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At least 721 records · Page 40Linked to original sources
PubMed1997

Human T-cell leukemia virus-1 encoded Tax protein transactivates alpha 1-->3 fucosyltransferase Fuc-T VII, which synthesizes sialyl Lewis X, a selectin ligand expressed on adult T-cell leukemia cells.

Leukemia cells in patients with adult T-cell leukemia (ATL) and related cell lines strongly express the carbohydrate determinant sialyl Lewis X, a ligand for selectins. Its expression is thought to be related closely to the extravascular infiltration of the leukemia cells. Human T-cell leukemia virus type 1 (HTLV-1), the etiological agent of ATL, produces Tax protein, which is implicated in leukemogenesis through its transactivating effect on various cellular genes. In this study we investigated the transactivating effect of HTLV-1 Tax on the alpha 1-->3 fucosyltransferase Fuc-T VII, the putative rate-limiting enzyme in the synthesis of sialyl Lewis X in human leukocytes using JPX-9 cells. JPX-9 is a subclone of a non-ATL human lymphocytic leukemia cell line, Jurkat, and was established by introducing a metallothionein promoter-driven Tax expression plasmid. The JPX-9 cells as well as parental Jurkat cells did not express Fuc-T VII mRNA under normal culture conditions. When cultured in the presence of 10 microM CdCl2, Tax was induced and a significant amount of the Fuc-T VII message was ascertained by Northern blotting. The amount of the message was 24.5 times as much as was detected in non-treated cells, and was comparable to that which appeared by TPA stimulation of the cells, which is supposed to simulate the sequence of events occurring in normal activation of T lymphocytes activated by more physiological stimuli. Sialyl Lewis X determinant was expressed at the surface of CdCl2-treated cells, while the determinant was not detectable on either unstimulated JPX-9 or parental Jurkat cells. These results indicate that expression of sialyl Lewis X on leukemic cells in patients with ATL is at least partly due to the transactivation of the Fuc-T VII gene induced by the HTLV-1 Tax, and suggest that this leads to the accelerated extravascular infiltration of ATL cells.

Cadmium Chloride↗
PubMed2000

Gender, Memory, and Hippocampal Volumes: Relationships in Temporal Lobe Epilepsy.

Previous research has suggested bilateral hippocampal support for verbal memory in women with early left-hemisphere injury and that women experience better verbal memory outcome following anterior temporal lobectomy (ATL). The present study investigated two issues: (1) Do women have better verbal memory outcome following ATL compared with men? (2) Are verbal memory abilities differentially supported by the right and left hippocampus in males and females? Verbal memory performance [Wechsler Memory Scale: Logical Memory (LM) savings score] was assessed in 70 patients who underwent ATL. MRI volumetric measurements of the left and right hippocampus were performed. No LM savings score difference was found between groups preoperatively although a statistically significant gender effect (P < 0.04) was found for postoperative LM savings scores. Females displayed better postoperative memory performance, regardless of side of surgery. Preoperative verbal memory performance was not associated with right or left hippocampal volumes in either left or right ATL females, although the right hippocampus was positively associated with memory performance for left ATL males. Hippocampal volumes were not associated with postoperative LM savings scores for any group. Results suggest that prose recall was only modestly influenced by gender and that bilateral hippocampal support for prose recall was not present in our female patients.

Journal Article↗
PubMed2002

Ipsilateral Reorganization of Language in Early-Onset Left Temporal Lobe Epilepsy.

Purpose. Decline in confrontation naming ability occurs in a subset of temporal lobe epilepsy (TLE) patients following left (dominant) anterior temporal lobectomy (ATL). Patients with late age of onset of seizures are most vulnerable to such decline. In addition, object names typically acquired later in language development are the words most likely to be inaccessible after ATL. Early-onset left TLE patients may be at lower risk for post-ATL dysnomia either because they have a limited preoperative lexicon that does not include most late-age-of-acquistion names or they undergo early ipsilateral language reorganization, which results in a lexicon similar to that of late-onset TLE patients but offers protection from post-ATL naming decline.Methods. Sixty-five left hemisphere speech dominant left TLE patients who had undergone ATL were assessed pre- and postoperatively on the Boston Naming Test (BNT).Results. The early- and late-onset groups performed similarly across three BNT age-of-acquisition categories at the preoperative assessment. Words acquired relatively later in life were most likely to become inaccessible postoperatively for both groups, but the early-onset patients showed significantly less overall postoperative decline in naming ability compared with the late-onset group.Conclusions. The more stable pre- to postoperative naming performance exhibited by early-onset patients cannot be attributed to lack of acquisition of the words shown to be most vulnerable to postoperative decline (i.e., late-age-of-acquisition words). Their object naming stability suggests that early-onset left TLE patients undergo intrahemispheric reorganization of language early in life that provides protective benefits.

