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Ian T. Magrath

Bio: Ian T. Magrath is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Lymphoma & Burkitt's lymphoma. The author has an hindex of 47, co-authored 107 publications receiving 8084 citations. Previous affiliations of Ian T. Magrath include Henry M. Jackson Foundation for the Advancement of Military Medicine & Tata Memorial Hospital.


Papers
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Journal ArticleDOI
TL;DR: Thymus-dependent regeneration of CD4+ T lymphocytes occurs primarily in children, whereas even young adults have deficiencies in this pathway, and the results suggest that rapid T-cell regeneration requires residual thymic function in patients receiving high-dose chemotherapy.
Abstract: Background Inadequate reconstitution of CD4+ T lymphocytes is an important clinical problem complicating chemotherapy, human immunodeficiency virus infection, and bone marrow transplantation, but relatively little is known about how CD4+ T lymphocytes regenerate. There are two main possibilities: bone marrow–derived progenitors could reconstitute the lymphocyte population using a thymus-dependent pathway, or thymus-independent pathways could predominate. Previous studies have suggested that the CD45RA glycoprotein on CD4+ T lymphocytes is a marker for progeny generated by a thymus-dependent pathway. Methods We studied 15 patients 1 to 24 years of age who had undergone intensive chemotherapy for cancer. The absolute numbers of CD4+ T lymphocytes in peripheral blood and the expression of CD45 isoforms (CD45RA and CD45RO) on these lymphocytes were studied serially during lymphocyte regeneration after the completion of therapy. Radiographic imaging of the thymus was performed concomitantly. Results There was ...

1,044 citations

Book ChapterDOI
TL;DR: This chapter discusses the evidence that deregulation of c-myc is a critical component of the pathogenesis of Burkitt's lymphoma, and consideration is given to the potential pathogenetic role of Epstein–Barr virus.
Abstract: Publisher Summary This chapter discusses the evidence that deregulation of c-myc is a critical component of the pathogenesis of Burkitt's lymphoma, and consideration is given to the potential pathogenetic role of Epstein–Barr virus (EBV). The clinical and epidemiological observations pertinent to the pathogenesis of this tumor are also presented. A consideration of the structural changes in c-myc provides strong, though indirect evidence that a major element in the pathogenesis of Burkitt's lymphoma is the deregulation of c-myc. The possibility of the structural changes in c-myc can be considered, if the c-myc allele involved in the translocation is the expressed allele in Burkitt's lymphoma. Evidence for this comes from two sources. First, in tumor cell lines in which there is a truncated c-myc gene that is, one in which the breakpoint on chromosome 8 is within the first intron, the first exon sequences cannot be detected by Northern blot in the messenger RNA. Second, somatic cell hybrid experiments have been performed in which the Burkitt's lymphoma cell lines were fused to mouse plasmacytoma cells and clones which contained either the derivative chromosomes or their normal alleles were isolated. In the case of hybrids in which one of the parents was a cell line bearing an 8;14 translocation four types of clone, each containing only one of the chromosomes 8, 14, derivative 8, or derivative 14, were isolated. Human c-myc expression was detectable only in clones bearing the derivative chromosome 14.

477 citations

Journal ArticleDOI
15 May 1997-Blood
TL;DR: Thymic-independent pathways of T-cell regeneration appear to rapidly regenerate substantial numbers of CD8+, but not CD4+ T cells, resulting in prolonged T- cell subset imbalance after T-cells depletion, which has significant implications for immunotherapeutic strategies undertaken to eradicate minimal residual neoplastic disease after cytoreductive chemotherapy.

391 citations

Journal ArticleDOI
01 Oct 1994-Blood
TL;DR: Based on the history of opportunistic complications in patients with other disorders who display similar degrees of CD4+ T-cell lymphopenia and preliminary observations in this population, immune incompetence could surface as a dose-limiting toxicity for highly dose-intensive chemotherapy regimens.

