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Autor     Colorectal cancer, one entity or three
Titel    Feng-ying LI, Mao-de LAI
Zeitschrift    Journal of Zhejiang University SCIENCE B
Jahr    2009
Seiten    219-229
ISSN    1862-1783
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650032/pdf/JZUSB10-0219.pdf

Literaturverz.   

ja
Fußnoten    ja
Fragmente    2


Fragmente der Quelle:
[1.] Shg/Fragment 021 18 - Diskussion
Zuletzt bearbeitet: 2014-11-02 08:57:03 Hindemith
Fragment, Gesichtet, Li Lai 2009, SMWFragment, Schutzlevel sysop, Shg, Verschleierung

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Seite: 21, Zeilen: 18-27
Quelle: Li Lai 2009
Seite(n): 219, Zeilen: right col., 3 ff.
According to the Surveillance, Epidemiology and End Results (SEER) Program database analysis, 5-year survival rates have risen from 56.5% for patients diagnosed in the early 1980s to as much as 63.2% for those diagnosed in the early 1990s and most recently to 64.9%, a trend due mostly to earlier diagnosis and treatment [Ries LAG, et al. 2008]. One reason for the improving trend is that the prognosis for patients with CRC is highly dependent on stage: 5-year survival rates are over 90% for Dukes A, but only 5% for Dukes D. Unfortunately, only 10% of CRCs are diagnosed early, most patients presenting themselves with the advanced disease [Rockville, MD. 1998].

Ries LAG, Melbert D, Krapcho M, et al. (2008). SEER Cancer Statistics Review. National Cancer Institute: 1975-2005.

Rockville, MD. (1998). Agency for Health Care Policy and Research. AHCPR Publication No. 98-003.

According to the Surveillance, Epidemiology and End Results (SEER) Program database analysis, 5-year survival rates have risen from 56.5% for patients diagnosed in the early 1980s to as much as 63.2% for those diagnosed in the early 1990s and most recently to 64.9%, a trend due mostly to earlier diagnosis and treatment (Ries et al., 2008). One reason for the improving trend is that the prognosis for patients with CRC is highly dependent on stage: 5-year survival rates are over 90% for Dukes A, but only 5% for Dukes D. Unfortunately, only 10% of CRCs are diagnosed early, most patients presenting themselves with advanced disease (AHCPR, 1998)

Ries, L.A.G., Melbert, D., Krapcho, M., Stinchcomb, D.G., Howlader, N., Horner, M.J., Mariotto, A., Miller, B.A., Feuer, E.J., Altekruse, S.F., Lewis, D.R., et al. (Eds.), 2008. SEER Cancer Statistics Review, 1975-2005 [WWW]. National Cancer Institute. Available from: http://seer.cancer.gov/csr/1975_2005/results_merged/topic_survival.pdf [Accessed 06/08/2008].

AHCPR (Agency for Health Care Policy and Research), 1998. Colorectal Cancer Screening. Technical Review 1. AHCPR Publication No. 98-0033. Agency for Health Care Policy and Research, Rockville, MD.

Anmerkungen

The source is not mentioned here.

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(SleepyHollow02), Hindemith

[2.] Shg/Fragment 022 13 - Diskussion
Zuletzt bearbeitet: 2014-11-02 09:01:06 Hindemith
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1.2.3. Genes

There is much progress which has been made in understanding the molecular mechanism of colorectal cancer. A progression from normal mucosa to adenoma to carcinoma was supported by the demonstration of accumulating mutations in genes as K-ras, adenomatous polyposis coli (APC), tumor protein P53 (TP53), and deleted in DCC, all of which are thought to be of significance, but are not able to successfully account for all colorectal cancers. There is heterogeneity in the pathogenetic pathway leading to CRCs, and there are two major tumorigenic pathways. The first is driven by chromosomal instability (CIN), the progress of which involves both oncogenes and tumor-suppressor genes including chromosomes 5q, 17p, and 18q [Fearon, E.R., Vogelstein, B. 1990; Gervaz, P., et al. 2001]. Chromosome 5q genes are responsible for APC, 17p for TP53, and 18q for DCC or Mothers against decapentaplegic homolog 4 (SMAD4). K-ras is the most common oncogene following this pattern. The tumor-suppressor genes APC, TP53, and DCC/SMAD4 play important roles in this sequential adenoma to carcinoma. Another genetic pathway may well be depicted as a consequence of the alteration in mismatch repair (MMR) genes. [Gervaz, P., et al. 2001] When the alteration happens in germinal cells, the hereditary cancer known as hereditary nonpolyposis colorectal cancer (HNPCC) occurs. When somatic cells are affected, microsatellite instability (MSI) would be [unavoidable. MSI is responsible for a subset of sporadic colorectal tumors. [Feng-ying LI, Mao-de LAI 2008]]


Fearon, E.R., Vogelstein, B. (1990). A genetic model for colorectal tumorigenesis. Cell, 61(5):759-76.

