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1
adul t cell leukem lymphoma 2005:2010[pubdate] *count=100
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Items 1 to 100 of about 802
1.
Kim YM, RamÃrez JA, Mick JE, Giebler HA, Yan JP, Nyborg JK:
Molecular characterization of the Tax-containing HTLV-1 enhancer complex reveals a prominent role for CREB phosphorylation in Tax transactivation.
J Biol Chem
; 2007 Jun 29;282(26):18750-7
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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
2.
Pais-Correia AM, Sachse M, Guadagnini S, Robbiati V, Lasserre R, Gessain A, Gout O, Alcover A, Thoulouze MI:
Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses.
Nat Med
; 2010 Jan;16(1):83-9
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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
The Lens.
Cited by Patents in
.
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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
3.
Yu Q, Minoda Y, Yoshida R, Yoshida H, Iha H, Kobayashi T, Yoshimura A, Takaesu G:
HTLV-1 Tax-mediated TAK1 activation involves TAB2 adapter protein.
Biochem Biophys Res Commun
; 2008 Jan 4;365(1):189-94
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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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4.
Ohsugi T, Kumasaka T, Okada S, Ishida T, Yamaguchi K, Horie R, Watanabe T, Umezawa K:
Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines.
Cancer Lett
; 2007 Nov 18;257(2):206-15
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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
5.
Toulza F, Nosaka K, Tanaka Y, Schioppa T, Balkwill F, Taylor GP, Bangham CR:
Human T-lymphotropic virus type 1-induced CC chemokine ligand 22 maintains a high frequency of functional FoxP3+ regulatory T cells.
J Immunol
; 2010 Jul 01;185(1):183-9
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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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OMIM: Data: Gene Annotation
.
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[Cites]
Blood. 2000 Feb 15;95(4):1386-92
[
10666215.001
]
[Cites]
Int J Cancer. 2009 Nov 15;125(10):2375-82
[
19544530.001
]
[Cites]
Blood. 2002 Mar 1;99(5):1505-11
[
11861261.001
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[Cites]
J Infect Dis. 2002 Oct 1;186(7):932-9
[
12232833.001
]
[Cites]
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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
6.
Saito M, Mori A, Irie T, Tanaka M, Morioka M, Uchiyama Y, Taukamoto E:
[Picture in clinical hematology no. 41: PET/ CT findings in case of ATLL ].
Rinsho Ketsueki
; 2009 Dec;50(12):1669-70
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[Title]
[Picture in
clinical
hematology no. 41: PET/ CT findings in case of
ATLL
].
[MeSH-major]
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ radiography.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ radionuclide imaging. Positron-Emission Tomography. Tomography, X-Ray Computed
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(PMID = 20068272.001).
[ISSN]
0485-1439
[Journal-full-title]
[Rinshō ketsueki] The Japanese journal of clinical hematology
[ISO-abbreviation]
Rinsho Ketsueki
[Language]
jpn
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
7.
Shiratori S, Yasumoto A, Tanaka J, Shigematsu A, Yamamoto S, Nishio M, Hashino S, Morita R, Takahata M, Onozawa M, Kahata K, Kondo T, Ota S, Wakasa K, Sugita J, Koike T, Asaka M, Kasai M, Imamura M:
A retrospective analysis of allogeneic hematopoietic stem cell transplantation for adult T cell leukemia/lymphoma (ATL): clinical impact of graft-versus-leukemia/lymphoma effect.
Biol Blood Marrow Transplant
; 2008 Jul;14(7):817-23
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[Title]
A retrospective analysis of allogeneic hematopoietic stem
cell
transplantation for
adult
T cell
leukemia
/
lymphoma
(
ATL
):
clinical
impact of graft-versus-
leukemia
/
lymphoma
effect.
Adult
T cell
leukemia
/
lymphoma
(
ATL
) is a highly aggressive
T cell
malignancy, and has a poor prognosis.
Recently, allogeneic-hematopoietic stem
cell
transplantation (allo-HSCT) has been suggested to improve the outcome.
We retrospectively analyzed 15 patients with
ATL
who had received allo-HSCT in 2 institutions in Hokkaido, Japan.
Calcineurin inhibitor dosage was reduced and administration was discontinued abruptly in 6 of the 15 patients for
disease
control; as a result, 4 (66.7%) of the 6 patients achieved complete response (CR) or partial response.
Therefore, a graft-versus-
leukemia
/
lymphoma
(GVL) effect might be induced by discontinuation of immunosuppression.
Thirteen of the 15 patients were followed up by monitoring
HTLV
-1 proviral DNA levels.
In 10 of the 11 patients with
positive HTLV
-1 proviral DNA before allo-HSCT,
HTLV
-1 proviral DNA became undetectable at least once after allo-HSCT, and only 1 of the 5 patients in whom
HTLV
-1 proviral DNA became detectable after allo-HSCT relapsed.
Compared to the results of past studies, these results show that allo-HSCT greatly improved the prognosis of
ATL
and suggest a contribution of the induction of a GVL effect.
[MeSH-major]
Graft vs
Leukemia
Effect. Hematopoietic Stem
Cell
Transplantation / methods.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ therapy
[MeSH-minor]
Adult
. Aged.
Disease
-Free Survival. Female. Follow-Up Studies.
HTLV
-I Infections / blood.
HTLV
-I Infections / therapy. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Remission Induction. Retrospective Studies. Transplantation, Homologous. Viral Load
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[ErratumIn]
Biol Blood Marrow Transplant. 2008 Sep;14(9):1079
(PMID = 18541202.001).
[ISSN]
1523-6536
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
United States
8.
Uphoff CC, Denkmann SA, Steube KG, Drexler HG:
Detection of EBV, HBV, HCV, HIV-1, HTLV-I and -II, and SMRV in human and other primate cell lines.
J Biomed Biotechnol
; 2010;2010:904767
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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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.
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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
9.
Okudaira T, Hirashima M, Ishikawa C, Makishi S, Tomita M, Matsuda T, Kawakami H, Taira N, Ohshiro K, Masuda M, Takasu N, Mori N:
A modified version of galectin-9 suppresses cell growth and induces apoptosis of human T-cell leukemia virus type I-infected T-cell lines.
Int J Cancer
; 2007 May 15;120(10):2251-61
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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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.
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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
10.
Peloponese JM, Yeung ML, Jeang KT:
Modulation of nuclear factor-kappaB by human T cell leukemia virus type 1 Tax protein: implications for oncogenesis and inflammation.
Immunol Res
; 2006;34(1):1-12
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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
11.
Sargent JT, Smith OP:
Haematological emergencies managing hypercalcaemia in adults and children with haematological disorders.
Br J Haematol
; 2010 May;149(4):465-77
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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
12.
Marzano AV, Vezzoli P, Fanoni D, Venegoni L, Berti E:
Primary cutaneous T-cell lymphoma expressing FOXP3: a case report supporting the existence of malignancies of regulatory T cells.
J Am Acad Dermatol
; 2009 Aug;61(2):348-55
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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
Genetic Alliance.
consumer health - Cutaneous T-Cell Lymphoma
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
Faculty of 1000.
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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
13.
Miyano-Kurosaki N, Kira J, Barnor JS, Maeda N, Misawa N, Kawano Y, Tanaka Y, Yamamoto N, Koyanagi Y:
Autonomous proliferation of HTLV-CD4+ T cell clones derived from human T cell leukemia virus type I (HTLV-I)-associated myelopathy patients.
Microbiol Immunol
; 2007;51(2):235-42
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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
14.
Tanaka Y, Nakasone H, Yamazaki R, Sato K, Sato M, Terasako K, Kimura S, Okuda S, Kako S, Oshima K, Tanihara A, Nishida J, Yoshikawa T, Nakatsura T, Sugiyama H, Kanda Y:
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.
Cancer Res
; 2010 Aug 1;70(15):6181-92
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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
Immune Epitope Database and Analysis Resource.
gene/protein/disease-specific - Related Immune Epitope Information
.
The Lens.
Cited by Patents in
.
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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
15.
Kobayashi H, Ngato T, Sato K, Aoki N, Kimura S, Tanaka Y, Aizawa H, Tateno M, Celis E:
In vitro peptide immunization of target tax protein human T-cell leukemia virus type 1-specific CD4+ helper T lymphocytes.
Clin Cancer Res
; 2006 Jun 15;12(12):3814-22
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[Title]
In vitro peptide immunization of target tax protein
human
T-
cell
leukemia virus
type 1-specific CD4+ helper T lymphocytes.
PURPOSE:
Adult
T-
cell
leukemia
/
lymphoma
induced by
human
T-
cell
leukemia virus
type 1 (
HTLV
-1) is usually a fatal lymphoproliferative malignant
disease
.
HTLV
-1 Tax protein plays a critical role in
HTLV
-1-
associated
leukemogenesis and is an attractive target for vaccine development.
Although
HTLV
-1 Tax is the most dominant antigen for
HTLV
-1-specific CD8(+) CTLs in
HTLV
-1-infected individuals, few epitopes recognized by CD4(+) helper T lymphocytes in
HTLV
-1 Tax protein have been described.
The aim of the present study was to study T-helper-
cell
responses to
HTLV
-1 Tax and to identify naturally processed MHC class II-restricted epitopes that could be used for vaccine development.
EXPERIMENTAL DESIGN: An MHC class II binding peptide algorithm was used to predict potential T-helper
cell
epitope peptides from
HTLV
-1 Tax.
We assessed the ability of the corresponding peptides to elicit helper T-
cell
responses by in vitro vaccination of purified CD4(+) T lymphocytes.
RESULTS: Peptides Tax(191-205) and Tax(305-319) were effective in inducing T-helper-
cell
responses.
Both these epitopes were found to be naturally processed by
HTLV
-1(+) T-
cell lymphoma
cells and by autologous antigen-presenting cells that were pulsed with
HTLV
-1 Tax(+) tumor lysates.
Notably, the two newly identified helper T-
cell
epitopes are found to lie proximal to known CTL epitopes, which will facilitate the development of prophylactic peptide-based vaccine capable of inducing simultaneous CTL and T-helper responses.
CONCLUSION: Our data suggest that
HTLV
-1 Tax protein could serve as tumor-
associated
antigen for CD4(+) helper T cells and that the present epitopes might be used for T-
cell
-based immunotherapy against tumors expressing
HTLV
-1.
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.
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(PMID = 16778109.001).
[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
[Grant]
United States / NCI NIH HHS / CA / R01 CA103921; United States / NCI NIH HHS / CA / R01CA80782; United States / NCI NIH HHS / CA / R01CA103921; United States / NCI NIH HHS / CA / R01 CA080782; United States / NCI NIH HHS / CA / P50CA91956; United States / NCI NIH HHS / CA / P50 CA091956
[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 / Gene Products, tax; 0 / HLA-D Antigens; 0 / Peptides
[Other-IDs]
NLM/ NIHMS14245; NLM/ PMC1986724
16.
Tözsér J, Weber IT:
The protease of human T-cell leukemia virus type-1 is a potential therapeutic target.
Curr Pharm Des
; 2007;13(12):1285-94
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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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.
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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
17.
Aiello A, Fattorusso E, Luciano P, Menna M, Calzado MA, Muñoz E, Bonadies F, Guiso M, Sanasi MF, Cocco G, Nicoletti R:
Synthesis of structurally simplified analogues of aplidinone A, a pro-apoptotic marine thiazinoquinone.
Bioorg Med Chem
; 2010 Jan 15;18(2):719-27
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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
18.
