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Background: The American Cancer Society, Centers for Disease Control and Prevention, National Cancer Institute, and North American Association of Central Cancer Registries provide annual updates on cancer occurrence and trends by cancer type, sex, race, ethnicity, and age in the United States. This year's report highlights the cancer burden among men and women age 20-49 years.Methods: Incidence data for the years 1999 to 2015 from the Centers for Disease Control and Prevention- and National Cancer Institute-funded population-based cancer registry programs compiled by the North American Association of Central Cancer Registries and death data for the years 1999 to 2016 from the National Vital Statistics System were used. Trends in age-standardized incidence and death rates, estimated by joinpoint, were expressed as average annual percent change.Results: Overall cancer incidence rates (per 100 000) for all ages during 2011-2015 were 494.3 among male patients and 420.5 among female patients; during the same time period, incidence rates decreased 2.1% (95% confidence interval [CI] = -2.6% to -1.6%) per year in men and were stable in females. Overall cancer death rates (per 100 000) for all ages during 2012-2016 were 193.1 among male patients and 137.7 among female patients. During 2012-2016, overall cancer death rates for all ages decreased 1.8% (95% CI = -1.8% to -1.8%) per year in male patients and 1.4% (95% CI = -1.4% to -1.4%) per year in females. Important changes in trends were stabilization of thyroid cancer incidence rates in women and rapid declines in death rates for melanoma of the skin (both sexes). Among adults age 20-49 years, overall cancer incidence rates were substantially lower among men (115.3 per 100 000) than among women (203.3 per 100 000); cancers with the highest incidence rates (per 100 000) among men were colon and rectum (13.1), testis (10.7), and melanoma of the skin (9.8), and among women were breast (73.2), thyroid (28.4), and melanoma of the skin (14.1). During 2011 to 2015, the incidence of all invasive cancers combined among adults age 20-49 years decreased -0.7% (95% CI = -1.0% to -0.4%) among men and increased among women (1.3%, 95% CI = 0.7% to 1.9%). The death rate for (per 100 000) adults age 20-49 years for all cancer sites combined during 2012 to 2016 was 22.8 among men and 27.1 among women; during the same time period, death rates decreased 2.3% (95% CI = -2.4% to -2.2%) per year among men and 1.7% (95% CI = -1.8% to -1.6%) per year among women.Conclusions: Among people of all ages and ages 20-49 years, favorable as well as unfavorable trends in site-specific cancer incidence were observed, whereas trends in death rates were generally favorable. Characterizing the cancer burden may inform research and cancer-control efforts. [ABSTRACT FROM AUTHOR]

Major clinical trials using prostate-specific antigen (PSA) as the screening test to detect localized early-stage prostate cancer and to attempt to change its natural history with early intervention have yielded conflicting interpretations. The US Prostate, Lung, Colorectal, and Ovarian (US PLCO) cancer screening trial concluded that PSA-based screening conferred no meaningful survival benefit, whereas the European Randomized Study of Screening for Prostate Cancer (ERSPC) and the GOTEBORG clinical trial (GOTEBORG) trials claimed statistically significant life-saving benefits. These divergent outcomes have not provided physicians with clarity on the best evidence-based treatment. To determine the extent to which these divergent outcomes are clinically meaningful, we evaluated these data and those of a long-term prospective cohort study in the context of the clinically documented harms of androgen deprivation therapy (ADT). We noted the unheralded fact that in both European trials far more patients received hormonal treatment in the control than the prostatectomy arm, whereas hormonal therapy in the US trial was balanced between arms. We examined this imbalance in ADT treatment and prostate cancer–related deaths in the contexts of contamination, stage migration, and attribution of cause of death, all of which impinge on data interpretation. The ERSPC and GOTEBORG data are compatible with the hypothesis that ADT treatment contributes differentially to an increase in prostate cancer deaths in control patients. If so, the claim of a reduction in prostate cancer deaths in the screened cohort requires reappraisal. The conventional interpretation that PSA screening and radical treatment intervention are the major contributors to the results of these two studies needs more rigorous scientific scrutiny, as does the role of ADT treatment of nonmetastatic disease. [ABSTRACT FROM PUBLISHER]

The article highlights a study on prostate-specific antigen (PSA) velocity, which is the rate of PSA level increases that is being used to determine when to conduct biopsy for prostate cancer. Using data from the Prostate Cancer Prevention Trial (PCPT), it was concluded that using PSA velocity, as the National Comprehensive Cancer Network (NCCN) guidelines suggest, would lead to many unnecessary biopsies. The guidelines require biopsy for men whose PSA is rising more than 0.35 ng/mL per year.

