Characteristics of chemotherapy-induced clinical remission in long survivors with aggressive adult T-cell leukemia/lymphoma

Tsukasaki, Kunihiro; Ikeda, Shu‐ichi; Murata, Ken T.; Maeda, Takahiro; Atogami, Sunao; Sohda, Hisashi; Momita, Saburo; T, Jubashi; Yamada, Yasuaki; Mine, Mariko; Kamihiri, Simeru; Tomonaga, Masao

doi:10.1016/0145-2126(93)90061-o

Cited by 68 publications

(35 citation statements)

References 13 publications

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“…Tsukasaki et al reviewed the outcome of their cohort of 114 patients presenting with acute or lymphomatous ATLL between 1975 and 1989. These patients were treated with combination chemotherapy with only 17.5% achieving CR, but a further 46.5% had a partial response (Tsukasaki et al, 1993). These data accord with the results of the Lymphoma Study Group in which CR was obtained in 17-18% of patients treated with CHOP (LSG-1) (Lymphoma Study Group, 1982;Shimoyama et al, 1988); in 37% of patients treated with CHOP plus methotrexate (Shimoyama et al, 1988).…”

Section: Chemotherapysupporting

confidence: 79%

Natural history of adult T-cell leukemia/lymphoma and approaches to therapy

2005

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After cell-to-cell transmission, HTLV-I increases its viral genome by de novo infection and proliferation of infected cells. Proliferation of infected cells is clonal and persistent in vivo. During the carrier state, infected cells are selected in vivo by the host's immune system, the genetic and epigenetic environment of proviral integration sites, and other factors. In leukemic cells, tax gene expression is frequently impaired by genetic and epigenetic mechanisms. Such loss of Tax expression enables ATL cells to escape the host immune system. On the other hand, ATL cells acquire the ability to proliferate without Tax by intracellular genetic and epigenetic changes. Despite advances in support and the development of novel treatment agents, the prognosis for ATLL remains poor. A number of therapies, however, do appear to improve prognosis compared to CHOP (VEPA). These include interferon-a plus zidovudine (probably after 1-2 cycles of CHOP), intensive chemotherapy as in LSG-15 with G-CSF support and Allo-SCT (which includes the potential for cure). Emerging novel approaches include HDAC inhibitors, monoclonal antibodies, and proteasome inhibitors. Comparison between different therapeutic approaches is complicated by the range of natural history of ATLL, different recruitments of naı¨ve-to-therapy, refractory or relapsed patients, and variations in the reporting of outcome that frequently excludes difficultto-evaluate patients. Moreover, results from relatively small proof-of-principle studies have not been extended with randomized, controlled trials. As a result, currently, there is no clear evidence to support the value of any particular treatment approach over others. To avoid further unnecessary patient suffering and to identify optimal therapy as rapidly as possible, large randomized, controlled trials encompassing multicenter, international collaborations will be necessary.

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Section: Chemotherapysupporting

confidence: 79%

Natural history of adult T-cell leukemia/lymphoma and approaches to therapy

2005

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“…3,19 An increased number of imbalances (0-2 versus Ͼ 2) on CGH analysis was associated with a significantly shorter survival in the total cohort of patients (P ϭ .0005; Figure 3) but not when either those with indolent ATL or those with aggressive ATL were analyzed separately. Analysis of prognostic factors showed that patients with an increased number of imbalances more frequently had poor prognostic factors, such as advanced PS or a high LDH value, and more aggressive clinical subtypes than other patients (Table 4).…”

Section: Clinical Importance Of Cgh Imbalancementioning

confidence: 99%

Comparative genomic hybridization analysis in adult T-cell leukemia/lymphoma: correlation with clinical course