Gómez-Acevedo H, Li MY:
Backward bifurcation in a model for HTLV-I infection of CD4+ T cells.
Bull Math Biol
; 2005 Jan;67(1):101-14
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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
19.
Mahieux R, Gessain A:
Adult T-cell leukemia/lymphoma and HTLV-1.
Curr Hematol Malig Rep
; 2007 Oct;2(4):257-64
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[Title]
Adult
T-
cell
leukemia
/
lymphoma
and
HTLV
-1.
Human
T-
cell
leukemia
/
lymphoma
virus
type 1 (
HTLV
-1) was the first oncogenic
human
retrovirus to be discovered, more than 25 years ago.
HTLV
-1 infects 15 to 20 million individuals worldwide.
HTLV
-1 causes two major diseases:
adult
T-
cell
leukemia
/
lymphoma
(
ATLL
) and tropical spastic paraparesis/
HTLV
-1-
associated
myelopathy (TSP/HAM).
ATLL
can be classified into four major subtypes: a smoldering type, a chronic type, a
lymphoma
type, and a leukemic type.
Because of intrinsic chemoresistance and severe immunosuppression, the survival rate of
ATLL
patients, especially those who develop the
acute
leukemic or
lymphoma
forms, is very poor, and such clonal malignant CD4 expansion remains one of the most severe lymphoproliferations.
[MeSH-major]
Human
T-
lymphotropic virus
1 / pathogenicity.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ virology
[MeSH-minor]
Adult
. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arsenicals / therapeutic use. CD4-
Positive
T-Lymphocytes / virology.
Clinical
Trials as Topic. Drug Resistance, Neoplasm. Endemic Diseases. Female. Gene Products, tax / physiology. Genes, pX. Humans. Immunoglobulin G / therapeutic use. Immunophenotyping. Immunotherapy. Infant, Newborn. Infectious
Disease
Transmission, Vertical. Interferon-alpha / therapeutic use. Male. Oxides / therapeutic use. Paraparesis, Tropical Spastic / epidemiology. Paraparesis, Tropical Spastic / virology. Pregnancy. Pregnancy Complications, Infectious. Zidovudine / therapeutic use
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[ISSN]
1558-822X
[Journal-full-title]
Current hematologic malignancy reports
[ISO-abbreviation]
Curr Hematol Malig Rep
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Gene Products, tax; 0 / Immunoglobulin G; 0 / Interferon-alpha; 0 / Oxides; 0 / tax protein, Human T-lymphotrophic virus 1; 3A189DH42V / alemtuzumab; 4B9XT59T7S / Zidovudine; CUJ2MVI71Y / daclizumab; S7V92P67HO / arsenic trioxide
[Number-of-references]
63
20.
Yoshie O:
Expression of CCR4 in adult T-cell leukemia.
Leuk Lymphoma
; 2005 Feb;46(2):185-90
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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
21.
Hieshima K, Nagakubo D, Nakayama T, Shirakawa AK, Jin Z, Yoshie O:
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.
J Immunol
; 2008 Jan 15;180(2):931-9
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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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.
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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
22.
D'Agostino DM, Silic-Benussi M, Hiraragi H, Lairmore MD, Ciminale V:
The human T-cell leukemia virus type 1 p13II protein: effects on mitochondrial function and cell growth.
Cell Death Differ
; 2005 Aug;12 Suppl 1:905-15
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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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[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
23.
Lyell V, Khatamzas E, Allain T:
Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report.
J Med Case Rep
; 2007;1:56
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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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1752-1947
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Journal of medical case reports
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J Med Case Rep
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC1950877
24.
Schlecht-Louf G, Renard M, Mangeney M, Letzelter C, Richaud A, Ducos B, Bouallaga I, Heidmann T:
Retroviral infection in vivo requires an immune escape virulence factor encrypted in the envelope protein of oncoretroviruses.
Proc Natl Acad Sci U S A
; 2010 Feb 23;107(8):3782-7
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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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]
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]
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]
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[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
25.
Miyamura F, Kako S, Yamagami H, Sato K, Sato M, Terasako K, Kimura S, Nakasone H, Aoki S, Okuda S, Yamazaki R, Oshima K, Yoshinaga K, Higuchi T, Nishida J, Demitsu T, Kakehashi A, Kanda Y:
Successful treatment of young-onset adult T cell leukemia/lymphoma and preceding chronic refractory eczema and corneal injury by allogeneic hematopoietic stem cell transplantation.
Int J Hematol
; 2009 Oct;90(3):397-401
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[Title]
Successful treatment of young-onset
adult
T cell
leukemia
/
lymphoma
and preceding chronic refractory eczema and corneal injury by allogeneic hematopoietic stem
cell
transplantation.
Only some carriers of
human
T cell
lymphotropic virus
type I (
HTLV
-1) develop
adult
T cell
leukemia
/
lymphoma
(
ATLL
) after a long latency period, and an association has been reported between chronic refractory eczema, known as infective dermatitis, and young-onset
ATLL
.
A 25-year-old female developed
ATLL
and underwent allogeneic hematopoietic stem
cell
transplantation (HSCT) in non-remission.
She had chronic refractory eczema and corneal injury at the onset of
ATLL
.
Remission of
ATLL
was achieved, and the
HTLV
-1 proviral load decreased after HSCT.
More than a year has passed since the transplantation was performed, and she has had no recurrence of either
ATLL
or lesions in the skin and eye.
Her
clinical
course suggests a possible association between skin and eye lesions and
HTLV
-1 infection.
Special attention is needed when
HTLV
-1 carriers develop eye or skin lesions.
[MeSH-major]
Corneal Diseases / therapy. Eczema / therapy. Hematopoietic Stem
Cell
Transplantation.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ therapy
[MeSH-minor]
Adult
. Chronic
Disease
. Female.
HTLV
-I Infections / complications.
Human
T-
lymphotropic virus
1. Humans. Transplantation, Homologous. Treatment Outcome. Viral Load
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.
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.
MedlinePlus Health Information.
consumer health - Eczema
.
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[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
26.
Nicot C, Harrod RL, Ciminale V, Franchini G:
Human T-cell leukemia/lymphoma virus type 1 nonstructural genes and their functions.
Oncogene
; 2005 Sep 5;24(39):6026-34
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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
27.
Patronas M, Smith JA, Levy-Clarke GA, Reed GF, Buggage RR:
Hypergammaglobulinemia and corneal opacities in patients with human T-cell lymphotrophic virus type-1.
Am J Ophthalmol
; 2006 Dec;142(6):1088-9
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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
28.
Wada T, Yoshinaga E, Oiso N, Kawara S, Kawada A, Kozuka T:
Adult T-cell leukemia-lymphoma associated with follicular mucinosis.
J Dermatol
; 2009 Dec;36(12):638-42
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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
29.
Shahnaz S, Reich D, Arévalo-Valencia D, Kucinska S, Tulczynska J, Fleischman J:
HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia.
J Gen Intern Med
; 2007 Mar;22(3):420-3
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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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[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
30.
Ohkura S, Yamashita M, Ishida T, Babu PG, Koyanagi Y, Yamamoto N, Miura T, Hayami M:
Phylogenetic heterogeneity of new HTLV type 1 isolates from southern India in subgroup A.
AIDS Res Hum Retroviruses
; 2005 Apr;21(4):325-30
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[Title]
Phylogenetic heterogeneity of new
HTLV
type 1 isolates from southern India in subgroup A.
Seven isolates of
human
T cell
leukemia virus
type 1 (
HTLV
-1) were taken in southern India and phylogenetically analyzed to gain new insights into the origin and dissemination of
HTLV
-1 in the subcontinent.
The new Indian
HTLV
-1s were found to be members of subgroup A (Transcontinental subgroup) of the Cosmopolitan group.
These results demonstrate that Indian
HTLV
-1s are genetically heterogeneous and include the most divergent strain of subgroup A.
On the basis of these results, we speculate that subgroup
A HTLV
- 1s may have been present for thousands of years in India.
[MeSH-major]
HTLV
-I Infections / virology.
Human
T-
lymphotropic virus
1 / genetics. Polymorphism, Genetic
[MeSH-minor]
Adult
. Child. DNA, Viral / chemistry. Female. Humans. India. Male. Middle Aged. Molecular Sequence Data. Phylogeny. Sequence Analysis, DNA. Terminal Repeat Sequences / genetics
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(PMID = 15943577.001).
[ISSN]
0889-2229
[Journal-full-title]
AIDS research and human retroviruses
[ISO-abbreviation]
AIDS Res. Hum. Retroviruses
[Language]
eng
[Databank-accession-numbers]
GENBANK/ AY607576/ AY607577/ AY607578/ AY607579/ AY607580/ AY607581/ AY607582
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Viral
31.
Phillips AA, Shapira I, Willim RD, Sanmugarajah J, Solomon WB, Horwitz SM, Savage DG, Bhagat G, Soff G, Zain JM, Alobeid B, Seshan VE, O'Connor OA:
A critical analysis of prognostic factors in North American patients with human T-cell lymphotropic virus type-1-associated adult T-cell leukemia/lymphoma: a multicenter clinicopathologic experience and new prognostic score.
Cancer
; 2010 Jul 15;116(14):3438-46
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[Title]
A critical analysis of prognostic factors in North American patients with
human
T-
cell
lymphotropic virus
type-1-
associated adult
T-
cell
leukemia
/
lymphoma
: a multicenter clinicopathologic experience and new prognostic score.
BACKGROUND: To define the clinicopathologic and prognostic features of patients with
human
T-
cell
lymphotropic virus
type-1 (
HTLV
-1)-
associated adult
T-
cell
leukemia
/
lymphoma
(
ATLL
) in North America, standard criteria were used to identify patients with
ATLL
.
The
acute
subtype predominated (68.5%).
Although the International Prognostic Index and Prognostic Index for peripheral T-
cell lymphoma
unspecified identified subsets of patients, these models were not completely predictive.
A recursive partitioning analysis was performed on the data, which successfully identified 3 prognostic categories based on Eastern Cooperative Oncology Group performance status, stage, age, and calcium level at
diagnosis
.
CONCLUSIONS: This series proposed a new prognostic model for patients with
HTLV
-1-
associated ATLL
and confirmed a poor outcome for these patients in North America.
[MeSH-major]
Human
T-
lymphotropic virus
1.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Male. Middle Aged. Prognosis. United States
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
COS Scholar Universe.
author profiles
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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[Copyright]
Copyright (c) 2010 American Cancer Society.
(PMID = 20564100.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
United States
32.
Hidaka T, Nakahata S, Hatakeyama K, Hamasaki M, Yamashita K, Kohno T, Arai Y, Taki T, Nishida K, Okayama A, Asada Y, Yamaguchi R, Tsubouchi H, Yokota J, Taniwaki M, Higashi Y, Morishita K:
Down-regulation of TCF8 is involved in the leukemogenesis of adult T-cell leukemia/lymphoma.
Blood
; 2008 Jul 15;112(2):383-93
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[Title]
Down-regulation of TCF8 is involved in the leukemogenesis of
adult
T-
cell
leukemia
/
lymphoma
.
Adult
T-
cell
leukemia
/
lymphoma
(
ATLL
) is caused by latent
human
T-
lymphotropic virus
-1 (
HTLV
-1) infection.
To clarify the molecular mechanism underlying leukemogenesis after viral infection, we precisely mapped 605 chromosomal breakpoints in 61
ATLL
cases by spectral karyotyping and identified frequent chromosomal breakpoints in 10p11, 14q11, and 14q32.
