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[Title] Sézary cell counts in erythrodermic cutaneous T-cell lymphoma: implications for prognosis and staging.

In this retrospective study, quantitative Sézary cell counts were performed at presentation on 192 patients with erythrodermic cutaneous T-cell lymphoma (E-CTCL).

Per recommendation of the International Society of Cutaneous Lymphomas (ISCL), the impact on staging of using an absolute Sézary cell count of 1.0 K microL-1 or more as equivalent to lymph node involvement was investigated.

Of 132 patients with disease initially classified at stage III using the current TNM staging system, 25% were up staged to IVa, resulting in a clearer separation of associated survival curves between the stages.

Furthermore, the current ISCL definition of B0, B1 and B2 ratings were improved using Sézary cell count levels of < 1.0 K microL-1, > or = 1.0 - 4.99 K microL-1 and > or = 5.0 K microL-1, respectively.

The clinical importance of these variables vis-à-vis the modified TNBM staging system will need to be clarified in future studies.

[MeSH-major] Dermatitis, Exfoliative / diagnosis. Lymphoma, T-Cell, Cutaneous / diagnosis. Sezary Syndrome / blood. Skin Neoplasms / diagnosis

[MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Count. Female. Humans. Lymph Nodes. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies

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(PMID = 17064997.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

   

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[Title] Molecular characterization of the Tax-containing HTLV-1 enhancer complex reveals a prominent role for CREB phosphorylation in Tax transactivation.

Transcriptional activation of human T-cell leukemia virus type 1 (HTLV-1) is mediated by the viral oncoprotein Tax, which utilizes cellular transcriptional machinery to perform this function.

The coactivator CREB-binding protein (CBP)/p300 binds to this promoter-bound ternary complex, which promotes the initiation of HTLV-1 transcription.

Consonant with a fundamental role for CREB phosphorylation in Tax recruitment to the complex, we found that CREB is highly phosphorylated in a panel of HTLV-1-infected human T-cell lines.

Because pCREB has been implicated in leukemogenesis, enhancement of CREB phosphorylation by the virus may play a role in the etiology of adult T-cell leukemia.

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(PMID = 17449469.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA055035; United States / NCI NIH HHS / CA / CA55035; United States / NCI NIH HHS / CA / CA055035-14S1; United States / NCI NIH HHS / CA / CA055035-14; United States / NCI NIH HHS / CA / R01 CA055035-14S1; United States / NCI NIH HHS / CA / CA55035-S1; United States / NCI NIH HHS / CA / R01 CA055035-14

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / CREB1 protein, human; 0 / Cyclic AMP Response Element-Binding Protein

   

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[Title] Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses.

Human T cell leukemia virus type 1 (HTLV-1) is a lymphotropic retrovirus whose cell-to-cell transmission requires cell contacts.

HTLV-1-infected T lymphocytes form 'virological synapses', but the mechanism of HTLV-1 transmission remains poorly understood.

We show here that HTLV-1-infected T lymphocytes transiently store viral particles as carbohydrate-rich extracellular assemblies that are held together and attached to the cell surface by virally-induced extracellular matrix components, including collagen and agrin, and cellular linker proteins, such as tetherin and galectin-3.

Extracellular viral assemblies rapidly adhere to other cells upon cell contact, allowing virus spread and infection of target cells.

Their removal strongly reduces the ability of HTLV-1-producing cells to infect target cells.

Our findings unveil a novel virus transmission mechanism based on the generation of extracellular viral particle assemblies whose structure, composition and function resemble those of bacterial biofilms.

HTLV-1 biofilm-like structures represent a major route for virus transmission from cell to cell.

[MeSH-major] CD4-Positive T-Lymphocytes / virology. Extracellular Matrix / virology. HTLV-I Infections / transmission. Human T-lymphotropic virus 1 / physiology

[MeSH-minor] Biofilms. Concanavalin A. Gene Products, env / metabolism. Humans. Microscopy, Electron, Transmission. Virus Assembly / physiology. Virus Attachment. Virus Internalization

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[CommentIn] Nat Med. 2010 Jan;16(1):25-7 [20057417.001]

(PMID = 20023636.001).

[ISSN] 1546-170X

[Journal-full-title] Nature medicine

[ISO-abbreviation] Nat. Med.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Gene Products, env; 11028-71-0 / Concanavalin A

   

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[Title] HTLV-1 Tax-mediated TAK1 activation involves TAB2 adapter protein.

Human T cell leukemia virus type 1 (HTLV-1) Tax is an oncoprotein that plays a crucial role in the proliferation and transformation of HTLV-1-infected T lymphocytes.

[MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. MAP Kinase Kinase Kinases / metabolism

[MeSH-minor] Binding Sites. Cell Line. Humans. NF-kappa B / metabolism. Ubiquitin-Protein Ligases / metabolism

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(PMID = 17986383.001).

[ISSN] 1090-2104

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / TAB2 protein, human; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP kinase kinase kinase 7; EC 6.3.2.19 / Ubiquitin-Protein Ligases

   

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[Title] Children and adults with acute lymphoblastic leukaemia have similar gene expression profiles.

OBJECTIVES: To compare the gene expression pattern in children and adults with acute lymphoblastic leukaemia (ALL) in order to improve our understanding of the difference in disease biology and prognosis.

RESULTS: Unsupervised hierarchical cluster analysis revealed that, in spite of differences in outcome, patients clustered irrespective of age, first by T-cell or B-precursor immunophenotype, and second by cytogenetic changes within the B-precursor group.

CONCLUSIONS: In spite of the difference in clinical outcome, the gene expression pattern in children and adults with ALL is very similar and is primarily dependent on immunophenotype and cytogenetic aberrations.

[MeSH-major] Gene Expression Regulation, Leukemic. Oligonucleotide Array Sequence Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adult. Child. Child, Preschool. Female. Fusion Proteins, bcr-abl / biosynthesis. Fusion Proteins, bcr-abl / genetics. Gene Deletion. Gene Expression Profiling. Genes, p16. Humans. Male. Philadelphia Chromosome

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(PMID = 15876250.001).

[ISSN] 0902-4441

[Journal-full-title] European journal of haematology

[ISO-abbreviation] Eur. J. Haematol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Denmark

[Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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[Title] Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines.

Adult T-cell leukemia (ATL) is an aggressive neoplasm caused by human T-cell leukemia virus type I (HTLV-I), which induces nuclear factor-kappaB (NF-kappaB), a molecule central to the ensuing neoplasia.

The NF-kappaB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) has been shown to inhibit NF-kappaB activation in Tax-expressing HTLV-I-infected cells.

In this study, we used NOD/SCID beta2-microglobulin(null) mice to show that intraperitoneal inoculation with Tax-deficient ATL cell lines caused rapid death, whereas DHMEQ-treated mice survived.

Furthermore, DHMEQ treatment after subcutaneous inoculation inhibited the growth of transplanted ATL cells.

These results demonstrate that DHMEQ has therapeutic efficacy on ATL cells, regardless of Tax expression.

[MeSH-major] Benzamides / pharmacology. Cyclohexanones / pharmacology. Gene Products, tax / deficiency. Leukemia, T-Cell / prevention & control. Xenograft Model Antitumor Assays / methods

[MeSH-minor] Adult. Animals. Apoptosis / drug effects. Cell Line, Tumor. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. Mice. Mice, Inbred NOD. Mice, Knockout. Mice, SCID. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Tumor Burden. beta 2-Microglobulin / genetics. beta 2-Microglobulin / metabolism

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(PMID = 17764832.001).

[ISSN] 0304-3835

[Journal-full-title] Cancer letters

[ISO-abbreviation] Cancer Lett.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Benzamides; 0 / Cyclohexanones; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / beta 2-Microglobulin; 0 / dehydroxymethylepoxyquinomicin

   

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[Title] Gene expression profiling reveals intrinsic differences between T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.

BACKGROUND: T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LL) and are often thought to represent a spectrum of a single disease.

The malignant cells in T-ALL and T-LL are morphologically indistinguishable, and they share the expression of common cell surface antigens and cytogenetic characteristics.

