PubMed · 9410958
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M Okuma. 1997-09-10. [Platelet dysfunction--from bedside clinical study to molecular study].. https://pubmed.ncbi.nlm.nih.gov/9410958/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Oxidative metabolism of polyunsaturated fatty acids through cyclooxygenases or lipoxygenases can generate various lipid peroxides and bioactive lipids, and regulate cellular proliferation, apoptosis, differentiation and senescence. The role of the second cyclooxygenase isoform (COX-2) has been demonstrated in a number of studies and is regarded as a promising target for chemoprevention and treatment. The involvement for lipoxygenases in tumor initiation and progression has been implicated in several studies but remains controversial. Among the many members of lipoxygenase family, both tumor promoting and suppressing activities have been described. For example, 15-lipoxygenase-1 has been implicated as a tumor promoter in prostate cancer, but it suppresses colon cancer. In this review, the role of cyclooxygenases and lipoxygenases in cancer will be described, with the hope of attracting further research to define their functions in cancer.
Explore the source record for details and available documents.
We report clinical and molecular findings in 20 patients from 11 families with autosomal recessive congenital ichthyosis (ARCI) linked to chromosome 17p13, and attributed to mutations in the ALOX gene cluster, which includes three lipoxygenase genes, ALOXE3, ALOX12B, and ALOX15B. We identified six novel missense mutations and one novel deletion leading to a premature stop codon in ALOX12B in only six out of the 11 families which led us to investigate a possible implication of ALOX15B. Mutation analysis of this gene, as well as ALOXE3, which is known to be mutated in some cases of ARCI, failed to reveal causative mutations in the five remaining ARCI families, indicating that other genes on chromosome 17p13 may be involved in this disease. However, by adding new variants to the repertoire of ALOX12B mutations in non-bullous congenital ichthyosiform erythroderma, our data contribute to an enlargement of the spectrum of mutations for the development of efficient molecular genetic tests for analysis of at risk individuals whose carrier status is unknown.