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Recent Research: Novel Treatment for Skin Lymphoma

Thursday, July 19, 2012

Filed under:  Case Studies/Studies | Treatments & Techniques | Oncology

Promising findings on a novel combination treatment approach for a chronic type of skin lymphoma were published in JAMA’s Archives of Dermatology by clinical researchers from Seidman Cancer Center at University Hospitals (UH) Case Medical Center and Case Western Reserve University School of Medicine.

The article outlines findings from a first-of-its-kind study showing that O6-benzylguanine is successful in treating cutaneous T-Cell lymphoma by enhancing the efficacy of topical chemotherapy (carmustine).

“Current therapy for cutaneous T-Cell lymphoma is suboptimal and this new study shows that adding O6-benzylguanine to carmustine is more effective and less toxic to the skin, allowing for more optimal treatments,” says Kevin Cooper, MD, Chairman of the Department of Dermatology at UH Case Medical Center and Case Western Reserve University School of Medicine. “This treatment essentially weakens the cancer cells to make the lymphoma more vulnerable to topical chemotherapy and has a lot of potential in alleviating patients’ disease burden in this chronic and progressive disease.”

Cutaneous T-cell lymphoma is a form of lymphoma which affects the skin and typically relapses and becomes increasingly challenging to treat. The new drug combination offers a potential new option for patients using skin-directed treatments, before the need to undergo systemic chemotherapy.

When used alone, carmustine attaches to the DNA in the patient’s cancer cells during the replication process, causing the cancer cells to die. Problems sometimes occur when an enzyme clips off the treatment from the DNA, allowing the cancer cells to replicate. O6-benzylguanine inhibits the enzyme from clipping off the carmustine from the DNA, so the drug can complete its mission and kill the cancer cells.

“By adding O6-benzylguanine, we can effectively lower the dosage of the topical treatment, carmustine, and render it less toxic on healthy cells but more effective at killing cancer cells,” says Dr. Cooper, who was senior author of the study. “This combination treatment has had excellent initial clinical results and we are following it up with additional ongoing studies.”

This study was funded by National Cancer Institute grants to Case Western Reserve University in conjunction with Keryx Pharmaceuticals Inc.

Genetic Cause of Thyroid Cancer Discovered

Cleveland Clinic researchers have discovered three genes that increase the risk of thyroid cancer, which has the largest incidence increase in cancers among both men and women. Research led by Charis Eng, MD, PhD, chair and founding director of the Genomic Medicine Institute of Cleveland Clinic’s Lerner Research Institute, included nearly 3,000 patients with Cowden syndrome (CS) or CS-like disease, which is related to an increased risk of breast and thyroid cancer.

Mutations in the PTEN gene are the foundation of Cowden syndrome. PTEN is a tumor suppressor gene, helping to direct the growth and division of cells. Inherited mutations in the PTEN gene have been found in approximately 80 percent of Cowden syndrome patients. These mutations prevent the PTEN protein from effectively regulating cell survival and division, which can lead to the formation of tumors.

The conclusions of this research, published in the Journal of Clinical Endocrinology & Metabolism, found that all six patients under age 18 had pathogenic PTEN mutations. The researchers recommend that the thyroids of children with PTEN mutation-causing CS-related disease receive increased surveillance.

Children with thyroid cancer are recommended to have testing for PTEN mutations, which could warrant surveillance for additional cancers or maladies. In contrast, alterations in the SDH and KLLN genes did not associate with thyroid cancer in children.

PTEN gene testing in the setting of genetic counseling is already routinely practiced, and has been a powerful gene-enabled diagnostic test which then personalizes clinical screening and treatment. Once SDH and KLLN findings are independently validated, the tests could be implemented as a clinical routine test as well. Importantly, these three genes belong to different cell pathways so that specific molecular-targeted treatments can be utilized depending on which gene is involved.

MD News Cleveland-Akron-Carton, May/June 2012