However, despite these similarities, differences in the clinical behavior of T-ALL and T-LL are observed.

CONCLUSIONS: Despite significant similarities between the malignant T-cell precursors, clear differences in the gene expression profiles were observed between T-ALL and T-LL implying underlying differences in the biology of the two entities.

[MeSH-major] Gene Expression Profiling. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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(PMID = 16358311.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / U01 CA88361

[Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

   

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[Title] Human T-lymphotropic virus type 1-induced CC chemokine ligand 22 maintains a high frequency of functional FoxP3+ regulatory T cells.

We recently reported that human T-lymphotropic virus type 1 (HTLV-1) infection is accompanied by a high frequency of CD4(+)FoxP3(+) cells in the circulation.

In asymptomatic carriers of HTLV-1 and in patients with HTLV-1-associated inflammatory and malignant diseases, a high FoxP3(+) cell frequency correlated with inefficient cytotoxic T cell-mediated killing of HTLV-1-infected cells.

In adult T cell leukemia/lymphoma (ATLL), the FoxP3(+) population was distinct from the leukemic T cell clones.

However, the cause of the increase in FoxP3(+) cell frequency in HTLV-1 infection was unknown.

In this study, we report that the plasma concentration of the chemokine CCL22 is abnormally high in HTLV-1-infected subjects and that the concentration is strongly correlated with the frequency of FoxP3(+) cells, which express the CCL22 receptor CCR4.

Further, we show that CCL22 is produced by cells that express the HTLV-1 transactivator protein Tax, and that the increased CCL22 enhances the migration and survival of FoxP3(+) cells in vitro.

Finally, we show that FoxP3(+) cells inhibit the proliferation of ex vivo, autologous leukemic clones from patients with ATLL.

We conclude that HTLV-1-induced CCL22 causes the high frequency of FoxP3(+) cells observed in HTLV-1 infection; these FoxP3(+) cells may both retard the progression of ATLL and HTLV-1-associated inflammatory diseases and contribute to the immune suppression seen in HTLV-1 infection, especially in ATLL.

[MeSH-major] Cell Proliferation. Chemokine CCL22 / physiology. Forkhead Transcription Factors / physiology. Human T-lymphotropic virus 1 / immunology. T-Lymphocytes, Regulatory / cytology. T-Lymphocytes, Regulatory / immunology

[MeSH-minor] CD4 Lymphocyte Count. Cell Survival / immunology. Cytotoxicity Tests, Immunologic. HTLV-I Infections / immunology. HTLV-I Infections / pathology. Humans. Jurkat Cells. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / pathology. T-Lymphocytes, Cytotoxic / cytology. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Cytotoxic / virology

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(PMID = 20525891.001).

[ISSN] 1550-6606

[Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)

[ISO-abbreviation] J. Immunol.

[Language] eng

[Grant] United Kingdom / Wellcome Trust / / 080871; United Kingdom / Medical Research Council / / G0501974; United Kingdom / Wellcome Trust / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / CCL22 protein, human; 0 / Chemokine CCL22; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors

[Other-IDs] NLM/ EMS51736; NLM/ PMC3575032

   

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[Title] [Molecular targeted therapy in adult T-cell leukemia/lymphoma].

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / drug therapy

[MeSH-minor] Adult. Antigens, Surface / immunology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Humans. NF-kappa B / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / antagonists & inhibitors

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(PMID = 17474481.001).

[ISSN] 0047-1852

[Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine

[ISO-abbreviation] Nippon Rinsho

[Language] jpn

[Publication-type] Journal Article; Review

[Publication-country] Japan

[Chemical-registry-number] 0 / Antigens, Surface; 0 / HSP90 Heat-Shock Proteins; 0 / NF-kappa B; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases

[Number-of-references] 30

   

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[Title] Indoleamine 2,3-dioxygenase is highly expressed in human adult T-cell leukemia/lymphoma and chemotherapy changes tryptophan catabolism in serum and reduced activity.

Adult T-cell leukemia/lymphoma (ATLL) is caused by human T-cell lymphotropic virus type 1 (HTLV-1).

In this study, we investigated the IDO expression in ATLL cells and the effect of chemotherapy on IDO-initiating l-TRP catabolism in patients with ATLL.

Serum l-kynurenine (l-KYN) concentrations, l-KYN/l-TRP ratio, and the level of IDO mRNA expression in ATLL cells were significantly increased in ATLL patients compared to those in healthy and HTLV-positive carrier subjects.

On the other hand, l-TRP level was significantly decreased in ATLL patients compared to that in healthy subjects.

In the immunohistochemical staining, IDO was strongly expressed in cytoplasm of ATLL cells.

These data provide evidence that IDO is highly expressed in ATLL cells, and that IDO-initiating l-TRP catabolism changes with chemotherapy.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Indoleamine-Pyrrole 2,3,-Dioxygenase / metabolism. Leukemia-Lymphoma, Adult T-Cell / enzymology. Tryptophan / blood

[MeSH-minor] Adult. Aged. Base Sequence. DNA Primers. Female. Humans. Immunohistochemistry. Male. Middle Aged. Treatment Outcome

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(PMID = 18639341.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / DNA Primers; 0 / Indoleamine-Pyrrole 2,3,-Dioxygenase; 8DUH1N11BX / Tryptophan

   

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[Title] Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function.

B cell lineage acute lymphoblastic leukemia (ALL) arises in virtually all cases from B cell precursors that are arrested at pre-B cell receptor-dependent stages.

The Philadelphia chromosome-positive (Ph(+)) subtype of ALL accounts for 25-30% of cases of adult ALL, has the most unfavorable clinical outcome among all ALL subtypes and is defined by the oncogenic BCR-ABL1 kinase and deletions of the IKAROS gene in >80% of cases.

Here, we demonstrate that the pre-B cell receptor functions as a tumor suppressor upstream of IKAROS through induction of cell cycle arrest in Ph(+) ALL cells.

Pre-B cell receptor-mediated cell cycle arrest in Ph(+) ALL cells critically depends on IKAROS function, and is reversed by coexpression of the dominant-negative IKAROS splice variant IK6.

IKAROS also promotes tumor suppression through cooperation with downstream molecules of the pre-B cell receptor signaling pathway, even if expression of the pre-B cell receptor itself is compromised.

In this case, IKAROS redirects oncogenic BCR-ABL1 tyrosine kinase signaling from SRC kinase-activation to SLP65, which functions as a critical tumor suppressor downstream of the pre-B cell receptor.

These findings provide a rationale for the surprisingly high frequency of IKAROS deletions in Ph(+) ALL and identify IKAROS-mediated cell cycle exit as the endpoint of an emerging pathway of pre-B cell receptor-mediated tumor suppression.

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(PMID = 19620627.001).

[ISSN] 1540-9538

[Journal-full-title] The Journal of experimental medicine

[ISO-abbreviation] J. Exp. Med.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / T32 CA009659-16; None / None / / R01 CA137060-01A1; United States / NCI NIH HHS / CA / T32 CA009659; United States / NCI NIH HHS / CA / R01 CA090321; United States / NCI NIH HHS / CA / R01CA090321; United States / NCI NIH HHS / CA / R21 CA152497; None / None / / R01 CA137060-02; None / None / / R01 CA139032-01; United States / NCI NIH HHS / CA / R01CA137060; United States / NCI NIH HHS / CA / R01 CA139032-02; None / None / / R01 CA139032-02; United States / NCI NIH HHS / CA / R01 CA139032-01; United States / NCI NIH HHS / CA / R21 CA152497-01; United States / NCI NIH HHS / CA / R01 CA137060-02; United States / NCI NIH HHS / CA / R01 CA137060-01A1; None / None / / R21 CA152497-01; United States / NCI NIH HHS / CA / R01 CA139032; United States / NCI NIH HHS / CA / R01CA139032; United States / NCI NIH HHS / CA / R01 CA137060

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / B cell linker protein; 0 / IKZF1 protein, human; 0 / Pre-B Cell Receptors; 148971-36-2 / Ikaros Transcription Factor

[Other-IDs] NLM/ PMC2722172

   

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[Title] Detection of EBV, HBV, HCV, HIV-1, HTLV-I and -II, and SMRV in human and other primate cell lines.

