Carcinogenesis, 肿瘤基本问题与肿瘤研究专题
本区主要讨论从正常细胞到肿瘤细胞转化的漫长过程，瘤性转化到肿瘤形成（如新生血管形成、新生淋巴管形成），以及肿瘤表型进行性恶变的过程（如转移等），一句话就是肿瘤的发生发展过程相关问题的集中讨论区。。。作为重要互补，本区同时欢迎就基本生命活动，如细胞增殖、分化、凋亡、移动等领域进行讨论！
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Carcinogenesis
[url]http://www.fsm.ac.fj/PWS/Resources/Lectures/Carcinogenesis.ppt[/url]
Radiation Induced Carcinogenesis
[url]http://www.medphys.mcgill.ca/mptexts/Radiation-Biology.ppt[/url]
The Process of Carcinogenesis
[url]http://classes.kumc.edu/son/nurs325/Student%20-%20Intro%20to%20Chemotherapy%20-%20basics.ppt[/url]
MOLECULAR CARCINOGENESIS
[url]http://www.zoey.med.howard.edu/2006/MOLECULAR%20CARCINOGENESIS.ppt[/url]
Environmental Carcinogenesis
[url]http://www.ucl.ac.uk/uro-neph/ppt/ec140303.ppt[/url]
The Stages of Chemical Carcinogenesis
[url]http://www.sph.uth.tmc.edu:8055/sa/Course_Pages/PHS2110/Class_Files/4risk%20assess.ppt[/url]
Viral Carcinogenesis
[url]http://www.kumc.edu/instruction/medicine/pathology/ed/ch_5/Dr.%20Pelling%20Viral%20Carcinogenesis.ppt[/url]
Chemical Carcinogens
[url]http://www.med.mcgill.ca/cancer/Course%20Material/Carcinogensis.ppt[/url]
Non-genotoxic carcinogenesis
[url]http://dmg.life.nottingham.ac.uk/teaching/cancer/cancer8.ppt[/url]
Causing Cancer
[url]http://phoenix.liunet.edu/~eduffy/cancercourse/presentations/2carcinogenesis.ppt[/url]
Carcinogenesis, Tumor Suppression, Gene Therapy
[url]http://www.sh.lsuhsc.edu/intragrad/foundations/219/Carcinogenesis.ppt[/url]
Nature Reviews Cancer 2003 10月的一篇综述：
Hypoxia-inducible factor 1 (HIF-1)刺激一些基因的转录，这些基因与肿瘤生物学的关键方面有关，包括肿瘤血管生成、细胞生存、糖代谢和肿瘤细胞的侵袭。肿瘤实质内的低氧和基因改变可导致HIF-1á的过表达，而HIF-1á的过表达会上升多种肿瘤患者的死亡率。一些临床前期研究表明，抑制HIF-1á活性对肿瘤的生长有显著效果。目前正致力于鉴定HIF-1á抑制剂，验证其抗肿瘤治疗的功效。
英文摘要：Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes that are involved in crucial aspects of cancer biology, including angiogenesis, cell survival, glucose metabolism and invasion.Intratumoral hypoxia and genetic alterations can lead to HIF-1á overexpression, which has been associated with increased patient mortality in several cancer types. In preclinical studies, inhibition of HIF-1 activity has marked effects on tumour growth. Efforts are underway to identify inhibitors of HIF-1 and to test their efficacy as anticancer therapeutics. HIF 表达可促进肿瘤的发展，HIF 不表达同样可促进肿瘤进展，这取决于肿瘤所在的微环境
The hypoxic response of tumors is dependent on their microenvironment
[url]http://www.cancercell.org/content/article/abstract?uid=PIIS1535610803001946[/url]
TUMORIGENESIS：Environmental impact
[url]http://www.nature.com/cgi-taf/DynaPage.taf?file=/nrc/journal/v3/n10/full/nrc1194_fs.html[/url]
Somatic Mutation Theory of Carcinogenesis
[url]http://www.institutnicod.org/Reduction/Molec-carc.pdf[/url]
Hormones and carcinogenesis
[url]http://journals.endocrinology.org/erc/005/0045/0050045.pdf[/url]
Role of DNA Transactions in Carcinogenesis
[url]http://www.acc.pref.aichi.jp/acc/english/sympo/1-3sympo/sympo2.pdf[/url]
Liver, Metabolism and Chemical Carcinogenesis
[url]http://mcardle.oncology.wisc.edu/bradfield/Liver%20Cancer%202.pdf[/url]
Mechanisms of carcinogenesis
[url]http://www.iarc.fr/pageroot/GENERAL/BIEN_REPORTS/ENG/Part4.pdf[/url]
FOURTH INTERNATIONAL SYMPOSIUM ON HORMONAL CARCINOGENESIS
[url]http://www.kumc.edu/hormonecancers/program.pdf[/url]
Radiation carcinogenesis Radiation genetics Radiation ...