Gervaz, P., Bouzourene, H., Cerottini, J.P., Chaubert, P., Benhattar, J., Secic, M., Wexner, S., Givel, J.C., Belin, B. (2001). Dukes B colorectal cancer: distinct genetic categories and clinical outcome based on proximal or distal tumor location. Dis. Colon Rectum. 44(3):364-372.

Feng-ying LI, Mao-de LAI (2008) Colorectal cancer, one entity or three. J Zhejiang Univ Sci. B 10(3):219-229.

GENETIC PATHWAY

Much progress has been made in understanding the molecular mechanism of CRC since 1990, when a genetic model for CRC tumorigenesis was proposed (Fearon and Vogelstein, 1990). A progression from normal mucosa to adenoma to carcinoma was supported by the demonstration of accumulating mutations in genes of K-ras, adenomatous polyposis coli (APC), tumor protein P53 (TP53), and deleted in colorectal carcinoma (DCC), all of which are thought to be of significance, but are not able successfully to account for all CRCs. There is heterogeneity in the pathogenetic pathway leading to CRCs, and there are two major tumorigenic pathways. The first is driven by chromosomal instability (CIN), namely the model mentioned above, the progress of which involves both oncogenes and tumor-suppressor genes including chromosomes 5q, 17p, and 18q (Delattre et al., 1989; Fearon and Vogelstein, 1990; Gervaz et al., 2001). Chromosome 5q genes are responsible for APC, 17p for TP53, and 18q for DCC or Mothers against decapentaplegic homolog 4 (SMAD4), respectively. K-ras is the most common oncogene following this pattern. As far as tumor-suppressor genes are concerned, genes of APC, TP53, DCC/SMAD4 play important roles in this sequential adenoma to carcinoma pattern. An alternative genetic pathway related to genetic instability may well be depicted as a consequence of

[Page 222]

the alteration in mismatch repair (MMR) genes (Gervaz et al., 2001; Miyakura et al., 2001; Thibodeau et al., 1993). When the alteration happens in germinal cells, the hereditary cancer known as hereditary nonpolyposis colorectal cancer (HNPCC) occurs. When somatic cells are affected, microsatellite instability (MSI) would be unavoidable, which is responsible for a subset of sporadic colorectal tumors.


Delattre, O., Olschwang, S., Law, D.J., Melot, T., Remvikos, Y., Salmon, R.J., Sastre, X., Validire, P., Feinberg, A.P., Thomas, G., 1989. Multiple genetic alterations in distal and proximal colorectal cancer. Lancet, 334(8659):353-356. [doi:10.1016/S0140-6736(89)90537-0]

Fearon, E.R., Vogelstein, B., 1990. A genetic model for colorectal tumorigenesis. Cell, 61(5):759-767. [doi:10.1016/0092-8674(90)90186-I]

Gervaz, P., Bouzourene, H., Cerottini, J.P., Chaubert, P., Benhattar, J., Secic, M., Wexner, S., Givel, J.C., Belin, B., 2001. Dukes B colorectal cancer: distinct genetic categories and clinical outcome based on proximal or distal tumor location. Dis. Colon Rectum, 44(3):364-372. [doi:10.1007/BF02234734]

Miyakura, Y., Sugano, K., Konishi, F., Ichikawa, A., Maekawa, M., Shitoh, K., Igarashi, S., Kotake, K., Koyama, Y., Nagai, H., 2001. Extensive methylation of hMLH1 promoter region predominates in proximal colon cancer with microsatellite instability. Gastroenterology, 121(6): 1300-1309. [doi:10.1053/gast.2001.29616]

Thibodeau, S.N., Bren, G., Schaid, D., 1993. Microsatellite instability in cancer of the proximal colon. Science, 260(5109):816-819. [doi:10.1126/science.8484122]

Anmerkungen

The source is mentioned in the end, but it does not become clear that the entire section including to references to the literature is taken from it.

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(SleepyHollow02), Hindemith

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