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1
acute myeloid leukemia m6 type 2005:2010[pubdate] *count=100
1058 results
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Items 1 to 100 of about 1058
1.
Witter DJ, Belvedere S, Chen L, Secrist JP, Mosley RT, Miller TA:
Benzo[b]thiophene-based histone deacetylase inhibitors.
Bioorg Med Chem Lett
; 2007 Aug 15;17(16):4562-7
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It was determined that substitution at the C6-position of the benzo[b]thiophene core with a three-atom spacer yielded optimal HDAC1 inhibition and anti-proliferative activity in murine
erythroleukemia
(SC-9) cells.
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(PMID = 17576064.001).
[ISSN]
0960-894X
[Journal-full-title]
Bioorganic & medicinal chemistry letters
[ISO-abbreviation]
Bioorg. Med. Chem. Lett.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Histone Deacetylase Inhibitors; 0 / Thiophenes
2.
Sun G, Guo H, Peterson J:
Seasonal odor, ammonia, hydrogen sulfide, and carbon dioxide concentrations and emissions from swine grower-finisher rooms.
J Air Waste Manag Assoc
; 2010 Apr;60(4):471-80
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The measured gas concentrations were generally below the
permissible exposure limits
(PELs) established by the Occupational Safety and Health Administration (OSHA) throughout the year except for the NH3 concentrations in cold weather (December, January, and February).
Hazardous Substances Data Bank.
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HYDROGEN SULFIDE
.
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(PMID = 20437782.001).
[ISSN]
1096-2247
[Journal-full-title]
Journal of the Air & Waste Management Association (1995)
[ISO-abbreviation]
J Air Waste Manag Assoc
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
142M471B3J / Carbon Dioxide; 7664-41-7 / Ammonia; YY9FVM7NSN / Hydrogen Sulfide
3.
Fukumoto T, Kubota Y, Kitanaka A, Yamaoka G, Ohara-Waki F, Imataki O, Ohnishi H, Ishida T, Tanaka T:
Gab1 transduces PI3K-mediated erythropoietin signals to the Erk pathway and regulates erythropoietin-dependent proliferation and survival of erythroid cells.
Cell Signal
; 2009 Dec;21(12):1775-83
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[Title]
Gab1 transduces PI3K-mediated erythropoietin signals to the Erk pathway and regulates erythropoietin-dependent proliferation and survival
of erythroid
cells.
Knockdown of Gab1 by the introduction of the Gab1 siRNA expression vector into F-36P human
erythroleukemia
(F-36P-Gab1-siRNA) cells resulted in a reduction of cell proliferation and survival in response to EPO.
LY294002 inhibited EPO-induced tyrosine phosphorylation of Gab1 and its association with Grb2 in human primary EPO-sensitive
erythroid
cells.
Taken together, these results suggest that Gab1 couples PI3K-mediated EPO signals with the Ras/Erk pathway and that Gab1 plays an important role in EPOR-mediated signal transduction involved in the proliferation and survival
of erythroid
cells.
[MeSH-major]
Adaptor Proteins, Signal Transducing / metabolism.
Erythroid
Cells / cytology. Erythropoietin / metabolism. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Phosphatidylinositol 3-Kinases / metabolism
[MeSH-minor]
Apoptosis. Cell Line, Tumor. Cell Proliferation. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. GRB2 Adaptor Protein / metabolism.
Gene
Knockdown Techniques. Humans. Janus Kinase 2 / antagonists & inhibitors. Janus Kinase 2 / metabolism.
Leukemia
,
Erythroblastic
,
Acute
/ metabolism. Morpholines / pharmacology. Protein Tyrosine Phosphatase, Non-Receptor
Type
11 / metabolism. Receptors, Erythropoietin / metabolism. SOS1 Protein / metabolism
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(PMID = 19665053.001).
[ISSN]
1873-3913
[Journal-full-title]
Cellular signalling
[ISO-abbreviation]
Cell. Signal.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / GAB1 protein, human; 0 / GRB2 Adaptor Protein; 0 / GRB2 protein, human; 0 / Morpholines; 0 / Receptors, Erythropoietin; 0 / SOS1 Protein; 11096-26-7 / Erythropoietin; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
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4.
Lim SH, Kemling JW, Feng L, Suslick KS:
A colorimetric sensor array of porous pigments.
Analyst
; 2009 Dec;134(12):2453-7
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The development
of a
low-cost, simple colorimetric sensor array capable of the detection and identification of toxic gases is reported.
Striking visual identification of 3 toxic gases has been shown at the IDLH (immediately dangerous to life and health) concentration, at the
PEL
(
permissible exposure level
), and at
a level
well below the
PEL
.
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.
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[Cites]
Nature. 2000 Aug 17;406(6797):710-3
[
10963592.001
]
[Cites]
Nat Mater. 2003 Jan;2(1):19-24
[
12652667.001
]
[Cites]
Acc Chem Res. 2004 Sep;37(9):663-72
[
15379582.001
]
[Cites]
MRS Bull. 2004 Oct;29(10):720-5
[
15991401.001
]
[Cites]
Angew Chem Int Ed Engl. 2005 Jul 18;44(29):4528-32
[
16003792.001
]
[Cites]
Anal Chem. 2009 Aug 1;81(15):6526-33
[
20337402.001
]
[Cites]
Anal Chem. 2006 Jun 1;78(11):3591-600
[
16737212.001
]
[Cites]
J Agric Food Chem. 2006 Jul 12;54(14):4925-31
[
16819897.001
]
[Cites]
J Agric Food Chem. 2007 Jan 24;55(2):237-42
[
17227048.001
]
[Cites]
J Org Chem. 2007 Feb 2;72(3):687-99
[
17253783.001
]
[Cites]
Org Lett. 2008 Oct 16;10(20):4405-8
[
18783231.001
]
[Cites]
J Am Chem Soc. 2005 Aug 24;127(33):11548-9
[
16104700.001
]
(PMID = 19918616.001).
[ISSN]
1364-5528
[Journal-full-title]
The Analyst
[ISO-abbreviation]
Analyst
[Language]
ENG
[Grant]
United States / NIEHS NIH HHS / ES / ES016011-03; United States / NIEHS NIH HHS / ES / U01 ES016011; United States / NIEHS NIH HHS / ES / U01 ES016011-03; United States / NIEHS NIH HHS / ES / U01ES016011
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Air Pollutants; 0 / Coloring Agents; 0 / Gases; 0 / Membranes, Artificial; 0UZA3422Q4 / Sulfur Dioxide; 4R7X1O2820 / Chlorine; 7664-41-7 / Ammonia
[Other-IDs]
NLM/ NIHMS229255; NLM/ PMC2947824
5.
Shaked Y, Cervi D, Neuman M, Chen L, Klement G, Michaud CR, Haeri M, Pak BJ, Kerbel RS, Ben-David Y:
The splenic microenvironment is a source of proangiogenesis/inflammatory mediators accelerating the expansion of murine erythroleukemic cells.
Blood
; 2005 Jun 1;105(11):4500-7
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Here we have used Friend murine
leukemia
virus (F-MuLV)-induced
erythroleukemia
to investigate factors of the splenic microenvironment that may make it fertile for the expansion and survival
of malignant
erythroblasts.