The high prevalence of contaminated cell cultures suggests that viral contaminations might be distributed among cultures.

We investigated more than 460 primate cell lines for Epstein-Barr (EBV), hepatitis B (HBV), hepatitis C (HCV), human immunodeficiency virus type 1 (HIV-1), human T-cell leukemia/lymphoma virus I and II (HTLV-I/-II), and squirrel monkey retrovirus (SMRV) infections for risk assessment.

None of the cell lines were infected with HCV, HIV-1, or HTLV-I/-II.

However, one cell line displayed reverse transcriptase activity.

Thirty-nine cell lines harbored EBV DNA sequences.

Studies on the lytic phase of EBV revealed that five cell lines produce EBV particles and six further cell lines produced EBV upon stimulation.

One cell line contained an integrated HBV genome fragment but showed no virus production.

Six cell lines were SMRV-infected.

Newly established cell lines should be tested for EBV infections to detect B-lymphoblastoid cell lines (B-LCL).

B-LCLs established with EBV from cell line B95-8 should be tested for SMRV infections.

[MeSH-major] Primates / virology. Viruses / genetics. Viruses / isolation & purification

[MeSH-minor] Animals. Blotting, Southern. Cell Line. DNA, Circular / analysis. HIV-1 / genetics. HIV-1 / isolation & purification. Hepacivirus / genetics. Hepacivirus / isolation & purification. Hepatitis B virus / genetics. Hepatitis B virus / isolation & purification. Herpesvirus 4, Human / genetics. Herpesvirus 4, Human / isolation & purification. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / isolation & purification. Human T-lymphotropic virus 2 / genetics. Human T-lymphotropic virus 2 / isolation & purification. Humans. In Situ Hybridization, Fluorescence. Polymerase Chain Reaction. Retroviruses, Simian / genetics. Retroviruses, Simian / isolation & purification. Saimiri / virology. Viral Proteins / analysis

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(PMID = 20454443.001).

[ISSN] 1110-7251

[Journal-full-title] Journal of biomedicine & biotechnology

[ISO-abbreviation] J. Biomed. Biotechnol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Circular; 0 / Viral Proteins

[Other-IDs] NLM/ PMC2861168

   

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[Title] A modified version of galectin-9 suppresses cell growth and induces apoptosis of human T-cell leukemia virus type I-infected T-cell lines.

ATL is a fatal malignancy of T lymphocytes caused by HTLV-I infection and remains incurable.

Galectins are a family of animal lectins that function both extracellularly (by interacting with cell surface and extracellular matrix glycoproteins and glycolipids) and intracellularly (by interacting with cytoplasmic and nuclear proteins) to modulate signaling pathways.

We found that protease-resistant galectin-9 by modification of its linker peptide, hG9NC(null), prevented cell growth of HTLV-I-infected T-cell lines and primary ATL cells.

The suppression of cell growth was inhibited by lactose, but not by sucrose, indicating that beta-galactoside binding is essential for hG9NC(null)-induced cell growth suppression. hG9NC(null) induced cell cycle arrest by reducing the expression of cyclin D1, cyclin D2, cyclin B1, Cdk1, Cdk4, Cdk6, Cdc25C and c-Myc, and apoptosis by reducing the expression of XIAP, c-IAP2 and survivin.

Most of these genes are regulated by NF-kappaB, which plays a critical role in oncogenesis by HTLV-I. hG9NC(null) suppressed IkappaBalpha phosphorylation, resulting in suppression of NF-kappaB.

Most importantly, treatment with hG9NC(null) (6.7 mg/kg injected intraperitoneally every day) reduced tumor formation from an HTLV-I-infected T-cell line when these cells were inoculated subcutaneously into SCID mice.

Our results suggest that hG9NC(null) could be a suitable agent for the management of ATL.

[MeSH-major] Apoptosis / drug effects. Galectins / pharmacology. HTLV-I Infections / drug therapy. Human T-lymphotropic virus 1 / growth & development. Leukemia-Lymphoma, Adult T-Cell / therapy. T-Lymphocytes / pathology. T-Lymphocytes / virology

[MeSH-minor] Animals. Caspases / metabolism. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Female. Galactosides / metabolism. Growth Inhibitors / pharmacology. Humans. Membrane Proteins. Mice. Mice, SCID. NF-kappa B / genetics. NF-kappa B / immunology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors, Virus / biosynthesis. beta-Galactosidase / metabolism

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[Copyright] (c) 2007 Wiley-Liss, Inc.

[RetractionIn] Int J Cancer. 2011 Dec 1;129(11):2762-3 [21960263.001]

(PMID = 17278100.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication

[Publication-country] United States

[Chemical-registry-number] 0 / Galactosides; 0 / Galectins; 0 / Growth Inhibitors; 0 / HAVCR2 protein, human; 0 / LGALS8 protein, human; 0 / LGALS9 protein, human; 0 / Membrane Proteins; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Receptors, Virus; 0 / beta-galactoside; EC 3.2.1.23 / beta-Galactosidase; EC 3.4.22.- / Caspases

   

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[Title] [Severe liver injury following nelarabine chemotherapy for T-cell lymphoblastic lymphoma].

A 41-year-old man received allogeneic hematopoietic stem cell transplantation for T-cell lymphoblastic lymphoma.

[MeSH-major] Antineoplastic Agents / adverse effects. Arabinonucleosides / adverse effects. Drug-Induced Liver Injury / etiology. Lymphoma, T-Cell / drug therapy. Mediastinal Neoplasms / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

[MeSH-minor] Adult. Humans. Male. Neoplasm Recurrence, Local. Severity of Illness Index

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(PMID = 19225230.001).

[ISSN] 0485-1439

[Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology

[ISO-abbreviation] Rinsho Ketsueki

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 60158CV180 / nelarabine

   

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[Title] Modulation of nuclear factor-kappaB by human T cell leukemia virus type 1 Tax protein: implications for oncogenesis and inflammation.

Human T cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL) and an inflammatory disease named tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM).

HTLV-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses.

[MeSH-major] Cell Transformation, Neoplastic / immunology. Gene Products, tax / immunology. HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / immunology. Inflammation / immunology. NF-kappa B / immunology

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(PMID = 16720895.001).

[ISSN] 0257-277X

[Journal-full-title] Immunologic research

[ISO-abbreviation] Immunol. Res.

[Language] eng

[Grant] United States / Intramural NIH HHS / /

[Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Gene Products, tax; 0 / NF-kappa B

[Number-of-references] 102

   

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Hypercalcaemia is a common metabolic complication of malignant disease often requiring emergency intervention.

Although it is more frequently associated with solid tumours, malignancy-associated hypercalcaemia (MAH) is seen in a significant number of patients with blood diseases.

Its association with myeloma and adult T-cell leukaemia/lymphoma is well recognized but the incidence of hypercalcaemia in other haematological neoplasms, affecting adults and children, is less clearly defined.

Haematologists need to be familiar with the clinical manifestations of, the differential diagnosis to be considered and the most effective management strategies that are currently available for MAH.

[MeSH-minor] Adult. Bone Density Conservation Agents / therapeutic use. Child. Diphosphonates / therapeutic use. Fluid Therapy / methods. Humans

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(PMID = 20377591.001).

[ISSN] 1365-2141

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates

[Number-of-references] 96

   

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[Title] Primary cutaneous T-cell lymphoma expressing FOXP3: a case report supporting the existence of malignancies of regulatory T cells.

Regulatory T (Treg) cells, which represent 5% to 10% of peripheral T cells, regulate the activities of T-cell subsets by performing immunosuppressive functions and thus preventing the development of autoimmune responses.

Recently, it has been demonstrated that the tumor cells in adult T-cell leukemia lymphomas can function as Treg, raising the question of whether any variant of primary cutaneous T-cell lymphoma may also express a regulatory phenotype.

