c-Myc Function in Neoplasia:
1. 1 SCOPE OF BOOK n explosion of novel findings in the past decade has contrib A uted to the great progress toward understanding the biology of human cancers. Much of this progress can be attributed to our abil ity to dissect many biological processes at the molecular level. Most spectacular is t...
Gespeichert in:
| Hauptverfasser: | , |
|---|---|
| Format: | Elektronisch E-Book |
| Sprache: | English |
| Veröffentlicht: |
Berlin, Heidelberg
Springer Berlin Heidelberg
1995
|
| Schriftenreihe: | Medical Intelligence Unit
|
| Schlagworte: | |
| Online-Zugang: | UBR01 URL des Erstveröffentlichers |
| Zusammenfassung: | 1. 1 SCOPE OF BOOK n explosion of novel findings in the past decade has contrib A uted to the great progress toward understanding the biology of human cancers. Much of this progress can be attributed to our abil ity to dissect many biological processes at the molecular level. Most spectacular is the technology of molecular biology that allows identi fication and characterization of genes that participate in the genesis of human cancers. Three major groups of genes appear to play out the drama of cancer development: tumor suppressor genes, mis match repair genes, and oncogenes. The tumor suppressor genes 1 encode products that are inhibitory to cell proliferation. The loss of these inhibitors, by mutation or deletion, can unleash cells from their restraints to proliferate. Mutations in the mismatch repair 2 10 genes also have been implicated in tumorigenesis. - The inability of cells to repair spontaneously occurring mutations leads to genom ic instability and could potentially result in the accumulation of car cinogenic DNA lesions. Finally, activation of proto-oncogenes, which are normal cellular genes, into oncogenes could accelerate the 11 processes of cell proliferation. c-myc was one of the very first proto oncogenes to be identified and because it normally plays pivotal roles in both cell proliferation and cell death has enticed many to investigate the molecular mechanisms by which it transforms cells |
| Beschreibung: | 1 Online-Ressource (IX, 201 p. 33 illus) |
| ISBN: | 9783662226810 |
| DOI: | 10.1007/978-3-662-22681-0 |
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| 520 | |a 1. 1 SCOPE OF BOOK n explosion of novel findings in the past decade has contrib A uted to the great progress toward understanding the biology of human cancers. Much of this progress can be attributed to our abil ity to dissect many biological processes at the molecular level. Most spectacular is the technology of molecular biology that allows identi fication and characterization of genes that participate in the genesis of human cancers. Three major groups of genes appear to play out the drama of cancer development: tumor suppressor genes, mis match repair genes, and oncogenes. The tumor suppressor genes 1 encode products that are inhibitory to cell proliferation. The loss of these inhibitors, by mutation or deletion, can unleash cells from their restraints to proliferate. Mutations in the mismatch repair 2 10 genes also have been implicated in tumorigenesis. - The inability of cells to repair spontaneously occurring mutations leads to genom ic instability and could potentially result in the accumulation of car cinogenic DNA lesions. Finally, activation of proto-oncogenes, which are normal cellular genes, into oncogenes could accelerate the 11 processes of cell proliferation. c-myc was one of the very first proto oncogenes to be identified and because it normally plays pivotal roles in both cell proliferation and cell death has enticed many to investigate the molecular mechanisms by which it transforms cells | ||
| 650 | 4 | |a Cancer Research | |
| 650 | 4 | |a Cell Biology | |
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Datensatz im Suchindex
| _version_ | 1804180484007133184 |
|---|---|
| any_adam_object | |
| author | Dang, Chi V. Lee, Linda A. |
| author_facet | Dang, Chi V. Lee, Linda A. |
| author_role | aut aut |
| author_sort | Dang, Chi V. |
| author_variant | c v d cv cvd l a l la lal |
| building | Verbundindex |
| bvnumber | BV046146264 |
| collection | ZDB-2-SME |
| ctrlnum | (ZDB-2-SME)978-3-662-22681-0 (OCoLC)1119066775 (DE-599)BVBBV046146264 |
| dewey-full | 614.5999 |
| dewey-hundreds | 600 - Technology (Applied sciences) |
| dewey-ones | 614 - Forensic medicine; incidence of disease |