Tsukasaki

Krebs

Nagai

et al. 2001

Blood

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103

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Sixty-four patients with adult T-cell leukemia/lymphoma (ATL; 18 patients with indolent subtype and 46 with aggressive subtype) associated with human T-lymphotropic virus type 1 (HTLV-1) were analyzed using comparative genomic hybridization (CGH). The most frequent observations were gains at chromosomes 14q, 7q, and 3p and losses at chromosomes 6q and 13q. Chromosome imbalances, losses, and gains were more frequently observed in aggressive ATL than in indolent ATL, with significant differences between the 2 ATL subtypes at gains of 1q and 4q. An increased number of chromosomal imbalances was associated with a significantly shorter survival in all patients. A high number of chromosomal losses was associated with a poor prognosis in indolent ATL, whereas the presence of 7q؉ was marginally associated with a good prognosis in aggressive ATL. Paired samples (ie, samples obtained at different sites from 4 patients) and sequential samples from 13 patients (from 6 during both chronic disease and acute crisis and from 7 during both acute onset and relapse) were examined by CGH and Southern blotting for HTLV-1. All but 2 paired samples showed differences on CGH assessment. Two chronic/crisis samples showed distinct results regarding both CGH and HTLV-1 integration sites, indicating clonal changes in ATL at crisis. In 11 patients, the finding of identical HTLV-1 sites and clonally related CGH results suggested a common origin of sequential samples. In contrast to chronic/ crisis samples, CGH results with all acute/ relapse sample pairs showed the presence of clonally related but not evolutional subclones at relapse, thereby suggesting marked chromosomal instability. In summary, clonal diversity is common during progression of ATL, and CGH alterations are associated with clinical course. (Blood. 2001;97:3875-3881)

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“…The diagnosis of ATL was based on clinical features, histologically and/or cytologically proven mature T-cell malignancy, the presence of anti-HTLV-1 antibody, and monoclonal integration of HTLV-1 proviral DNA into tumor cells as described previously. 2,[7][8][9] The subtypes of ATL were classified according to criteria established by the Lymphoma Study Group of Japan Clinical Oncology Group. 2 Clinical data included date of diagnosis, complications at diagnosis, therapy regimens if applicable, date of death, cause of death, and date of latest contact.…”

Section: Patientsmentioning

confidence: 99%

Long-term study of indolent adult T-cell leukemia-lymphoma

Takasaki

Iwanaga

Imaizumi

et al. 2010

Blood

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153

115

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The long-term prognosis of indolent adult T-cell leukemia-lymphoma (ATL) is not clearly elucidated. From 1974 to 2003, newly diagnosed indolent ATL in 90 patients (65 chronic type and 25 smoldering type) was analyzed. The median survival time was 4.1 years; 12 patients remained alive for more than 10 years, 44 progressed to acute ATL, and 63 patients died. The estimated 5-, 10-, and 15-year survival rates were 47.2%, 25.4%, and 14.1%, respectively, with no plateau in the survival curve. Although most patients were treated with watchful waiting, 12 patients were treated with chemotherapy. Kaplan-Meier analyses showed that advanced performance status (PS), neutrophilia, high concentration of lactate dehydrogenase, more than 3 extranodal lesions, more than 4 total involved lesions, and receiving chemotherapy were unfavorable prognostic factors for survival. Multivariate Cox analysis showed that advanced PS was a borderline significant independent factor in poor survival (hazard ratio, 2.1, 95% confidence interval, 1.0-4.6; P ‫؍‬ .06), but it was not a factor when analysis was limited to patients who had not received chemotherapy. The prognosis of indolent ATL in this study was poorer than expected.

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Characteristics of chemotherapy-induced clinical remission in long survivors with aggressive adult T-cell leukemia/lymphoma

Cited by 68 publications

References 13 publications

Natural history of adult T-cell leukemia/lymphoma and approaches to therapy

Natural history of adult T-cell leukemia/lymphoma and approaches to therapy

Comparative genomic hybridization analysis in adult T-cell leukemia/lymphoma: correlation with clinical course

Long-term study of indolent adult T-cell leukemia-lymphoma

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