We describe an extraordinary case of primary cutaneous T-cell lymphoma clinically characterized by protean cutaneous manifestations and histologically showing a pattern consistent with epidermotropic pleomorphic medium-/large-cell primary cutaneous T-cell lymphoma.

[MeSH-major] CD4-Positive T-Lymphocytes / immunology. Forkhead Transcription Factors / immunology. Lymphoma, T-Cell, Cutaneous / pathology. Skin Neoplasms / pathology. T-Lymphocytes, Regulatory / immunology

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(PMID = 19615546.001).

[ISSN] 1097-6787

[Journal-full-title] Journal of the American Academy of Dermatology

[ISO-abbreviation] J. Am. Acad. Dermatol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers; 0 / Forkhead Transcription Factors

   

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[Title] Autonomous proliferation of HTLV-CD4+ T cell clones derived from human T cell leukemia virus type I (HTLV-I)-associated myelopathy patients.

That HTLV-I infects CD4(+) T cells and enhances their cell growth has been shown as successful long-term in vitro proliferation in the presence of IL-2.

It is known that T cells isolated from HAM patients possess strong ability for cell proliferation in vitro and mRNA of various cytokines are abundantly expressed in CNS tissues of HAM patients.

In this study, we examined the relationship between cell proliferation and ability of in vitro cytokine production of CD4(+) T cell clones isolated from HAM patients.

We started a culture from a single cell to isolate cell clones immediately after drawing blood from the patients using limiting dilution method, which could allow the cell to avoid in vitro HTLV-I infection after initiation of culture.

Many cell clones were obtained and the rate of proliferation efficiency from a single cell was as high as 80%, especially in the 4 weeks' culture cells from HAM patients.

Our results indicate that the ability of cell proliferation in HAM patients is not restricted in HTLV-I-infected T cells.

HTLV-Iuninfected CD4(+) T cells, mainly Th0 cells, also have a strong ability to respond to IL-2-stimulation, showing that unusual immune activation on T cells has been observed in HAM patients.

[MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / virology. Human T-lymphotropic virus 1 / immunology. Paraparesis, Tropical Spastic / immunology

[MeSH-minor] Adult. Aged. Clone Cells. Cytokines / genetics. Cytokines / immunology. DNA, Viral / chemistry. DNA, Viral / genetics. Female. Humans. Lymphocyte Activation. Male. Middle Aged. Polymerase Chain Reaction. Receptors, Antigen, T-Cell / immunology

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(PMID = 17310092.001).

[ISSN] 0385-5600

[Journal-full-title] Microbiology and immunology

[ISO-abbreviation] Microbiol. Immunol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Cytokines; 0 / DNA, Viral; 0 / Receptors, Antigen, T-Cell

   

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[Title] Risk factors before autologous stem-cell transplantation for lymphoma predict for secondary myelodysplasia and acute myelogenous leukemia.

PURPOSE: The risk factors for treatment-related myelodysplastic syndrome (t-MDS) and acute myelogenous leukemia (AML) after autologous stem-cell transplantation (ASCT) are similar to those that increase the risk of difficult stem-cell harvests.

We reviewed our experience in 526 patients with lymphoma treated by ASCT to determine whether difficult stem-cell harvests predict for an increased risk of t-MDS/AML.

Pretransplantation characteristics, including age, diagnosis of non-Hodgkin's lymphoma or Hodgkin's disease, bone marrow involvement, prior radiation therapy, prior exposure to chemotherapy, lactate dehydrogenase at the time of ASCT, disease status, and method of stem-cell mobilization, were then analyzed with respect to the subsequent development of t-MDS/AML.

[MeSH-major] Leukemia, Myeloid, Acute / etiology. Lymphoma / surgery. Myelodysplastic Syndromes / etiology. Peripheral Blood Stem Cell Transplantation

[MeSH-minor] Actuarial Analysis. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Hematopoietic Stem Cell Mobilization / methods. Humans. Incidence. Male. Middle Aged. Multivariate Analysis. Predictive Value of Tests. Retrospective Studies. Risk Factors. Survival Analysis. Transplantation, Autologous

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(PMID = 16877727.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor

   

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[Title] Dermatological findings in 3 generations of a family with a high prevalence of human T cell lymphotropic virus type 1 infection in Brazil.

BACKGROUND: Dermatologic manifestations are quite common in patients with adult T cell leukemia and lymphoma and patients with myelopathy and/or tropical spastic paraparesis associated with human T cell lymphotropic virus type 1 (HTLV-1).

The aim of this study was to investigate dermatological findings presented by 30 members of a Brazilian family, half of whom are infected with HTLV-1 (as confirmed by enzyme-linked immunosorbent assay and Western blot).

METHODS: The subjects underwent dermatologic examination and laboratory assessment, which included the search for the HTLV-1 genome in peripheral blood mononuclear cells (PBMCs) by qualitative and semiquantitative polymerase chain reaction (PCR) and in skin samples by nested qualitative PCR and immunofluorescence assay.

One HTLV-1-infected individual presented with concurrently acquired ichthyosis, impetigo, scabies, dermatophytosis, and seborrheic dermatitis.

Additionally, the HTLV-1 proviral load was higher in patients with >1 skin lesion.

Finally, HTLV-1 could be identified in the skin by immunofluorescence assay, which, by use of PCR as the gold standard, showed a sensitivity and specificity of 61.5% and 100%, respectively.

CONCLUSIONS: Altogether, these clinical and laboratory findings point to an HTLV-1 tropism toward the skin, even in HTLV-1 carriers without adult T cell leukemia/lymphoma or HTLV-1-associated myelopathy and/or tropical spastic paraparesis.

[MeSH-major] HTLV-I Infections / epidemiology. Human T-lymphotropic virus 1

[MeSH-minor] Adult. Brazil / epidemiology. Carrier State / virology. Family Health. Female. Humans. Leukemia-Lymphoma, Adult T-Cell / etiology. Male. Paraparesis, Tropical Spastic / etiology. Polymerase Chain Reaction. Skin Diseases / epidemiology. Skin Diseases / physiopathology

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(PMID = 17051489.001).

[ISSN] 1537-6591

[Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America

[ISO-abbreviation] Clin. Infect. Dis.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

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[Title] Adult T-cell leukemia/lymphoma with multiple integration of HTLV-1 provirus presenting as an isolated paranasal sinus tumor: a case report.

BACKGROUND: Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive T-cell lymphoma and etiologically associated with human T-lymphotropic virus type 1 (HTLV-1).

Patients with ATLL commonly present with leukemic changes, systemic lymphadenopathy, and/or extranodal lesion and have very poor prognosis.

METHODS AND RESULTS: We describe a rare case of ATLL presenting as an isolated paranasal mass.

Southern blot analysis of the biopsied specimens demonstrated multiple integration bands of HTLV-1 provirus of different intensities.

Thereafter, the patient showed an indolent clinical course with leukemic changes and pulmonary and cutaneous ATLL lesions and remains alive more than 5 years from diagnosis.

CONCLUSION: ATLL should be included in the differential diagnosis of sinonasal lymphoma, although the event is rare.

Multiple HTLV-1 provirus integrations of different intensities may be indicative of good prognosis for ATLL.

[MeSH-major] Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Paranasal Sinus Neoplasms / diagnosis. Proviruses / physiology

[MeSH-minor] Adult. Humans. Male. Virus Integration

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(PMID = 18023035.001).

[ISSN] 1043-3074

[Journal-full-title] Head & neck

[ISO-abbreviation] Head Neck

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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[Title] Single-cell analysis of T-cell receptor repertoire of HTLV-1 Tax-specific cytotoxic T cells in allogeneic transplant recipients with adult T-cell leukemia/lymphoma.

Adult T-cell leukemia (ATL) is a lymphoproliferative malignancy associated with human T-cell lymphotropic virus type 1 (HTLV-1) infection.