Single nucleotide polymorphism (SNP) array-comparative genomic hybridization (CGH), genetic, and expression analyses of the genes mapped within a common breakpoint cluster region in 10p11.2 revealed that in
ATLL
cells, transcription factor 8 (TCF8) was frequently disrupted by several mechanisms, including mainly epigenetic dysregulation.
TCF8 mutant mice frequently developed invasive CD4(+) T-
cell
lymphomas
in the
thymus
or in ascitic fluid in vivo.
Down-regulation of TCF8 expression in
ATLL
cells in vitro was
associated
with resistance to transforming growth factor beta1 (TGF-beta1), a well-known characteristic of
ATLL
cells, suggesting that escape from TGF-beta1-mediated growth inhibition is important in the pathogenesis of
ATLL
.
These findings indicate that TCF8 has a tumor suppressor role in
ATLL
.
[MeSH-major]
Homeodomain Proteins / physiology.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ etiology. Transcription Factors / physiology. Transforming Growth Factor beta1 / physiology
[MeSH-minor]
Animals. Chromosome Breakage. Chromosomes,
Human
, Pair 10. Chromosomes,
Human
, Pair 14. Down-Regulation / genetics. Humans. Karyotyping. Mice. Tumor Cells, Cultured
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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(PMID = 18467597.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / Transcription Factors; 0 / Transforming Growth Factor beta1; 0 / ZEB1 protein, human
33.
Javier RT:
Cell polarity proteins: common targets for tumorigenic human viruses.
Oncogene
; 2008 Nov 24;27(55):7031-46
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[Title]
Cell
polarity proteins: common targets for tumorigenic
human viruses
.
Loss of polarity and disruption of
cell
junctions are common features of epithelial-
derived
cancer cells, and mounting evidence indicates that such defects have a direct function in the pathology of cancer.
Supporting this idea, results with several different
human
tumor
viruses
indicate that their oncogenic potential depends in part on a common ability to inactivate key
cell
polarity proteins.
For example, adenovirus (Ad) type 9 is unique among
human
Ads by causing exclusively estrogen-dependent mammary tumors in experimental animals and in having E4 region-encoded open reading frame 1 (E4-ORF1) as its primary oncogenic determinant.
Most notably, the E4-ORF1 PBM mediates interactions with a selected group of cellular PDZ proteins, three of which include the
cell
polarity proteins Dlg1, PATJ and ZO-2.
Data further indicate that these interactions promote disruption of
cell
junctions and a loss of
cell
polarity.
In addition, one or more of the E4-ORF1-interacting
cell
polarity proteins, as well as the
cell
polarity protein Scribble, are common targets for the high-risk
human
papillomavirus (HPV) E6 or
human
T-
cell
leukemia virus
type 1 (
HTLV
-1) Tax oncoproteins.
Underscoring the significance of these observations, in humans, high-risk HPV and
HTLV
-1 are causative agents for cervical cancer and
adult
T-
cell
leukemia
, respectively.
Consequently,
human
tumor
viruses
should serve as powerful tools for deciphering mechanisms whereby disruption of
cell
junctions and loss of
cell
polarity contribute to the development of many
human
cancers.
This review article discusses evidence supporting this hypothesis, with an emphasis on the
human
Ad E4-ORF1 oncoprotein.
[MeSH-major]
Cell
Polarity. Membrane Proteins / physiology. Neoplasms / etiology.
Virus
Attachment.
Virus
Diseases / complications
[MeSH-minor]
Adenovirus Infections,
Human
/ virology. Adenoviruses,
Human
/ physiology. Animals.
Cell
Transformation, Viral / physiology. Gene Products, tax / physiology.
Human
T-
lymphotropic virus
1 / metabolism.
Human
T-
lymphotropic virus
1 / physiology.
Human
papillomavirus 6 / metabolism.
Human
papillomavirus 6 / physiology. Humans. Models, Biological. Oncogene Proteins, Viral / metabolism. Oncogene Proteins, Viral / physiology. Protein Binding
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[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA058541
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / E4 protein, Adenovirus 9; 0 / Gene Products, tax; 0 / Membrane Proteins; 0 / Oncogene Proteins, Viral; 0 / tax protein, Human T-lymphotrophic virus 1
[Number-of-references]
233
[Other-IDs]
NLM/ NIHMS411909; NLM/ PMC3501650
34.
Masuda M, Maruyama T, Ohta T, Ito A, Hayashi T, Tsukasaki K, Kamihira S, Yamaoka S, Hoshino H, Yoshida T, Watanabe T, Stanbridge EJ, Murakami Y:
CADM1 interacts with Tiam1 and promotes invasive phenotype of human T-cell leukemia virus type I-transformed cells and adult T-cell leukemia cells.
J Biol Chem
; 2010 May 14;285(20):15511-22
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[Title]
CADM1 interacts with Tiam1 and promotes invasive phenotype of
human
T-
cell
leukemia virus
type I-transformed cells and
adult
T-
cell
leukemia
cells.
CADM1 encodes a multifunctional immunoglobulin-like
cell
adhesion molecule whose cytoplasmic domain contains a type II PSD95/Dlg/ZO-1 (PDZ)-binding motif (BM) for associating with other intracellular proteins.
Although CADM1 lacks expression in T lymphocytes of healthy individuals, it is overexpressed in
adult
T-
cell
leukemia
-
lymphoma
(
ATL
) cells.
It has been suggested that the expression of CADM1 protein promotes infiltration of leukemic cells into various organs and tissues, which is one of the frequent
clinical
manifestations of
ATL
.
Amino acid sequence alignment revealed that Tiam1 (T-
lymphoma
invasion and metastasis 1), a Rac-specific guanine nucleotide exchange factor, has a type II PDZ domain similar to those of membrane-
associated
guanylate kinase homologs (MAGUKs) that are known to bind to the PDZ-BM of CADM1.
In this study, we demonstrated that the cytoplasmic domain of CADM1 directly interacted with the PDZ domain of Tiam1 and induced formation of lamellipodia through Rac activation in
HTLV
-I-transformed
cell
lines as well as
ATL
cell
lines.
Our results indicate that Tiam1 integrates signals from CADM1 to regulate the actin cytoskeleton through Rac activation, which may lead to tissue infiltration of leukemic cells in
ATL
patients.
[MeSH-major]
Guanine Nucleotide Exchange Factors / metabolism.
Human
T-
lymphotropic virus
1 / pathogenicity. Immunoglobulins / metabolism.
Leukemia
, T-
Cell
/ pathology. Membrane Proteins / metabolism. Neoplasm Invasiveness. Tumor Suppressor Proteins / metabolism
[MeSH-minor]
Amino Acid Sequence. Base Sequence.
Cell
Adhesion Molecules.
Cell
Line, Tumor. Humans. Immunohistochemistry. Microscopy, Confocal. Molecular Sequence Data. Protein Binding. RNA Interference. RNA, Small Interfering. Sequence Homology, Amino Acid
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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[ISSN]
1083-351X
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Guanine Nucleotide Exchange Factors; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / RNA, Small Interfering; 0 / TIAM1 protein, human; 0 / Tumor Suppressor Proteins
[Other-IDs]
NLM/ PMC2865322
35.
Sugita S, Takase H, Yoshida T, Sugamoto Y, Watanabe T, Mochizuki M:
Intraocular soluble IL-2 receptor alpha in a patient with adult T cell leukaemia with intraocular invasion.
Br J Ophthalmol
; 2006 Sep;90(9):1204-6
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[Source]
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[Title]
Intraocular soluble IL-2 receptor alpha in a patient with
adult
T cell
leukaemia
with intraocular invasion.
[MeSH-major]
Biomarkers, Tumor / analysis. Eye / pathology.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ pathology. Leukemic Infiltration / immunology. Receptors, Interleukin-2 / analysis
MedlinePlus Health Information.
consumer health - Eye Care
.
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[ISSN]
0007-1161
[Journal-full-title]
The British journal of ophthalmology
[ISO-abbreviation]
Br J Ophthalmol
[Language]
eng
[Publication-type]
Case Reports; Letter; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / IL2RA protein, human; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Receptors, Interleukin-2
[Other-IDs]
NLM/ PMC1857395
36.
Zhang J, Yamada O, Matsushita Y, Chagan-Yasutan H, Hattori T:
Transactivation of human osteopontin promoter by human T-cell leukemia virus type 1-encoded Tax protein.
Leuk Res
; 2010 Jun;34(6):763-8
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[Title]
Transactivation of
human
osteopontin promoter by
human
T-
cell
leukemia virus
type 1-encoded Tax protein.
We report here that OPN gene is transactivated by Tax protein of
human
T-
cell
leukemia virus
type 1 (
HTLV
-1).
This study suggests that OPN is one of the downstream mediators of aberrantly activated PI3K/AKT signaling by Tax, which may partially contribute to
HTLV
-1-
associated
leukemogenesis.
[MeSH-minor]
Base Sequence. Binding Sites. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology.
Cell
Line, Tumor.
Cell
Transformation, Viral / genetics. Gene Expression Regulation, Neoplastic.
Human
T-
lymphotropic virus
1 / genetics.
Human
T-
lymphotropic virus
1 / physiology. Humans. Liver Neoplasms / genetics. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Phosphatidylinositol 3-Kinases / metabolism. Phosphatidylinositol 3-Kinases / physiology. Promoter Regions, Genetic / physiology. Proto-Oncogene Proteins c-akt / metabolism. Proto-Oncogene Proteins c-akt / physiology. Signal Transduction / genetics. Transcription Factor AP-1 / metabolism
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[Copyright]
Copyright 2009 Elsevier Ltd. All rights reserved.
(PMID = 19767100.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Gene Products, tax; 0 / Transcription Factor AP-1; 0 / tax protein, Human T-lymphotrophic virus 1; 106441-73-0 / Osteopontin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
37.
Peloponese JM Jr, Yeung ML, Jeang KT:
Modulation of nuclear factor-ϰB by human T cell leukemia virus type 1 tax protein : Implications for oncogenesis and inflammation.
Immunol Res
; 2006 Jan;34(1):1-12
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[Title]
Modulation of nuclear factor-ϰB 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.
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[ISSN]
0257-277X
[Journal-full-title]
Immunologic research
[ISO-abbreviation]
Immunol. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Keywords]
NOTNLM ; Adult T cell leukemia (ATL) / HTLV-1 Tax / Human T cell leukemia virus (HTLV-1) / IKK / Inflammation / NF-ϰB / NIK
38.
Fahim S, Prokopetz R, Jackson R, Faught C, McCarthy AE, Andonov A, Coulthart M, Daw Z, Olberg B, Giulivi A, Padmore R:
Human T-cell lymphotropic virus type 1-associated adult T-cell leukemia/lymphoma in the Inuit people of Nunavut.
CMAJ
; 2006 Sep 12;175(6):579
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[Title]
Human
T-
cell
lymphotropic virus
type 1-
associated adult
T-
cell
leukemia
/
lymphoma
in the Inuit people of Nunavut.
[MeSH-major]
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ ethnology
[MeSH-minor]
Adult
. Aged. Fatal Outcome. Female. Humans. Indians, North American. Lymphocytosis / blood. Medical History Taking. Middle Aged. Physical Examination. Practice Guidelines as Topic
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[Cites]
Tissue Antigens. 1998 Nov;52(5):444-51
[
9864034.001
]
[Cites]
CMAJ. 2006 Jan 17;174(2):150-1
[
16415454.001
]
[Cites]
Am J Hematol. 2005 Mar;78(3):232-9
[
15726602.001
]
(PMID = 16966657.001).
