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      HIV-Associated Lymphomas: Progress and New Challenges

      Author(s): ,
      Publication date Created:
      Publication date (Electronic):
      Journal: Journal of Clinical Medicine
      Publisher: MDPI AG

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          Abstract

          The association of human immunodeficiency virus (HIV) and aggressive lymphomas was first reported in 1982. Before the development of effective HIV antiviral therapy, the incidence and the mortality of these lymphomas was high, with patients frequently succumbing to the disease. More lately, the combination of cART with chemoimmunotherapy significantly improved the survival outcome of the HIV-lymphomas. In this review, we discuss on describing the incidence of HIV-associated lymphomas, their clinical features, and the latest advances in the management of the various lymphoma subtypes.

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          Cancer statistics, 2020

          Rebecca Siegel, Kimberly D Miller, Ahmedin Jemal (2020)
          Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States and compiles the most recent data on population-based cancer occurrence. Incidence data (through 2016) were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data (through 2017) were collected by the National Center for Health Statistics. In 2020, 1,806,590 new cancer cases and 606,520 cancer deaths are projected to occur in the United States. The cancer death rate rose until 1991, then fell continuously through 2017, resulting in an overall decline of 29% that translates into an estimated 2.9 million fewer cancer deaths than would have occurred if peak rates had persisted. This progress is driven by long-term declines in death rates for the 4 leading cancers (lung, colorectal, breast, prostate); however, over the past decade (2008-2017), reductions slowed for female breast and colorectal cancers, and halted for prostate cancer. In contrast, declines accelerated for lung cancer, from 3% annually during 2008 through 2013 to 5% during 2013 through 2017 in men and from 2% to almost 4% in women, spurring the largest ever single-year drop in overall cancer mortality of 2.2% from 2016 to 2017. Yet lung cancer still caused more deaths in 2017 than breast, prostate, colorectal, and brain cancers combined. Recent mortality declines were also dramatic for melanoma of the skin in the wake of US Food and Drug Administration approval of new therapies for metastatic disease, escalating to 7% annually during 2013 through 2017 from 1% during 2006 through 2010 in men and women aged 50 to 64 years and from 2% to 3% in those aged 20 to 49 years; annual declines of 5% to 6% in individuals aged 65 years and older are particularly striking because rates in this age group were increasing prior to 2013. It is also notable that long-term rapid increases in liver cancer mortality have attenuated in women and stabilized in men. In summary, slowing momentum for some cancers amenable to early detection is juxtaposed with notable gains for other common cancers.
          Article 0 comments Cited 8912 times – based on 0 reviews     Review now
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            Global, Regional, and National Cancer Incidence, Mortality, Years of Life Lost, Years Lived With Disability, and Disability-Adjusted Life-Years for 29 Cancer Groups, 1990 to 2017

            Christina Fitzmaurice, Degu Abate, Naghmeh Abbasi … (2020)
            This systematic analysis describes cancer burden for 29 cancer groups across 195 countries from 1990 through 2017 to provide data needed for cancer control planning.
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              Decade-long safety and function of retroviral-modified chimeric antigen receptor T cells.

              John Scholler, Troy Brady, Gwendolyn Binder-Scholl … (2012)
              The success of adoptive T cell gene transfer for treatment of cancer and HIV is predicated on generating a response that is both durable and safe. We report long-term results from three clinical trials to evaluate gammaretroviral vector-engineered T cells for HIV. The vector encoded a chimeric antigen receptor (CAR) composed of CD4 linked to the CD3ζ signaling chain (CD4ζ). CAR T cells were detected in 98% of samples tested for at least 11 years after infusion at frequencies that exceeded average T cell levels after most vaccine approaches. The CD4ζ transgene retained expression and function. There was no evidence of vector-induced immortalization of cells; integration site distributions showed no evidence of persistent clonal expansion or enrichment for integration sites near genes implicated in growth control or transformation. The CD4ζ T cells had stable levels of engraftment, with decay half-lives that exceeded 16 years, in marked contrast to previous trials testing engineered T cells. These findings indicate that host immunosuppression before T cell transfer is not required to achieve long-term persistence of gene-modified T cells. Further, our results emphasize the safety of T cells modified by retroviral gene transfer in clinical application, as measured in >500 patient-years of follow-up. Thus, previous safety issues with integrating viral vectors are hematopoietic stem cell or transgene intrinsic, and not a general feature of retroviral vectors. Engineered T cells are a promising form of synthetic biology for long-term delivery of protein-based therapeutics. These results provide a framework to guide the therapy of a wide spectrum of human diseases.
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                Author and article information

                Journal
                Journal ID (publisher-id): JCMOHK
                Title: Journal of Clinical Medicine
                Abbreviated Title: JCM
                Publisher: MDPI AG
                ISSN (Electronic): 2077-0383
                Publication date Created: March 2022
                Publication date (Electronic): March 07 2022
                Volume: 11
                Issue: 5
                Page: 1447
                Article
                DOI: 10.3390/jcm11051447
                PubMed ID: 35268547
                SO-VID: 64996dbe-371d-47fd-a23d-bad583fafff2
                Copyright © © 2022
                License:

                https://creativecommons.org/licenses/by/4.0/

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