Recently, it has been shown that allogeneic hematopoietic stem cell transplantation (allo-HSCT) is an effective treatment for ATL, and that HTLV-1 Tax-specific CD8(+) cytotoxic T cells (CTL) contribute to the graft-versus-ATL effect.

In the present study, we, for the first time, analyzed the T-cell receptor (TCR) repertoire of isolated Tax(301-309) (SFHSLHLLF)-specific CTLs in HLA-A*2402(+) ATL patients before and after allo-HSCT by single-cell reverse transcription-PCR.

In addition, a unique conserved amino acid motif of "P-D/P-R" in TCR-beta complementarity-determining region 3 in either BV7- or BV18-expressing CTLs was observed not only in all of the samples from ATL patients, but also in samples from the same patient before and after HSCT.

Furthermore, the P-D/P-R motif-bearing CTL clones established from peripheral blood samples after HSCT exhibited strong killing activity against the HTLV-1-infected T cells of the patient.

Hence, Tax(301-309)-specific CTLs in ATL patients might have a preference for TCR construction and induce strong immune responses against the HTLV-1-infected T cells of patients, which contribute to the graft-versus-ATL effects after allo-HSCT.

[MeSH-major] Gene Products, tax / immunology. Hematopoietic Stem Cell Transplantation. Human T-lymphotropic virus 1 / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes, Cytotoxic / immunology

[MeSH-minor] Amino Acid Motifs. HLA-A Antigens / immunology. HLA-A24 Antigen. Humans. Peptide Fragments / immunology. Receptors, Antigen, T-Cell / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology

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(PMID = 20647322.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Gene Products, tax; 0 / HLA-A Antigens; 0 / HLA-A*24:02 antigen; 0 / HLA-A24 Antigen; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / tax protein, Human T-lymphotrophic virus 1

   

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[Title] Anti-Tac (daclizumab, Zenapax) in the treatment of leukemia, autoimmune diseases, and in the prevention of allograft rejection: a 25-year personal odyssey.

In addition, we demonstrated that daclizumab is of value in the treatment of patients with noninfectious uveitis, multiple sclerosis, and the neurological disease human T-cell lymphotropic virus I associated myelopathy/tropical spastic paraparesis (HAM/TSP).

Others demonstrated therapeutic efficacy with daclizumab in patients with pure red cell aplasia, aplastic anemia, and psoriasis.

Thus, translation of basic insights concerning the IL-2/IL-2 receptor system obtained using the monoclonal antibody daclizumab provided a useful strategy for the prevention of organ allograft rejection and the treatment of patients with select autoimmune diseases or T-cell leukemia/lymphoma.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Autoimmune Diseases / drug therapy. Graft Rejection / prevention & control. Immunoglobulin G / therapeutic use. Immunosuppressive Agents / therapeutic use. Leukemia / drug therapy. Receptors, Interleukin-2 / drug effects

[MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Binding, Competitive / immunology. Humans. Interleukin-2 / antagonists & inhibitors. Interleukin-2 / immunology. Interleukin-2 Receptor alpha Subunit / antagonists & inhibitors. Interleukin-2 Receptor alpha Subunit / immunology. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Mice. Paraparesis, Tropical Spastic / drug therapy. Uveitis / drug therapy

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(PMID = 17216565.001).

[ISSN] 0271-9142

[Journal-full-title] Journal of clinical immunology

[ISO-abbreviation] J. Clin. Immunol.

[Language] eng

[Grant] United States / Intramural NIH HHS / /

[Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; 0 / Interleukin-2; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Receptors, Interleukin-2; CUJ2MVI71Y / daclizumab

[Number-of-references] 94

   

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[Title] Transplantation in adult ALL.

The value of the allogeneic graft-versus-leukemia effect in adult acute lymphoblastic leukemia (ALL) has now been conclusively demonstrated and confirmed.

While this is true for adults in all age groups, it may not be the best clinical option for young adults for whom increasingly intensive pediatric protocols are clearly of benefit.

As in childhood ALL minimal residual disease studies may be extremely useful in predicting outcome and, therefore, strategy, but at present there are less definite data in adults.

Clinical indications to harness the allogeneic effect will mature as the true value of pediatric protocols in adult patients and the safety and efficacy of a sibling, unrelated and reduced intensity transplant emerge in this disease.

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(PMID = 20008244.001).

[ISSN] 1520-4383

[Journal-full-title] Hematology. American Society of Hematology. Education Program

[ISO-abbreviation] Hematology Am Soc Hematol Educ Program

[Language] ENG

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Neoplasm Proteins

[Number-of-references] 44

   

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The Haematological Malignancy Research Network (HMRN) was established in 2004 to provide robust generalizable data to inform clinical practice and research.

With an emphasis on primary-source data, prognostic factors, sequential treatment/response history, and socio-demographic details are recorded to clinical trial standards.

HMRN captures all diagnoses (adult and paediatric) and the diagnostic age ranged from 4 weeks to 99 years (median 70.4 years).

In line with published estimates, first-line clinical trial entry varied widely by disease subtype and age, falling from 59.5% in those aged <15 years to 1.9% in those aged over 75 years - underscoring the need for contextual population-based treatment and response data of the type collected by HMRN.

The critical importance of incorporating molecular and prognostic markers into comparative survival analyses is illustrated with reference to diffuse-large B-cell lymphoma, acute myeloid leukaemia and myeloma.

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Health Services Research. Humans. Infant. Infant, Newborn. Male. Middle Aged. Young Adult

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(PMID = 19958356.001).

[ISSN] 1365-2141

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Other-IDs] NLM/ PMC3066245

[Investigator] Ackroyd S; Ali S; Allsup D; Ashcroft J; Bashi R; Bond L; Bynoe G; Bowen D; Carter C; Chapple M; Ciepluch H; Cook G; Cuthbert A; Czyz J; Edwards A; Feyler S; Gilleece M; Gilson D; Hall C; Harris E; Hill A; Hill Q; Hillmen P; Howard M; Jalihal S; Johnson R; Kinsey S; Kraemer D; Kwok-Williams M; Mcverry T; Moreton P; Munro L; Newton L; Norfolk D; Parapia L; Patil K; Patmore R; Richards M; Sayala H; Sherton G; Smith G; Speed K; Steed A; Subash C; Thomas E; Williams A; Wieczorek A; Wright D; Barrans S; Blythe D; Burton C; Cullen M; Dickinson H; Evans P; Jack A; Jones R; O'Connor S; Owen R; Rawstron A; Richards S; Swirsky D; Tooze R; Worrillow L; Ansell P; Blase J; Cope I; Cox H; Crouch S; Curson W; Doughty J; Farish J; Griffiths S; Howell D; James B; Johnston T; Kane E; Lewis C; Lightfoot T; Newton R; Oliver S; O'Sullivan J; Painter D; Roman E; Simpson J; Sinclair V; Smith A; Thomson A

   

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[Title] The protease of human T-cell leukemia virus type-1 is a potential therapeutic target.

Human T-cell leukemia virus type-1 (HTLV-1) is associated with a number of human diseases.

Although the mechanism by which the virus causes diseases is still not known, studies indicate that viral replication is critical for the development of HTLV-1 associated myelopathy, and initial studies suggested that blocking replication with reverse transcriptase inhibitors had a therapeutic effect.

Therefore, based on the success of HIV-1 protease inhibitors, the HTLV-1 protease is also a potential target for chemotherapy.

Furthermore, mutated residues in HIV-1 protease that confer drug resistance are frequently seen in equivalent positions of other retroviral proteases, like HTLV-1 protease.

Therefore, comparison of HTLV-1 and HIV-1 proteases is expected to aid the rational design of broad spectrum inhibitors effective against various retroviral proteases, including the mutant HIV-1 enzymes appearing in drug resistance.

This review describes the characteristics of HTLV-1 protease, makes comparison with HIV-1 protease, and discusses the status of inhibitor development for the HTLV-1 protease.

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(PMID = 17504236.001).

[ISSN] 1873-4286

[Journal-full-title] Current pharmaceutical design

[ISO-abbreviation] Curr. Pharm. Des.