Cytokine protein arrays revealed that F-MuLV-infected splenocytes secreted elevated
levels of
interleukin-6 (IL-6), vascular endothelial growth factor-A (VEGF-A), macrophage chemoattractant protein-5 (MCP-5), soluble tumor necrosis factor receptor-1 (sTNFR1), IL-12p70, tumor necrosis factor-alpha (TNF-alpha), and IL-2 over normal splenocytes.
Furthermore, in vivo administration
of a
neutralizing antibody to VEGF-A extended survival times of erythroleukemic mice in comparison with controls.
These findings suggest that VEGF-A and MCP-5 are potentially pivotal paracrine mediators occurring within the diseased splenic microenvironment capable of promoting
disease
acceleration and expansion of erythroleukemic blasts.
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[Cites]
Blood Cells. 1981;7(1):133-44
[
7187746.001
]
[Cites]
Clin Haematol. 1983 Jun;12(2):505-16
[
6352114.001
]
[Cites]
Curr Top Microbiol Immunol. 1989;148:1-42
[
2684547.001
]
[Cites]
Exp Hematol. 1990 Aug;18(7):775-84
[
1696206.001
]
[Cites]
Leuk Lymphoma. 1993 Jul;10(4-5):245-64
[
8220125.001
]
[Cites]
Eur J Haematol. 1996 Jan-Feb;56(1-2):45-53
[
8599993.001
]
[Cites]
J Exp Med. 1997 Jan 6;185(1):99-109
[
8996246.001
]
[Cites]
Am J Pathol. 1997 Mar;150(3):815-21
[
9060819.001
]
[Cites]
Leukemia. 1997 Apr;11 Suppl 3:474-7
[
9209429.001
]
[Cites]
Virchows Arch. 1997 Jun;430(6):433-43
[
9230908.001
]
[Cites]
Eur J Cell Biol. 1997 Dec;74(4):321-8
[
9438127.001
]
[Cites]
Leuk Lymphoma. 1997 Nov;27(5-6):375-86
[
9477120.001
]
[Cites]
Blood. 1998 Mar 1;91(5):1548-55
[
9473219.001
]
[Cites]
Blood. 1998 Dec 15;92(12):4798-807
[
9845547.001
]
[Cites]
Mol Cell Biol. 1999 Jun;19(6):4452-64
[
10330185.001
]
[Cites]
Virology. 1964 Nov;24:513-8
[
14227060.001
]
[Cites]
Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):712-9
[
15701860.001
]
[Cites]
Exp Hematol. 2000 Jun;28(6):700-6
[
10880756.001
]
[Cites]
Clin Cancer Res. 2000 Aug;6(8):3282-9
[
10955814.001
]
[Cites]
J Immunol Methods. 2001 Jun 1;252(1-2):131-8
[
11334972.001
]
[Cites]
Nature. 2001 May 17;411(6835):375-9
[
11357145.001
]
[Cites]
Blood. 2001 Jun 1;97(11):3658-61
[
11369666.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10857-62
[
11553814.001
]
[Cites]
Ann Hematol. 2001 Dec;80(12):695-705
[
11797109.001
]
[Cites]
Blood. 2002 Mar 15;99(6):2179-84
[
11877295.001
]
[Cites]
Blood. 2002 Apr 1;99(7):2532-40
[
11895790.001
]
[Cites]
Cancer Res. 2002 Mar 15;62(6):1838-46
[
11912163.001
]
[Cites]
Am J Hematol. 2002 May;70(1):22-30
[
11994978.001
]
[Cites]
J Mol Med (Berl). 2003 Jan;81(1):20-31
[
12545246.001
]
[Cites]
APMIS. 2002 Dec;110(12):899-912
[
12645669.001
]
[Cites]
Nat Med. 2003 Jun;9(6):653-60
[
12778163.001
]
[Cites]
Anticancer Res. 2003 May-Jun;23(3A):2159-66
[
12894591.001
]
[Cites]
Cancer Res. 2003 Aug 1;63(15):4342-6
[
12907602.001
]
[Cites]
Cancer Sci. 2003 Dec;94(12):1034-41
[
14662017.001
]
[Cites]
Cancer. 1978 Aug;42(2 Suppl):946-56
[
356959.001
]
[Cites]
Exp Hematol. 1985 Aug;13(7):623-8
[
3861325.001
]
(PMID = 15701719.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA-41233
[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.
[Publication-country]
United States
[Chemical-registry-number]
0 / Angiogenic Proteins; 0 / Antibodies, Monoclonal; 0 / Cytokines; 0 / Inflammation Mediators; 0 / Monocyte Chemoattractant Proteins; 0 / Vascular Endothelial Growth Factor A
[Other-IDs]
NLM/ PMC1895028
6.
Xie SQ, Wu YL, Liu GC, Cheng PF, Wang MW, Ma YF, Zhao J, Wang CJ:
[Apoptosis induced by NNAMB, a novel polyamine conjugate, in human erythroleukemia K562 cells and its mechanism].
Zhonghua Zhong Liu Za Zhi
; 2008 Jul;30(7):490-3
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[Title]
[Apoptosis induced by NNAMB, a novel polyamine conjugate, in human
erythroleukemia
K562 cells and its mechanism].
OBJECTIVE: To investigate the apoptosis-inducing effects of NNAMB, a novel polyamine conjugate, in
erythroleukemia
K562 cells and its molecular mechanism.
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(PMID = 19062712.001).
[ISSN]
0253-3766
[Journal-full-title]
Zhonghua zhong liu za zhi [Chinese journal of oncology]
[ISO-abbreviation]
Zhonghua Zhong Liu Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Anthracenes; 0 / NNAMB compound; 0 / Polyamines; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9; U87FK77H25 / Spermidine
7.
Scher W, Jing Y, Lu M, Bishop DF, Scher BM:
Sequences of polycythemia-type Friend spleen focus-forming virus in clone-745-derived mouse erythroleukemia cells.
Arch Virol
; 2009;154(5):895-8
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[Title]
Sequences of polycythemia-
type
Friend spleen focus-forming virus in clone-745-derived mouse
erythroleukemia
cells.
Friend
leukemia
virus complex consists
of a
replication-competent virus plus one of two replication-incompetent viruses, spleen focus-forming virus anemia virus or spleen focus-forming virus polycythemia virus.
The replication-incompetent viruses induce rapid
malignant
transformation
of erythroid
precursor cells.
However, lines containing the anemia-
type
virus require erythropoietin and another agent such as dimethyl sulfoxide for optimal erythrodifferentiation, whereas those containing the polycythemia-
type
virus do not require or respond to erythropoietin.
Sequence analysis demonstrates that they contain the polycythemia-
type
virus and not the anemia-
type
virus.
[MeSH-minor]
Animals. Cell Differentiation. Cell Line, Transformed.
Leukemia
, Experimental / virology. Mice. Molecular Sequence Data. RNA, Viral / genetics. Retroviridae Infections / virology. Sequence Analysis, RNA. Tumor Virus Infections / virology
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(PMID = 19347245.001).