Journal Article↗
PubMed1987

Studies of human retroviruses in relation to adult T-cell leukaemia, acquired immune deficiency syndrome, and multiple sclerosis.

Studies of adult T-cell leukaemia virus/human T-cell leukaemia/lymphotropic viruses (ATLV/HTLV-I) in Japan indicate that the virus is involved only with the development of ATL. By contrast, reports from the U.S.A. about HTLV have from time to time claimed that related HTLV are concerned not only with ATL of black persons, but also with a wide range of diseases, such as mycosis fungoides/Sezary's syndrome, T-cell hairy cell leukaemia, acquired immune deficiency syndrome (AIDS) and also multiple sclerosis. Using morphological, biological, serological and molecular hybridisation studies, we were able to confirm that the viruses implicated in the development of ATL and AIDS are distinct and that ATLV/HTLV-I is involved only in ATL, and HIV/LAV/HTLV-III only in AIDS. In vitro, ATLV/HTLV-I transformed and immortalised T-cells, while HIV/LAV/HTLV-III killed our T-cells. Failure to detect any serological cross-reaction indicates that all the structural proteins are different. Likewise, Southern blot studies failed to reveal any cross-hybridisation. Sixty patients with multiple sclerosis failed to reveal any association with ATLV/HTLV-I or with HIV/LAV/HTLV-III. Our conclusion is that ATLV/HTLV-I is involved only in ATL of Japanese and of some black persons of African origin, and that HIV/LAV/HTLV-III is associated only in AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Pancreatic tumor formed by infiltration of adult T-cell leukemia cells.

CONCLUSION: We have described a case of pancreatic tumor formed by adult T-cell leukemia (ATL) cell infiltration. BACKGROUND: The patient was diagnosed as chronic ATL hematologically with the findings of increased number of atypical lymphocytes, ATL cells in the peripheral blood, and positive human T-cell leukemia virus type I (HTLV-I) antibody in the serum. The pancreatic tumor was identified by ultrasonography and computed tomography as a diffusely swollen tumor from the body to the tail of the pancreas. Biopsy specimen confirmed the ATL cell infiltration into the pancreas immunohistochemically, and Southern blot analysis showed the integration of HTLV-I proviral DNA both in the pancreas and in the peripheral blood. RESULTS: The pancreatic tumor diminished spontaneously without chemotherapy when ATL cells in the peripheral blood disappeared by spontaneous regression.

Aged↗
PubMed2003

Deoxycoformycin-containing combination chemotherapy for adult T-cell leukemia-lymphoma: Japan Clinical Oncology Group Study (JCOG9109).

Aggressive adult T-cell leukemia-lymphoma (ATL) generally has a very poor prognosis. Deoxycoformycin (DCF, pentostatin), an inhibitor of adenosine deaminase, has shown promising therapeutic efficacy for ATL. To develop a new effective therapy against aggressive ATL, we carried out a multicenter phase II study of DCF-containing combination chemotherapy. Sixty-two previously untreated patients with ATL (34, 21, and 7 patients with diseases of the acute, lymphoma, and unfavorable chronic types, respectively) were enrolled, but 2 were ineligible because they were judged to be favorable chronic types. A regimen of 1 mg/m2 vincristine intravenously on days 1 and 8, 40 mg/m2 doxorubicin intravenously on day 1, 100 mg/m2 etoposide intravenously on days 1 through 3, 40 mg/m2 prednisolone orally on days 1 and 2, and 5 mg/m2 DCF intravenously on days 8, 15, and 22 was administered every 28 days for 10 cycles unless disease progression or toxic complications occurred. Fifty-two percent of 60 eligible patients responded (95% confidence interval [CI], 38%-65%), with 17 patients (28%) achieving a complete response (CR) (95% CI, 17%-41%) and 14 achieving a partial response. The CR rate was inferior to those of both the previous Japan Clinical Oncology Group (JCOG) study (JCOG8701, 43%), a 9-drug combination chemotherapy of the second generation, and the subsequent JCOG9303 study (35%), a granulocyte colony-stimulating factor-supported, dose-intensified, 9-drug regimen. The median survival time of the 60 eligible patients in JCOG9109 was 7.4 months, and the estimated 2-year survival rate was 15.5%; these results were identical with those of JCOG8701 but inferior to those of JCOG9303. Grade 4 neutropenia and infection of grade 3 or greater were frequent (67% and 22%, respectively), and treatment-related death was observed in 4 patients (7%), septicemia in 2, and cytomegalovirus pneumonia in 2. We conclude that DCF-containing combination chemotherapy is not a promising regimen against aggressive ATL.

