Search: onr:"swepub:oai:DiVA.org:kth-219965" > Benign clonal kerat...
Fältnamn | Indikatorer | Metadata |
---|---|---|
000 | 03225naa a2200349 4500 | |
001 | oai:DiVA.org:kth-219965 | |
003 | SwePub | |
008 | 171214s1997 | |||||||||||000 ||eng| | |
024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-2199652 URI |
040 | a (SwePub)kth | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Ren, Z. P.4 aut |
245 | 1 0 | a Benign clonal keratinocyte patches with p53 mutations show no genetic link to synchronous squamous cell precancer or cancer in human skin |
264 | 1 | b American Society for Investigative Pathology and the Association for Molecular Pathology,c 1997 |
338 | a print2 rdacarrier | |
500 | a QC 20171215 | |
520 | a Ultraviolet light, which is the major etiology of human skin cancer, will cause mutations in the p53 gene. We and others have found that such mutations occur in more than one-half of non-melanoma squamous cell cancer and precancer. Immunostaining for p53 has disclosed a characteristic compact pattern not only in cancer/precancer but also in areas of microscopically normal epidermis termed p53 patches. By microdissection, sequence analysis of the p53 gene, and analysis of loss of heterozygosity (LOH) at the site of this gene, we have now extended previous data to ascertain whether these p53 patches are precursors of simultaneously present squamous cell cancer or its morphologically recognized precancerous stages (dysplasia, carcinoma in situ). In none of 11 instances with co-existence of a p53 patch with dysplasia or in situ or invasive cancer were the mutations identical. We conclude that p53 patches, estimated to be approximately 100,000 times as common as dysplasia, have a very small or even no precancerous potential. Their common presence demonstrates that human epidermis contains a large number of p53 mutations apparently without detrimental effect. The only result of the mutation may be a clandestine benign clonal keratinocyte proliferation. The importance of p53 mutations for such benign cell multiplication on one band and malignant transformation on the other is unclear. Although the spectrum, type, and multiplicity of mutations were similar in both types of proliferative responses, there was a clear difference with respect to LOH. No LOH was found in 17 p53 patches. By contrast 11 of 30 precancers/cancers had LOH. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaper0 (SwePub)3012 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Basic Medicine0 (SwePub)3012 hsv//eng |
700 | 1 | a Ahmadian, A.4 aut |
700 | 1 | a Pontén, F.4 aut |
700 | 1 | a Nistér, M.4 aut |
700 | 1 | a Berg, Cecilia,d 1969-u KTH,Biokemi och biokemisk teknologi4 aut0 (Swepub:kth)u1ygqmuy |
700 | 1 | a Lundeberg, J.4 aut |
700 | 1 | a Uhlén, M.4 aut |
700 | 1 | a Pontén, J.4 aut |
710 | 2 | a KTHb Biokemi och biokemisk teknologi4 org |
773 | 0 | t American Journal of Pathologyd : American Society for Investigative Pathology and the Association for Molecular Pathologyg 150:5, s. 1791-803q 150:5<1791-803x 0002-9440x 1525-2191 |
856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-219965 |
Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.