18 research outputs found

    Performance of Self-Report to Establish Cancer Diagnoses in Disaster Responders and Survivors, World Trade Center Health Registry, New York, 2001–2007

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    Objective. Large-scale disasters may disrupt health surveillance systems, depriving health officials and researchers of timely and accurate information needed to assess disaster-related health effects and leading to use of less reliable self-reports of health outcomes. In particular, ascertainment of cancer in a population is ordinarily obtained through linkage of self-reported data with regional cancer registries, but exclusive reliance on these sources following a disaster may result in lengthy delays or loss of critical data. To assess the impact of such reliance, we validated self-reported cancer in a cohort of 59,340 responders and survivors of the World Trade Center disaster against data from 11 state cancer registries (SCRs). Methods. We focused on residents of the 11 states with SCRs and on cancers diagnosed from September 11, 2001, to the date of their last survey participation. Medical records were also sought in a subset of 595 self-reported cancer patients who were not recorded in an SCR. Results. Overall sensitivity and specificity of self-reported cancer were 83.9% (95% confidence interval [CI] 81.9, 85.9) and 98.5% (95% CI 98.4, 98.6), respectively. Site-specific sensitivities were highest for pancreatic (90.9%) and testicular (82.4%) cancers and multiple myeloma (84.6%). Compared with enrollees with true-positive reports, enrollees with false-negative reports were more likely to be non-Hispanic black (adjusted odds ratio [aOR] 5 1.8, 95% CI 1.2, 2.9) or Asian (aOR52.2, 95% CI 1.2, 4.1). Among the 595 cases not recorded in an SCR, 13 of 62 (21%) cases confirmed through medical records were reportable to SCRs. Conclusion. Self-report of cancer had relatively high sensitivity among adults exposed to the World Trade Center disaster, suggesting that self-reports of other disaster-related conditions less amenable to external validation may also be reasonably valid

    Genome-wide copy number alterations in subtypes of invasive breast cancers in young white and African American women.

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    Genomic copy number alterations (CNA) are common in breast cancer. Identifying characteristic CNAs associated with specific breast cancer subtypes is a critical step in defining potential mechanisms of disease initiation and progression. We used genome-wide array comparative genomic hybridization to identify distinctive CNAs in breast cancer subtypes from 259 young (diagnosed with breast cancer at 40%) for TN breast tumors at 10q, 11p, 11q, 16q, 20p, and 20q. In addition, we report CNAs that differ in frequency between TN breast tumors of AA and CA women. This is of particular relevance because TN breast cancer is associated with higher mortality and young AA women have higher rates of TN breast tumors compared to CA women. These data support the possibility that higher overall frequency of genomic alteration events as well as specific focal CNAs in TN breast tumors might contribute in part to the poor breast cancer prognosis for young AA women

    Estrogen-related genes and their contribution to racial differences in breast cancer risk.

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    Racial differences in breast cancer risk, including the risks of hormone receptor subtypes of breast cancer, have been previously reported. We evaluated whether variation in genes related to estrogen metabolism (COMT, CYP1A1, CYP1B1, CYP17A1, CYP19A1, ESR1, GSTM1, GSTP1, GSTT1, HSD17B1, SULT1A1, and UGT1A1) contributes to breast cancer risk and/or racial differences in risk within the CARE study, a multi-centered, population-based case–control study of breast cancer. Genetic variation was assessed as single nucleotide polymorphisms (SNPs), haplotypes, and SNP–hormone therapy (HT) interactions within a subset of 1,644 cases and 1,451 controls, including 949 Black women (493 cases and 456 controls), sampled from the CARE study population. No appreciable associations with breast cancer risk were detected for single SNPs or haplotypes in women overall. We detected SNP–HT interactions in women overall within CYP1B1 (rs1800440; p(het) = 0.003) and within CYP17A1 (rs743572; p(het) = 0.009) in which never users of HT were at a decreased risk of breast cancer, while investigated among racial groups, we detected evidence of an SNP–HT interaction with CYP1B1 in White women (p value = 0.02) and with CYP17A1 in Black women (p value = 0.04). This analysis suggests that HT use may modify the effect of variation in estrogen-related genes on breast cancer risk, which may affect Black and White women to a different extent
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