MedicalResearch.com Interview with:
A low magnification image of a germ cell tumor, called a teratocarcinoma, from a new mouse model developed to study testicular cancer. A cluster of cancer stem cells, termed embryonal carcinoma, is shown at higher magnification at the bottom.
Amy M. Lyndaker, Ph.D.
Assistant Professor of Biology
Division of Mathematics and Natural Sciences
This work was completed when I was a Research Associate in the laboratory of
Dr. Robert S. Weiss at:
Department of Biomedical Sciences College of Veterinary Medicine
Cornell University Ithaca, NY
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: There has been this puzzle in the field of cancer biology that testicular cancers, even after they have spread to the brain or the lungs, are often able to be cured with radiation and chemotherapy (think of Lance Armstrong, for instance), whereas the majority of cancers are not curable with similar treatments. We thought that this could be due to the unique properties of the cells from which the cancers are derived; testicular cancers arise from germ cells (which later go on to make sperm), whereas most cancers arise from somatic cells (body cells). We proposed that maybe the germ cells and somatic cells were hard-wired to respond differently to DNA damage, and that because of this, cancers derived from these two distinct types of cells might then respond differently to chemotherapies (which typically kill cancer cells by creating DNA damage).
To test this, we generated a novel genetic mouse model that develops cancers similar to the malignant testicular cancers seen in young men. We then used standard chemotherapies (cisplatin alone, or combined bleomycin/etoposide/cisplatin), and found that treatment with DNA-damaging chemotherapies specifically killed the cancer stem cells within the tumors. Thus, we were able to show that testicular cancers are curable with standard DNA-damaging chemotherapies because their stem cells are highly sensitive to DNA damage. This is in contrast to most cancers, where the cancer stem cells are refractory to treatment and are responsible for tumor recurrence and metastasis.
MedicalResearch.com Interview with:
M. Minhaj Siddiqui, MD
Director of Urologic Robotic Surgery
Assistant Professor of Surgery – Urology
University of Maryland School of Medicine
Baltimore MD 21201
Medical Research: What is the background for this study?
Response: A history of testicular cancer has been suggested to have an association with an increased risk of developing prostate cancer (PCa) in epidemiologic studies. We hypothesized that there may be an increased risk of developing intermediate to high-risk prostate cancer as well.
Medical Research: What are the main findings?
Response: 147,044 men with melanoma and 32,435 men with testicular cancer were identified. Prostate cancer was diagnosed in 3,205 men in total. The cumulative incidence of all prostate cancer by age 80 was 2.8% in the control melanoma cohort and 12.6% in the case cohort of men with history of testicular cancer (p<0.0001 for KM survival curves, Figure 1). For intermediate/high-risk disease, the incidence was 1.1% versus 5.8% for each cohort respectively (p<0.0001 for KM survival curves, Figure 2). No association with prostate cancer was seen with non-seminomatous versus seminomatous germ cell tumors. Upon multivariate analysis, testis cancer was associated with an increased risk of all prostate cancer (HR 4.7, p<0.0001) and intermediate/high-risk PCa (HR 5.2, p<0.0001) when controlling for race and radiation history.
MedicalResearch.com Interview with
Rebecca H. Johnson, MD
Assistant Professor, Clinical Genetics
University of Washington
Medical Research: What are the main findings of the study?
Dr. Johnson: We observed that, over the past two decades, there has been an increase in the incidence of testicular cancer in Hispanic American adolescents and young adults (AYAs) between 15 and 39 years of age. This increase is seen in both major subtypes of testicular cancer and affects Hispanic AYA patients with all stages of disease at the time of diagnosis. No comparable increase was observed in non-Hispanic white AYA,s or in older American men regardless of Hispanic ethnicity. Between 1992 and 2010, the incidence of testicular cancer in AYA Hispanics has increased 58% in contrast to just 7% in non-Hispanic white AYAs.