[ISSN]
1432-8798
[Journal-full-title]
Archives of virology
[ISO-abbreviation]
Arch. Virol.
[Language]
eng
[Databank-accession-numbers]
GENBANK/ FJ556972/ FJ556973
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Austria
[Chemical-registry-number]
0 / RNA, Viral
8.
Terano T, Zhong Y, Toyokuni S, Hiai H, Yamada Y:
Transcriptional control of fetal liver hematopoiesis: dominant negative effect of the overexpression of the LIM domain mutants of LMO2.
Exp Hematol
; 2005 Jun;33(6):641-51
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OBJECTIVE: The LIM-finger protein LMO2 forms a transcription factor complex with other hematopoietic regulator proteins, such as TAL1 (SCL), LDB1, GATA1, 2, and 3, in the promoters of several
erythroid genes
.
In vivo hematopoiesis in transgenic mice with wild-
type
and LIM-modified Lmo2 was studied morphologically and by measuring the progenitor cells in fetal liver.
Their effects on the
erythroid
differentiation of the dimethylsulfoxide (DMSO)-induced murine
erythroleukemia
(MEL) cells were evaluated.
Overexpression of wild-
type
LMO2 is known to have dominant negative inhibitory effects on erythropoietic development.
DMSO-induced
erythroid
differentiation of the MEL cells was inhibited by the overexpressed LMO2 with mutant LIM2 but not by the LMO2 with modified LIM1.
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 = 15911088.001).
[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 / Adaptor Proteins, Signal Transducing; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins
9.
Tang ZK, Zhai JP, Tong YY, Hu XJ, Saito R, Feng YJ, Sheng P:
Resonant Raman scattering of the smallest single-walled carbon nanotubes.
Phys Rev Lett
; 2008 Jul 25;101(4):047402
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These ultrasmall SWNTs are fabricated in the elliptical nanochannels of an AlPO-11 (
AEL
) single crystal.
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(PMID = 18764364.001).
[ISSN]
0031-9007
[Journal-full-title]
Physical review letters
[ISO-abbreviation]
Phys. Rev. Lett.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
10.
Novoselov SS, Novoselova TV, Verbova MV, Margulis BA, Guzhova IV:
[The balance between Hsp70 and its cochaperones Hdj1 and Bag1 determines its substrate-binding activity].
Tsitologiia
; 2005;47(3):220-9
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The accumulation of Hsp70 and Hdj 1 in human
erythroleukemia
K562 cells was stimulated by heat stress (43 degrees C, 60 min).
The
level of
Hsp70 chaperone activity in cell extracts was estimated using original technique.
The results of the study indicate that Hsp70 chaperone activity is regulated by the
level of
its cochaperones, especially Hdj 1.
This
finding
confirms the possibility of using peptide approach for regulation of Hsp70 function at the cellular and organismal
levels
.
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(PMID = 16706166.001).
[ISSN]
0041-3771
[Journal-full-title]
Tsitologiia
[ISO-abbreviation]
Tsitologiia
[Language]
rus
[Publication-type]
Comparative Study; English Abstract; Journal Article
[Publication-country]
Russia (Federation)
[Chemical-registry-number]
0 / BCL2-associated athanogene 1 protein; 0 / Culture Media; 0 / DNA-Binding Proteins; 0 / DNAJB1 protein, human; 0 / HSP40 Heat-Shock Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Transcription Factors; 8L70Q75FXE / Adenosine Triphosphate
11.
Zhang Y, Yao W, Zeng Z, Wang X, Sun D, Ka W, Zhou S, He D, Wen Z, Chien S:
Exogenous wild-type p53 gene improved survival of nude mice injected with murine erythroleukemia cell line through amelioration of hemorheological changes.
Microcirculation
; 2007 Feb;14(2):155-66
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[Title]
Exogenous wild-
type
p53
gene
improved survival of nude mice injected with murine
erythroleukemia
cell line through amelioration of hemorheological changes.
OBJECTIVES: Previous investigations have shown that human wild-
type
p53
gene
(WTp53) inhibits the growth of
leukemia
and tumor cells in vitro.
In the present study, the authors used nude mice and examined the therapeutic role of p53
gene
for
erythroleukemia
in vivo in the absence of MHC effects.
METHODS: The nude mice were injected with murine
erythroleukemia
cells (MEL), MEL cells transfected with wild-
type
p53
gene
(MEL-W), and MEL cells transfected with mutated p53
gene
(MEL-M).
RESULTS: The results showed that WTp53 restrained the growth
of erythroleukemia
cells in vivo and reduced the
erythroleukemia
tumorigenesis in the microcirculation by improving the hemorheological and biophysical properties of MEL cells, which helped to prolong the life span of nude mice suffering from
erythroleukemia
.
CONCLUSION: These results contribute to our knowledge on the use of wild-
type
p53
gene
for the treatment
of erythroleukemia disease
.
[MeSH-major]
Leukemia
,
Erythroblastic
,
Acute
/ pathology.
Leukemia
,
Erythroblastic
,
Acute
/ physiopathology. Tumor Suppressor Protein p53 / genetics
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(PMID = 17365670.001).
[ISSN]
1073-9688
[Journal-full-title]
Microcirculation (New York, N.Y. : 1994)
[ISO-abbreviation]
Microcirculation
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Tumor Suppressor Protein p53
12.
Catani MV, Fezza F, Baldassarri S, Gasperi V, Bertoni A, Pasquariello N, Finazzi-Agrò A, Sinigaglia F, Avigliano L, Maccarrone M:
Expression of the endocannabinoid system in the bi-potential HEL cell line: commitment to the megakaryoblastic lineage by 2-arachidonoylglycerol.
J Mol Med (Berl)
; 2009 Jan;87(1):65-74
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We investigated whether human
erythroleukemia
(HEL) cells were able to bind, metabolise and transport the main endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol (2-AG).
Indeed, 2-AG itself drove HEL cells towards megakaryocytic differentiation, as it enhanced expression of beta3 integrin subunit, a megakaryocyte/platelet surface antigen, and glycoprotein VI, a late marker of megakaryocytes; in parallel, it reduced the amount of messenger RNA encoding for glycophorin A, a marker
of erythroid
phenotype.
In addition, classical inducers of megakaryocyte differentiation reduced 2-AG synthesis (although they did not affect the binding efficiency of CB(2) receptors), suggesting that
levels of
this endocannabinoid may be critical for committing HEL cells towards the megakaryocytic lineage.
[MeSH-major]
Arachidonic Acids / pharmacology. Cannabinoid Receptor Modulators / biosynthesis. Cannabinoid Receptor Modulators / pharmacology. Cell Differentiation / drug effects. Endocannabinoids.