Testicular cancer represents the most curable solid tumor, with a 10-year survival rate of more than 95%. Given the young average age at diagnosis, it is estimated that effective treatment approaches, in particular, platinum-based chemotherapy, have resulted in an average gain of several decades of life. This success, however, is offset by the emergence of considerable long-term morbidity, including second malignant neoplasms, cardiovascular disease, neurotoxicity, nephrotoxicity, pulmonary toxicity, hypogonadism, decreased fertility, and psychosocial problems. Data on underlying genetic or molecular factors that might identify those patients at highest risk for late sequelae are sparse. Genome-wide association studies and other translational molecular approaches now provide opportunities to identify testicular cancer survivors at greatest risk for therapy-related complications to develop evidence-based long-term follow-up guidelines and interventional strategies. We review research priorities identified during an international workshop devoted to testicular cancer survivors. Recommendations include 1) institution of lifelong follow-up of testicular cancer survivors within a large cohort setting to ascertain risks of emerging toxicities and the evolution of known late sequelae, 2) development of comprehensive risk prediction models that include treatment factors and genetic modifiers of late sequelae, 3) elucidation of the effect(s) of decades-long exposure to low serum levels of platinum, 4) assessment of the overall burden of medical and psychosocial morbidity, and 5) the eventual formulation of evidence-based long-term follow-up guidelines and interventions. Just as testicular cancer once served as the paradigm of a curable malignancy, comprehensive follow-up studies of testicular cancer survivors can pioneer new methodologies in survivorship research for all adult-onset cancer. [ABSTRACT FROM PUBLISHER]

Background: Two prostate cancer genome-wide scans in populations of European ancestry identified several genetic variants that are strongly associated with prostate cancer risk. The effect of these risk variants and their cumulative effect in other populations are unknown. [ABSTRACT FROM PUBLISHER]

Background: The mitogenic and growth-stimulatory effects of insulin-like growth factors appear to play a role in prostate carcinogenesis, yet any direct association of circulating insulin levels and risk of prostate cancer remains unclear. [ABSTRACT FROM PUBLISHER]

Background: The frequently indolent nature of early-stage prostate cancer in older men and in men with low- or moderate-grade tumors and the demonstration that the survival benefits of radical prostatectomy are primarily among men younger than 65 years have led to concerns about prostate cancer overtreatment. Methods: Using data from 13 Surveillance, Epidemiology, and End Results registries, we performed a retrospective cohort study of 71 602 men who were diagnosed with localized or regional prostate cancer between 2000 and 2002. We quantified the incidence of initial curative therapy (i.e., surgery or radiation therapy) among men with lower-risk cancers as defined by their limited likelihood of either dying from expectantly managed prostate cancer or achieving a survival benefit from local therapy. Stratified analyses and multinomial logistic regression models were used to quantify the absolute and relative rates of curative therapy among men in various age-grade strata. All statistical tests were two-sided. Results: We identified 24405 men with lower-risk prostate cancers and complete data for the first course of treatment. Initial curative therapy was undertaken in 13 537 of these men (55%); 81% of treated men received radiation therapy. The likelihood of curative therapy, relative to expectant management, varied statistically significantly among lower-risk age-grade strata (all P<.05). Assuming that initial expectant management is appropriate for all lower-risk cancers, 2564 men (10%) in this population-based sample were overtreated with radical prostatectomy and 10973 (45%) with radiation therapy. Conclusions: These data quantify a target population for whom greater use of expectant approaches may reduce overtreatment and improve the quality of localized prostate cancer care. [ABSTRACT FROM AUTHOR]

