence of Cancer Stem Cells in Bone: Role of Bone Morphogenetic Proteins

27.  Role of Microenvironment in Regulating Stem Cell and Tumor Initiating Cancer Cell Behavior and its Potential Therapeutic Implications

 Index.       

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 11 countries.



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