Gene
Expression Regulation / drug effects. Glycerides / pharmacology. Megakaryocytes / metabolism
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[Cites]
Blood. 2004 Jul 15;104(2):526-34
[
15039279.001
]
[Cites]
Cell. 1995 Jan 27;80(2):179-85
[
7834738.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10819-24
[
12136125.001
]
[Cites]
Pharmacol Ther. 1997;74(2):129-80
[
9336020.001
]
[Cites]
J Clin Endocrinol Metab. 2006 Aug;91(8):3171-80
[
16684820.001
]
[Cites]
Eur J Biochem. 2004 May;271(10 ):1827-34
[
15128293.001
]
[Cites]
Blood. 2002 Dec 1;100(12 ):4040-8
[
12393387.001
]
[Cites]
Eur J Pharmacol. 2004 Jan 26;484(2-3):249-57
[
14744610.001
]
[Cites]
Neuroscience. 2003;119(2):481-96
[
12770562.001
]
[Cites]
Trends Pharmacol Sci. 2006 Mar;27(3):134-40
[
16476494.001
]
[Cites]
Thromb Haemost. 2003 Feb;89(2):340-7
[
12574815.001
]
[Cites]
Nature. 2000 Mar 9;404(6774):193-7
[
10724173.001
]
[Cites]
Free Radic Biol Med. 2007 Mar 1;42(5):608-16
[
17291984.001
]
[Cites]
Blood. 1987 Dec;70(6):1764-72
[
3676512.001
]
[Cites]
Curr Pharm Des. 2006;12 (18):2319-25
[
16787257.001
]
[Cites]
J Cell Sci. 2005 Oct 1;118(Pt 19):4393-404
[
16144868.001
]
[Cites]
Eur J Biochem. 2001 Feb;268(3):819-25
[
11168423.001
]
[Cites]
J Neurochem. 1997 Aug;69(2):631-8
[
9231721.001
]
[Cites]
EMBO J. 1984 Feb;3(2):453-9
[
6201359.001
]
[Cites]
Handb Exp Pharmacol. 2005;(168):599-625
[
16596789.001
]
[Cites]
Nat Rev Neurosci. 2003 Nov;4(11):873-84
[
14595399.001
]
[Cites]
Science. 2005 Oct 14;310(5746):329-32
[
16224028.001
]
[Cites]
AAPS J. 2006;8(2):E409-12
[
16808043.001
]
[Cites]
J Exp Med. 1981 Jul 1;154(1):88-100
[
6788894.001
]
[Cites]
J Pharmacol Exp Ther. 2002 Jan;300(1):339-45
[
11752134.001
]
[Cites]
FEBS Lett. 1999 Mar 26;447(2-3):277-82
[
10214961.001
]
[Cites]
J Biol Chem. 2000 Jan 7;275(1):605-12
[
10617657.001
]
[Cites]
J Cell Biol. 2003 Nov 10;163(3):463-8
[
14610053.001
]
[Cites]
Mini Rev Med Chem. 2006 Mar;6(3):257-68
[
16515464.001
]
[Cites]
Annu Rev Biochem. 2005;74:411-32
[
15952893.001
]
[Cites]
Nature. 2006 Nov 9;444(7116):208-12
[
17093448.001
]
[Cites]
J Biol Chem. 2004 Feb 13;279(7):5298-305
[
14634025.001
]
[Cites]
Cell Biol Int. 2004;28(5):403-10
[
15193284.001
]
[Cites]
Blood. 2003 Feb 15;101(4):1336-43
[
12406867.001
]
(PMID = 18820887.001).
[ISSN]
0946-2716
[Journal-full-title]
Journal of molecular medicine (Berlin, Germany)
[ISO-abbreviation]
J. Mol. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, Differentiation; 0 / Arachidonic Acids; 0 / Cannabinoid Receptor Modulators; 0 / Endocannabinoids; 0 / Glycerides; 0 / Polyunsaturated Alkamides; 8D239QDW64 / glyceryl 2-arachidonate; UR5G69TJKH / anandamide
13.
Davis DA, Singer KE, Reynolds IP, Haque M, Yarchoan R:
Hypoxia enhances the phosphorylation and cytotoxicity of ganciclovir and zidovudine in Kaposi's sarcoma-associated herpesvirus infected cells.
Cancer Res
; 2007 Jul 15;67(14):7003-10
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Primary effusion lymphoma (
PEL
) is a rare B-cell lymphoma caused by Kaposi's sarcoma-associated herpesvirus (KSHV).
PEL
is poorly responsive to standard cytotoxic chemotherapy and portends a poor survival.
It is known that KSHV encodes two lytic
genes
, ORF36 (phosphotransferase) and KSHV ORF21 (thymidine kinase), which can phosphorylate ganciclovir and azidothymidine, respectively.
Here, we have explored whether these
genes
can be used as therapeutic targets for
PEL
.
PEL
arises in pleural spaces and other effusions that provide a hypoxic environment.
Based on Northern blot analysis,
exposure of PEL
cells to hypoxia up-regulated the expression of both ORF36 and ORF21.
Using a newly developed nonradioactive reverse-phase high-performance liquid chromatography/mass spectrometry method to separate and quantify the phosphorylated forms of ganciclovir and azidothymidine, we found that
PEL
cells exposed to hypoxia produced increased amounts of the toxic triphosphates of these drugs.
Moreover, we found that hypoxia increased the cell toxicity of ganciclovir and azidothymidine in
PEL
cells but had no significant effect on the herpesvirus-negative cell line CA46.
These findings may have clinical applicability in the development of effective therapies for
PEL
or other KSHV-related malignancies.
MedlinePlus Health Information.
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Hazardous Substances Data Bank.
ZIDOVUDINE
.
Hazardous Substances Data Bank.
GANCICLOVIR
.
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(PMID = 17638913.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antiviral Agents; 4B9XT59T7S / Zidovudine; P9G3CKZ4P5 / Ganciclovir
14.
Zhang M, Qi C, Chen WH, Lu Y, Du XY, Li WJ, Meng CS:
[Re-analysis of occupational hazards in foundry].
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
; 2010 Apr;28(4):280-5
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The mean concentration of silica before 1986 was an extremely high
level of
8.6 mg/m(3), and then remarkably dropped after 1986, with the
level of
2.4 mg/m(3) from 1986 to 1989, 2.7 mg/m(3) from 1990 to 2002 and 2.7 mg/m(3) from 2003 to 2008.
Silica concentrations among jobs were significantly different, with highest
level
in melting (4.4 mg/m(3)), followed by cast shakeout and finishing (3.4 mg/m(3)), pouring (3.4 mg/m(3)), sand preparation (2.4 mg/m(3)), moulding (2.1 mg/m(3)) and core-making (1.7 mg/m(3)).
Mean concentration of asbestos dust in melting was a relative high
level of
2.0 mg/m(3).
Benzene and its homologues existed in cast shakeout and finishing, and the
level of
benzene, toluene, xylene was 0.2 mg/m(3), 0.1 mg/m(3) and 1.3 mg/m(3), respectively.
Mean concentration of benzo(a) pyrene was a low
level of
1.80 x 10(-4) microg/m(3).
Intensity of heat stress was high in melting, pouring and cast shakeout and finishing, with the
level of
30 degrees C, 29 degrees C and 26 degrees C, respectively.
Noise was high in cast shakeout and finishing and core-making, with the
level of
93.1 dB(A) and 89.5 dB(A), respectively.
CONCLUSION: Occupational hazards in environment of the foundry are diversified and their concentrations exceed
permissible exposure limits
stipulated by the national occupational hygienic standards.