Background: In the Prostate Cancer Prevention Trial (PCPT), men receiving finasteride had a 24.8% lower risk of prostate cancer than men receiving placebo but a higher risk of high-grade cancer. We examined the impact of finasteride on the sensitivity and area under the receiver operating characteristic curve (AUC) of prostate-specific antigen (PSA) for detecting prostate cancer. Methods: We studied men in the placebo and finasteride groups of the PCPT who had a prostate biopsy and concurrent PSA tests during the 7-year study. We compared the placebo and finasteride groups for sensitivity and AUC of PSA for the detection of all prostate cancer, of Gleason grade 7 or higher prostate cancer, and of Gleason grade 8 or higher prostate cancer. All statistical tests were two-sided. Results: Of 5112 men in the placebo group, prostate cancer was detected in 1111. Gleason tumor grade was available for 1100 men, of whom 240 had grade 7 or higher and 55 had grade 8 or higher. Of 4579 men in the finasteride group, 695 had prostate cancer. Gleason grade was available for 686 men, of whom 264 had grade 7 or higher and 81 had grade 8 or higher. The AUC of PSA for all outcomes was greater for the finasteride group than the placebo group. For detecting prostate cancer versus no cancer, the AUCs were 0.757 and 0.681, respectively (P<.001); for detecting Gleason grade ≥7 versus ≤6 or no cancer, the AUCs were 0.838 and 0.781, respectively (P = .003); and for detecting Gleason grade ≥8 versus ≤7 or no cancer, the AUCs were 0.886 and 0.824, respectively (P = .071). The sensitivity of PSA was higher for men in the finasteride group than in the placebo group at all PSA cutoffs matched by specificity. Conclusions: PSA had statistically significantly better sensitivity and AUC for detecting prostate cancer in the finasteride arm of the PCPT than in the placebo arm. This bias would be expected to contribute to greater detection of all grades of prostate cancer with finasteride. [ABSTRACT FROM AUTHOR]

Background: Vitamin D has potent anticancer properties, especially against digestive-system cancers. Many human studies have used geographic residence as a marker of solar ultraviolet B and hence vitamin D exposure. Here, we considered multiple determinants of vitamin D exposure (dietary and supplementary vitamin D, skin pigmentation, adiposity, geographic residence, and leisure-time physical activity—to estimate sunlight exposure) in relation to cancer risk in the Health Professionals Follow-Up Study. Methods: Among 1095 men of this cohort, we quantified the relation of these six determinants to plasma 25-hydroxy-vitamin D [25(OH)D] level by use of a multiple linear regression model. We used results from the model to compute a predicted 25(OH)D level for each of 47800 men in the cohort based on these characteristics. We then prospectively examined this variable in relation to cancer risk with multivariable Cox proportional hazards models. Results: From 1986 through January 31, 2000, we documented 4286 incident cancers (excluding organ-confined prostate cancer and nonmelanoma skin cancer) and 2025 deaths from cancer. From multivariable models, an increment of 25 nmol/L in predicted 25(OH)D level was associated with a 17% reduction in total cancer incidence (multivariable relative risk [RR] = 0.83, 95% confidence interval [CI] = 0.74 to 0.92), a 29% reduction in total cancer mortality (RR = 0.71, 95% CI = 0.60 to 0.83), and a 45% reduction in digestive-system cancer mortality (RR = 0.55, 95% CI = 0.41 to 0.74). The absolute annual rate of total cancer was 758 per 100000 men in the bottom decile of predicted 25(OH)D and 674 per 100000 men for the top decile; these respective rates were 326 per 100000 and 277 per 100000 for total cancer mortality and 128 per 100000 and 78 per 100000 for digestive-system cancer mortality. Results were similar when we controlled further for body mass index or physical activity level. Conclusions: Low levels of vitamin D may be associated with increased cancer incidence and mortality in men, particularly for digestive-system cancers. The vitamin D supplementation necessary to achieve a 25(OH)D increment of 25 nmol/L may be at least 1500 IU/day. [ABSTRACT FROM AUTHOR]

