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p53 mutations are present in colorectal cancer with cytoplasmic p53 accumulation
Linköpings universitet, Institutionen för biomedicin och kirurgi, Onkologi. Linköpings universitet, Hälsouniversitetet.
Linköpings universitet, Institutionen för biomedicin och kirurgi, Onkologi. Linköpings universitet, Hälsouniversitetet.
Linköpings universitet, Institutionen för biomedicin och kirurgi, Onkologi. Linköpings universitet, Hälsouniversitetet.
2001 (engelsk)Inngår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 92, nr 3, s. 338-341Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Previous studies have shown that nuclear p53 over-expression is an indicator of p53 mutations whereas cytoplasmic p53 accumulation is related to wild-type p53 in several kinds of tumors. Cytoplasmic p53 accumulation has been demonstrated to be an independent prognostic factor in colorectal adenocarcinomas. The purpose was to examine whether mutations occur in cases with p53 accumulated in the cytoplasm and whether there are any differences in the frequency and characteristics of p53 mutations in different staining patterns. In the present study, we identified p53 mutations using PCR single-strand conformation polymorphism (SSCP) and DNA sequencing in 75 primary colorectal adenocarcinomas with different staining patterns (negative, nucleus, cytoplasm, nucleus and cytoplasm). The results show that the frequency and nature of mutations in tumors with cytoplasmic p53 accumulation were similar to those with nuclear p53 expression. However, the tumors with accumulation in both the nucleus and cytoplasm demonstrated a higher mutation rate. We suppose that the role of cytoplasmic p53 accumulation in predicting prognosis in patients with colorectal cancer may be dependent on both mutational and non-mutational mechanisms.

sted, utgiver, år, opplag, sider
2001. Vol. 92, nr 3, s. 338-341
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-25033DOI: 10.1002/ijc.1189Lokal ID: 9456OAI: oai:DiVA.org:liu-25033DiVA, id: diva2:245359
Tilgjengelig fra: 2009-10-07 Laget: 2009-10-07 Sist oppdatert: 2017-12-13bibliografisk kontrollert
Inngår i avhandling
1. Molecular alterations in colorectal cancer
Åpne denne publikasjonen i ny fane eller vindu >>Molecular alterations in colorectal cancer
2002 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Colorectal cancer is one of the most common causes to death due to cancer in the world. It is important to understand the molecular mechanisms behind tumour development for both prognostic and therapeutic applications. In this thesis, we have focused on genes and proteins related to tumour suppressor function, apoptosis and DNA repair in patients with colorectal adenocarcinomas. In Paper I, the pattern of mutations affecting the tumour suppressor p53 was investigated in 75 cases in order to determine whether there were any specific mutations in the cases with p53 accumulated in the cytoplasm. We found that the frequency and pattern of mutation were similar to those with nuclear p53 expression, suggesting that the prognostic importance of cytoplasmic p53 accumulation may depend on both mutational and non-mutational mechanisms. In Paper II we investigated the protein expression of the pro-apoptotic gene Bax from normal mucosa to primary tumour and to regional lymph node metastases in 135 patients. We further examined Bax mutations and the microsatellite status in the primary tumours. Bax expression was stronger from normal to tumour tissue, but decreased in the metastases. The matched cases with lower expression in the metastastases than in the primary tumour showed a more infiltrative growth pattern and more distal metastases. In paper III the mRNA expression of the pro-apoptotic gene Noxa was examined with real-time PCR and mutations searched for in 94 colorectal tumours and the corresponding normal mucosa. Noxa mRNA expression was weak in 9% and strong in 2% of the tumours and decreased in 9% and increased in 16% of the tumours compared to the normal mucosa. The expression was not related to clinicopathological features. We did not find any mutations in the gene. In Paper IV we studied the biological and clinicopathological importance of protein expression of the mismatch repair genes hMLHJ, hMSH2, hMSH3 and hMSH6 individually or combined in 301 colorectal cancers. When analysed individually, hMLH1 and hMSH2 were more important and the combined groups were more related to the mutator pathway, suggesting that the combined deficiencies of the proteins are more efficiently involved in the mutator pathway. Our result from comparing weak versus strong staining may suggest that the intensity of staining should be considered in future studies on the expression of mismatch repair proteins.

sted, utgiver, år, opplag, sider
Linköping: Linköpings universitet, 2002. s. 92
Serie
Linköping University Medical Dissertations, ISSN 0345-0082 ; 743
HSV kategori
Identifikatorer
urn:nbn:se:liu:diva-25665 (URN)10041 (Lokal ID)91-7373-183-8 (ISBN)10041 (Arkivnummer)10041 (OAI)
Disputas
2002-10-04, Administrationsbyggnadens aula, Hälsouniversitetet, Linköping, 09:00 (svensk)
Opponent
Tilgjengelig fra: 2009-10-08 Laget: 2009-10-08 Sist oppdatert: 2012-09-20bibliografisk kontrollert

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