[MeSH-major]
Dust / analysis. Hazardous Substances / analysis. Occupational
Exposure
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(PMID = 20465956.001).
[ISSN]
1001-9391
[Journal-full-title]
Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases
[ISO-abbreviation]
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Dust; 0 / Hazardous Substances
15.
Patnayak R, Paul TR, Uppin SG, K G, Rajappa S, Rao DR:
Acute erythroid leukemia (AML-M6) - Is it rare?
Turk J Haematol
; 2009 Mar 5;26(1):38-9
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[Title]
Acute
erythroid
leukemia
(
AML
-
M6
) - Is it rare?
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(PMID = 27265109.001).
[ISSN]
1300-7777
[Journal-full-title]
Turkish journal of haematology : official journal of Turkish Society of Haematology
[ISO-abbreviation]
Turk J Haematol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Turkey
16.
Adkins JN, Monroe ME, Auberry KJ, Shen Y, Jacobs JM, Camp DG 2nd, Vitzthum F, Rodland KD, Zangar RC, Smith RD, Pounds JG:
A proteomic study of the HUPO Plasma Proteome Project's pilot samples using an accurate mass and time tag strategy.
Proteomics
; 2005 Aug;5(13):3454-66
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This analysis highlighted both known differences in serum and citrated plasma such as fibrinogens, and reproducible differences in peptide abundances from proteins such as soluble activin receptor-like kinase 7b and glycoprotein
m6b
.
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[Cites]
Nat Biotechnol. 2001 Mar;19(3):242-7
[
11231557.001
]
[Cites]
Proteomics. 2004 Mar;4(3):656-68
[
14997489.001
]
[Cites]
Lancet. 2002 Feb 16;359(9306):572-7
[
11867112.001
]
[Cites]
Proteomics. 2002 Mar;2(3):288-305
[
11921445.001
]
[Cites]
Proteomics. 2002 May;2(5):513-23
[
11987125.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Aug 20;99(17):11049-54
[
12177431.001
]
[Cites]
Anal Chem. 2002 Oct 15;74(20):5383-92
[
12403597.001
]
[Cites]
Anal Chem. 2002 Nov 1;74(21):5593-9
[
12433093.001
]
[Cites]
Mol Cell Proteomics. 2002 Nov;1(11):845-67
[
12488461.001
]
[Cites]
Mol Cell Proteomics. 2002 Dec;1(12):947-55
[
12543931.001
]
[Cites]
Nat Biotechnol. 2003 Mar;21(3):247-54
[
12610571.001
]
[Cites]
J Proteome Res. 2003 Jan-Feb;2(1):43-50
[
12643542.001
]
[Cites]
J Proteome Res. 2002 Sep-Oct;1(5):459-65
[
12645918.001
]
[Cites]
J Mol Diagn. 2003 May;5(2):73-81
[
12707371.001
]
[Cites]
EHP Toxicogenomics. 2003 Jan;111(1T):1-5
[
12735104.001
]
[Cites]
Proteomics. 2003 Jul;3(7):1345-64
[
12872236.001
]
[Cites]
J Proteome Res. 2003 Jul-Aug;2(4):383-93
[
12938928.001
]
[Cites]
Mol Cell Proteomics. 2003 Oct;2(10):1096-103
[
12917320.001
]
[Cites]
Nature. 2003 Oct 30;425(6961):905
[
14586448.001
]
[Cites]
Anal Chem. 2003 Sep 1;75(17):4646-58
[
14632076.001
]
[Cites]
Mol Cell Proteomics. 2004 Jan;3(1):1-9
[
14608001.001
]
[Cites]
J Am Soc Mass Spectrom. 2004 Feb;15(2):212-32
[
14766289.001
]
[Cites]
Anal Chem. 2004 Feb 15;76(4):1134-44
[
14961748.001
]
[Cites]
J Proteome Res. 2004 Jan-Feb;3(1):68-75
[
14998165.001
]
[Cites]
Mol Cell Proteomics. 2004 Apr;3(4):311-26
[
14718574.001
]
[Cites]
Mol Cell Proteomics. 2004 Apr;3(4):298-301
[
14747694.001
]
[Cites]
J Proteome Res. 2004 Mar-Apr;3(2):163
[
15113090.001
]
[Cites]
Proteomics. 2004 May;4(5):1235-40
[
15188391.001
]
[Cites]
Mol Cell Proteomics. 2004 Jun;3(6):608-14
[
15034119.001
]
[Cites]
Proteomics. 2004 Jul;4(7):2125-50
[
15221774.001
]
[Cites]
J Proteome Res. 2004 May-Jun;3(3):364-82
[
15253417.001
]
[Cites]
Nat Biotechnol. 2004 Aug;22(8):985-92
[
15258593.001
]
[Cites]
J Proteome Res. 2004 Jul-Aug;3(4):760-9
[
15359729.001
]
[Cites]
Anal Chem. 2004 Sep 15;76(18):5345-53
[
15362891.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Sep 14;101(37):13417-22
[
15347803.001
]
[Cites]
Rapid Commun Mass Spectrom. 2004;18(19):2201-7
[
15384137.001
]
[Cites]
Proc Natl Acad Sci U S A. 1977 Dec;74(12):5421-5
[
271964.001
]
[Cites]
EMBO J. 1990 Mar;9(3):797-803
[
2311582.001
]
[Cites]
Methods Mol Biol. 1999;112:553-69
[
10027276.001
]
[Cites]
Nat Biotechnol. 1999 Jul;17(7):676-82
[
10404161.001
]
[Cites]
Biotechniques. 2004 Oct;37(4):621-4, 626-33, 636 passim
[
15517975.001
]
[Cites]
Anal Chem. 2004 Dec 1;76(23):6853-60
[
15571333.001
]
[Cites]
IEEE Comput Graph Appl. 2004 Sep-Oct;24(5):10-5
[
15628094.001
]
[Cites]
Anal Chem. 2005 Jan 15;77(2):400-6
[
15649034.001
]
[Cites]
J Proteome Res. 2005 Jan-Feb;4(1):53-62
[
15707357.001
]
[Cites]
Mol Cell Proteomics. 2005 May;4(5):700-9
[
15753121.001
]
[Cites]
Anal Chem. 2001 Dec 1;73(23):5683-90
[
11774908.001
]
(PMID = 16052625.001).
[ISSN]
1615-9853
[Journal-full-title]
Proteomics
[ISO-abbreviation]
Proteomics
[Language]
ENG
[Grant]
United States / NCRR NIH HHS / RR / P41 RR018522; United States / NCI NIH HHS / CA / CA78722; United States / NCRR NIH HHS / RR / RR18522
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
Germany
[Chemical-registry-number]
0 / Blood Proteins; 0 / Ions; 0 / Peptides; 0 / Proteins; 0 / Proteome; 9001-32-5 / Fibrinogen; EC 3.4.21.4 / Trypsin
[Other-IDs]
NLM/ NIHMS15646; NLM/ PMC2041806
17.