Adult↗
PubMed2003

Leukemogenesis of adult T-cell leukemia.

Adult T-cell leukemia (ATL) is one of the most aggressive hematologic malignancies and is caused by human T-cell leukemia virus type I (HTLV-I). Tax, encoded by the HTLV-I pX region, has been recognized by its pleiotropic actions as a critical accessory protein playing a central role in leukemogenesis. However, fresh ATL cells frequently lose Tax protein expression via several mechanisms, such as genetic and epigenetic changes in the provirus. Furthermore, there is a long latency period before the onset of ATL, indicating the multistep mechanisms of leukemogenesis. Therefore, additional factors, including other viral proteins, genetic and epigenetic changes of the host genome, and alterations in the gene expression and immune systems of the host cells, may be implicated in ATL leukemogenesis. This review summarizes recent advances in the understanding of ATL leukemogenesis.

Gene Expression Regulation, Viral↗
PubMed2002

Central nervous system lesions in adult T-cell leukaemia: MRI and pathology.

Adult T-cell leukaemia (ATL) is a T-cell lymphoid neoplasm caused by human T-cell leukaemia virus type I (HTLV-I). Radiological findings in central nervous system (CNS) involvement have not been well characterised. We reviewed the MRI of 18 patients with ATL who developed new neurological symptoms or signs, and pathology specimens from a 53-year-old woman who died of ATL. MRI findings were divided into three categories: definite, probable, and other abnormal. Definite and probable findings were defined as ATL-related. The characteristic findings were multiple parenchymal masses with or without contrast enhancement adjacent to cerebrospinal fluid (CSF) spaced and the deep grey matter of both cerebral hemispheres, plus leptomeningeal lesion. One patient had both cerebral and spinal cord lesions. Other abnormal findings in eight patients included one case of leukoencephalopathy caused by methotrexate. The histology findings consisted of clusters of tumour cells along perivascular spaces, and scattered infiltration of the parenchyma, with nests of tumour cells. Leptomeningeal infiltration by tumour spread into the parenchyma and secondary degeneration of the neuronal tracts was observed. MRI was useful for detecting CNS invasion by ATL and differentiating it from other abnormalities. The MRI findings seemed to correlate well with the histological changes.

Adult↗
PubMed2001

Bone resorption associated with uncoupling of osteoclastic and osteoblastic activities in adult T cell leukemia with hypercalcemia: case report.

A 64-year-old woman with adult T cell leukemia (ATL) was admitted to our hospital with severe hypercalcemia. The serum calcium level was elevated to 14.9 mg/dl. Biochemical parameters for bone formation including serum osteocalcin (bone Gla protein, BGP) and alkaline phosphatase (ALP) were normal. The serum levels of tartrate-resistant acid phosphatase (TRAP), a parameter for bone resorption, were increased (4.6 KAU). The serum level of parathyroid hormone-related protein (PTHrP) was elevated (343 pmol/l). The cytokines with stimulatory effects on bone resorption, such as interleukin (IL)-1alpha, IL-1beta, IL-6, and tumor necrosis factor-alpha, were not detected. Serum Ca levels, PTHrP levels, and TRAP levels decreased with the decrease in ATL cells after chemotherapy, while serum BGP levels and ALP levels increased. On the 29th hospital day, ATL cells began to increase again. Then serum PTHrP levels, Ca levels, and TRAP levels increased, while serum BGP levels and ALP levels decreased. A marked excessive bone resorption with suppressed bone formation (uncoupling) occurred in this patient. The ATL cells produced not only PTHrP but also IL-1alpha and IL-1beta. These results suggest that PTHrP may act as a humoral factor and IL-1 may act as a local factor in bone metabolism of ATL patients.