[ISSN]
1488-2329
[Journal-full-title]
CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne
[ISO-abbreviation]
CMAJ
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Canada
[Other-IDs]
NLM/ PMC1559419
39.
Mesnard JM, Barbeau B, Devaux C:
HBZ, a new important player in the mystery of adult T-cell leukemia.
Blood
; 2006 Dec 15;108(13):3979-82
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[Title]
HBZ, a new important player in the mystery of
adult
T-
cell
leukemia
.
Adult
T-
cell
leukemia
(
ATL
) was first described in 1977.
A link between
ATL
and
human
T-
cell
leukemia virus
type 1 (
HTLV
-1) was clearly established in the early 1980s.
Over the years, many aspects of
HTLV
-1-induced cellular dysfunctions have been clarified.
However, the detailed mechanism behind
ATL
occurrence remains unsolved.
Presently, we are still unable to explain the absence of viral Tax protein (thought to play a central role in T-
cell
transformation) in more than 50% of
ATL
cells.
A novel
HTLV
-1 HBZ protein, encoded on the negative strand, was characterized by our group and is currently the subject of intensive research efforts to determine its function in viral replication and/or pathophysiology.
Recently, 4 studies reported on the existence of different HBZ isoforms and have investigated on their function in both
ATL
cells or animal models.
[MeSH-major]
Basic-Leucine Zipper Transcription Factors / genetics.
Cell
Transformation, Viral / genetics.
Human
T-
lymphotropic virus
1 / genetics.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ genetics. Viral Proteins / genetics.
Virus
Replication / genetics
[MeSH-minor]
Animals.
Cell
Proliferation.
Disease
Models, Animal. Gene Products, tax / deficiency. Gene Products, tax / immunology. Humans. Protein Isoforms / genetics. Protein Isoforms / immunology. RNA, Messenger / genetics. RNA, Messenger / immunology. RNA, Viral / genetics. RNA, Viral / immunology. T-Lymphocytes / immunology. T-Lymphocytes / pathology. T-Lymphocytes / virology
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(PMID = 16917009.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / RNA, Viral; 0 / Viral Proteins
[Number-of-references]
102
40.
Ariumi Y, Trono D:
Ataxia-telangiectasia-mutated (ATM) protein can enhance human immunodeficiency virus type 1 replication by stimulating Rev function.
J Virol
; 2006 Mar;80(5):2445-52
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[Title]
Ataxia-telangiectasia-mutated (ATM) protein can enhance
human
immunodeficiency
virus
type 1 replication by stimulating Rev function.
The ataxia-telangiectasia-mutated (ATM) kinase plays a central role in responses to various forms of DNA damage and has been suggested to facilitate
human
immunodeficiency
virus
type 1 (HIV-1) integration.
Notably, ATM overexpression did not stimulate the HIV-1 late gene expression within the context of Rev-independent constructs or the Rex-dependent production of capsid from
human
T-
cell
leukemia virus
type 1 proviral constructs.
[MeSH-major]
Cell
Cycle Proteins / physiology. DNA-Binding Proteins / physiology. Gene Expression Regulation, Viral. Gene Products, rev / physiology. HIV-1 / physiology. Protein-Serine-Threonine Kinases / physiology. Tumor Suppressor Proteins / physiology.
Virus
Replication
[MeSH-minor]
Ataxia Telangiectasia Mutated Proteins. Caffeine.
Cell
Line. Gene Silencing. Genes, Reporter. HIV Core Protein p24 / analysis. Humans. Luciferases / analysis. Luciferases / genetics. rev Gene Products,
Human
Immunodeficiency
Virus
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[ISSN]
0022-538X
[Journal-full-title]
Journal of virology
[ISO-abbreviation]
J. Virol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Gene Products, rev; 0 / HIV Core Protein p24; 0 / Tumor Suppressor Proteins; 0 / rev Gene Products, Human Immunodeficiency Virus; 3G6A5W338E / Caffeine; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
[Other-IDs]
NLM/ PMC1395391
41.
Yoshida M, Satou Y, Yasunaga J, Fujisawa J, Matsuoka M:
Transcriptional control of spliced and unspliced human T-cell leukemia virus type 1 bZIP factor (HBZ) gene.
J Virol
; 2008 Oct;82(19):9359-68
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[Title]
Transcriptional control of spliced and unspliced
human
T-
cell
leukemia virus
type 1 bZIP factor (HBZ) gene.
The
human
T-
cell
leukemia virus
type 1 (
HTLV
-1) basic leucine zipper factor (HBZ) gene is encoded by the minus strand of the
HTLV
-1 provirus and transcribed from the 3' long terminal repeat (LTR).
We compared the functions of the proteins
derived
from the sHBZ and usHBZ transcripts. sHBZ showed a stronger suppression of Tax-mediated transcriptional activation through the 5' LTR than did usHBZ; the level of suppression correlated with the level of protein produced.
The expression of sHBZ had a growth-promoting function in a T-
cell
line, while usHBZ expression did not.
[MeSH-major]
Basic-Leucine Zipper Transcription Factors / chemistry.
Human
T-
lymphotropic virus
1 / genetics. Sp1 Transcription Factor / metabolism. Transcription, Genetic. Viral Proteins / genetics. Viral Proteins / physiology
[MeSH-minor]
Alternative Splicing. Base Sequence.
Cell
Proliferation. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Humans. Molecular Sequence Data. Promoter Regions, Genetic. RNA, Viral / metabolism. Terminal Repeat Sequences
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[Cites]
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[ISSN]
1098-5514
[Journal-full-title]
Journal of virology
[ISO-abbreviation]
J. Virol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Viral; 0 / Sp1 Transcription Factor; 0 / Viral Proteins
[Other-IDs]
NLM/ PMC2546946
42.
Kress AK, Schneider G, Pichler K, Kalmer M, Fleckenstein B, Grassmann R:
Elevated cyclic AMP levels in T lymphocytes transformed by human T-cell lymphotropic virus type 1.
J Virol
; 2010 Sep;84(17):8732-42
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[Title]
Elevated cyclic AMP levels in T lymphocytes transformed by
human
T-
cell
lymphotropic virus
type 1.
Human
T-
cell
lymphotropic virus
type 1 (
HTLV
-1), the cause of
adult
T-
cell
leukemia
/
lymphoma
(
ATLL
), transforms CD4(+) T cells to permanent growth through its transactivator Tax.
HTLV
-1-transformed cells share phenotypic properties with memory and regulatory T cells (T-reg).
This led us to determine cAMP levels in
HTLV
-1-transformed cells.
We found elevated cAMP concentrations as a consistent feature of
all HTLV
-1-transformed
cell
lines, including in vitro-
HTLV
-1-transformed, Tax-transformed, and patient-
derived
cells.
We found specific downregulation of the cAMP-degrading phosphodiesterase 3B (PDE3B) in
HTLV
-1-transformed cells, which was independent of Tax in transient expression experiments.
Overexpression of PDE3B led to a decrease of cAMP in
HTLV
-1-transformed cells.
Decreased expression of PDE3B was
associated
with inhibitory histone modifications at the PDE3B promoter and the PDE3B locus.
This shows that
HTLV
-1-transformed cells assume biological features of long-lived T-
cell
populations that potentially contribute to viral persistence.
[MeSH-major]
Cell
Transformation, Viral. Cyclic AMP / metabolism.
HTLV
-I Infections / metabolism.
Human
T-
lymphotropic virus
1 / physiology.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ metabolism
[MeSH-minor]
Cell
Line, Transformed. Cells, Cultured. Cyclic Nucleotide Phosphodiesterases, Type 3 / genetics. Cyclic Nucleotide Phosphodiesterases, Type 3 / metabolism. Gene Products, tax / genetics. Gene Products, tax / metabolism. Humans. T-Lymphocytes / metabolism. T-Lymphocytes / virology
SciCrunch.
ArrayExpress: Data: Microarray
.
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[ISSN]
1098-5514
[Journal-full-title]
Journal of virology
[ISO-abbreviation]
J. Virol.
[Language]
eng
[Databank-accession-numbers]
GEO/ GSE17718
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Gene Products, tax; 0 / tax protein, Human T-lymphotrophic virus 1; E0399OZS9N / Cyclic AMP; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 3; EC 3.1.4.17 / PDE3B protein, human
[Other-IDs]
NLM/ PMC2918996
43.
Masutani H, Ueda S, Yodoi J:
The thioredoxin system in retroviral infection and apoptosis.
Cell Death Differ
; 2005 Aug;12 Suppl 1:991-8
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Human
thioredoxin (TRX) was first identified in
human
T-
cell
leukemia virus
type I (
HTLV
-I)-
positive
T-
cell
lines and is
associated
with the pathophysiology of retroviral infections.
Thioredoxin binding protein-2/vitamin D(3) upregulated protein 1 is a growth suppressor and its expression is suppressed in
HTLV
-I-transformed cells.
Studies of these molecules of the TRX system provide novel insights into the apoptosis
associated
with retroviral diseases.
[MeSH-minor]
Animals. Glutathione / metabolism. HIV Infections / metabolism.
HTLV
-I Infections / metabolism. Humans. MAP Kinase Kinase Kinase 5 / metabolism. Membrane Proteins / metabolism. Peroxidases / metabolism. Peroxiredoxins
NCI CPTAC Assay Portal.
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.
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.
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Cited by Patents in
.
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(PMID = 15818395.001).
[ISSN]
1350-9047
[Journal-full-title]
Cell death and differentiation
[ISO-abbreviation]
Cell Death Differ.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Membrane Proteins; 52500-60-4 / Thioredoxins; EC 1.11.1.- / Peroxidases; EC 1.11.1.15 / Peroxiredoxins; EC 2.7.11.25 / MAP Kinase Kinase Kinase 5; GAN16C9B8O / Glutathione
[Number-of-references]
93
44.
Mukherjee S, Negi VS, Keitany G, Tanaka Y, Orth K:
In vitro activation of the IkappaB kinase complex by human T-cell leukemia virus type-1 Tax.
J Biol Chem
; 2008 May 30;283(22):15127-33
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[Title]
In vitro activation of the IkappaB kinase complex by
human
T-
cell
leukemia virus
type-1 Tax.
Human
T-
cell
leukemia virus
type-I expresses Tax, a 40-kDa oncoprotein that activates IkappaB kinase (IKK), resulting in constitutive activation of NFkappaB.
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
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[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / R01 AI 056404; United States / NIDDK NIH HHS / DK / R21 DK 072134
[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 / Bacterial Proteins; 0 / Gene Products, tax; 0 / HSP90 Heat-Shock Proteins; 0 / Multiprotein Complexes; 0 / NF-kappa B; 0 / Recombinant Proteins; 0 / YopP protein, Yersinia; EC 2.7.11.10 / I-kappa B Kinase; EC 3.1.3.16 / Phosphoprotein Phosphatases
[Other-IDs]
NLM/ PMC2397464
45.
Chiba K, Hashino S, Izumiyama K, Toyoshima N, Suzuki S, Kurosawa M, Asaka M:
Multiple osteolytic bone lesions with high serum levels of interleukin-6 and CCL chemokines in a patient with adult T cell leukemia.
