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A study to examine the degree of breast cancer risk among individuals who were carriers of the BRC1 and BRC 2 mutated genes is conducted. Results show that definite variations existed in the incidence of carriers developing unilateral or contralateral breast cancer when carrying the mentioned genes.

Studies were conducted to examine the impact of screening for lung cancer by computed tomography (CT) on lung cancer outcomes. Results revealed that screening for lung cancer with low-dose CT might increase the rate of lung cancer diagnosis and treatment by lung cancer resection, but might not significantly reduce the risk of advanced lung cancer or death from lung cancer.

The study aims to address whether studies of care rendered to patients prior to their death produce an accurate portrait of care provided to patients who are dying. It concluded that studying care received prior to death could lead to invalid conclusions about the quality or type of care provided to dying patients.

Blood levels of prostate-specific antigen (PSA) may change from month to month and year to year, according to a study of 972 men. Men who had an abnormal PSA test result during one visit had a normal one during a follow-up visit. This is especially likely to happen in men with only a moderate elevation, between 4 and 10 nanograms per mililiter. PSA is a test for prostate cancer.

Black cancer patients have the same outcome as white cancer patients provided they receive the same treatments, according to researchers who analyzed 54 studies covering 189,877 white patients and 32,004 black patients with 14 different cancers. This supports the idea that black cancer patients have higher mortality rates because they do not receive adequate treatment, not because there is some biological difference between the races., Context in recent years a theory that cancer biology is different in blacks and whites has gained prominence in reaction to epidemiologic observations that blacks have poorer survival than whites, even when diagnosed with cancer of similar severity. Yet, few studies have evaluated whether lower-quality treatment and shorter overall life expectancy due to a greater burden of other illnesses may explain the survival discrepancy. Objective To estimate the magnitude of overall and cancer-specific survival differences between blacks and whites who receive comparable treatment for similar-stage cancer. Data Sources We searched MEDLINE for English-language articles published from 1966 to January 2002 that reported on overall survival for black and white patients treated similarly for cancer. Study Selection The abstracts or titles for 891 citations were independently examined by 2 authors. The full text was retrieved if the abstract mentioned both black and white patients, made some comment regarding either similarity of treatment received or presented an analysis based on the treatment received, and commented on survival. Studies were included if they included data for at least 10 black and 10 white patients; specified the cohort ascertainment method and what measures were undertaken to minimize loss to follow-up; summarized survival of both blacks and whites using actuarial measures; presented outcomes within stage, adjusted for stage, or based on cohorts with balanced stage distributions; and specified that blacks and whites in the study received similar treatment. We identified 89 unique cohorts in 54 articles that met our inclusion criteria. Data Extraction Overall survival rates and hazard ratios (HRs) for death for blacks relative to whites were calculated. These were subsequently adjusted for rates of death due to causes other than the cancer under study to determine cancer-specific survival and cancer-specific HRs. Data Synthesis Results represent 189877 white and 32004 black patients with 14 different cancers. Compared with whites, blacks had an overall excess risk of death (HR, 1.16; 95% confidence interval [Cl], 1.12-1.20). After correction for deaths due to other causes, the cancer-specific HR was 1.07 (95% Cl, 1.02-1.13). Of the 14 cancers, blacks were at a significantly higher risk of cancer-specific death only for cancer of the breast, uterus, or bladder. Conclusions Only modest cancer-specific survival differences are evident for blacks and whites treated comparably for similar-stage cancer. Therefore, differences in cancer biology between racial groups are unlikely to be responsible for a substantial portion of the survival discrepancy. Differences in treatment, stage at presentation, and mortality from other diseases should represent the primary targets of research and interventions designed to reduce disparities in cancer outcomes.

Men with prostate cancer can lower their risk of a surgical complication if they have the operation at a hospital where this type of operation is done frequently and the surgeons have a lot of experience doing the operation. Urinary incontinence and other damage to the urinary tract are frequent complications of prostate surgery.

Patients with lung cancer may survive longer if they have surgery at a hospital whose surgeons have experience doing these types of procedures. This was the conclusion of a study of 2,118 lung cancer patients who had surgery at 76 different hospitals.

The lower survival rates among black patients with non-small-cell lung cancer can be explained by the fact that they are less likely to have surgery. Surgery can cure non-small-cell lung cancer if it is diagnosed in its early stages. In a study of 10,984 patients with non-small-cell lung cancer, 64% of the black patients had surgery compared with 77% of the white patients. Only 26% of blacks were alive five years later compared to 34% of the whites. However, survival rates were similar when black and white patients who had surgery were compared, as well as those who didn't have surgery.

It is increasingly common clinically for cancer specimens to be examined using techniques that identify somatic mutations. In principle, these mutational profiles can be used to diagnose the tissue of origin, a critical task for the 3% to 5% of tumors that have an unknown primary site. Diagnosis of primary site is also critical for screening tests that employ circulating DNA. However, most mutations observed in any new tumor are very rarely occurring mutations, and indeed the preponderance of these may never have been observed in any previous recorded tumor. To create a viable diagnostic tool we need to harness the information content in this "hidden genome" of variants for which no direct information is available. To accomplish this we propose a multilevel meta‐feature regression to extract the critical information from rare variants in the training data in a way that permits us to also extract diagnostic information from any previously unobserved variants in the new tumor sample. A scalable implementation of the model is obtained by combining a high‐dimensional feature screening approach with a group‐lasso penalized maximum likelihood approach based on an equivalent mixed‐effect representation of the multilevel model. We apply the method to the Cancer Genome Atlas whole‐exome sequencing data set including 3702 tumor samples across seven common cancer sites. Results show that our multilevel approach can harness substantial diagnostic information from the hidden genome. [ABSTRACT FROM AUTHOR]

Genome-wide association studies (GWAS) and candidate pathway studies have identified low-penetrant genetic variants associated with cutaneous melanoma. We investigated the association of melanoma-risk variants with primary melanoma tumor prognostic characteristics and melanoma-specific survival. The Genes, Environment, and Melanoma Study enrolled 3285 European origin participants with incident invasive primary melanoma. For each of 47 melanoma-risk single nucleotide polymorphisms (SNPs), we used linear and logistic regression modeling to estimate, respectively, the per allele mean changes in log of Breslow thickness and odds ratios for presence of ulceration, mitoses, and tumor-infiltrating lymphocytes (TILs). We also used Cox proportional hazards regression modeling to estimate the per allele hazard ratios for melanoma-specific survival. Passing the false discovery threshold (p = 0.0026) were associations of IRF4 rs12203592 and CCND1 rs1485993 with log of Breslow thickness, and association of TERT rs2242652 with presence of mitoses. IRF4 rs12203592 also had nominal associations (p < 0.05) with presence of mitoses and melanomaspecific survival, as well as a borderline association (p = 0.07) with ulceration. CCND1 rs1485993 also had a borderline association with presence of mitoses (p = 0.06). MX2 rs45430 had nominal associations with log of Breslow thickness, presence of mitoses, and melanoma-specific survival. Our study indicates that further research investigating the associations of these genetic variants with underlying biologic pathways related to tumor progression is warranted. [ABSTRACT FROM AUTHOR]