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- Pontén, F, et al.
(författare)
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Molecular pathology in basal cell cancer with p53 as a genetic marker.
- 1997
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Ingår i: Oncogene. - : Springer Science and Business Media LLC. - 0950-9232 .- 1476-5594. ; 15:9
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Tidskriftsartikel (refereegranskat)abstract
- Human basal cell cancer (BCC) has unique growth characteristics with virtual inability to metastasize. We investigated clonality and genetic progression using p53 mutations as marker. Sampling was done through microdissection of frozen immunohistochemically stained 16 microm slices of tumors. From 11 BCC tumors 78 samples were analysed. Direct DNA sequencing of exons 5-8 was performed, haplotypes were determined after cloning of p53 exons and loss of heterozygosity (LOH) ascertained by microsatellite analysis. All tumors had p53 mutations and in a majority both p53 alleles were affected, commonly through missense mutations. Microdissection of small parts (50-100 cells) of individual tumors showed BCC to be composed of a dominant cell clone and prone to genetic progression with appearance of subclones with a second and even third p53 mutation. Samples from normal immunohistochemically negative epidermis always showed wild type sequence, except for a case of previously unknown germline p53 mutation. Our analysis also included p53 immunoreactive patches i.e. morphologically normal epidermis with a compact pattern of p53 immunoreactivity. Mutations within those were never the same as in the adjacent BCC. This detailed study of only one gene thus uncovered a remarkable heterogeneity within a tumor category famous for its benign clinical behavior.
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- Ren, Z. P., et al.
(författare)
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Benign clonal keratinocyte patches with p53 mutations show no genetic link to synchronous squamous cell precancer or cancer in human skin
- 1997
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Ingår i: American Journal of Pathology. - : American Society for Investigative Pathology and the Association for Molecular Pathology. - 0002-9440 .- 1525-2191. ; 150:5, s. 1791-803
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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- Sun, L C, et al.
(författare)
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Binuclear ruthenium-manganese complexes as simple artificial models for photosystem II in green plants
- 1997
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Ingår i: Journal of the American Chemical Society. - : American Chemical Society (ACS). - 1520-5126 .- 0002-7863. ; 119:30, s. 6996-7004
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Tidskriftsartikel (refereegranskat)abstract
- As part of a project aimed at developing models for photosystem II (PSII) in green plants, we have prepared a series of model compounds (7, 8, and 13). In these compounds, a photosensitizer, ruthenium(II) tris(bipyridyl) complex (to mimic the function of P-680 in PSII), was covalently linked to a manganese(II) ion through different bridging ligands. The structures of the compounds were characterized by electron paramagnetic resonance measurements and electrospray ionization mass spectrometry. The interaction between the ruthenium and manganese moieties within the complex was probed by steady-state and time-resolved emission measurements. When the binuclear complexes are exposed to flash photolysis in the presence of an electron acceptor such as methylviologen (MV2+), it could be shown that after the initial electron transfer from the excited state of Ru(II) in compound 7, forming Ru(III) and MV+., an intramolecular electron transfer from coordinated Mn(II) to the photogenerated Ru(III) occurred with a first-order rate constant of 1.8 x 10(5) s(-1), regenerating Ru(II). This is believed to be the first supramolecular system where a manganese complex has been used as an electron donor to a photo-oxidized photosensitizer, Possible extensions to develop the manganese donor, and thus to approach the function of reaction center in PSII, are indicated.
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