Int J Lab Hematol
; 2009 Jun;31(3):368-71
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[Title]
Multiple osteolytic bone lesions with high serum levels of interleukin-6 and CCL chemokines in a patient with
adult
T cell
leukemia
.
A 37-year-old woman was diagnosed as having chronic
adult
T-
cell
leukemia
(
ATL
) of the skin by a skin biopsy and
human
T-
cell
leukemia virus
type-1 serology at our hospital in August 1992.
The skin lesions of
ATL
were improved by treatment with psoralen ultraviolet ray A.
[MeSH-major]
Chemokines / blood. Interleukin-6 / blood.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ blood.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ complications. Osteolysis / blood. Osteolysis / etiology
[MeSH-minor]
Adult
. Chronic
Disease
. Fatal Outcome. Female. Humans
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 18177436.001).
[ISSN]
1751-553X
[Journal-full-title]
International journal of laboratory hematology
[ISO-abbreviation]
Int J Lab Hematol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Chemokines; 0 / Interleukin-6
46.
Fan J, Ma G, Nosaka K, Tanabe J, Satou Y, Koito A, Wain-Hobson S, Vartanian JP, Matsuoka M:
APOBEC3G generates nonsense mutations in human T-cell leukemia virus type 1 proviral genomes in vivo.
J Virol
; 2010 Jul;84(14):7278-87
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[Title]
APOBEC3G generates nonsense mutations in
human
T-
cell
leukemia virus
type 1 proviral genomes in vivo.
Human
T-
cell
leukemia virus
type 1 (
HTLV
-1) induces
cell
proliferation after infection, leading to efficient transmission by
cell
-to-
cell
contact.
After a long latent period, a fraction of carriers develop
adult
T-
cell
leukemia
(
ATL
).
Genetic changes in the tax gene in
ATL
cells were reported in about 10% of
ATL
cases.
To determine genetic changes that may occur throughout the provirus, we determined the entire sequence of the
HTLV
-1 provirus in 60
ATL
cases.
Abortive genetic changes, including deletions, insertions, and nonsense mutations, were frequent in all viral genes except the HBZ gene, which is transcribed from the minus strand of the
virus
.
G-to-A base substitutions were the most frequent mutations in
ATL
cells.
The sequence context of G-to-A mutations was in accordance with the preferred target sequence of
human
APOBEC3G (hA3G).
The target sequences of hA3G were less frequent in the plus strand of the HBZ coding region than in other coding regions of the
HTLV
-1 provirus.
HTLV
-1-infected cells likely take advantage of hA3G to escape from the host immune system by losing expression of viral proteins.
[MeSH-major]
Cytidine Deaminase / metabolism. Genome, Viral.
HTLV
-I Infections / virology.
Human
T-
lymphotropic virus
1 / genetics.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ virology. Mutation. Proviruses / genetics
[MeSH-minor]
Base Sequence.
Cell
Line. Genes, Reporter. Genetic Variation. Genetic Vectors. Humans. Molecular Sequence Data. Mutagenesis
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(PMID = 20463074.001).
[ISSN]
1098-5514
[Journal-full-title]
Journal of virology
[ISO-abbreviation]
J. Virol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / APOBEC3G protein, human; EC 3.5.4.5 / Cytidine Deaminase
[Other-IDs]
NLM/ PMC2898234
47.
Mizobe T, Tsukada J, Higashi T, Mouri F, Matsuura A, Tanikawa R, Minami Y, Yoshida Y, Tanaka Y:
Constitutive association of MyD88 to IRAK in HTLV-I-transformed T cells.
Exp Hematol
; 2007 Dec;35(12):1812-22
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[Title]
Constitutive association of MyD88 to IRAK in
HTLV
-I-transformed T cells.
OBJECTIVE: Constitutive activation of nuclear factor (NF)-kappaB is a common feature of
human
T-
cell
leukemia virus
type I (
HTLV
-I)-transformed T cells.
Inhibition of NF-kappaB activity reduces
cell
growth and induces apoptosis of
HTLV
-I-transformed T cells, suggesting a central role of NF-kappaB in their proliferation and survival.
In this study, we investigated whether MyD88, an adaptor protein of Toll-like receptor (TLR) signaling, contributes to constitutive NF-kappaB activation in
HTLV
-I-transformed T cells.
MATERIALS AND METHODS: Activation status of MyD88 and interleukin (IL)-1R-
associated
kinase 1 (IRAK1) in
HTLV
-I-transformed
human
T cells, MT2, MT4, and HUT102 was examined by using Western blot and immunoprecipitation.
An expression vector encoding a dominant negative MyD88 with a deletion of its death domain (MyD88dn) was transfected into MT2 cells to evaluate roles of MyD88 in spontaneous activation of cytokine gene promoters and transcription factors, proliferation, and apoptosis in
HTLV
-I-transformed T cells.
RESULTS: Constitutive association of MyD88 with IRAK1 was observed in all three of
HTLV
-I-transformed T cells, but not in
HTLV
-I-negative T cells, such as Jurkat, HUT78, and MOLT4.
HTLV
-I Tax enhanced TLR expression and synergistically activated NF-kappaB with wild-type MyD88.
CONCLUSION: Our results show a novel pathway in NF-kappaB activation in
HTLV
-I-transformed T cells and further demonstrate a critical role of MyD88 in their dysregulated gene activation, survival, and proliferation.
[MeSH-major]
Human
T-
lymphotropic virus
1 / physiology. Interleukin-1 Receptor-
Associated
Kinases / metabolism. Myeloid Differentiation Factor 88 / metabolism
[MeSH-minor]
Base Sequence.
Cell
Line, Transformed.
Cell
Transformation, Viral. DNA Primers. Humans. Protein Binding. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / metabolism
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(PMID = 17920759.001).
[ISSN]
0301-472X
[Journal-full-title]
Experimental hematology
[ISO-abbreviation]
Exp. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / DNA Primers; 0 / MYD88 protein, human; 0 / Myeloid Differentiation Factor 88; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases
48.
Park CW, Kim A, Cha SW, Jung SH, Yang HW, Lee YJ, Lee HIe, Kim SH, Kim YH:
A case of phlegmonous gastritis associated with marked gastric distension.
Gut Liver
; 2010 Sep;4(3):415-8
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[Title]
A case of phlegmonous gastritis
associated
with marked gastric distension.
Phlegmonous gastritis is an
acute
and severe infectious
disease
that is occasionally fatal if the
diagnosis
is delayed.
Alcohol consumption, an immunocompromised state (e.g., due to HIV infection, rheumatoid arthritis, diabetes mellitus, or
adult
T-
cell lymphoma
), and mucosal injury of the stomach are reported to be predisposing factors.
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(PMID = 20981225.001).
[ISSN]
2005-1212
[Journal-full-title]
Gut and liver
[ISO-abbreviation]
Gut Liver
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Korea (South)
[Other-IDs]
NLM/ PMC2956360
[Keywords]
NOTNLM ; Gastric outlet obstruction / Phlegmonous gastritis
49.
Arisawa K, Soda M, Ono M, Uemura H, Hiyoshi M, Suyama A:
Trends of incidence rate of adult T-cell leukemia/lymphoma in an HTLV-1 endemic area in Japan.
Int J Cancer
; 2009 Aug 1;125(3):737-8
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[Title]
Trends of incidence rate of
adult
T-
cell
leukemia
/
lymphoma
in an
HTLV
-1 endemic area in Japan.
[MeSH-major]
Endemic Diseases.
HTLV
-I Infections / epidemiology.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ epidemiology
[MeSH-minor]
Adult
. Age Distribution. Aged. Aged, 80 and over. Female. Humans. Incidence. Japan / epidemiology. Male. Middle Aged. Odds Ratio. Registries. Risk Assessment. Risk Factors. Time Factors
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(PMID = 19437534.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Comparative Study; Letter
[Publication-country]
United States
50.
Venkitaraman R, Sagar TG, George MK:
Adult T-cell lymphoma with HTLV-I and HTLV-II infection.
South Med J
; 2007 Nov;100(11):1178-9
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[Title]
Adult
T-
cell lymphoma
with
HTLV
-I and
HTLV
-II infection.
[MeSH-major]
HTLV
-I Infections /
diagnosis
.
HTLV
-II Infections /
diagnosis
.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/
diagnosis
.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ virology
[MeSH-minor]
Diagnosis
, Differential. Fatal Outcome. Humans. Male. Middle Aged
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(PMID = 17984755.001).
[ISSN]
0038-4348
[Journal-full-title]
Southern medical journal
[ISO-abbreviation]
South. Med. J.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
51.
Miyagi T, Nagasaki A, Taira T, Shinhama A, Suzuki M, Ohshima K, Takasu N:
Extranodal adult T-cell leukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature.
Leuk Lymphoma
; 2009 Feb;50(2):187-95
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[Title]
Extranodal
adult
T-
cell
leukemia
/
lymphoma
of the head and neck: a clinicopathological study of nine cases and a review of the literature.
Extranodal
adult
T-
cell
leukemia
/
lymphoma
(
ATLL
) of the head and neck is a rare
disease
.
We studied the clinicopathological features of nine patients with
ATLL
involving extranodal head and neck sites and conducted a literature review.
Histopathology included diffuse pleomorphic-type (with angiocentric features), Hodgkin-like and anaplastic large
cell
-type.
Five patients with localised
disease
showed prolonged survival regardless of unfavourable histology and/or aberrant provirus status, including integration of multiple copies or defective provirus.
Patients with localised
disease
documented in the literature, including our study series, had a reduced frequency of elevated lactate dehydrogenase, no hypercalcemia and longer survival.
ATLL
should be included in the differential
diagnosis
of extranodal head and neck
lymphoma
.
Localised extranodal
ATLL
of the head and neck may exhibit indolent
clinical
behaviours.
[MeSH-major]
Head and Neck Neoplasms / pathology.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ pathology
[MeSH-minor]
Adult
. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Tomography, X-Ray Computed
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[CommentIn]
Leuk Lymphoma. 2009 Feb;50(2):148-9
[
19235009.001
]
[CommentIn]
Leuk Lymphoma. 2009 Feb;50(2):150-1
[
19235010.001
]
(PMID = 19197730.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
England
[Number-of-references]
50
52.
Janik JE, Morris JC:
Survivin(g) adult T-cell leukemia/lymphoma.
Oncology (Williston Park)
; 2009 Dec;23(14):1256, 1261, 1266
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[Title]
Survivin(g)
adult
T-
cell
leukemia
/
lymphoma
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm / genetics. Hematopoietic Stem
Cell
Transplantation.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ drug therapy.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ therapy. Microtubule-
Associated
Proteins / genetics
[MeSH-minor]
Adult
. Female. Gene Expression Profiling. Humans. Inhibitor of Apoptosis Proteins. Male. Transplantation, Homologous
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[CommentOn]
Oncology (Williston Park). 2009 Dec;23(14):1250-6
[
20120837.001
]
(PMID = 20120838.001).
[ISSN]
0890-9091
[Journal-full-title]
Oncology (Williston Park, N.Y.)
[ISO-abbreviation]
Oncology (Williston Park, N.Y.)
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Comment; Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins
53.
Nascimento MC, Primo J, Bittencourt A, Siqueira I, de Fátima Oliveira M, Meyer R, Schriefer A, Santos SB, Carvalho EM:
Infective dermatitis has similar immunological features to human T lymphotropic virus-type 1-associated myelopathy/tropical spastic paraparesis.
