June is Men’s Health Awareness Month. Learn about testicular cancer, who’s at risk and how to perform a self exam! 

June is Men’s Health Awareness Month. Learn about testicular cancer, who’s at risk and how to perform a self exam!

June is Men’s Health Awareness Month. In this blog, Barbara Zoltick, RN, discusses testicular cancer, who is at risk and how to perform a self-exam to check for the most common cancer for men between the ages of 15 and 35.

Though it can occur in older men, testicular cancer generally occurs in young men, at the time of life when they are completing their education, finding new jobs, and creating families.

Who is at Risk for Testicular Cancer?

The incidence of testicular cancer has been increasing over the past 40 years for reasons which remain unclear. Testicular cancer is more prevalent in white men than in black, Asian, or other nonwhite ethnic groups. Historically, the incidence has been found to be greater in men of any ethnicity with higher socio-economic status and more education, though more recent studies have found this difference has diminished.

The risk factors associated with the development of testicular cancer are not well established. However, cryptorchidism, or an undescended testicle, is currently the most recognized risk factor. Cryptorchidism increases the risk of developing testicular cancer by ten-fold, though only about 5% of testicular cancers can be attributed to this condition. Additional risk factors include prenatal exposure to estrogen; other testicular abnormalities, such as underdeveloped testicles; and genetic disorders that affect sexual development, such as Kleinfelter’s Syndrome.

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

What Testicular Cancer Looks Like

The most common sign of testicular cancer is a lump, swelling or enlargement of a testicle. This may be accompanied by tenderness, pain or a feeling of heaviness. Unfortunately, after noticing a change in a testicle, some 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. Monthly testicular self-examinations can help, by making a mental note of and becoming more familiar with how testicles normally feel.

It is also important to note that not every change or discomfort indicates cancer — seeking medical evaluation can provide reassurance that cancer is not the cause.

How to Perform a Testicular Self-Exam

• Check for any swelling on the scrotum. You may need to do this in front of a mirror.
• Examine one testicle at a time, using both hands. Put your index and middle fingers under the testicle with thumbs on top. Roll the testicle gently between your fingers. It can be normal for one testicle to be slightly larger than the other.
• You will notice a soft, tube-like area behind the testicles. This is the epididymis, where sperm is stored.
• Any testicular changes, pain, swelling, lump or tender area should be evaluated by a health care professional, preferably a urologist as soon as possible. It may not be cancer, but needs to be evaluated to be sure.

Neuroblastoma is the most common extracranial solid tumor of childhood, and survival remains poor for patients with advanced disease. Novel immune therapies are currently in development, but clinical outcomes have not matched preclinical results. Here, we describe key mechanisms in which neuroblastoma inhibits the immune response. We show that murine and human neuroblastoma tumor cells suppress T-cell proliferation through increased arginase activity. Arginase II is the predominant isoform expressed and creates an arginine-deplete local and systemic microenvironment. Neuroblastoma arginase activity results in inhibition of myeloid cell activation and suppression of bone marrow CD34+ progenitor proliferation. Finally, we demonstrate that the arginase activity of neuroblastoma impairs NY-ESO-1–specific T-cell receptor and GD2-specific chimeric antigen receptor–engineered T-cell proliferation and cytotoxicity. High arginase II expression correlates with poor survival for patients with neuroblastoma. The results support the hypothesis that neuroblastoma creates an arginase-dependent immunosuppressive microenvironment in both the tumor and blood that leads to impaired immunosurveillance and suboptimal efficacy of immunotherapeutic approaches. Cancer Res; 75(15); 1–11. ©2015 AACR.

Neuroblastoma is the most common extra cranial solid tumour of childhood, and survival remains poor for patients with advanced disease. Novel immune therapies are currently in development, but clinical outcomes have not matched preclinical results. Here, we describe key mechanisms in which neuroblastoma inhibits the immune response. We show that murine and human neuroblastoma tumour cells suppress T cell proliferation, through increased arginase activity. Arginase II is the predominant isoform expressed and creates an arginine deplete local and systemic microenvironment. Neuroblastoma arginase activity results in inhibition of myeloid cell activation and suppression of bone marrow CD34+ progenitor proliferation. Finally we demonstrate that the arginase activity of neuroblastoma impairs NY-ESO-1 specific TCR and GD2-specific CAR engineered T cell proliferation and cytotoxicity. High arginase II expression correlates with poor survival for neuroblastoma patients. The results support the hypothesis that neuroblastoma creates an arginase-dependent immunosuppressive microenvironment in both the tumour and blood that leads to impaired immune surveillance and sub-optimal efficacy of immunotherapeutic approaches.