Bone Resorption↗
PubMed2000

Intracellular pH in isolated rat renal papillary thin limbs of Henle's loop.

Intracellular pH (pHi) was measured in isolated, nonperfused and perfused rat papillary thin limbs of Henle's loops in N-2-hydroxyethylpiperazine-N'-2-ethansulfonic acid (HEPES)- or HEPES/bicarbonate-buffered medium at pH 7.4 using the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF). Resting pHi was about 6.7 in descending thin limbs (DTL) and about 6.9 in ascending thin limbs (ATL), even with a medium pH of 7.4. These values appeared to reflect the acid pH of the blood in the neighboring vasa recta found in vivo. The resting pHi did not differ whether or not the medium contained bicarbonate although the total buffering capacity of the tubule cells was increased in the presence of bicarbonate. In nonperfused DTL and ATL, pHi was further acidified following an NH4Cl pulse. The rate of recovery of pHi from this level to the resting pHi was reduced by Na+ removal from the bath in both DTL and ATL and by the addition of ethylisopropylamiloride (EIPA) to the bath in the presence of Na+ in DTL. The rate of recovery was not affected by Cl- removal from the bath or K+ (75 mM) or 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS) addition to the bath in either DTL or ATL. These results suggest that the common, amiloride-sensitive, basolateral Na+/H+ exchanger plays a role in the regulation of pHi in rat papillary DTL but that a different basolateral Na+/H+ exchanger or a luminal Na+/H+ exchanger is important in rat papillary ATL.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2000

Cycloleucine fluxes during rat vasa recta and loop microinfusions in vivo and loop microperfusions in vitro.

Amino acids are apparently recycled between loops of Henle and vasa recta in rat papilla in vivo. To examine this process in the absence of metabolism, we performed continuous microinfusions of rat renal papillary ascending thin limbs (ATLs) and vasa recta in vivo, and microperflusions of isolated rat renal papillary descending thin limbs (DTLs) and ATLs in vitro using the nonmetabolizable, synthetic, neutral amino acid cycloleucine. Like naturally occurring amino acids, approximately = 25% of radiolabeled cycloleucine microinfused into ATLs in vivo was reabsorbed by a process that was not saturable or inhibitable. Also, like naturally occurring amino acids, approximately = 47% (relative to inulin) of radiolabeled cycloleucine microinfused into ascending vasa recta in vivo was transferred directly into ipsilateral tubular structures (probably DTLs) by a saturable and inhibitable process. In DTLs perfused in vitro, unidirectional bath-to-lumen fluxes (Jbl) tended to exceed unidirectional lumen-to-bath fluxes (Jlb), whereas in ATLs perfused in vitro Jlb tended to exceed Jbl, but the differences were not statistically significant. Moreover, none of the unidirectional fluxes was saturable or inhibitable, an observation compatible with apparent reabsorption from ATLs in vivo but incompatible with apparent movement from vasa recta to DTLs in vivo. These in vitro observations are like those made previously for the naturally occurring neutral amino acid L-alanine. The lack of saturation and inhibition, like the previous data on L-alanine, suggest that transepithelial movement of amino acids in thin limbs of Henle's loop may occur via a paracellular route and that regulation of amino acid movement in vivo may involve vasa recta, not DTLs. They also suggest that cycloleucine is a good nonmetabolizable surrogate for the study of neutral amino acid transport in the kidney.

Alanine↗
PubMed2006

TCR variable gene involvement in chromosome inversion between 14q11 and 14q24 in adult T-cell leukemia.