Li D, He G, Xu Y, Duan Y, Gu N, Li X, Shi Y, Qin W, Feng G, He L:
Schizophrenia is not associated with the ERBB3 gene in a Han Chinese population sample: Results from case-control and family-based studies.
Genet Mol Biol
; 2009 Oct;32(4):729-30
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[Title]
Schizophrenia is not associated with the ERBB3
gene
in a Han Chinese population sample: Results from case-control and family-based studies.
ERBB3 (v-erb-b2
erythroblastic
leukemia
viral oncogene homolog 3), encoding a receptor of neuregulin-1 (NRG1), has been considered a functional candidate
gene
for schizophrenia susceptibility.
In order to investigate a relationship between ERBB3
gene
and schizophrenia in the Chinese population, case-control and family-based studies were carried out in 470 cases matched by controls, and in 532 family trios.
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[Cites]
Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4746-51
[
11296301.001
]
[Cites]
Nat Genet. 2001 Aug;28(4):386-8
[
11455389.001
]
[Cites]
Lancet. 2003 Sep 6;362(9386):798-805
[
13678875.001
]
[Cites]
Biochem Biophys Res Commun. 2005 Sep 2;334(3):817-23
[
16023997.001
]
[Cites]
Ann Hum Genet. 1995 Jan;59(Pt 1):97-105
[
7762987.001
]
[Cites]
Am J Med Genet B Neuropsychiatr Genet. 2007 Jan 5;144B(1):113-6
[
16958035.001
]
[Cites]
Neurosci Res. 2007 Apr;57(4):574-8
[
17275115.001
]
[Cites]
Behav Brain Funct. 2007;3:31
[
17598910.001
]
[Cites]
Hum Mol Genet. 2006 Jun 15;15(12):1995-2002
[
16687441.001
]
(PMID = 21637446.001).
[ISSN]
1678-4685
[Journal-full-title]
Genetics and molecular biology
[ISO-abbreviation]
Genet. Mol. Biol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Brazil
[Other-IDs]
NLM/ PMC3036886
[Keywords]
NOTNLM ; ERBB3 gene / schizophrenia
18.
Tanaka PY, Atala MM, Pereira J, Caterino-de-Araujo A:
Primary effusion lymphoma with cardiac involvement in HIV positive patient-complete response and long survival with chemotherapy and HAART.
J Clin Virol
; 2009 Jan;44(1):84-5
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Primary effusion lymphoma (
PEL
) is a rare
type
of lymphoma related to herpesvirus-8 (HHV-8), and considered an AIDS-defining condition.
The authors describe a case
of PEL
with cardiac involvement occurring in an HIV-positive patient treated with HAART and chemotherapy, who achieved complete
remission
and long survival.
[MeSH-major]
Antiretroviral Therapy, Highly Active. HIV Infections / complications. HIV Infections / drug therapy. HIV Long-Term Survivors. Heart Neoplasms / secondary. Lymphoma, Primary Effusion / complications. Lymphoma, Primary Effusion /
diagnosis
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consumer health - HIV
.
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consumer health - HIV/AIDS
.
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consumer health - HIV/AIDS Medicines
.
HIV InSite.
treatment guidelines - Cardiac Cardiac Manifestations of HIV
.
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(PMID = 18845471.001).
[ISSN]
1386-6532
[Journal-full-title]
Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
[ISO-abbreviation]
J. Clin. Virol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Netherlands
19.
Barnard DR, Alonzo TA, Gerbing RB, Lange B, Woods WG, Children's Oncology Group:
Comparison of childhood myelodysplastic syndrome, AML FAB M6 or M7, CCG 2891: report from the Children's Oncology Group.
Pediatr Blood Cancer
; 2007 Jul;49(1):17-22
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[Title]
Comparison of childhood myelodysplastic
syndrome
,
AML FAB
M6
or M7, CCG 2891: report from the Children's Oncology Group.
BACKGROUND: Myelodysplastic
syndromes
(MDS),
acute
erythroleukemia
(
FAB
M6
), and
acute
megakaryocytic
leukemia
(
FAB
M7) have overlapping features.
PROCEDURE: Children without Down
syndrome
or
acute
promyelocytic
leukemia
who were newly diagnosed with primary myelodysplastic
syndrome
or
acute myeloid leukemia
(
AML
)
M6
or M7 were compared to children with
de
novo
AML
M0-M5.
RESULTS: The presentation and outcomes of the 132 children diagnosed with MDS (60 children),
AML FAB
M6
(19 children), or
AML FAB
M7 (53 children) were similar.
Children with
AML FAB
M7 were diagnosed at a significantly younger age (P = 0.001).
Children with MDS,
M6
, or M7 had significantly lower white blood cell (WBC) counts (P = 0.001), lower peripheral blast counts (P < 0.001), and an increased frequency of -7/7q- (P = 0.003) at presentation.
All three groups had significantly inferior overall survival (OS) (P < 0.001) and event free survival (P < 0.001) compared with the 748 children diagnosed with
AML FAB
M0-M5 when assessed from entry on study.
However, when assessed from successful completion of induction therapy, the 5-year OS (P = 0.090)(49.1 vs. 56.9%) and
disease
-free survival (DFS) (P = 0.113)(38.0 vs. 46.3%) therapy were not significantly different from other children with
AML
.
CONCLUSIONS: Childhood
AML FAB
M6
and
AML
M7 resemble MDS in presentation, poor induction success rates, and outcomes.
[MeSH-major]
Leukemia
,
Erythroblastic
,
Acute
/
diagnosis
.
Leukemia
, Megakaryoblastic,
Acute
/
diagnosis
. Myelodysplastic
Syndromes
/
diagnosis
[MeSH-minor]
Acute
Disease
. Child. Child, Preschool.
Diagnosis
, Differential.
Disease
-Free Survival. Female. Humans. Male. Prognosis.
Remission
Induction. Survival Rate. Treatment Outcome
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(PMID = 16856158.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
20.
Schneider DJ, Taatjes-Sommer HS:
Augmentation of megakaryocyte expression of FcgammaRIIa by interferon gamma.
Arterioscler Thromb Vasc Biol
; 2009 Jul;29(7):1138-43
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METHODS AND RESULTS: Effects of selected cytokines and growth factors on megakaryocyte expression of FcgammaRIIa were assessed with phorbol 12-myristate 13-acetate (PMA)-differentiated human
erythroleukemia
(HEL) cells and with thrombopoietin-differentiated CD34 stem cells and compared with those obtained with myelocytic cell lines and a monocytic cell lines.
This effect of IFNgamma may contribute to greater platelet expression of FcgammaRIIa in patients with atherosclerotic vascular
disease
.
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(PMID = 19372459.001).
[ISSN]
1524-4636
[Journal-full-title]
Arteriosclerosis, thrombosis, and vascular biology
[ISO-abbreviation]
Arterioscler. Thromb. Vasc. Biol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Fc gamma receptor IIA; 0 / Receptors, IgG; 82115-62-6 / Interferon-gamma
21.
Chen C, Zhou Z, Liu R, Li Y, Azmi PB, Seth AK:
The WW domain containing E3 ubiquitin protein ligase 1 upregulates ErbB2 and EGFR through RING finger protein 11.