379 citations

Journal ArticleDOI
TL;DR: At the present time, only seven of the 43 patients who responded to the chemotherapy regimen have relapsed, with a median follow-up of 10 weeks after the response.
Abstract: One hundred twenty-four children and young adults with recurrent tumors, predominantly sarcomas, were treated with the combination of ifosfamide, etoposide, and the uroprotector, mesna (2-mercaptoethane sulphonate), in a phase II trial. The treatment regimen consisted of 12 cycles of therapy administered every 3 weeks. After evaluation of the tumor response to chemotherapy alone, radiation or surgery was used to eradicate residual sites of metastatic disease where possible. At the present time, 77 patients are evaluable for response to the chemotherapy; 43 of the patients have experienced a significant reduction in the tumor size in response to the chemotherapy alone (39 partial responses [PR] and four complete responses [CR]). Sixteen of 17 patients with Ewing's sarcoma, nine of 13 with rhabdomyosarcoma, four of eight with peripheral neuroepithelioma, three of eight with osteosarcoma, and 11 of 31 with other tumors have responded with a PR or CR. The toxicity of the regimen was acceptable. Moderate or severe toxicity evaluated on a per cycle basis included: neutropenia, 97%; thrombocytopenia, 32%; nephrotoxicity, less than 1%; mucositis, 1%; neurologic toxicity, 2%; nausea and vomiting, 13%; hemorrhagic cystitis, less than 1%. Fever was present after 33% of cycles and sepsis following 7%. One patient died due to sepsis and pancytopenia. At the present time, only seven of the 43 patients who responded to the chemotherapy regimen have relapsed, with a median follow-up of 10 weeks after the response. This drug combination is highly active in the treatment of recurrent sarcomas and other tumors in children and young adults.

302 citations


Cited by
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Journal ArticleDOI
TL;DR: The fraction of the different types of cancer, and of all cancers worldwide and in different regions, has been estimated using several methods; primarily by reviewing the evidence for the strength of the association (relative risk) and the prevalence of infection in different world areas.
Abstract: Several infectious agents are considered to be causes of cancer in humans. The fraction of the different types of cancer, and of all cancers worldwide and in different regions, has been estimated using several methods; primarily by reviewing the evidence for the strength of the association (relative risk) and the prevalence of infection in different world areas. The estimated total of infection-attributable cancer in the year 2002 is 1.9 million cases, or 17.8% of the global cancer burden. The principal agents are the bacterium Helicobacter pylori (5.5% of all cancer), the human papilloma viruses (5.2%), the hepatitis B and C viruses (4.9%), Epstein-Barr virus (1%), human immunodeficiency virus (HIV) together with the human herpes virus 8 (0.9%). Relatively less important causes of cancer are the schistosomes (0.1%), human T-cell lymphotropic virus type I (0.03%) and the liver flukes (0.02%). There would be 26.3% fewer cancers in developing countries (1.5 million cases per year) and 7.7% in developed countries (390,000 cases) if these infectious diseases were prevented. The attributable fraction at the specific sites varies from 100% of cervix cancers attributable to the papilloma viruses to a tiny proportion (0.4%) of liver cancers (worldwide) caused by liver flukes.

2,770 citations

Journal ArticleDOI
22 Aug 1997-Cell
TL;DR: It is demonstrated that p53 can be modified by acetylated both in vivo and in vitro, indicating a novel pathway for p53 activation and providing an example of an acetylation-mediated change in the function of a nonhistone regulatory protein.

2,583 citations

Journal Article

2,378 citations

01 Jan 2014
TL;DR: Lymphedema is a common complication after treatment for breast cancer and factors associated with increased risk of lymphedEMA include extent of axillary surgery, axillary radiation, infection, and patient obesity.

1,988 citations

Journal ArticleDOI
TL;DR: This work presents a meta-analyses of the immune system’s response to chemotherapy, which shows clear patterns of decline in the immune systems of patients diagnosed with central giant cell cancer.
Abstract: Walter T. Hughes, Donald Armstrong, Gerald P. Bodey, Eric J. Bow, Arthur E. Brown, Thierry Calandra, Ronald Feld, Philip A. Pizzo, Kenneth V. I. Rolston, Jerry L. Shenep, and Lowell S. Young St. Jude Children’s Research Hospital, Memphis, Tennessee; Memorial Sloan-Kettering Cancer Center, New York, New York; University of Texas M. D. Anderson Cancer Center, Houston; Harvard Medical School, Boston, Massachusetts; Stanford University School of Medicine, Palo Alto, and Kuzell Institute for Arthritis, San Francisco, California; University of Manitoba, Winnipeg, and Princess Margaret Hospital, Toronto, Canada; and Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

1,881 citations