[Language] ENG

[Grant] United States / NIGMS NIH HHS / GM / R01 GM062920; United States / NIGMS NIH HHS / GM / GM 062920; United States / FIC NIH HHS / TW / TW01001

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Protease Inhibitors; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.- / HTLV-1 protease

[Number-of-references] 45

   

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[Title] [Immunological aspects of human retrovirus infection].

[MeSH-major] HIV Infections / immunology. HIV-1. HTLV-I Infections / immunology

[MeSH-minor] AIDS Vaccines. Animals. Antiretroviral Therapy, Highly Active. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / immunology. Humans. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Leukemia-Lymphoma, Adult T-Cell / therapy. Mutation. Paraparesis, Tropical Spastic / immunology. Paraparesis, Tropical Spastic / physiopathology. Paraparesis, Tropical Spastic / therapy. Receptors, CCR5 / genetics. Risk

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(PMID = 15861703.001).

[ISSN] 0047-1852

[Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine

[ISO-abbreviation] Nippon Rinsho

[Language] jpn

[Publication-type] Journal Article; Review

[Publication-country] Japan

[Chemical-registry-number] 0 / AIDS Vaccines; 0 / Receptors, CCR5

[Number-of-references] 60

   

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[Title] [ATL].

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell

[MeSH-minor] Adult. Humans

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(PMID = 20962495.001).

[ISSN] 0485-1439

[Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology

[ISO-abbreviation] Rinsho Ketsueki

[Language] jpn

[Publication-type] Journal Article; Review

[Publication-country] Japan

   

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The study evidenced one of the synthetic analogues (11) as a potent cytotoxic and pro-apoptotic agent against several tumor cell lines which also inhibits the TNFalpha-induced NF-kappaB activation in a human leukemia T cell line.

[MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Computer Simulation. Drug Screening Assays, Antitumor. Humans. Molecular Structure. NF-kappa B / metabolism. Structure-Activity Relationship. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / pharmacology

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[Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.

(PMID = 20031419.001).

[ISSN] 1464-3391

[Journal-full-title] Bioorganic & medicinal chemistry

[ISO-abbreviation] Bioorg. Med. Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Quinones; 0 / Tumor Necrosis Factor-alpha; 0 / aplidinone A

   

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[Title] Backward bifurcation in a model for HTLV-I infection of CD4+ T cells.

Human T-cell Lymphotropic Virus Type I (HTLV-I) primarily infects CD4+ helper T cells.

HTLV-I infection is clinically linked to the development of Adult T-cell Leukemia/Lymphoma and of HTLV-I Associated Myelopathy/Tropical Spastic Paraparesis, among other illnesses.

HTLV-I transmission can be either horizontal through cell-to-cell contact, or vertical through mitotic division of infected CD4+ T cells.

It has been observed that HTLV-I infection has a high proviral load but a low rate of proviral genetic variation.

We consider and analyze a mathematical model for HTLV-I infection of CD4+ T cells that incorporates both horizontal and vertical transmission.

[MeSH-major] CD4-Positive T-Lymphocytes / virology. Computer Simulation. Human T-lymphotropic virus 1 / growth & development. Models, Biological

[MeSH-minor] Algorithms. Cell Death. Cell Proliferation. Humans

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(PMID = 15691541.001).

[ISSN] 0092-8240

[Journal-full-title] Bulletin of mathematical biology

[ISO-abbreviation] Bull. Math. Biol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

   

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[Title] Expression of CCR4 in adult T-cell leukemia.

Adult T-cell leukemia (ATL) is a malignancy of mature T cells that is etiologically associated with human T-cell leukemia virus type 1 (HTLV-1).

The frequent manifestation of ATL is infiltration of leukemic cells into various organs.

Besides certain cell adhesion molecules and matrix metalloproteineses, chemokine receptors may play important roles in tissue infiltration of ATL.

Identification of a unique set of chemokine receptors expressed by ATL would thus provide valuable information about the molecular mechanism of tissue infiltration of ATL.

This may also reveal that ATL frequently develops from a certain subset of T cells that express a particular set of chemokine receptors.

Since HTLV-1 encodes a potent viral transcriptional activator Tax, which is known to induce various cellular genes, expression of some chemokine receptors may be affected by Tax.

This, however, may relate more to HTLV-1-infected T cells, since ATL cells usually do not express Tax.

Finally, identification of a unique set of chemokine receptors expressed by ATL may also provide a new therapeutic target.

These considerations prompted us to examine the chemokine receptor expression in ATL.

We found that in the majority of ATL cases, leukemic cells consistently express CCR4.

Since CCR4 is known to be involved in T cell migration into skin, this may in part explain the frequent skin infiltration in ATL.

Thus, the majority of ATL may predominantly originate from either Th2 or regulatory T cells.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Receptors, Chemokine / analysis

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(PMID = 15621800.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / CCR4 protein, human; 0 / Receptors, CCR4; 0 / Receptors, Chemokine

[Number-of-references] 44

   

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[Title] Short intensive sequential therapy followed by autologous stem cell transplantation in adult Burkitt, Burkitt-like and lymphoblastic lymphoma.

The feasibility and efficacy of up-front high-dose sequential chemotherapy followed by autologous stem cell transplantation (ASCT) in previously untreated adults (median age 33 years; range 15-64) with Burkitt lymphoma (BL), Burkitt-like lymphoma (BLL) or lymphoblastic lymphoma (LyLy), both without central nervous system or extensive bone marrow involvement was investigated in a multicenter phase II study.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Burkitt Lymphoma / drug therapy. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

[MeSH-minor] Adolescent. Adult. Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / adverse effects. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / adverse effects. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Follow-Up Studies. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Prednisone / administration & dosage. Prednisone / adverse effects. Transplantation, Autologous

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(PMID = 15800666.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; VB0R961HZT / Prednisone

   

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[Title] Tax-inducible production of CC chemokine ligand 22 by human T cell leukemia virus type 1 (HTLV-1)-infected T cells promotes preferential transmission of HTLV-1 to CCR4-expressing CD4+ T cells.

Adult T cell leukemia is a mature CD4+ T cell malignancy which predominantly expresses CCR4 and is etiologically associated with human T cell leukemia virus type 1 (HTLV-1).

Because HTLV-1 transmission depends on close cell-cell contacts, HTLV-1-infected T cells may preferentially interact with CCR4+CD4+ T cells for efficient viral transmission.

In terms of gene expression and protein secretion, we found a strong correlation between HTLV-1 Tax oncoprotein and CCL22, a CCR4 ligand, in HTLV-1-infected T cells.

Transient Tax expression in an HTLV-1-negative T cell line activated the CCL22 promoter and induced CCL22.

In chemotaxis assays, the culture supernatants of HTLV-1-infected T cells selectively attracted CCR4+CD4+ T cells in PBMCs.

Finally, anti-CCL22 Ab treatment also blocked HTLV-1 transmission to primary CD4+ T cells in coculture experiments with HTLV-1 producer cells.

Thus, HTLV-1-infected T cells produce CCL22 through Tax and selectively interact with CCR4+CD4+ T cells, resulting in preferential transmission of HTLV-1 to CCR4+CD4+ T cells.

[MeSH-major] CD4-Positive T-Lymphocytes / virology. Chemokine CCL22 / genetics. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / physiology. Virus Internalization

[MeSH-minor] Cell Adhesion / drug effects. Cell Adhesion / genetics. Cell Line. Humans. Pertussis Toxin / pharmacology. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Receptors, CCR4 / antagonists & inhibitors. Receptors, CCR4 / metabolism. T-Lymphocytes / immunology. T-Lymphocytes / virology

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[ErratumIn] J Immunol. 2008 Jun 15;180(12):8470

(PMID = 18178833.001).

[ISSN] 0022-1767

[Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)

[ISO-abbreviation] J. Immunol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / CCL22 protein, human; 0 / CCR4 protein, human; 0 / Chemokine CCL22; 0 / Gene Products, tax; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, CCR4; EC 2.4.2.31 / Pertussis Toxin

   

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[Title] The human T-cell leukemia virus type 1 p13II protein: effects on mitochondrial function and cell growth.

p13(II) of human T-cell leukemia virus type 1 (HTLV-1) is an 87-amino-acid protein that is targeted to the inner mitochondrial membrane. p13(II) alters mitochondrial membrane permeability, producing a rapid, membrane potential-dependent influx of K(+).