Chromosomal translocations in T-cell malignancies frequently involve the T-cell receptor (TCR)alpha/delta locus at chromosome 14q11. Although 14q11 abnormalities are found in about 10% of adult T-cell leukemia (ATL) cases, until now there has been no direct evidence showing involvement of the TCR locus in ATL-a malignancy closely associated with HTLV-1 infection. The breakpoints of T-cell malignancies most commonly occur within the Jalpha or Jdelta region of the TCR locus. In ATL, however, despite extensive searching no breakpoint has yet been found in that region. Using fluorescence in situ hybridization with a panel of cosmid and bacterial artificial chromosome probes derived from chromosome 14, including the variable region of the TCRalpha locus, comprehensive analysis of an ATL patient carrying inv(14)(q11q32) revealed that the TCR locus was indeed involved in this inversion. Molecular cloning of the breakpoint revealed the juxtaposition of TCR Valpha to the 14q24 region as a result of two consecutive inversions: inv(14)(q11q32) and inv(14)(q11q24). We also found a gene near the breakpoint at the 14q24 region that is downregulated in this ATL patient and is assigned in the database as a pseudogene of ADAM21 (a disintegrin and metalloproteinase domain 21). Our expression analysis, however, showed that this pseudogene was actually expressed and was capable of encoding a protein similar to ADAM21; thus we have named this gene ADAM21-like (ADAM21-L).

ADAM Proteins↗
PubMedDate not supplied

Retinal vasculitis caused by adult T-cell leukemia/lymphoma.

BACKGROUND: To report a case of lymphomatous infiltration and bilateral retinal vasculitis observed among 83 cases of adult T-cell leukemia (ATL) treated in the University Hospital Center in Fort-de-France (Martinique, French West Indies) between 1984 and 2003. CASE: A complete clinical ophthalmologic examination was performed in this patient along with fluorescein angiography. OBSERVATIONS: After being checked for diffuse adenopathies, myodesopsias, and phosphenes, the 35-year-old patient was diagnosed with ATL. The ocular impairment, present since the onset of ATL as peripheral subretinal infiltrates, spread progressively and afferently to the rest of the retina in the form of an essentially venous vasculitis. Impairment of the vitreous was noted only in the end stages of disease progression. As ocular lesions progressed, the general state of the patient degraded at the same time despite chemotherapeutic measures. CONCLUSION: Among the more than 300 seropositive for human T-cell lymphotropic virus type 1 (HTLV-1) or patients with HTLV-1-associated myelopathy/tropical spastic paraparesis treated at our hospital in the last 20 years, and among the 83 cases of ATL, only this single case of retinal vasculitis associated with HTLV-1 was observed (1/83, 1.2%) in Martinique, confirming the geographic variability of the clinical phenotype of HTLV-1 infection. The incidence of retinal vasculitis in ATL patients may signify an even worse prognosis than initially indicated.

Adult↗
PubMed1989

Concurrent infections with Strongyloides and T-cell leukemia virus and their possible effect on immune responses of host.

Sera from 91 patients with strongyloidiasis in Okinawa prefecture, Japan, were examined for the presence of the concurrent infection with adult T-cell leukemia (ATL) virus by detecting the antibody to ATL-associated virus antigen (anti-ATLA). As high as 73.6% of the patients were found to be positive for the anti-ATLA antibody, whereas in 38 Strongyloides-negative controls, the positive rate was only 18.4% A significant increase of OKT 4+ cells and a decrease of OKT 8+ cells were noted among the patients positive for anti-ATLA antibody. A considerable rise of spontaneous proliferation of peripheral lymphocytes and a depression of mitogen-induced proliferative responses were also found in the patients. The increase of background mitogenesis was considered to be due to the concurrent infection with the ATL virus, but the depressed responses to mitogenic stimuli seemed to have no relation with the presence of the viral infection. The possible contribution of strongyloidiasis as a cofactor predisposing to ATL viral infection or leading the virus carriers to ATL patients was discussed.

Adult↗
PubMed1985

Clinical features of OKT4+/OKT8+ adult T-cell leukemia.

Adult T-cell leukemia (ATL) has a range of clinical characteristics. Phenotypically the leukemic cells usually express the helper/inducer associated antigen OKT4 with lack of OKT8. We have observed three patients with acute ATL cytologically indistinguishable from OKT4+/OKT8- ATL but whose neoplastic cells had the unusual phenotype, OKT3+, OKT4+, OKT6-, OKT8+ OKT9+/-, OKT11+, Tac+/-, TdT-. All patients had abnormal karyotypes and antibodies against anti-ATL associated antigens as well as proviral DNA of human T-cell leukemia virus in the leukemic cells. The clinical course was complicated by skin eruptions, hypercalcemia, pulmonary infection and disseminated intravascular coagulopathy. All died of complications shortly after diagnosis. The clinical features of these patients were similar to those of OKT4+/OKT8- ATL. However, their acute course suggests that co-expression surface antigens OKT4 and OKT8 may be a sign of aggressive nature of the disease with poor prognosis.

