June is Men’s Health Awareness Month. In this blog post, we’ll explore the top three cancer types affecting men of all ages in the United States, as well as some of the important screenings men should be aware of to help stay one step ahead of cancer. 

Screening for Prostate Cancer

Prostate cancer is the most common cancer found in American men, and sits as the second leading cause of cancer-related death in men. The American Cancer Society estimates that one in seven men will get prostate cancer during his lifetime. 

While over 230,000 new cases of prostate cancer are diagnosed each year in the United States, tests like PSA screenings and digital rectal exams can dramatically increase your chance of survival.The prostate gland produces a protein known as prostate-stimulating antigen, or PSA.

As these levels are known to rise before other symptoms of prostate cancer appear, it is important to seek out a regular exam starting in the mid-twenties.

Learn more in our PSA levels and prostate cancer.

Screening and Self-Exams for Testicular Cancer

Testicular cancer is most common in men between 15 and 35 years of age. The American Cancer Society estimates that in 2014  8,820 men will be diagnosed, with only about 380 men dying as a result.

Fortunately, testicular cancer is one of the most curable cancers. Men diagnosed and treated when the disease is in an early stage have a 97 to 100 percent chance of being cured. Therefore, early detection is critical – and relatively easy to do frequently, and at home.

The most common way to check is to perform a monthly testicular self-exam. Unfortunately, after noticing a change in a testicle, many men wait several months before seeking a medical evaluation. The disease is then more advanced upon diagnosis, possibly requiring more intensive treatment and potentially decreasing the chance of a cure.

Learn more about testicular cancer and how to perform a self-exam. 

Checking for Colorectal Cancer

Colorectal cancer is the third most common cancer type found in both men and women (outside of skin cancers) in the United States, but thanks to awareness around colonoscopy screenings, the death rate from this cancer has dropped in recent years. Typically it affects people over 50 years old, as well as those those with a hereditary history of colorectal cancer.

Colorectal cancer is often beatable when detected and treated in its early stages and can even be prevented altogether when polyps are removed before they develop into cancer. It’s important to know that symptoms of colorectal cancer –  can look like symptoms of other conditions.

Roughly 80 percent of colorectal cancer cases can be prevented with adequate colonoscopy screening – often saving lives. We encourage everyone to begin a dialogue about colorectal cancer screening with their physicians. While no screening test is 100 percent perfect, colonoscopy remains the best method of screening for most individuals.

Request a colonoscopy appointment at Penn Medicine today.

A new study suggests what scientists have long suspected about the protective effects of breast milk against one of the leading killers of children.

The anaplastic lymphoma kinase ALK is chromosomally rearranged in a subset of certain cancers, including 2-7% non-small cell lung cancers (NSCLC) and ~70% of anaplastic large cell lymphomas (ALCL). The ALK kinase inhibitors crizotinib and ceritinib are approved for relapsed ALK+ NSCLC, but acquired resistance to these drugs limits median progression-free survival on average to ~10 months. Kinase domain mutations are detectable in 25-37% of resistant NSCLC samples, with activation of bypass signaling pathways detected frequently with or without concurrent ALK mutations. Here we report that, in contrast to NSCLC cells, drug resistant ALCL cells show no evidence of bypassing ALK by activating alternate signaling pathways. Instead, drug resistance selected in this setting reflects upregulation of ALK itself. Notably, in the absence of crizotinib or ceritinib, we found that increased ALK signaling rapidly arrested or killed cells, allowing a prolonged control of drug-resistant tumors in vivo with the administration of discontinuous rather than continuous regimens of drug dosing. Furthermore, even when drug resistance mutations were detected in the kinase domain, overexpression of the mutant ALK was toxic to tumor cells. We confirmed these findings derived from human ALCL cells in murine pro-B cells that were transformed to cytokine independence by ectopic expression of an activated NPM-ALK fusion oncoprotein. In summary, our results show how ALK activation functions as a double-edged sword for tumor cell viability, with potential therapeutic implications.

Glioblastoma (GBM) is often treated with the cytotoxic drug temozolomide, but the disease inevitably recurs in a drug-resistant form after initial treatment. Here, we report that in GBM cells, even a modest decrease in the mismatch repair (MMR) components MSH2 and MSH6 have profound effects on temozolomide sensitivity. RNAi-mediated attenuation of MSH2 and MSH6 showed that such modest decreases provided an unexpectedly strong mechanism of temozolomide resistance. In a mouse xenograft model of human GBM, small changes in MSH2 were sufficient to suppress temozolomide-induced tumor regression. Using The Cancer Genome Atlas to analyze mRNA expression patterns in tumors from temozolomide-treated GBM patients, we found that MSH2 transcripts in primary GBM could predict patient responses to initial temozolomide therapy. In recurrent disease, the absence of microsatellite instability (the standard marker for MMR deficiency) suggests a lack of involvement of MMR in the resistant phenotype of recurrent disease. However, more recent studies reveal that decreased MMR protein levels occur often in recurrent GBM. In accordance with our findings, these reported decreases may constitute a mechanism by which GBM evades temozolomide sensitivity while maintaining microsatellite stability. Overall, our results highlight the powerful effects of MSH2 attenuation as a potent mediator of temozolomide resistance and argue that MMR activity offers a predictive marker for initial therapeutic response to temozolomide treatment. Cancer Res; 75(15); 1–12. ©2015 AACR.

Glioblastoma (GBM) is often treated with the cytotoxic drug temozolomide (TMZ) but the disease inevitably recurs in a drug-resistant form after initial treatment. Here we report that in GBM cells even a modest decrease in the mismatch repair (MMR) components MSH2 and MSH6 have profound effects on TMZ sensitivity. RNAi-mediated attenuation of MSH2 and MSH6 showed that such modest decreases provided an unexpectedly strong mechanism of TMZ resistance. In a mouse xenograft model of human GBM, small changes in MSH2 were sufficient to suppress TMZ-induced tumor regression. Using the Cancer Genome Atlas to analyze mRNA expression patterns in tumors from TMZ-treated GBM patients, we found that MSH2 transcripts in primary GBM could predict patient responses to initial TMZ therapy. In recurrent disease, the absence of microsatellite instability (the standard marker for MMR deficiency) suggests a lack of involvement of MMR in the resistant phenotype of recurrent disease. However, more recent studies reveal that decreased MMR protein levels occur often in recurrent GBM. In accordance with our findings, these reported decreases may constitute a mechanism by which GBM evades TMZ sensitivity while maintaining microsatellite stability. Overall, our results highlight the powerful effects of MSH2 attenuation as a potent mediator of TMZ resistance, and argue that MMR activity offers a predictive marker for initial therapeutic response to TMZ treatment.