Abstract
e22039 Background: The only known human cancer retrovirus, HTLV1 causes adult T-cell leukemia/lymphoma of which some respond to AZT+ alpha interferon. The existence of human retroviruses originating from murine leukemia viruses (MLVs) and their role in human cancer has been debated since the 1970s. A previously untreated 68 y.o. Oncologist with B-cell CLL and Cancer-Related Fatigue (CRF) was studied for retrovirus to determine if he could be treated with anti-retroviral drugs (arvs). His history included autoimmune disorders. Methods: Antibody detection: Alter et al. 2012. Gag detection: Mikovits et al. 2010. Results: Antibody to MLV envelope antigen and Gag RNA was detected. The Gag sequence was similar to MLVs but sufficiently different from the laboratory generated, XMRV which has no natural history in Man to rule it out. Proinflammatory cytokines were elevated. Trisomy 12 was present. By day 571 of his CLL the ALC doubling time decreased to < 1 year and he developed disabling CRF. AZT and raltegravir were started day 899. ALC, cytokine levels and CRF improved. After 9 months CLL parameters relapsed and then responded to adding tenofovir. This response lasted 3 months and then relapsed. Addition of lopinavir induced a response of parameters now ongoing 9 months. Total time on treatment is 29 months without toxicity and with improved CRF. In addition to his CLL there was a measurable T-cell clone and monocytosis both of which rose and fell with relapses and responses of the CLL to arvs but at different rates. Conclusions: A common human neoplasm was successfully treated with arvs. The drugs used were 2 Reverse Transcriptase inhibitors, an Integrase inhibitor and a Protease inhibitor developed for HIV treatment. There is nothing unusual or unique about this patient’s neoplasm and his case should stimulate further research. The role of retrovirus in cancer and CRF and whether arvs could be beneficial to patients identified as having a retroviral associated cancer and CRF should be studied. In addition, the significance of this patient’s clonal T-cell expansion and monocytosis and their production of cytokines should be examined. [Table: see text]
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