At the cellular level, p13(II) has been found to interfere with cell proliferation and transformation and to promote apoptosis induced by ceramide and Fas ligand.

Assays carried out in T cells (the major targets of HTLV-1 infection in vivo) demonstrate that p13(II)-mediated sensitization to Fas ligand-induced apoptosis can be blocked by an inhibitor of Ras farnesylation, thus implicating Ras signaling as a downstream target of p13(II) function.

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(PMID = 15761473.001).

[ISSN] 1350-9047

[Journal-full-title] Cell death and differentiation

[ISO-abbreviation] Cell Death Differ.

[Language] ENG

[Grant] United States / PHS HHS / / 100730; United States / FIC NIH HHS / TW / TW005705-03; United States / FIC NIH HHS / TW / TW 05705; United States / FIC NIH HHS / TW / R03 TW005705; United States / FIC NIH HHS / TW / R03 TW005705-01A1; United States / FIC NIH HHS / TW / TW005705-01A1; United States / FIC NIH HHS / TW / TW005705-02; United States / FIC NIH HHS / TW / R03 TW005705-03; United States / FIC NIH HHS / TW / R03 TW005705-02

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review

[Publication-country] England

[Chemical-registry-number] 0 / Retroviridae Proteins; 0 / rof protein, Human T-lymphotropic virus 1; 0 / tof protein, Human T-lymphotropic virus 1; SY7Q814VUP / Calcium

[Number-of-references] 84

[Other-IDs] NLM/ NIHMS183534; NLM/ PMC3057663

   

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[Title] [Experimental and selected clinical aspects of active immunotherapy in leukemia].

The aim of the review is to summarize current knowledge concerning active immunotherapy in leukemia.

The molecular mechanisms and selected clinical implications of different cancer vaccines used in pediatric and adult leukemias are discussed.

Cells of acute lymphoblastic leukemia and chronic lymphocytic leukemia can be induced into antigen-presenting cells with the CD40 ligation system.

In many studies it was confimed that these cells stimulate auto- and/or allogeneic T-cell response.

Similar effects using different cytokines such as GM-CSF, TNF-alpha, and IL-4 can be observed in acute myeloid leukemia and myelodysplastic syndromes.

Clinical experience with such vaccines is limited, but the results of some preliminary reports are quite promising.

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(PMID = 16885908.001).

[ISSN] 1732-2693

[Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)

[ISO-abbreviation] Postepy Hig Med Dosw (Online)

[Language] POL

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Poland

[Chemical-registry-number] 0 / Cancer Vaccines

[Number-of-references] 51

   

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[Title] [Clinical and laboratory characteristics of two acute lymphoblastic leukemia patients with dicentric (9; 20) (p11 - 13; q11)].

OBJECTIVE: To explore the morphologic, immunophenotypic, cytogenetic and clinical features of acute lymphoblastic leukemia (ALL) patients with dicentric (9;.

RESULTS: The two ALL patients were positive for CD10 and HLA-DR, showing of B cell origin.

q11) is a rare recurring chromosome abnormality associated with ALL.

Because of the subtle nature of the translocation, FISH is essential for the detection of this abnormality.

[MeSH-major] Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

[MeSH-minor] Adult. Base Sequence. Chromosome Banding. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Molecular Sequence Data. Sequence Analysis, DNA

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(PMID = 16875578.001).

[ISSN] 0253-2727

[Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] China

   

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[Title] Phase II study of immunomodulation with granulocyte-macrophage colony-stimulating factor, interleukin-2, and rituximab following autologous stem cell transplant in patients with relapsed or refractory lymphomas.

High-dose chemotherapy followed by autologous stem cell transplant (ASCT) leads to durable remissions in approximately half of patients with chemosensitive relapsed or refractory aggressive lymphomas; however, many will relapse despite ASCT secondary to persistent minimal residual disease (MRD) or malignant graft contamination.

Forty-six patients with relapsed non-Hodgkin lymphoma (NHL) or Hodgkin lymphoma (HL) were enrolled.

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(PMID = 20496994.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / K24 CA116471; United States / NCI NIH HHS / CA / K23CA133196; United States / NCI NIH HHS / CA / K24CA116471

[Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Interleukin-2; 4F4X42SYQ6 / Rituximab; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor

   

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[Title] Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report.

Human T cell lymphotrophic virus type-1 infection is endemic in the Afro-Caribbean community in Britain, with carriage rates of about 3%.

Although there is a long latency, carriers have a 1-5% chance of developing adult T cell leukaemia/lymphoma, a condition frequently complicated by marked and refractory hypercalcaemia, and with a poor prognosis.

We present the case of an elderly Jamaican woman with severe hypercalcaemia and a raised PTHrP who was found to have lymphoma and was positive for HTLV-1.

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(PMID = 17651486.001).

[ISSN] 1752-1947

[Journal-full-title] Journal of medical case reports

[ISO-abbreviation] J Med Case Rep

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC1950877

   

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Here, we genetically "switched off' the envelope-mediated immunosuppression of an infectious retrovirus, the Friend murine leukemia virus, while preserving mutant envelope infectivity both ex vivo and in vivo, thus allowing us to test the functional importance of envelope-mediated immunosuppression in retrovirus physiology.

Remarkably, we show, in vivo, that the non-IS mutant virus displays the same propagation kinetics as its WT counterpart in irradiated immunocompromised mice but that it is rapidly and totally cleared from normal immunocompetent mice, which become fully protected against a challenge with the WT retrovirus.

Using cell depletion strategies, we further establish that envelope-mediated immunosuppression enables the retrovirus to escape innate (natural killer cells) and adaptive (CD8 T cells) antiviral effectors.

In conclusion, our work demonstrates the critical role of Env-induced immunosuppression for retrovirus propagation in vivo and identifies a unique definite target for antiretroviral therapies and vaccine strategies, also characterized in the human T-cell leukemia virus (HTLV) and xenotropic murine leukemia virus-related virus (XMRV) retroviruses, opening unprecedented prospects for the treatment of retroviral diseases.

[MeSH-major] Friend murine leukemia virus / immunology. Immune Tolerance. Leukemia, Experimental / immunology. Retroviridae Infections / immunology. Tumor Virus Infections / immunology. Viral Envelope Proteins / immunology. Virulence Factors / immunology

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(PMID = 20142478.001).

[ISSN] 1091-6490

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Viral Envelope Proteins; 0 / Viral Vaccines; 0 / Virulence Factors

[Other-IDs] NLM/ PMC2840525

   

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[Title] [Analysis of clinical feature and treatment outcome in 42 patients with lymphoblastic lymphoma].

OBJECTIVE: To investigate the clinical features and treatment outcomes of different regimens in Chinese patients with lymphoblastic lymphoma (LBL).

The RR and CR rates in patients treated with regimens for ALL (ALL-like group) and those treated with regimens for NHL (NHL-like group) were 94.4%, 68.4% and 83.3%, 52.6%, respectively. (3) The estimated median overall survival (OS) and progression free survival (PFS) of hematopoietic stem cell transplantation (HSCT) group were significant longer than those of ALL-like group (P=0.018, P=0.025) and NHL-like group (P=0.016, P=0.011).

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

[MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Male. Middle Aged. Retrospective Studies. Treatment Outcome. Young Adult

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(PMID = 21678570.001).

[ISSN] 0253-2727

[Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

   

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[Title] Human T-cell leukemia/lymphoma virus type 1 nonstructural genes and their functions.

The human T-cell leukemia/lymphoma virus (HTLV) genome, in addition to the structural Gag and Env proteins and retroviral enzymes, carries a region at its 3' end originally designated pX.

To date, we know that this region encodes two essential transcriptional and post-transcriptional positive regulators of viral expression, the Tax and Rex proteins, respectively (reviewed elsewhere in this issue).