| dewey-raw | 614.5999 |
| dewey-search | 614.5999 |
| dewey-sort | 3614.5999 |
| dewey-tens | 610 - Medicine and health |
| discipline | Medizin |
| doi_str_mv | 10.1007/978-3-662-22681-0 |
| format | Electronic eBook |
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| id | DE-604.BV046146264 |
| illustrated | Not Illustrated |
| indexdate | 2024-07-10T08:36:29Z |
| institution | BVB |
| isbn | 9783662226810 |
| language | English |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-031526449 |
| oclc_num | 1119066775 |
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| physical | 1 Online-Ressource (IX, 201 p. 33 illus) |
| psigel | ZDB-2-SME ZDB-2-SME_1990/2004 ZDB-2-SME ZDB-2-SME_1990/2004 |
| publishDate | 1995 |
| publishDateSearch | 1995 |
| publishDateSort | 1995 |
| publisher | Springer Berlin Heidelberg |
| record_format | marc |
| series2 | Medical Intelligence Unit |
| spelling | Dang, Chi V. Verfasser aut c-Myc Function in Neoplasia by Chi V. Dang, Linda A. Lee Berlin, Heidelberg Springer Berlin Heidelberg 1995 1 Online-Ressource (IX, 201 p. 33 illus) txt rdacontent c rdamedia cr rdacarrier Medical Intelligence Unit 1. 1 SCOPE OF BOOK n explosion of novel findings in the past decade has contrib A uted to the great progress toward understanding the biology of human cancers. Much of this progress can be attributed to our abil ity to dissect many biological processes at the molecular level. Most spectacular is the technology of molecular biology that allows identi fication and characterization of genes that participate in the genesis of human cancers. Three major groups of genes appear to play out the drama of cancer development: tumor suppressor genes, mis match repair genes, and oncogenes. The tumor suppressor genes 1 encode products that are inhibitory to cell proliferation. The loss of these inhibitors, by mutation or deletion, can unleash cells from their restraints to proliferate. Mutations in the mismatch repair 2 10 genes also have been implicated in tumorigenesis. - The inability of cells to repair spontaneously occurring mutations leads to genom ic instability and could potentially result in the accumulation of car cinogenic DNA lesions. Finally, activation of proto-oncogenes, which are normal cellular genes, into oncogenes could accelerate the 11 processes of cell proliferation. c-myc was one of the very first proto oncogenes to be identified and because it normally plays pivotal roles in both cell proliferation and cell death has enticed many to investigate the molecular mechanisms by which it transforms cells Cancer Research Cell Biology Oncology Cytology Protoonkogen (DE-588)4256457-8 gnd rswk-swf Myc (DE-588)4267356-2 gnd rswk-swf Onkogen (DE-588)4131118-8 gnd rswk-swf Krebs Medizin (DE-588)4073781-0 gnd rswk-swf Krebs Medizin (DE-588)4073781-0 s Protoonkogen (DE-588)4256457-8 s Myc (DE-588)4267356-2 s DE-604 Onkogen (DE-588)4131118-8 s Lee, Linda A. aut Erscheint auch als Druck-Ausgabe 9783662226834 Erscheint auch als Druck-Ausgabe 9783662226827 Erscheint auch als Druck-Ausgabe 9783540606321 https://doi.org/10.1007/978-3-662-22681-0 Verlag URL des Erstveröffentlichers Volltext |
| spellingShingle | Dang, Chi V. Lee, Linda A. c-Myc Function in Neoplasia Cancer Research Cell Biology Oncology Cytology Protoonkogen (DE-588)4256457-8 gnd Myc (DE-588)4267356-2 gnd Onkogen (DE-588)4131118-8 gnd Krebs Medizin (DE-588)4073781-0 gnd |
| subject_GND | (DE-588)4256457-8 (DE-588)4267356-2 (DE-588)4131118-8 (DE-588)4073781-0 |
| title | c-Myc Function in Neoplasia |
| title_auth | c-Myc Function in Neoplasia |
| title_exact_search | c-Myc Function in Neoplasia |
| title_full | c-Myc Function in Neoplasia by Chi V. Dang, Linda A. Lee |
| title_fullStr | c-Myc Function in Neoplasia by Chi V. Dang, Linda A. Lee |
| title_full_unstemmed | c-Myc Function in Neoplasia by Chi V. Dang, Linda A. Lee |
| title_short | c-Myc Function in Neoplasia |
| title_sort | c myc function in neoplasia |
| topic | Cancer Research Cell Biology Oncology Cytology Protoonkogen (DE-588)4256457-8 gnd Myc (DE-588)4267356-2 gnd Onkogen (DE-588)4131118-8 gnd Krebs Medizin (DE-588)4073781-0 gnd |
| topic_facet | Cancer Research Cell Biology Oncology Cytology Protoonkogen Myc Onkogen Krebs Medizin |
| url | https://doi.org/10.1007/978-3-662-22681-0 |
| work_keys_str_mv | AT dangchiv cmycfunctioninneoplasia AT leelindaa cmycfunctioninneoplasia |