Oncogene
; 2008 Nov 20;27(54):6845-55
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The WW domain containing E3 ubiquitin protein ligase 1 (WWP1) is a homologous to the E6-associated protein C terminus-
type
E3 ligase frequently overexpressed in human prostate and breast cancers due to
gene
amplification.
Here, we showed that WWP1 upregulates and maintains
erythroblastic
leukemia
viral oncogene homolog 2 (ErbB2) and epithelial growth factor receptor (EGFR) in multiple cell lines.
[MeSH-major]
Genes
, erbB-2. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / genetics. Ubiquitin-Protein Ligases / metabolism
[MeSH-minor]
Breast Neoplasms / genetics. Breast Neoplasms / pathology. Carrier Proteins / genetics. Carrier Proteins / physiology. Cell Division. Cell Line, Tumor. Cell Survival. Epidermal Growth Factor / physiology. Extracellular Signal-Regulated MAP Kinases / metabolism. Female.
Gene
Amplification.
Gene
Deletion.
Gene
Expression Regulation, Neoplastic. Humans. Male. Phosphorylation. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology
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(PMID = 18724389.001).
[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[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]
England
[Chemical-registry-number]
0 / Carrier Proteins; 0 / RNF11 protein, human; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / WWP1 protein, human
22.
Shimada Y, Fukuda T, Aoki K, Yukawa T, Iwamuro S, Ohkawa K, Takada K:
A protocol for immunoaffinity separation of the accumulated ubiquitin-protein conjugates solubilized with sodium dodecyl sulfate.
Anal Biochem
; 2008 Jun 1;377(1):77-82
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The application of this method was tested on ubiquitin-protein conjugates in the brains of Niemann-Pick
type
C
disease
mouse and in heat-shocked K562
erythroleukemia
cells.
Hazardous Substances Data Bank.
SODIUM LAURYL SULFATE
.
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(PMID = 18358228.001).
[ISSN]
1096-0309
[Journal-full-title]
Analytical biochemistry
[ISO-abbreviation]
Anal. Biochem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Detergents; 0 / Membrane Proteins; 0 / Npc1 protein, mouse; 0 / Proteins; 0 / Ubiquitin; 0 / flotillins; 368GB5141J / Sodium Dodecyl Sulfate
23.
Lan K, Murakami M, Choudhuri T, Kuppers DA, Robertson ES:
Intracellular-activated Notch1 can reactivate Kaposi's sarcoma-associated herpesvirus from latency.
Virology
; 2006 Aug 1;351(2):393-403
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Importantly, during latency, only a small number of viral encoded
genes
are expressed.
This viral
gene
expression pattern contributes to the establishment of long-term infection as well as the ability of the virus to evade the immune system.
Previous studies have been shown that the replication and transcription activator (RTA) encoded by ORF50 activates it downstream
genes
and initiates viral lytic reactivation through functional interaction with RBP-Jkappa, the major downstream effector of the Notch signaling pathway.
This indicates that RTA can usurp the conserved Notch signaling pathway and mimic the activities of intracellular Notch1 to modulate
gene
expression.
In this report, we show that the activated intracellular domain of Notch1 (ICN) is aberrantly accumulated in KSHV latently infected pleural effusion lymphoma (
PEL
) cells.
[MeSH-minor]
B-
Lymphocytes
. Cell Line.
Gene
Expression Regulation, Viral. Humans. Promoter Regions, Genetic. Protein Binding. Sarcoma, Kaposi / metabolism. Sarcoma, Kaposi / virology. Transcriptional Activation
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(PMID = 16701788.001).
[ISSN]
0042-6822
[Journal-full-title]
Virology
[ISO-abbreviation]
Virology
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 072510; United States / NCI NIH HHS / CA / CA 091792; United States / NIDCR NIH HHS / DE / DE 01436
[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 / Receptor, Notch1
24.
Cirone M, Lucania G, Aleandri S, Borgia G, Trivedi P, Cuomo L, Frati L, Faggioni A:
Suppression of dendritic cell differentiation through cytokines released by Primary Effusion Lymphoma cells.
Immunol Lett
; 2008 Oct 30;120(1-2):37-41
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Primary effusion lymphoma (
PEL
) is a Human Herpesvirus-8 (HHV-8)-associated tumor, which releases several cytokines such as IL-6, IL-10 and VEGF and its growth seems to be dependent on them in vitro or in vivo.
The iDC obtained in the presence
of PEL
supernatants showed reduction of FITC-dextran uptake, reduction of MLR allostimulatory activity and altered expression of surface molecules, suggesting that cytokines released by
PEL
adversely affect DC differentiation.
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(PMID = 18680763.001).
[ISSN]
0165-2478
[Journal-full-title]
Immunology letters
[ISO-abbreviation]
Immunol. Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Culture Media, Conditioned; 0 / Cytokines
25.
Binelli A, Sarkar SK, Chatterjee M, Riva C, Parolini M, Bhattacharya Bd, Bhattacharya AK, Satpathy KK:
A comparison of sediment quality guidelines for toxicity assessment in the Sunderban wetlands (Bay of Bengal, India).
Chemosphere
; 2008 Oct;73(7):1129-37
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The characterization
of exposure
was conducted by means of an extensive survey of several persistent organic pollutants (PAHs, PCBs, DDTs, PBDEs, HCHs, HCB) measured in seven core sediments from the Sunderban wetlands, obtaining a dataset with more than 2200 analyses.
The three different approaches chosen for risk assessment of the Sunderban were the consensus SQGs obtained by TEC (threshold effect concentration), PEC (probable effect concentration) and EEC (extreme effect concentration), the threshold/probable effect
level
(TEL/
PEL
) approach and, finally, the ERL-ERM guidelines, including the m-ERM-Q (mean ERM quotient).
A different sensitivity for toxicity assessment due to quality guidelines was obtained, as the consensus SQGs based on TEC were less conservative and protective than the TEL and ERL approaches, while the use
of m
-ERM-Q seems to be the most powerful tool to predict the toxicity related to a contaminant mixture.
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(PMID = 18718633.001).
[ISSN]
1879-1298
[Journal-full-title]
Chemosphere
[ISO-abbreviation]
Chemosphere
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Soil Pollutants; 0 / Water Pollutants, Chemical
26.
Harada H, Suzu S, Ito T, Okada S:
Selective expansion and engraftment of human CD16+ NK cells in NOD/SCID mice.
Eur J Immunol
; 2005 Dec;35(12):3599-609
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NK cells are large granular
lymphocytes
that represent a critical component of the innate immunity.
Significant numbers of CD56dimCD16+ cytotoxic and CD56-CD16+ immature NK cells appeared in peripheral blood (PB),
peritoneal
cavity, spleen, bone marrow and liver of the mice.
The NOD/SCID mice engrafted with human NK cells exhibited antitumor activity against K562
erythroleukemia
in vitro and in vivo.
[MeSH-minor]
Animals. Cell Death / immunology. Cell Line, Tumor. Cells, Cultured. Fetal Blood / cytology. Fetal Blood / transplantation. GPI-Linked Proteins. Humans. Immunity, Innate. K562 Cells.