[MeSH-major] Human T-lymphotropic virus 1 / genetics. Viral Nonstructural Proteins / genetics

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(PMID = 16155609.001).

[ISSN] 0950-9232

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

[Grant] United States / NIAID NIH HHS / AI / R01 AI058944; United States / NCI NIH HHS / CA / R01 CA106258

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review

[Publication-country] England

[Chemical-registry-number] 0 / Viral Nonstructural Proteins

[Number-of-references] 54

   

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[Title] Hypergammaglobulinemia and corneal opacities in patients with human T-cell lymphotrophic virus type-1.

PURPOSE: To investigate the relationship between serum immunoglobulin levels and corneal opacities in a cohort of patients with human T-cell lymphotrophic virus type-1 (HTLV-1).

METHODS: Complete ophthalmologic examination was performed on 44 patients with HTLV-1 infection (25 patients with adult T-cell leukemia/lymphoma [ATL], 18 patients with HTLV-1 that was associated myelopathy/tropical spastic paraparesis [HAM/TSP], and one patient who was asymptomatic).

RESULTS: Corneal opacities were identified in 15 of 25 patients (60%) with ATL and five of 18 patients (28%) with HAM/TSP.

The prevalence of corneal opacities was associated statistically with elevated IgG level (P = .023) in patients with ATL, but not in patients with HAM/TSP (P > .99).

CONCLUSION: Although the mechanism remains unclear, hypergammaglobulinemia is associated with the development of the corneal opacities in patients of African descent with ATL.

[MeSH-major] Corneal Opacity / etiology. HTLV-I Infections / complications. Hypergammaglobulinemia / etiology

[MeSH-minor] Human T-lymphotropic virus 1 / isolation & purification. Humans. Immunoglobulin A / blood. Immunoglobulin G / blood. Immunoglobulin M / blood. Nephelometry and Turbidimetry. Prevalence. Retrospective Studies

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(PMID = 17157606.001).

[ISSN] 0002-9394

[Journal-full-title] American journal of ophthalmology

[ISO-abbreviation] Am. J. Ophthalmol.

[Language] eng

[Grant] United States / Intramural NIH HHS / /

[Publication-type] Journal Article; Research Support, N.I.H., Intramural

[Publication-country] United States

[Chemical-registry-number] 0 / Immunoglobulin A; 0 / Immunoglobulin G; 0 / Immunoglobulin M

   

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[Title] Adult T-cell leukemia-lymphoma associated with follicular mucinosis.

Follicular mucinosis (alopecia mucinosa) is often associated with malignancies including mycosis fungoides and Sézary syndrome, but not adult T-cell leukemia-lymphoma (ATLL).

The patient showed 11% of flower-shaped atypical lymphocytes in blood examination and positive human T-cell leukemia virus type 1 antibody in serology, consistent with the chronic type of ATLL.

This case seems to be a very rare association of follicular mucinosis and chronic ATLL, suggesting that malignant T cells may have a feature of folliculotropism as well as epidermotropism.

[MeSH-major] Leukemia-Lymphoma, Adult T-Cell / complications. Mucinosis, Follicular / complications

[MeSH-minor] DNA, Viral / genetics. DNA, Viral / isolation & purification. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / isolation & purification. Humans. Male. Middle Aged

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(PMID = 19958447.001).

[ISSN] 1346-8138

[Journal-full-title] The Journal of dermatology

[ISO-abbreviation] J. Dermatol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / DNA, Viral

   

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[Title] HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia.

BACKGROUND: Since the initial description of human T cell lymphotropic virus (HTLV-1), clusters of this infection have been detected globally.

Unlike HIV infection, most patients infected with HTLV-1 remain asymptomatic throughout their lifetime.

CASE REPORT: We report the case of a 39-year-old Afro-Caribbean man with HTLV-1 infection presenting as hypercalcemia and granulomatous pneumocystis jiroveci pneumonia.

HTLV-1-associated adult T cell leukemia lymphoma (ATLL) was diagnosed in this patient by bone marrow and lymph node biopsy.

This is believed to be the first description of this type of reaction to pneumocystis jiroveci in a HTLV-1-infected ATLL patient.

[MeSH-major] HTLV-I Infections / diagnosis. Hypercalcemia / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Pneumocystis jirovecii. Pneumonia, Pneumocystis / diagnosis

[MeSH-minor] Aged. Diagnosis, Differential. Female. Humans

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(PMID = 17356979.001).

[ISSN] 1525-1497

[Journal-full-title] Journal of general internal medicine

[ISO-abbreviation] J Gen Intern Med

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Other-IDs] NLM/ PMC1824742

   

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[Title] Defucosylated humanized anti-CCR4 monoclonal antibody KW-0761 as a novel immunotherapeutic agent for adult T-cell leukemia/lymphoma.

PURPOSE: Adult T-cell leukemia/lymphoma (ATLL) has a very poor prognosis.

The first aim of the present study was to evaluate whether the antitumor activity of KW-0761 would likely be sufficient for therapeutic clinical application against ATLL.

EXPERIMENTAL DESIGN: The antitumor activity of KW-0761 against ATLL cell lines was evaluated in vitro using human cells and in mice in vivo.

Primary ATLL cells from 23 patients were evaluated for susceptibility to autologous ADCC with KW-0761 by two independent methods.

RESULTS: KW-0761 showed potent antitumor activity against ATLL cell lines both in vitro and in the ATLL mouse model in vivo.

In addition, KW-0761 showed potent antitumor activity mediated by highly enhanced ADCC against primary ATLL cells both in vitro and ex vivo in an autologous setting.

The degree of KW-0761 ADCC against primary ATLL cells in an autologous setting was mainly determined by the amount of effector natural killer cells present, but not the amount of the target molecule CCR4 on the ATLL cell surface.

CONCLUSION: KW-0761 should be sufficiently active for therapeutic clinical application for ATLL.

In addition, combination treatment strategies that augment natural killer cell activity should be promising for amplifying the effect of KW-0761.

In the near future, the actual efficacy of KW-0761 will be established in pivotal clinical trials.

[MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Immunotherapy / methods. Leukemia-Lymphoma, Adult T-Cell / drug therapy

[MeSH-minor] Adult. Animals. Antibodies, Monoclonal, Humanized. Antibody-Dependent Cell Cytotoxicity / drug effects. Antibody-Dependent Cell Cytotoxicity / immunology. Biosensing Techniques. Cell Separation. Flow Cytometry. Humans. Male. Mice. Mice, SCID. Receptors, CCR4 / immunology

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(PMID = 20160057.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / CCR4 protein, human; 0 / Receptors, CCR4; 0 / mogamulizumab

   

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[Title] [Clinical and molecular biologic characteristics of 36 cases of leukemia with 11q23/mll].

This study was aimed to analyze the clinical and cytogenetic characteristics of acute leukemia with 11q23/mll rearrangement and explore the reasonable therapeutic principles.

Characteristics in general situation, morphology, immunology, molecular biology, cytogenetics, treatment and overall survival of 36 cases of acute leukemias with mll gene rearrangement were studied and analyzed.

The results showed that 36 cases with mll gene rearrangement were found positive (7.2%) in 494 patients with acute leukemia.

Among the 36 cases of mll rearrangement positive, 32 cases were diagnosed as acute myeloid leukemia (AML) with myeloid antigen expression, of which 5 cases expressed lymphoblastic differentiation antigen; 4 cases were classified as B-lineage acute lymphoblastic leukemia (ALL), of which non-lineage myeloid expression pattern were found in 3 cases.

Of the responded patients, 10 cases relapsed within 6 months, with a recurrence rate of 40%; 9 cases received hematopoietic stem cell transplantation (HSCT), 7 cases of which survived after transplantation.

It is concluded that acute leukemia patients with mll gene rearrangement show poor response to chemotherapy, high recurrence rate and poor prognosis.

Hematopoietic stem cell transplantation may be a reasonable treatment principle to improve these patients' survival situation.

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(PMID = 21176334.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase