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Which are the Wellness Consequences associated with Up Freedom?
Androgen receptor signaling is crucial to prostate cancer aggressiveness. check details Members of the solute carrier family of the organic anion transporting peptides (SLCO) are potential regulators of androgen availability in prostate tissue. It remains unknown whether genetic variations in SLCOs contribute to the differences in prostate cancer aggressiveness in African Americans (AA) and European Americans (EA).

SNPs in 11 SLCO members were selected, with addition of 139 potentially functional SNPs and 128 ancestry informative markers. A total of 1,045 SNPs were genotyped and analyzed in 993 AAs and 1,057 EAs from the North Carolina-Louisiana Prostate Cancer Project. Expression and cellular localization of SLCOs were examined using qRT-PCR, IHC, and
RNA hybridization in independent sets of prostate cancer cases.

Significant associations with prostate cancer characteristics were found for SNPs in
and
. The associations differed by race (

< 0.05). SNPs in
were associated with reduced tumor aggressiveness and low Gleason score in AAs; whereas, SNPs in
were associated with high clinical stage in EAs. In prostate tissue, SLCO2A1 and SLCO5A1 were the most expressed SLCOs at the mRNA level and were expressed predominantly in prostate endothelial and epithelial cells at the protein level, respectively.

SLCO2A1 and SLCO5A1 play important but different roles in prostate cancer aggressiveness in AAs versus EAs.

The finding calls for consideration of racial differences in biomarker studies of prostate cancer and for investigations on functions of SLCO2A1 and SLCO5A1 in prostate cancer.
The finding calls for consideration of racial differences in biomarker studies of prostate cancer and for investigations on functions of SLCO2A1 and SLCO5A1 in prostate cancer.
A growing body of evidence suggests that alterations of dietary fatty acid (FA) profiles are associated with colorectal cancer risk. However, data from large-scale epidemiologic studies using circulating FA measurements to objectively assess individual FA and FA categories are scarce.

We investigate the association between red blood cell (RBC) membrane FAs and risk of colorectal cancer in a case-control study nested within a large prospective cohort. After a median follow-up of 6.4 years, 1,069 incident colorectal cancer cases were identified and matched to 1,069 controls among participants of the European Prospective Investigation into Cancer and Nutrition (EPIC). The FA composition of RBC phospholipids (in mol%) was analyzed by gas chromatography, and their association with risk of colorectal cancer was estimated by multivariable adjusted conditional logistic regression models.

After correction for multiple testing, subjects with higher concentrations of RBC stearic acid were at higher risk for colorectal cancer (OR = 1.23; 95% CI = 1.07-1.42, per 1 mol%). Conversely, colorectal cancer incidence decreased with increasing proportions of RBC n-3 PUFA, particularly eicosapentaenoic acid (0.75; 0.62-0.92, per 1 mol%). The findings for the n-6 PUFA arachidonic acid were inconsistent.

The positive association between prediagnostic RBC stearic acid and colorectal cancer reflects putative differences in FA intake and metabolism between cancer cases and matched controls, which deserve further investigation. The inverse relationship between EPA and colorectal cancer is in line with the repeatedly reported protective effect of fish consumption on colorectal cancer risk.

These findings add to the evidence on colorectal cancer prevention.
These findings add to the evidence on colorectal cancer prevention.
The cancer registry of Bulawayo (Zimbabwe) operated for 15 years in the preindependence period (1963-77), and was restarted in 2011. This allows comparison of incidence of cancers over a period of almost 50 years.

Age-standardized rates, with SEs, were calculated for 1963-1972 and 2011-2015. Detailed results are presented for those cancers for which there was a significant (
< 0.05) change in the rates between the two periods.

There were declines in the rates of those cancers previously known to be common in East and Southern Africa (esophagus, liver, bladder), and the emergence of cancers associated with "westernization" of lifestyles (breast, prostate, large bowel). Cancers related to infection with HIV-AIDS (Kaposi sarcoma, non-Hodgkin lymphoma, eye cancers) have come to comprise a much larger proportion of the total burden, and cancer of the cervix (also AIDS-related) has shown a large increase in incidence-as elsewhere in sub-Saharan Africa (SSA). More surprising is the decline in cancer of the lung-formerly very high, but by 2011-2015, despite little change in the prevalence of smoking, rates were low-close to the average for SSA. This may relate, in part, to a decline in the numbers of miners, and ex-miners, residing in the city.

The changes in incidence are largely explained by differences in past exposure to environmental risk factors.

Few datasets from SSA can document temporal changes in the cancer epidemic on the continent. There are some anticipated observations, as well as unexpected findings meriting further investigation.
Few datasets from SSA can document temporal changes in the cancer epidemic on the continent. There are some anticipated observations, as well as unexpected findings meriting further investigation.
The risk of breast cancer among hypertensive patients who use beta-blockers has attracted attention. However, the evidence is inconsistent and investigation of the dose-specific associations for subtypes of beta-blockers is limited.

By incorporating Swedish national registers, breast cancer risk was estimated in women with hypertension who used nonselective beta-blockers and beta-1 selective blockers compared with propensity score-matched nonusers. The cumulative defined daily dose was used to study the dose-response association. Test of interaction between beta-blocker use and other antihypertensive medications was performed.

Hypertensive patients taking beta-1 selective blockers (metoprolol, atenolol, bisoprolol) had an increased risk of breast cancer with a HR and 95% confidence interval (CI) of 2.39 (1.95-2.94), 2.31 (1.46-3.64), and 3.02 (2.09-4.36), respectively. All of the observed associations were dose-dependent (

< 0.0001). No significant association was found for the nonselective beta-blocker (propranolol) except that among users of agents acting on the renin-angiotensin system, those who used propranolol had increased breast cancer risk.
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