[url]http://www.roc.wayne.edu/med_phys/rad7060/rad7060f2000.pdf[/url]
Molecular Mechanisms of Metal Toxicity and Carcinogenesis
[url]http://www.neutrino.co.jp/abi_dmcb/0-7923-7498-3.PDF[/url]
Section of Molecular Carcinogenesis
[url]http://www.icr.ac.uk/research_pdf/mol_carc.pdf[/url]
Multistage carcinogenesis and radiation
[url]http://www.iop.org/EJ/article/0952-4746/22/3A/308/jr2c08.pdf[/url]
Cancer, apoptosis, and nonimmune surveillance
Cell Death and Differentiation (2004) 11, 13-17.
All organisms have powerful surveillance mechanisms that prevent the outgrowth of potentially cancerous cells. Many of them are highly conserved by evolution. To this end, the C. elegans animal model has been essential.
Believed for a long time as the most important safeguard, immunological surveillance now occupies a relatively minor place. It is still a powerful restraint against the outgrowth of virally transformed cells, however. This is the reason why tumorigenesis by Epstein-Barr virus, the papillomaviruses, and HHV-8, the Kaposi sarcoma herpes virus, is either restricted to or more pronounced in the immunodefectives.
Non-immune surveillance is of four different kinds:
(i) Genetic surveillance is largely based on DNA repair. It is the first line of defense, robustly built on a multitude of repair mechanisms. Defects in repair enzymes lead to specific cancer syndromes, several of them associated with multicancer families.
(ii) The evidence for epigenetic surveillance is not yet firmly established. Preliminary evidence indicates the existence of inherited differences in the stringency of imprinting, possibly related to cancer risk.
(iii) Intracellular surveillance prevents the outgrowth of cells driven by illegitimately activated oncogenes. Growth arrest and apoptosis are its two main arms. They are related but distinct. Growth arrest can be assigned to specific tumor-suppressor genes, some of which are also linked to apoptotic pathways. Apoptosis is a firmly built multipathway system, as tightly controlled as cell division. Tumor development includes impairment or damage to one or several apoptotic pathways. Tumor cells use multiple escapes from apoptosis, including both debilitation of proapoptotic pathways (e.g. p53) and activation of antiapoptotic mechanisms, for example, AKT/PI3 K. Nevertheless, no tumor cell is completely resistant to apoptosis. 'Genotoxic' agents such as irradiation or chemotherapy act by inducing apoptosis in relatively apoptosis-resistant cells.
Many therapeutic approaches, including clinical trials, aim at the reactivation of apoptosis. Partial or full restoration of a pathway that has been damaged in a given tumor cell is most likely to succeed. The 'Achilles heel' approach involves mRNA or protein targeting, to reduce abnormally high enzyme levels and/or amplified oncoproteins.
(iv) Intercellular surveillance is less well explored. It is clear, however, that loss of contact by epithelial cells leads to anoikis, a special form of apoptosis. Inhibition of tumor growth by adjacent normal cells is another phenomenon of great interest, largely unexplored by molecular methods. It may explain long-range dormancy and counteract the outgrowth of disseminated tumor cells.
Fusion genes and rearranged genes in carcinogenesis
It has long been the accepted view of cancer researchers that there is a difference between the mechanism behind the development of leukemias, on the one hand, and solid tumors like breast cancer, prostate cancer, gastrointestinal cancer, etc, on the other. A research team at the Section for Clinical Genetics at Lund University is now claiming just the opposite: the same mechanism gives rise to all non-hereditary forms of cancer. These findings are being published in Nature Genetics.
[url]http://www.eurekalert.org/pub_releases/2004-04/src-rtt040604.php[/url]
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Fusion genes and rearranged genes as a linear function of chromosome aberrations in cancer- Perspective
Nature Genetics 36, 331 - 334 (2004)
Cytogenetic aberrations have been reported in 45,000 human neoplasms. Structural balanced rearrangements are associated with distinct tumor subtypes with remarkable specificity and have been essential for identifying genes involved in tumorigenesis. All balanced rearrangements that have been characterized molecularly act by deregulating a gene in one of the breakpoints or by creating a fusion gene. Because most recurrent aberrations and rearranged genes have been found in hematological disorders, whereas numerous genomic imbalances have been identified in solid tumors7, 8, it has become generally accepted that there are pathogenetic differences between these neoplasms. We here show that in every tumor type, the numbers of recurrent balanced chromosome abnormalities, fusion genes and genes rearranged as a consequence of balanced aberrations are simply a function of the number of cases with an abnormal karyotype. Hence, there may not be any fundamental tissue-specific differences in the genetic mechanisms by which neoplasia is initiated.
[url]http://www.nature.com/cgi-taf/DynaPage.taf?file=/ng/journal/v36/n4/abs/ng1335.html[/url] drs与非Mt通路凋亡
The release of cytochrome c from the mitochondria into the cytoplasm was not observed in apoptosis by drs, .........
Drs protein can interact with ASY/Nogo-B/RTN-xS, an apoptosis-inducing protein localized in the endoplasmic reticulum, and that coexpression of these genes increased the efficiency of apoptosis. These results indicated that Drs induces apoptosis by a novel pathway mediated by ASY/Nogo-B/RTN-xS, caspase-12, -9, and -3.
[url]http://www.nature.com/cgi-taf/DynaPage.taf?file=/onc/journal/v23/n17/abs/1207419a.html[/url]
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