000 03896nam a22004815i 4500
001 978-1-4020-6016-8
003 DE-He213
005 20161121230756.0
007 cr nn 008mamaa
008 100301s2007 ne | s |||| 0|eng d
020 _a9781402060168
_9978-1-4020-6016-8
024 7 _a10.1007/978-1-4020-6016-8
_2doi
050 4 _aRC261-271
072 7 _aMJCL
_2bicssc
072 7 _aMED062000
_2bisacsh
082 0 4 _a614.5999
_223
100 1 _aWeber, Georg F.
_eauthor.
245 1 0 _aMolecular Mechanisms of Cancer
_h[electronic resource] /
_cby Georg F. Weber.
264 1 _aDordrecht :
_bSpringer Netherlands,
_c2007.
300 _aXIV, 645 p.
_bonline resource.
336 _atext
_btxt
_2rdacontent
337 _acomputer
_bc
_2rdamedia
338 _aonline resource
_bcr
_2rdacarrier
347 _atext file
_bPDF
_2rda
505 0 _aGeneral Mechanisms of Transformation -- Theories of Carcinogenesis -- Physiologic Correlates of Malignancy -- Alterations Intrinsic to the Tumor Cells -- Cell Division and Survival -- Cellular Senescence -- Invasiveness -- Mechanisms of Regulation of Cancer-related Genes -- DNA Repair -- Epigenetic Regulation of Cancer-Associated Gene Products -- Interaction of the Groups of Cancer-Related Gene Products -- Interactions Between Host and Tumor -- Structural Growth Control -- The Organ Preference of Metastasis Formation -- Angiogenesis -- Interactions with the Immune System -- Endocrine Dysregulation -- Dormancy and Minimal Residual Disease -- Molecular Mechanisms of Individual Malignancies -- Epithelial Tumors -- Hematologic Malignancies -- Mesenchymal Tumors -- Neurologic Tumors -- Tumors of Serous Cavities -- Embryonic Tumors.
520 _aCancer may constitute the most extensively studied functions constitute a second line of defense that disease entity of our time. Nevertheless, our com- protects against transforming defects in oncogenes prehension of the cellular and molecular pathology or tumor-suppressor genes and are here considered of malignant transformation is incomplete. In view as metasuppressor genes. Advances in the molecular of the diverse clinical presentations of various explanations of growth dysregulation, metastasis malignancies, doubts may be raised as to whether it formation, extension of life span, and loss of ma- is appropriate to refer to cancer as one group of dis- tenance of genomic and epigenetic integrity in ease states. The notion of malignant tumors as a cancer suggest models for their causal connection. pathologic and pathophysiologic class of conditions The mechanisms of growth control, senescence, and begs the question for defining criteria that charac- anchorage dependence are linked on the molecular terize all malignant growths, regardless of their tis- level (Chapter 8). In cells that are not fully differ- sue of origin. Toward this goal, the recognition that tiated, the overactivation of oncogene pathways tumor development is caused by the dysregulation also induces the expression of metastasis genes. of growth-controlling genes (oncogenes and tumor- Telomerase, the enzyme that prevents cell sen- suppressor genes) has advanced our mechanistic cence, is expressed in these precursor cells and may understanding of oncology (Chapter 3). However, be further activated by growth factor signaling.
650 0 _aMedicine.
650 0 _aCancer research.
650 0 _aMolecular biology.
650 0 _aOncology.
650 0 _aCell biology.
650 1 4 _aBiomedicine.
650 2 4 _aCancer Research.
650 2 4 _aMolecular Medicine.
650 2 4 _aCell Biology.
650 2 4 _aOncology.
710 2 _aSpringerLink (Online service)
773 0 _tSpringer eBooks
776 0 8 _iPrinted edition:
_z9781402060151
856 4 0 _uhttp://dx.doi.org/10.1007/978-1-4020-6016-8
912 _aZDB-2-SBL
950 _aBiomedical and Life Sciences (Springer-11642)
999 _c503802
_d503802