Aged↗
PubMed1986

Dissociation of interleukin-2-mediated cell proliferation and interleukin-2 receptor upregulation in adult T-cell leukemia cells.

We studied cell proliferation and interleukin-2 (IL-2) receptor upregulation mediated by exogenous IL-2 in leukemic cells from adult T-cell leukemia (ATL) patients to characterize some aspects of abnormal IL-2 receptor expression in ATL. Leukemic cells from 7 ATL patients examined showed no or very poor proliferative response to IL-2 though they expressed IL-2 receptors without any stimulation. In contrast, ATL leukemic cells cultured with IL-2 for 2 days expressed about twice as many IL-2 receptors as those of cells cultured without IL-2. Thus, in ATL leukemic cells, there seems to be a dissociation between the signal(s) for two different effects mediated by IL-2, cell proliferation and IL-2 receptor upregulation.

Adult↗
PubMed1987

Expression of the HT462 antigen on fresh leukemic T cells and on cells of HTLV-I infected lines.

We have examined expression of antigens defined by HT462 monoclonal antibody (mAb), together with other HTLV-I related antigens using phorbol 12-myristate 13-acetate treated leukemic mature T cells. Thirteen patients with adult T-cell leukemia (ATL), 3 patients in remission states of ATL and 5 patients with non-ATL were examined. All ATL cells expressed the HT462 antigen, however cells from patients in remission did not express the HT462 antigen. A low percentage of cells from 2 out of 5 patients with non-ATL mature leukemic T cells expressed the HT462 antigen, although these cells did not express other HTLV-I related antigens. Cells of HTLV-I infected human cell lines expressed the HT462 antigen. Three HTLV-I infected rat cell lines (TARS-1, TART-1, TARL-2) did not express the HT462 antigen, although cells of these lines expressed other HTLV-I related antigens. Characterization of the HT462 antigen by strip radioimmunoassay based on western blotting technique using cell lysates of HUT102 cells revealed two additional bands (p68, p35) together with previously reported proteins (gp52, p42). Only p68 was seen in western blots using cell lysates of the rat cell lines. These findings further suggest that the HT462 antigen is a cellular component induced in virus transformed human cells and not a virus encoded protein.

Animals↗
PubMed1988

Increase in cytoplasmic free calcium concentration initiated by T3 antigen stimulation is imparied in adult T-cell leukemia cells.

We studied the change in cytoplasmic free calcium ion concentration ([Ca2+]i) in the peripheral blood leukemic cells from adult T-cell leukemia (ATL) patients stimulated by anti-T3 (CD3) or anti-T11 (CD2) antibodies in order to see whether there is an abnormal response in the early activation processes following T3 or T11 antigen stimulation. Peripheral blood mononuclear cells (PBMC) from four T-cell chronic lymphocytic leukemia (T-CLL) patients showed a rapid and clear increase in [Ca2+]i (from 165 +/- 26 nM to more than 299 nM) when stimulated by OKT3 antibody and anti-mouse IgG antibody. This response was comparable to that of PBMC from 10 normal individuals (from 151 +/- 20 nM to 252 +/- 34 nM). In contrast, PBMC from 10 ATL patients showed only a slight increase in [Ca2+]i (from 137 +/- 21 nM to 176 +/- 32 nM) following T3 stimulation. The experiments with higher concentrations of OKT3 antibody suggested that this attenuated increase in [Ca2+]i in ATL cells was not exclusively due to impaired expression of T3 antigen. The [Ca2+]i increase in ATL cells induced by the stimulation with two anti-T11 antibodies recognizing different epitopes of the T11 antigen, however, was comparable to that of normal PBMC. The abnormal response of [Ca2+]i to the T-cell receptor/T3 antigen stimulation in ATL may be related to dysfunction or leukemogenesis of HTLV-I-infected cells.

Adult↗