Clin Exp Immunol
; 2009 Jun;156(3):455-62
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[Title]
Infective dermatitis has similar immunological features to
human
T
lymphotropic virus
-type 1-
associated
myelopathy/tropical spastic paraparesis.
Human
T
lymphotropic virus
-type 1 (
HTLV
-1) is the causal agent of the
HTLV
-1-
associated
myelopathy/tropical spastic paraparesis (HAM/TSP),
adult
T cell
leukaemia
/
lymphoma
and infective dermatitis
associated
with
HTLV
-1 (IDH).
Over-production of proinflammatory cytokines and an increase in
HTLV
-1 proviral load are features of HAM/TSP, but the immunological basis of IDH has not been established.
In this study we determined the immune response in patients with IDH measuring interleukin (IL)-4, IL-5, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels as well as the
HTLV
-1 proviral load.
HTLV
-1 carriers and patients with HAM/TSP served as controls.
TNF-alpha and IFN-gamma levels were higher in IDH than in
HTLV
-1 carriers.
There was a tendency for higher IL-4 mRNA expression and immunoglobulin E (IgE) levels in IDH than in
HTLV
-1 carriers, but the difference did not reach statistical significance.
The
HTLV
-1 proviral load was significantly higher in IDH patients than in
HTLV
-1 carriers.
IDH is characterized by an exaggerated Th1 immune response and high
HTLV
-1 proviral load.
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[
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]
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[
17051489.001
]
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[
17119343.001
]
[Cites]
J Immunol. 2001 Feb 15;166(4):2602-9
[
11160322.001
]
(PMID = 19438598.001).
[ISSN]
1365-2249
[Journal-full-title]
Clinical and experimental immunology
[ISO-abbreviation]
Clin. Exp. Immunol.
[Language]
ENG
[Grant]
United States / FIC NIH HHS / TW / D43 TW007127; United States / FIC NIH HHS / TW / TW007127-05; United States / FIC NIH HHS / TW / D43 TW007127-05
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cytokines; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 37341-29-0 / Immunoglobulin E; 82115-62-6 / Interferon-gamma
[Other-IDs]
NLM/ PMC2691974
54.
Mizuguchi M, Asao H, Hara T, Higuchi M, Fujii M, Nakamura M:
Transcriptional activation of the interleukin-21 gene and its receptor gene by human T-cell leukemia virus type 1 Tax in human T-cells.
J Biol Chem
; 2009 Sep 18;284(38):25501-11
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[Title]
Transcriptional activation of the interleukin-21 gene and its receptor gene by
human
T-
cell
leukemia virus
type 1 Tax in
human
T-cells.
At the incipient stages of the development of
adult
T-
cell
leukemia
, T-cells infected with
human
T-
cell
leukemia virus
type 1 (
HTLV
-1) suffer disregulation in
cell
growth caused by aberrant expression of host genes by the
HTLV
-1 transactivator protein Tax (Tax1).
Tax1-mediated growth promotion is thought to result from, at least in part, up-regulation of genes for growth factors and their receptors that induce T-
cell
growth.
In the present study, we demonstrate that Tax1 transactivates the interleukin-21 (IL-21) and its receptor (IL-21R) genes in
human
T-cells.
Chromatin immunoprecipitation assay and gel mobility shift assay exhibited that the IL-21 promoter elements bound transcription factors AP-1 and NF-kappaB, and the IL-21R promoter elements were
associated
with AP-1 and interferon regulatory factor.
The related
virus HTLV
-2 with Tax2 similar to Tax1 is known not to be pathogenic.
The study suggests insights into cytokine-dependent aberrant growth of
HTLV
-1-infected T-cells and the molecular basis of different pathogenicity between
HTLV
-1 and
HTLV
-2.
[MeSH-major]
CD4-
Positive
T-Lymphocytes / metabolism. Gene Products, tax / metabolism.
Human
T-
lymphotropic virus
1 / metabolism. Interleukin-21 Receptor alpha Subunit / biosynthesis. Interleukins / biosynthesis. Response Elements. Transcriptional Activation
[MeSH-minor]
Adenoviridae.
HTLV
-I Infections / genetics.
HTLV
-I Infections / metabolism.
Human
T-
lymphotropic virus
2 / genetics.
Human
T-
lymphotropic virus
2 / metabolism.
Human
T-
lymphotropic virus
2 / pathogenicity. Humans. Jurkat Cells. NF-kappa B / genetics. NF-kappa B / metabolism. Transcription Factor AP-1 / genetics. Transcription Factor AP-1 / metabolism. Transduction, Genetic
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 19617351.001).
[ISSN]
1083-351X
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[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 / IL21R protein, human; 0 / Interleukin-21 Receptor alpha Subunit; 0 / Interleukins; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 0 / interleukin-21; 0 / tax protein, Human T-lymphotrophic virus 1; 0 / tax protein, Human T-lymphotrophic virus 2
[Other-IDs]
NLM/ PMC2757951
55.
Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Nair R, Sengar M, Nair C:
Immunophenotyping of mature T/NK cell neoplasm presenting as leukemia.
Indian J Cancer
; 2010 Apr-Jun;47(2):189-93
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[Title]
Immunophenotyping of mature T/NK
cell
neoplasm presenting as
leukemia
.
INTRODUCTION: Mature T/NK
cell
lymphomas
(MTNKL) presenting as
leukemia
are rare and show considerable overlapping of
clinical
, morphological and immunophenotypic features.
MATERIALS AND METHODS: We reviewed 380 consecutive cases of mature lymphoid neoplasm that presented as
leukemia
and were diagnosed on morphology and immunophenotyping of bone marrow and/or peripheral blood samples.
MTNKL constituted 4% (nine cases) of all mature lymphoid neoplasms presenting as
leukemia
.
It included four cases of T-large granular
leukemia
(T-LGL), two of T-
cell
prolymphocytic
leukemia
small
cell
variant (T-PLL), two of
adult
T-
cell
leukemia
/
lymphoma
(
ATLL
) and one of primary cutaneous gamma delta T-
cell lymphoma
(PCGDTCL).
One case of T- PLL small
cell
variant showed CD4+/CD8- phenotype, while the other revealed CD4-/CD8+ phenotype.
Both cases of
ATLL
showed CD4+/CD8+/CD25+ phenotype.
TCRalpha/beta was performed in three cases of T-LGL and was
positive
in all.
CONCLUSION: Mature nodal T/NK
cell
neoplasms are rare and MTNKL presenting as
leukemia
are even rarer.
There is an overlap between the immunophenotypic profiles of different MTNKL subtypes and elaborate T/NK
cell
panels are required for their evaluation.
[MeSH-major]
Killer Cells, Natural / pathology.
Leukemia
, Prolymphocytic, T-
Cell
/
diagnosis
.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/
diagnosis
.
Lymphoma
, T-
Cell
/
diagnosis
[MeSH-minor]
Adult
. Aged. Bone Marrow / immunology. Bone Marrow / pathology.
Diagnosis
, Differential. Female. Flow Cytometry. Humans. Male. Middle Aged. Prognosis
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(PMID = 20448385.001).
[ISSN]
1998-4774
[Journal-full-title]
Indian journal of cancer
[ISO-abbreviation]
Indian J Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
56.
Silveira-Lacerda Ede P, Vilanova-Costa CA, Hamaguchi A, Pavanin LA, Goulart LR, Homsi-Brandenburgo MI, Dos Santos WB, Soares AM, Nomizo A:
The ruthenium complex cis-(dichloro)tetraammineruthenium(III) chloride presents selective cytotoxicity against murine B cell lymphoma (A-20), murine ascitic sarcoma 180 (S-180), human breast adenocarcinoma (SK-BR-3), and human T cell leukemia (Jurkat) tumor cell lines.
Biol Trace Elem Res
; 2010 Jun;135(1-3):98-111
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[Title]
The ruthenium complex cis-(dichloro)tetraammineruthenium(III) chloride presents selective cytotoxicity against murine B
cell lymphoma
(A-20), murine ascitic sarcoma 180 (S-180),
human
breast adenocarcinoma (SK-BR-3), and
human
T cell
leukemia
(Jurkat) tumor
cell
lines.
The aim of present study was to verify the in vitro antitumor activity of a ruthenium complex, cis-(dichloro)tetraammineruthenium(III) chloride (cis-[RuCl(2)(NH(3))(4)]
Cl
) toward different tumor
cell
lines.
The antitumor studies showed that ruthenium(III) complex presents a relevant cytotoxic activity against murine B
cell lymphoma
(A-20), murine ascitic sarcoma 180 (S-180),
human
breast adenocarcinoma (SK-BR-3), and
human
T cell
leukemia
(Jurkat)
cell
lines and a very low cytotoxicity toward
human
peripheral blood mononuclear cells.
The cytotoxic activity of a high concentration (2 mg mL(-1)) of cis-[RuCl(2)(NH(3))(4)]
Cl
toward Jurkat cells correlated with an increased number of annexin V-
positive
cells and also the presence of DNA fragmentation, suggesting that this compound induces apoptosis in tumor cells.
Thus, a mechanistic understanding of how metal complexes achieve their activities is crucial to their
clinical
success and to the rational design of new compounds with improved potency.
[MeSH-minor]
Animals. Breast Neoplasms / drug therapy.
Cell
Cycle / drug effects.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Cytotoxicity, Immunologic / drug effects. Female. Humans. Jurkat Cells / drug effects.
Lymphoma
, B-
Cell
/ drug therapy. Mice. Ruthenium / therapeutic use. Sarcoma 180 / drug therapy
MedlinePlus Health Information.
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(PMID = 19727575.001).
[ISSN]
1559-0720
[Journal-full-title]
Biological trace element research
[ISO-abbreviation]
Biol Trace Elem Res
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / (dichloro)tetraammineruthenium(III); 0 / Antineoplastic Agents; 0 / Ruthenium Compounds; 7UI0TKC3U5 / Ruthenium
57.
Lepoutre V, Jain P, Quann K, Wigdahl B, Khan ZK:
Role of resident CNS cell populations in HTLV-1-associated neuroinflammatory disease.
Front Biosci (Landmark Ed)
; 2009 Jan 01;14:1152-68
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[Title]
Role of resident CNS
cell
populations in
HTLV
-1-
associated
neuroinflammatory
disease
.
Human
T cell
leukemia virus
type 1 (
HTLV
-1), the first
human
retrovirus discovered, is the etiologic agent for a number of disorders; the two most common pathologies include
adult
T cell
leukemia
(
ATL
) and a progressive demyelinating neuroinflammatory
disease
,
HTLV
-1-
associated
myelopathy/tropical spastic paraparesis (HAM/TSP).
The neurologic dysfunction
associated
with HAM/TSP is a result of viral intrusion into the central nervous system (CNS) and the generation of a hyperstimulated host response within the peripheral and central nervous system that includes expanded populations of CD4+ and CD8+ T cells and proinflammatory cytokines/chemokines in the cerebrospinal fluid (CSF).
The mechanisms of neurological degeneration in HAM/TSP have yet to be fully delineated in vivo and may involve the immunogenic properties of the
HTLV
-1 transactivator protein Tax.
This comprehensive review characterizes the available knowledge to date concerning the effects of
HTLV
-1 on CNS resident
cell
populations with emphasis on both viral and host factors contributing to the genesis of HAM/TSP.
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(PMID = 19273122.001).
