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Objectives: We examined the effect of New York's HIV Reporting and Partner Notification law on HIV testing levels and on the HIV testing decisions of high-risk individuals., Methods: In-person interviews were administered to 761 high-risk individuals to assess their knowledge, attitudes, and behaviors regarding HIV testing and reporting. Trends in HIV testing were also assessed in publicly funded HIV counseling and testing programs, Medicaid, and New York's Maternal Pediatric Newborn Prevention and Care Program., Results: High-risk individuals had limited awareness of the reporting and notification law, and few cited concern about named reporting as a reason for avoiding or delaying HIV testing. HIV testing levels, posttest counseling rates, and anonymous-to-confidential conversion rates among those who tested HIV positive were not affected by the law. Medicaid-related HIV testing rates also remained stable. HIV testing during pregnancy continued to trend upward following implementation of the law. Findings held true within demographic and risk-related subgroups., Conclusions: HIV reporting has permitted improved monitoring of New York's HIV/AIDS epidemic. This benefit has not been offset by decreases in HIV testing behavior, including willingness to test among those at high risk of acquiring HIV.

An activating point mutation in codon 12 of the HRAS gene was the first somatic point mutation identified in a human cancer and established the role of somatic mutations as the common driver of oncogenesis. Since then, there have been over 11,000 mutations in the three RAS (HRAS, KRAS and NRAS) genes in codons 12, 13 and 61 reported in the literature. We report here the identification of recurrent somatic missense mutations at alanine 146, a highly conserved residue in the guanine nucleotide binding domain. In two independent series of colorectal cancers from Hong Kong and the United States we detected KRAS A146 mutations in 7/126 and 2/94 cases, respectively, giving a combined frequency of 4%. We also detected KRAS A146 mutations in 2/40 (5%) colorectal cell lines, including the NCI-60 colorectal cancer line HCC2998. Codon 146 mutations thus are likely to make an equal or greater contribution to colorectal cancer than codon 61 mutations (4.2% in our combined series, 1% in the literature). Lung adenocarcinomas and large cell carcinomas did not show codon 146 mutations. We did, however, identify a KRAS A146 mutation in the ML-2 acute myeloid leukemia cell line and an NRAS A146 mutation in the NALM-6 B-cell acute lymphoblastic leukemia line, suggesting that the contribution of codon 146 mutations is not entirely restricted to colorectal cancers or to KRAS.