Background: Adiponectin is an insulin-sensitizing hormone secreted by adipocytes. Levels of adiponectin are inversely associated with adiposity and insulin resistance. Because both adiposity and insulin resistance have been associated with risk of colorectal cancer, we hypothesized that adiponectin is associated with colorectal carcinogenesis. Methods: We evaluated the association between adiponectin and colorectal cancer among 18 225 men in the Health Professionals Follow-up Study who provided blood samples in 1994. Between blood collection and January 31, 2002, 179 incident colorectal cancer cases occurred. Each case patient was matched to two control subjects on year of birth and date of blood draw. Information on lifestyle factors and diet was collected using biennial questionnaires and food frequency questionnaires. Logistic regression models were used to estimate relative risks (RRs) and confidence intervals (CIs). All statistical tests were two-sided. Results: We observed a statistically significant inverse association between plasma adiponectin levels and risk of colorectal cancer (for the highest quintile [Q5] versus the lowest quintile [QI], RR = 0.42, 95% CI = 0.23 to 0.78; Ptrend = .01). The association was only slightly attenuated after adjustment for body mass index (Q5 versus Q1, RR = 0.48, 95% CI = 0.25 to 0.90; Ptrend = .04) or for body mass index and other major risk factors for colorectal cancer (family history, physical activity, multivitamin use, smoking, alcohol, aspirin use, history of endoscopy, dietary calcium, folate, vitamin E, and vitamin D; Q5 versus Q1, multivariable RR = 0.50, 95% CI = 0.26 to 0.97; Ptrend = .08). Relative risks were not linear in any of the analyses; the second quintile had a lower relative risk than the lowest quintile, but further decreases in risk were not evident with increasing levels of adiponectin. Conclusions: In this prospective nested case-control study, men with low plasma adiponectin levels had a higher risk of colorectal cancer than men with higher levels. More prospective observational studies, particularly in women, and mechanistic studies are required to fully understand the relationship between adiponectin and carcinogenesis. [ABSTRACT FROM AUTHOR]

Background: Although risk estimates for synchronous and metachronous contralateral testicular cancers vary widely, many clinicians recommend routine biopsy of the contralateral testis for patients diagnosed with unilateral testicular cancer. We evaluated the risk of contralateral testicular cancer and survival in a large population-based cohort of men diagnosed with testicular cancer before age 55 years. Methods: For 29515 testicular cancer cases reported to the National Cancer Institute's Surveillance, Epidemiology and End Results Program from 1973 through 2001, we estimated the prevalence of synchronous contralateral testicular cancer, the observed-to-expected ratio (O/E) and 15-year cumulative risk of metachronous contralateral testicular cancer, and the 10-year overall survival rate of both synchronous and metachronous contralateral testicular cancer, using the Kaplan- Meier method for the two latter assessments. Age-adjusted multivariable analyses were used to examine risk according to histologic type of the original cancer. Results: A total of 175 men presented with synchronous contralateral testicular cancer; 287 men developed metachronous contralateral testicular cancer (O/E = 12.4 195% confidence interval {CI} = 11.0 to 13.91; 15-year cumulative risk = 1.9% [95% CI = 1.7% to 2.1%]). In the multivariable analysis, only nonseminomatous histology of the first testicular cancer was associated with a statistically significantly decreased risk of metachronous contralateral testicular cancer (hazard ratio [HR] =0.60,95% confidence interval [CI] = 0.46 to 0.79; P < .001). Increasing age at first testicular cancer diagnosis was associated with decreasing risk of nonseminomatous metachronous contralateral testicular cancer (odds ratio = 0.90, 95% CI = 0.86 to 0.94). The 10-year overall survival rate after metachronous contralateral testicular cancer diagnosis was 93% (95% CI = 88% to 96%), and that after synchronous contralateral testicular cancer was 85% (95% CI = 78% to 90%). Conclusions: The low cumulative risk of metachronous contralateral testicular cancer and favorable overall survival of patients diagnosed with metachronous contralateral testicular cancer is in accordance with the current U.S. approach of not performing a biopsy on the contralateral testis. [ABSTRACT FROM AUTHOR]