[ISSN]
1093-4715
[Journal-full-title]
Frontiers in bioscience (Landmark edition)
[ISO-abbreviation]
Front Biosci (Landmark Ed)
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA054559; United States / NCI NIH HHS / CA / CA054559-14; United States / NCI NIH HHS / CA / R01 CA054559-14; United States / NCI NIH HHS / CA / 2R1 CA054559; United States / NCI NIH HHS / CA / CA054559-15; United States / NCI NIH HHS / CA / CA054559-13A1; United States / NCI NIH HHS / CA / CA054559; United States / NIAID NIH HHS / AI / AI077414-01A2; United States / NIAID NIH HHS / AI / R01 AI077414; United States / NIAID NIH HHS / AI / R01 AI077414-01A2; United States / NCI NIH HHS / CA / R01 CA054559-13A1; United States / NCI NIH HHS / CA / R01 CA054559-15
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
181
[Other-IDs]
NLM/ NIHMS126265; NLM/ PMC2739244
58.
Pezeshkpoor F, Yazdanpanah MJ, Shirdel A:
Specific cutaneous manifestations in adult T-cell leukemia/lymphoma.
Int J Dermatol
; 2008 Apr;47(4):359-62
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[Title]
Specific cutaneous manifestations in
adult
T-
cell
leukemia
/
lymphoma
.
BACKGROUND:
Adult
T-
cell
leukemia
/
lymphoma
(
ATLL
) is an aggressive malignancy which may occur in individuals infected with
human
T-
cell
lymphotropic virus
type-I (
HTLV
-I).
HTLV
-I is endemic in Khorasan, with a frequency of 2.3% in the general population.
As specific cutaneous manifestations of
lymphoma
may occur in a significant number of patients, we studied these manifestations in
ATLL
patients admitted to the Hematology and Dermatology Departments of Ghaem Hospital, Mashhad, Iran, during 1995-2004.
METHODS: In this descriptive study, demographic and
clinical
information was obtained from 23 patients suffering from
ATLL
with specific cutaneous lesions (atypical lymphocytes on histopathology of cutaneous lesions), and was analyzed statistically.
CONCLUSION: The most common type of specific skin lesion in
ATLL
was maculopapular eruption, especially with a generalized distribution.
[MeSH-major]
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ pathology. Leukemic Infiltration. Skin / pathology
[MeSH-minor]
Adolescent.
Adult
. Aged. Female.
Human
T-
lymphotropic virus
1 / isolation & purification. Humans. Iran. Male. Middle Aged
Genetic Alliance.
consumer health - Cutaneous T-Cell Lymphoma
.
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(PMID = 18377598.001).
[ISSN]
1365-4632
[Journal-full-title]
International journal of dermatology
[ISO-abbreviation]
Int. J. Dermatol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
59.
Tsuji Y, Hatanaka M, Maeda T, Seya T, Takenaka H, Shimizu A:
Differential-expression and tyrosine-phosphorylation profiles of caveolin isoforms in human T cell leukemia cell lines.
Int J Mol Med
; 2005 Nov;16(5):889-93
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[Title]
Differential-expression and tyrosine-phosphorylation profiles of caveolin isoforms in
human
T cell
leukemia
cell
lines.
Caveolin-1 and -2 are expressed in most
cell
types, but are not expressed in normal blood cells and
cell
lines.
We previously demonstrated that caveolin-1 is expressed in a panel of
human leukemia
cell
lines that show an activated
T cell
phenotype.
Using this method we detected caveolin-1beta, -2alpha and -2beta, but not caveolin-3 in the
leukemia
cell
lines.
This modification is likely to cause the lack of reactivity of caveolin-1alpha to the mAb, and suggests a possible close relationship to
cell
activation.
[MeSH-major]
Leukemia
, T-
Cell
/ metabolism. Tyrosine / metabolism
[MeSH-minor]
Antibodies / immunology. Antibodies, Monoclonal / immunology.
Cell
Line, Tumor. Humans. Phosphorylation. Protein Isoforms / analysis. Protein Isoforms / immunology. Protein Isoforms / metabolism
Hazardous Substances Data Bank.
L-TYROSINE
.
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(PMID = 16211260.001).
[ISSN]
1107-3756
[Journal-full-title]
International journal of molecular medicine
[ISO-abbreviation]
Int. J. Mol. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antibodies; 0 / Antibodies, Monoclonal; 0 / Protein Isoforms; 42HK56048U / Tyrosine
60.
Jin Q, Alkhatib B, Cornetta K, Alkhatib G:
Alternate receptor usage of neuropilin-1 and glucose transporter protein 1 by the human T cell leukemia virus type 1.
Virology
; 2010 Jan 20;396(2):203-12
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[Title]
Alternate receptor usage of neuropilin-1 and glucose transporter protein 1 by the
human
T cell
leukemia virus
type 1.
Recent studies have demonstrated that neuropilin 1 (NP-1) is involved in
HTLV
-1 entry; however, the role NP-1 plays in this process is not understood.
We demonstrated that ectopic expression of
human
NP-1 but not NP-2 cDNA increased susceptibility to
HTLV
-1.
SiRNA-mediated inhibition of NP-1 expression correlated with significant reduction of
HTLV
-1 Env-mediated fusion.
The vascular endothelial growth factor (VEGF(165)) caused downmodulation of surface NP-1 and inhibited
HTLV
-1 infection of U87 cells.
HTLV
-1 Env forms complexes with both NP-1 and GLUT-1 in primary
human
astrocytes.
The alternate usage of these two cellular receptors may have important implications regarding
HTLV
-1 neuro-tropism.
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
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author profiles
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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[ISSN]
1096-0341
[Journal-full-title]
Virology
[ISO-abbreviation]
Virology
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R21 CA098095-01; United States / NCI NIH HHS / CA / CA098095-01; United States / NCI NIH HHS / CA / R21 CA098095-02; United States / NCI NIH HHS / CA / 1R21CA98095-01; United States / NCI NIH HHS / CA / CA098095-02; United States / NCI NIH HHS / CA / R21 CA098095
[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 / Glucose Transporter Type 1; 0 / Vascular Endothelial Growth Factor A; 0 / Viral Envelope Proteins; 144713-63-3 / Neuropilin-1
[Other-IDs]
NLM/ NIHMS154887; NLM/ PMC2789895
61.
Shimizu D, Taki T, Utsunomiya A, Nakagawa H, Nomura K, Matsumoto Y, Nishida K, Horiike S, Taniwaki M:
Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma.
Int J Hematol
; 2007 Apr;85(3):212-8
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[Title]
Detection of NOTCH1 mutations in
adult
T-
cell
leukemia
/
lymphoma
and peripheral T-
cell lymphoma
.
We analyzed NOTCH1 gene mutation in 53 adults with mature T-
cell
leukemia
/
lymphoma
: 21 patients with
adult
T-
cell
leukemia
(
ATL
), 25 with T-
cell
non-Hodgkin's
lymphoma
(T-NHL), and 7 with T-
cell
prolymphocytic
leukemia
.
We detected a nonsense mutation, C7249T (resulting in Q2417X, where X is a termination codon) in the PEST domain of NOTCH1 in an
ATL
patient and detected a 3-bp deletion (positions 7234-7236) that resulted in deletion of a proline codon at codon 2412 in the PEST domain of NOTCH1 in a patient with a T-NHL, peripheral T-
cell lymphoma
-unspecified (PTCL-u).
We also analyzed the expression of NOTCH1 target genes (HES1, CCND1, and MYC), all of which were expressed in the sample of the PTCL-u patient with the NOTCH1 mutation, but found only MYC to be expressed in the sample from the
ATL
patient.
These findings suggest that nonsense mutation in the PEST domain in the
ATL
case was
associated
with NOTCH1 signaling through a pathway different from that for T-
cell
acute
lymphoblastic
leukemia
(T-ALL).
Although NOTCH1 mutation occurs infrequently in mature T-
cell
leukemia
/
lymphoma
, NOTCH1 may be involved in leukemogenesis
associated
with various forms of T-
cell
leukemia
/
lymphoma
rather than only with T-ALL.
[MeSH-major]
Codon, Nonsense.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ genetics.
Lymphoma
, T-
Cell
, Peripheral / genetics. Receptor, Notch1 / genetics
[MeSH-minor]
Adult
. DNA Mutational Analysis. Humans
Genetic Alliance.
consumer health - Peripheral T-cell lymphoma
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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]
(PMID = 17483057.001).
[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Codon, Nonsense; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
62.
Kohno T, Yamada Y, Akamatsu N, Kamihira S, Imaizumi Y, Tomonaga M, Matsuyama T:
Possible origin of adult T-cell leukemia/lymphoma cells from human T lymphotropic virus type-1-infected regulatory T cells.
Cancer Sci
; 2005 Aug;96(8):527-33
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[Title]
Possible origin of
adult
T-
cell
leukemia
/
lymphoma
cells from
human
T
lymphotropic virus
type-1-infected regulatory T cells.
Adult
T-
cell
leukemia
/
lymphoma
(
ATLL
) is a lymphoproliferative
disorder
caused by
human
T
lymphotropic virus
type 1 (
HTLV
-I).
Although
ATLL
cells display an activated helper/inducer T-
cell
phenotype, CD4+ and CD25+, they are known to exhibit strong immunosuppressive activity.
As regulatory T cells (Treg cells) express CD4+ and CD25+ molecules and possess potent immune response suppressive activity, we investigated a possible link between
ATLL
cells and Treg cells.
In primary
ATLL
cells, the expression levels of the Treg
cell
marker molecules Foxp3 and glucocorticoid-induced tumor necrosis factor receptor family related protein (GITR) were significantly higher than in those from healthy adults.
Furthermore,
ATLL
cells are unresponsive in vitro to concanavalin A stimulation and suppress the proliferation of normal T cells.
GITR mRNA expression was induced by the
HTLV
-I transactivator Tax, and GITR promoter analyses revealed that this induction depends on the kappaB site from -431 bp to -444 bp upstream of the putative transcription site.
Taken together,
ATLL
cells may originate from
HTLV
-I-infected Treg cells, and GITR seems to be involved in the progression to
ATLL
.
[MeSH-major]
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ immunology. T-Lymphocytes / immunology
[MeSH-minor]
Adult
.
Cell
Division.
Cell
Line, Tumor. Concanavalin A. DNA-Binding Proteins / genetics. Forkhead Transcription Factors. Gene Expression Regulation, Neoplastic. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Glucocorticoid-Induced TNFR-Related Protein. Humans. Lymphocyte Activation. Receptors, Nerve Growth Factor / genetics. Receptors, Tumor Necrosis Factor / genetics. Reverse Transcriptase Polymerase Chain Reaction
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
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(PMID = 16108835.001).
[ISSN]
1347-9032
[Journal-full-title]
Cancer science
[ISO-abbreviation]
Cancer Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Gene Products, tax; 0 / Glucocorticoid-Induced TNFR-Related Protein; 0 / Receptors, Nerve Growth Factor; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF18 protein, human; 11028-71-0 / Concanavalin A
63.
Ramos JC, Ruiz P Jr, Ratner L, Reis IM, Brites C, Pedroso C, Byrne GE Jr, Toomey NL, Andela V, Harhaj EW, Lossos IS, Harrington WJ Jr:
IRF-4 and c-Rel expression in antiviral-resistant adult T-cell leukemia/lymphoma.
Blood
; 2007 Apr 1;109(7):3060-8
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[Title]
IRF-4 and c-Rel expression in antiviral-resistant
adult
T-
cell
leukemia
/
lymphoma
.
Adult
T-
cell
leukemia
/
lymphoma
(
ATLL
) is a generally fatal malignancy.