Background: Men treated for clinically localized prostate cancer with either radical prostatectomy or external beam radiotherapy usually survive many years with the side effects of these treatments. We present treatment-specific quality-of-life outcomes for prostate cancer patients 5 years after initial diagnosis. Methods: The cohort consisted of men aged 55-74 years who were newly diagnosed with clinically localized prostate cancer in 1994-1995 and were treated with radical prostatectomy (n = 901) or external beam radiotherapy (n = 286). We used clinical and quality-of-life data previously collected at the time of diagnosis (i.e., baseline) and at the 2-year follow-up and data newly collected at 5 years after diagnosis to compare urinary, bowel, and sexual function and to examine temporal changes in those functions. Odds ratios (ORs) and adjusted percentages were calculated by logistic regression. All statistical tests were two-sided. Results: At 5 years after diagnosis, overall sexual function declined in both groups to approximately the same level. However, at 5 years after diagnosis, erectile dysfunction was more prevalent in the radical prostatectomy group than in the external beam radiotherapy group (79.3% versus 63.5%; OR = 2.5, 95% confidence interval [CI] = 1.6 to 3.8). Approximately 14%-16% of radical prostatectomy and 4% of external beam radiotherapy patients were incontinent at 5 years (OR = 4.4, 95% CI = 2.2 to 8.6). Bowel urgency and painful hemorrhoids were more common in the external beam radiotherapy group than in the radical prostatectomy group. All of these differences remained statistically significant after adjustment for confounders and for differences between treatment groups in some baseline characteristics. Conclusions: At 5 years after diagnosis, men treated with radical prostatectomy for localized prostate cancer continue to experience worse urinary incontinence than men treated with external beam radiotherapy. However, the two treatment groups were more similar to each other with respect to overall sexual function, mostly because of a continuing decline in erectile function among the external beam radiotherapy patients between years 2 and 5. [ABSTRACT FROM AUTHOR]

Background: Accumulating epidemiologic and molecular evidence suggest that inflammation is an important component in the etiology of prostate cancer. Macrophage-inhibitory cytokine-1 (MIC-1), a member of the transforming growth factor β superfamily, is thought to play an important role in inflammation by regulating macrophage activity. We examined whether sequence variants in the MIC-1 gene are associated with the risk of prostate cancer. Methods: The study population, a population-based case-control study in Sweden, consisted of 1383 prostate cancer case patients and 780 control subjects. From 94 of the control subjects, we constructed gene-specific haplotypes of MIC-1 and identified four haplotype-tagging single-nucleotide polymorphisms (SNPs): Exon1+25 (V9L), Exon1+142 (S48T), IVS1+1809, and Exon2+2423 (H6D). All study subjects were genotyped for the four SNPs, and conditional logistic regression analysis was used to estimate odds ratios (ORs) with 95% confidence intervals (CIs). Results: A statistically significant difference (P = .006) in genotype frequency was observed for the nonsynonymous change H6D (histidine to aspartic acid at position 6) between prostate cancer patients and control subjects. Carriers of the GC genotype, which results in the H6D change, experienced a lower risk of sporadic prostate cancer (OR = 0.80, 95% CI = 0.66 to 0.97) and of familial prostate cancer (OR = 0.61, 95% CI = 0.42 to 0.89) than the CC genotype carriers. In the study population, the proportion of prostate cancer cases attributable to the CC genotype was 7.2% for sporadic cancer and 19.2% for familial cancer. None of the other SNPs or haplotypes was associated with prostate cancer. Conclusion: This study shows an association between a nonsynonymous change (H6D) in the MIC-1 gene and prostate cancer. This finding supports the hypothesis that genetic variation in the inflammatory process contributes to prostate cancer susceptibility. [ABSTRACT FROM AUTHOR]

Background: Prostate cancer represents a substantial public health burden worldwide. It is the second leading cause of cancer death among men in the United States. A family history of the disease is among the most well-established risk factors for prostate cancer. Efforts to localize prostate cancer susceptibility alleles by using genetic linkage analysis methods have been hindered by genetic heterogeneity, incomplete penetrance, disease phenocopies, and the lack of DNA samples from parents of individuals with late-onset prostate cancer. Methods: We performed a combined genome-wide linkage analysis among 426 families from four existing hereditary prostate cancer (HPC) study populations to systematically search for prostate cancer susceptibility genes. To decrease the degree of locus heterogeneity, we analyzed subsets of families with similar clinical and demographic characteristics. Nonparametric multipoint linkage was the primary method of analysis. Results are presented as allele-sharing logarithm of the odds (LOD) scores, and all reported P values are two-sided. Results: The strongest evidence for prostate cancer linkage was found at chromosome region 17q22 (nonparametric multipoint Kong and Cox allele-sharing LOD score = 3.16 at marker D17S787; P = .00007). Stratified analyses revealed several additional chromosomal regions that are likely to segregate prostate cancer susceptibility genes among specific subsets of HPC families, including 15q11 among families with late-onset disease (allele-sharing LOD = 5.57 at marker D15S128; P < .00001) and 4q35 among families with four or more affected family members (allele-sharing LOD = 3.10 at marker D4S1615; P = .00008). Conclusion: Fine mapping studies to facilitate identification of prostate cancer susceptibility genes in these linked regions are warranted. [ABSTRACT FROM AUTHOR]

Background: Colorectal cancer and type 2 diabetes share many risk factors, and hyperinsulinemia appears to be associated with an increased risk of colorectal cancer. We used the concentration of plasma C-peptide (an indicator of insulin production) to determine whether insulin and insulin resistance are associated with the risk of developing colorectal cancer. Methods: We conducted a nested case-control study in the Physicians' Health Study. Plasma samples were collected from 14 916 cancer-free men from August 1982 through December 1984. Plasma C-peptide concentration, measured with an enzyme-linked immunosorbent assay, was available for 176 case patients who developed incident colorectal cancer through December 31, 1995, and 294 age- and smoking status-matched control subjects. Information on four other insulin resistance-related factors at baseline was obtained. We used conditional logistic regression models to investigate associations. All statistical tests were two-sided. Results: Plasma C-peptide concentration was positively associated with age, body mass index (BMI), and number of insulin resistance-related factors, and it was inversely associated with fasting time before the blood draw, alcohol consumption, and vigorous exercise. An increased concentration of plasma C-peptide was statistically significantly associated with an increased risk of colorectal cancer (relative risk [RR] for the highest versus lowest quintile of plasma C-peptide = 2.7, 95% confidence interval [CI] = 1.2 to 6.2; Ptrend = .047), after adjusting for age, smoking status, fasting, BMI, alcohol consumption, vigorous exercise, and aspirin assignment in the Physicians' Health Study. The association became even stronger when the analysis was further adjusted for factors related to insulin resistance other than insulin levels (RR for the highest versus lowest quintile = 3.4, 95% CI = 1.4 to 8.3; Ptrend = .02) or when data from case patients who were diagnosed during the first 5 years of follow-up were excluded (RR for the highest versus the lowest quintile = 3.4, 95% CI = 1.3 to 8.8; Ptrend = .03). Adjusting for plasma levels of insulin-like growth factor I (IGF-I) and its binding protein 3 (IGFBP-3) did not materially change the results. There was no apparent modification of risk by BMI, insulin resistancerelated factors, or vigorous exercise. Conclusion: Elevated insulin production, as reflected by elevated concentrations of plasma C-peptide, may predict the risk of developing colorectal cancer, independently of BMI, factors related to insulin resistance, or levels of IGF-I and IGFBP-3. [ABSTRACT FROM AUTHOR]

The article reports on the association between estrogen level and the outcomes in lung cancer patients. It is mentioned that lung cancer has been known to manifest differently in men and women and studies point out that estrogen is the key factor in such difference. Results of studies made on the issue are also presented in the article along with information on the influence of estrogen as a possible initiator of cancer in both sexes.

Discusses various aspects related to testicular cancer. Occurrence of testicular cancer before or during the peak reproductive period of life in men; Effect of testicular cancer and its associated therapy on fertility; Application of aggressive therapy on testicular cancer.

Reports on the controversy on the research about gender risk in lung cancer in the U.S. Comparison of the incidence of lung cancer in women and men; Susceptibility of women to the carcinogenic effects of cigarette smoke; Debate on the research.

The article offers information regarding the application of active surveillance as a standard management practice for some men with prostate cancer. It discusses several studies examining active surveillance' safety as well as determining cancer-specific survival rates of patients. Information about prostate-specific antigen and positive biopsy is presented.

This article focuses on a debate on whether testicular cancer patients should be monitored with active surveillance or adjuvant treatments to minimize likelihood of recurrence, referencing two studies published in the October 1, 2013 issue of the "Journal of Clinical Oncology." One study argued that guidelines should recommend active surveillance after architect or surgery. The other study concluded that active surveillance does not fully consider the treatment consequences of relapse.

The authors looks at congenital abnormalities as long-term health effects of cancer treatment. They note the emergence of major congenital abnormalities as a potential outcome linked with a paternal cancer diagnosis, based on a study using Danish and Swedish national registries by O. Stahl et al published within the issue. Inherent flaws to the use of these registries to address the study hypotheses are cited. Also mentioned are possible explanations behind the increased prevalence of these abnormalities among the children of male cancer survivors.

In this article, the author comments on a study published within the issue which analyzed data on long-term outcomes for patients diagnosed with localized prostate cancer and possible implications for health care providers. The incorporation of prostate-specific antigen (PSA) and Gleason score data into the statistical models utilized by the researchers is noted. The author references a similar study conducted in the U.S. On final note, the author contends that the research study highlighted several health interventions that are often neglected.

A graph is presented depicting percentage of new prostate cancer case by age group in the U.S. from 2008-2012.

The article discusses the causes in the development of prostate cancer among men. Trichomonas vaginalis infection is inferred to be as a possible environmental factor in the said disease. It also mentions that one of the most dynamic factors in the development of prostate cancer is the testing for prostate-specific antigen (PSA). The study of Stark et al evaluates potential effect of a specific variable T. vaginalis infection on prostate cancer with the help of "Physician's Health Study."

A correction to the article "Anthropometric and Hormonal Risk Factors for Male Breast Cancer: Male Breast Cancer Pooling Project Results" that was first published online in the April 10, 2014 issue is presented.

The article discusses a study on the effectiveness of flexible sigmoidoscopy (FSG) in detecting of colorectal cancer or advanced adenoma. Conducted by Joel L. Weissfeld et al., the study analyzed data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) cancer screening trial. It found that repeated screening by FSG increased the diagnosis of the disorders in both women and men.

A correction to the article "Risk of Colorectal Cancer in Men on Long-term Androgen Deprivation Therapy for Prostate Cancer" in an issue is presented.

The article states that the incidence of major congenital birth abnormalities was slightly higher in the children of male cancer survivors than the offspring of fathers with no history of this disease, based on a study by O. Stahl et al published online in the "JNCI: Journal of the National Cancer Institute" on February 8, 2011. It notes that the study was aimed at determining the effects of paternal cancer and assisted reproductive technologies (ARTs) on pregnancy outcomes. Also mentioned are the inherent shortcomings of this study.

The article focuses on the estimated total cost of cancer care in the U.S., based on a study by Angela Maritto and colleagues from the National Cancer Institute published in the January 12, 2011 issue of the "Journal of the National Cancer Institute." The researchers examined the national medical cost of cancer care in men and women through the year 2020. They considered future incidence and survival, as well as projected costs by phase of care.

The article presents statistics on the incidence of lung cancer among men and women from the year 1975 to 2003.

Reports on the estimated number of mortality among men diagnosed with cancer worldwide in 2002. Commonality of prostate cancer in men; Risks of cancer.

Presents statistics from the American Cancer Society showing annual cancer deaths by site among men aged 35 or older attributable to smoking.

Reports that men with low-grade prostate cancer have a low risk of dying from the disease, according to results from a long-term study. Retrospective, population-based cohort study of men diagnosed with clinically localized prostate cancer between 1971 and 1984; Observation that the data do not support aggressive treatment.

Reports on the findings of a study about the association of rapid increased in prostate-specific antigen levels with risk of death from prostate cancer. Spread of tumor; Increased risk of dying even after prostatectomy; Relative risk of death.