Most
ATLL
patients fare poorly with conventional chemotherapy; however, antiviral therapy with zidovudine (AZT) and interferon alpha (IFN-alpha) has produced long-term
clinical
remissions.
We studied primary
ATLL
tumors and identified molecular features linked to sensitivity and resistance to antiviral therapy.
This
finding
was independent of the
disease
form.
Elevated expression of the putative c-Rel target, interferon regulatory factor-4 (IRF-4), was observed in 10 (91%) of 11 nonresponders and in all tested patients with c-Rel+ tumors and occurred in the absence of the
HTLV
-1 oncoprotein Tax.
Gene rearrangement studies demonstrated the persistence of circulating T-
cell
clones in long-term survivors maintained on antiviral therapy.
The expression of nuclear c-Rel and IRF-4 occurs in the absence of Tax in primary
ATLL
and is
associated
with antiviral resistance.
AZT and IFN-alpha is a suppressive rather than a curative regimen, and patients in
clinical
remission should remain on maintenance therapy indefinitely.
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.
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[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U01 CA070058; United States / NCI NIH HHS / CA / CA-10521; United States / NCI NIH HHS / CA / R01 CA082274; United States / NCI NIH HHS / CA / CA-082274; United States / NCI NIH HHS / CA / U01-CA-070058
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antiviral Agents; 0 / DNA-Binding Proteins; 0 / HIVEN86A protein, human; 0 / Interferon Regulatory Factors; 0 / Interferon Type I; 0 / NF-kappa B; 0 / Nuclear Proteins; 0 / Recombinant Proteins; 0 / interferon regulatory factor-4; 4B9XT59T7S / Zidovudine
[Other-IDs]
NLM/ PMC1852214
64.
Ishikawa C, Tafuku S, Kadekaru T, Sawada S, Tomita M, Okudaira T, Nakazato T, Toda T, Uchihara JN, Taira N, Ohshiro K, Yasumoto T, Ohta T, Mori N:
Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol.
Int J Cancer
; 2008 Dec 1;123(11):2702-12
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[Title]
Anti-
adult
T-
cell
leukemia
effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol.
Adult
T-
cell
leukemia
(
ATL
) is a fatal malignancy of T lymphocytes caused by
human
T-
cell
leukemia virus
type 1 (
HTLV
-1) infection and remains incurable.
We evaluated the anti-
ATL
effects of fucoxanthin and its metabolite, fucoxanthinol.
Both carotenoids inhibited
cell
viability of
HTLV
-1-infected T-
cell
lines and
ATL
cells, and fucoxanthinol was approximately twice more potent than fucoxanthin.
In contrast, other carotenoids, beta-carotene and astaxanthin, had mild inhibitory effects on
HTLV
-1-infected T-
cell
lines.
Importantly, uninfected
cell
lines and normal peripheral blood mononuclear cells were resistant to fucoxanthin and fucoxanthinol.
Both carotenoids induced
cell
cycle arrest during G(1) phase by reducing the expression of cyclin D1, cyclin D2, CDK4 and CDK6, and inducing the expression of GADD45alpha, and induced apoptosis by reducing the expression of Bcl-2, XIAP, cIAP2 and survivin.
The induced apoptosis was
associated
with activation of caspase-3, -8 and -9.
Mice with severe combined immunodeficiency harboring tumors induced by inoculation of
HTLV
-1-infected T cells responded to treatment with fucoxanthinol with suppression of tumor growth, showed extensive tissue distribution of fucoxanthinol, and the presence of therapeutically effective serum concentrations of fucoxanthinol.
Our preclinical data suggest that fucoxanthin and fucoxanthinol could be potentially useful therapeutic agents for patients with
ATL
.
[MeSH-major]
Antineoplastic Agents / therapeutic use.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ drug therapy.
Leukemia
-
Lymphoma
,
Adult
T-
Cell
/ pathology. Phaeophyta / chemistry. Xanthophylls / therapeutic use. beta Carotene / analogs & derivatives
[MeSH-minor]
Acetylation. Animals. Caspases / metabolism.
Cell
Survival / drug effects. Female.
Human
T-
lymphotropic virus
1 / drug effects. Humans. Mice. NF-kappa B / metabolism. Transcription Factor AP-1 / metabolism. Tumor Cells, Cultured. Xenograft Model Antitumor Assays
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.
NCI CPTC Antibody Characterization Program.
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.
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.
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NCI CPTC Antibody Characterization Program
.
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[Copyright]
(c) 2008 Wiley-Liss, Inc.
(PMID = 18798263.001).
[ISSN]
1097-0215
[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
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 0 / Xanthophylls; 01YAE03M7J / beta Carotene; 06O0TC0VSM / fucoxanthin; 7176-02-5 / fucoxanthinol; EC 3.4.22.- / Caspases
65.
Mirsaliotis A, Nurkiyanova K, Lamb D, Kuo CW, Brighty DW:
An antibody that blocks human T-cell leukemia virus type 1 six-helix-bundle formation in vitro identified by a novel assay for inhibitors of envelope function.
J Gen Virol
; 2007 Feb;88(Pt 2):660-9
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[Title]
An antibody that blocks
human
T-
cell
leukemia virus
type 1 six-helix-bundle formation in vitro identified by a novel assay for inhibitors of envelope function.
Fusion of the viral and cellular membranes is a critical step in the infection of cells by the
human
T-
cell
leukemia virus
type 1 (
HTLV
-1) and this process is catalysed by the viral envelope glycoproteins.
Importantly, synthetic peptides that interfere with the conformational changes of TM are potent inhibitors of membrane fusion and
HTLV
-1 entry, suggesting that the pre-hairpin motif is a valid target for antiviral therapy.
However, the mAb failed to neutralize
HTLV
-1 envelope-mediated membrane fusion, suggesting that, on native viral envelope, the epitope recognized by the mAb is obscured during fusion.
This novel mAb will be of value in the immunological characterization of fusion-active structures of
HTLV
-1 TM.
Moreover, the assay developed here will aid the search for therapeutic antibodies, peptides and small-molecule inhibitors targeting envelope and the
HTLV
-1 entry process.
[MeSH-major]
Antibodies, Monoclonal / pharmacology. Glycoproteins / metabolism.
Human
T-
lymphotropic virus
1 / metabolism. Membrane Fusion / drug effects. Viral Envelope Proteins / metabolism
[MeSH-minor]
Amino Acid Sequence.
Cell
Membrane / drug effects.
Cell
Membrane / metabolism. HeLa Cells. Humans. Models, Molecular. Molecular Sequence Data. Peptides / chemical synthesis. Peptides / chemistry. Peptides / metabolism. Peptides / pharmacology. Protein Conformation
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(PMID = 17251585.001).
[ISSN]
0022-1317
[Journal-full-title]
The Journal of general virology
[ISO-abbreviation]
J. Gen. Virol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Glycoproteins; 0 / Peptides; 0 / Viral Envelope Proteins
66.
Cunha L, Plouzeau C, Ingrand P, Gudo JP, Ingrand I, Mondlane J, Beauchant M, Agius G:
Use of replacement blood donors to study the epidemiology of major blood-borne viruses in the general population of Maputo, Mozambique.
J Med Virol
; 2007 Dec;79(12):1832-40
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[Title]
Use of replacement blood donors to study the epidemiology of major blood-borne
viruses
in the general population of Maputo, Mozambique.
The seroprevalence rates of
human
immunodeficiency
virus
(HIV),
human
T-
cell
leukemia
/
lymphoma
virus
(
HTLV
), hepatitis B
virus
(HBV), hepatitis D
virus
(HDV), and hepatitis
C virus
(HCV) in Mozambique are poorly documented.
All donors attending the blood bank during the study period were interviewed and underwent serological and molecular tests for markers of
virus
exposure.
The age-standardized prevalence rates among 15- to 49-year-old men and women were, respectively, 12.3 and 15.4% for HIV and 0.9 and 1.2% for
HTLV
.
The age-adjusted prevalence rates of markers of hepatotropic
virus
among men and women were, respectively, 10.6 and 4.5% for hepatitis B surface antigen (HBsAg), 1.2 and 1.0% for anti-HCV, and 0 and 0% for anti-HDV.
HBsAg was
associated
with the place of birth (P = 0.011) and a history of transfusion (P = 0.069).
[MeSH-minor]
Adolescent.
Adult
. Aged. Aged, 80 and over. Antibodies, Viral / blood. Antigens, Viral / blood. Cross-Sectional Studies. Female. Hepacivirus / genetics. Hepatitis B
virus
/ genetics. Humans. Male. Middle Aged. Mozambique / epidemiology. Seroepidemiologic Studies
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.
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.
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.
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[Copyright]
(c) Wiley-Liss, Inc.
(PMID = 17935167.001).
[ISSN]
0146-6615
[Journal-full-title]
Journal of medical virology
[ISO-abbreviation]
J. Med. Virol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Viral; 0 / Antigens, Viral
67.
Shanmugam H, Eow GI, Nadarajan VS:
A case report of adult T-cell leukaemia/lymphoma.
Malays J Pathol
; 2009 Jun;31(1):63-6
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[Title]
A case report of
adult
T-
cell
leukaemia
/
lymphoma
.
Adult
T-
cell
leukaemia
/
lymphoma
(
ATLL
) is a rare T lymphoproliferative
disorder
which is aetiologically linked with
human
T-
cell
lymphotropic virus
type-1 (
HTLV
-1).
HTLV
-1 is endemic in Japan, Caribbean and Africa.
The highest incidence of
ATLL
is in Japan although sporadic cases have been reported elsewhere in the world.
We describe a case of
ATLL
with an unusual presentation which we believe is the first reported case of
ATLL
in Malaysia based on our literature search.
A 51-year-old Indian lady was referred to University Malaya Medical Centre for an incidental
finding
of lymphocytosis while being investigated for pallor and giddiness.
Clinical
examination revealed bilateral shotty cervical lymph nodes with no hepato-splenomegaly or skin lesions.
Immunophenotyping of the bone marrow mononuclear cells showed CD3+, CD4+, CD5+, CD7- and CD25+ which is characteristic of
ATLL
phenotype.
HTLV
-1 infection was confirmed by the presence of
HTLV
-1 proviral DNA in the tumor cells using conventional Polymerase Chain Reaction (PCR) and real-time PCR.
Here, we discuss the pathogenesis and characteristics of
ATLL
as well as the detection of
HTLV
-1 by real time PCR.
[MeSH-major]
Leukemia
, T-
Cell
/ pathology.
Lymphoma
, T-
Cell
/ pathology
[MeSH-minor]
Antigens, CD / metabolism. Bone Marrow Cells / pathology. Bone Marrow Cells / virology. DNA, Viral / analysis. Female. Flow Cytometry.
HTLV
-I Infections / complications.
HTLV
-I Infections / pathology.
Human
T-
lymphotropic virus
1 / genetics.
Human
T-
lymphotropic virus
1 / isolation & purification. Humans. Immunophenotyping. L-Lactate Dehydrogenase / blood. Leukocytosis / etiology. Leukocytosis / pathology. Lymph Nodes / metabolism. Lymph Nodes / pathology. Lymph Nodes / virology. Middle Aged. Monocytes / pathology. Polymerase Chain Reaction
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(PMID = 19694316.001).
[ISSN]
0126-8635
[Journal-full-title]
The Malaysian journal of pathology
[ISO-abbreviation]
Malays J Pathol
[Language]
eng
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