Lymphocyte
Activation / immunology. Mice. Mice, Inbred NOD. Mice, SCID. Transduction, Genetic
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(PMID = 16304638.001).
[ISSN]
0014-2980
[Journal-full-title]
European journal of immunology
[ISO-abbreviation]
Eur. J. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, CD; 0 / FCGR3B protein, human; 0 / GPI-Linked Proteins; 0 / Receptors, IgG
27.
Marcelin AG, Motol J, Guihot A, Caumes E, Viard JP, Dussaix E, Cadranel J, Frances C, Carcelain G, Calvez V, Dupin N:
Relationship between the quantity of Kaposi sarcoma-associated herpesvirus (KSHV) in peripheral blood and effusion fluid samples and KSHV-associated disease.
J Infect Dis
; 2007 Oct 15;196(8):1163-6
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[Title]
Relationship between the quantity of Kaposi sarcoma-associated herpesvirus (KSHV) in peripheral blood and effusion fluid samples and KSHV-associated
disease
.
The Kaposi sarcoma-associated herpesvirus (KSHV)-DNA
level
was determined in samples from 71 patients with Kaposi sarcoma (KS), 28 patients with multicentric Castleman
disease
(MCD), and 8 patients with primary effusion lymphoma (
PEL
).
KSHV-DNA
levels
were higher in patients with active KS or MCD than in those with KS or MCD in
remission
.
Among patients with active
disease
, the highest KSHV-DNA
levels
were observed in effusion fluid samples from patients with
PEL
(7.2 log(10) copies/150,000 cells), followed by blood samples from patients with MCD and
PEL
(4.86 and 3.83 log(10) copies/150,000 cells, respectively), and the lowest
levels
were observed in blood samples from patients with KS (2.63 log(10) copies/150,000 cells).
Determining the KSHV-DNA
level
may be useful in diagnosing KSHV-associated
disease
and for following up patients with KS when the development of MCD or
PEL
is suspected.
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Ascitic Fluid / virology. CD4
Lymphocyte
Count. Female. HIV Infections / complications. Humans. Male. Middle Aged. Pleural Effusion / virology. Retrospective Studies
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.
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(PMID = 17955434.001).
[ISSN]
0022-1899
[Journal-full-title]
The Journal of infectious diseases
[ISO-abbreviation]
J. Infect. Dis.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Viral
28.
Li X, Jia X, Xie C, Lin Y, Cao R, He Q, Chen P, Wang X, Liang S:
Development of cationic colloidal silica-coated magnetic nanospheres for highly selective and rapid enrichment of plasma membrane fractions for proteomics analysis.
Biotechnol Appl Biochem
; 2009 Dec;54(4):213-20
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In the present study, an improved PM isolation technique involving coating intact cells with synthesized cationic silica-coated magnetic nanospheres was developed and applied to the proteomic analysis of the PM from human
erythroleukaemia
K562 cells.
[MeSH-minor]
Blotting, Western. Cations / chemistry. Cell Line, Tumor. Colloids / chemistry. Humans.
Leukemia
,
Erythroblastic
,
Acute
/ metabolism
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(PMID = 19860738.001).
[ISSN]
1470-8744
[Journal-full-title]
Biotechnology and applied biochemistry
[ISO-abbreviation]
Biotechnol. Appl. Biochem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cations; 0 / Colloids; 0 / Membrane Proteins; 7631-86-9 / Silicon Dioxide
29.
Carbone A, Gloghini A, Vaccher E, Cerri M, Gaidano G, Dalla-Favera R, Tirelli U:
Kaposi's sarcoma-associated herpesvirus/human herpesvirus type 8-positive solid lymphomas: a tissue-based variant of primary effusion lymphoma.
J Mol Diagn
; 2005 Feb;7(1):17-27
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[Title]
Kaposi's sarcoma-associated herpesvirus/human herpesvirus
type
8-positive solid lymphomas: a tissue-based variant of primary effusion lymphoma.
Kaposi's sarcoma-associated herpesvirus (KSHV), also termed human herpesvirus
type
8, is consistently identified in Kaposi's sarcoma, primary effusion lymphoma (
PEL
), and multicentric Castleman'
s disease
.
All KSHV-positive solid lymphomas exhibited
PEL
-like cell morphology.
To investigate the relationship of these disorders to
PEL
and to other AIDS-associated diffuse large cell lymphomas, KSHV-positive solid lymphomas were tested for the expression
of a
set
of genes
that were previously shown by
gene
profiling analysis to define
PEL
tumor cells.
The results showed that expression of this set
of genes
in KSHV-positive lymphomas is similar to that
of PEL
but distinct from KSHV-negative AIDS-associated diffuse large cell lymphomas.
Because pathobiological features of KSHV-positive solid lymphomas closely mimic those
of PEL
, our results suggest that KSHV-positive solid lymphomas should be considered as a tissue-based variant of classical
PEL
, irrespective of HIV status.
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HIV InSite.
treatment guidelines - Human Herpesvirus-8
.
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[Cites]
Mod Pathol. 2000 Jan;13(1):77-85
[
10658913.001
]
[Cites]
Am J Surg Pathol. 1999 Oct;23(10):1208-16
[
10524521.001
]
[Cites]
Leuk Lymphoma. 1999 Oct;35(3-4):379-87
[
10706463.001
]
[Cites]
AIDS. 2000 Aug 18;14(12):1675-88
[
10985303.001
]
[Cites]
Adv Cancer Res. 2001;80:115-46
[
11034542.001
]
[Cites]
Blood. 2001 Feb 1;97(3):744-51
[
11157493.001
]
[Cites]
J Mol Diagn. 2001 Feb;3(1):32-8
[
11227070.001
]
[Cites]
Methods. 2001 Dec;25(4):402-8
[
11846609.001
]
[Cites]
Blood. 2002 Apr 1;99(7):2331-6
[
11895764.001
]
[Cites]
AIDS Patient Care STDS. 2002 Apr;16(4):139-45
[
12015867.001
]
[Cites]
Hum Pathol. 2002 Aug;33(8):846-9
[
12203218.001
]
[Cites]
Am J Surg Pathol. 2002 Oct;26(10):1363-7
[
12360052.001
]
[Cites]
Blood. 2002 Nov 1;100(9):3415-8
[
12384445.001
]
[Cites]
Blood. 2003 May 15;101(10):4115-21
[
12531789.001
]
[Cites]
Mod Pathol. 2003 May;16(5):424-9
[
12748248.001
]
[Cites]
Blood. 2003 Nov 15;102(10):3775-85
[
12907442.001
]
[Cites]
J Mol Diagn. 2004 Nov;6(4):290-6
[
15507667.001
]
[Cites]
Cancer Res. 1971 Nov;31(11):1860-1
[
5121694.001
]
[Cites]
J Histochem Cytochem. 1984 Feb;32(2):219-29
[
6198355.001
]
[Cites]
J Clin Oncol. 1985 Sep;3(9):1202-16
[
4031967.001
]
[Cites]
N Engl J Med. 1993 Feb 4;328(5):327-35
[
8093551.001
]
[Cites]
Lancet. 1993 Feb 13;341(8842):441
[
8094208.001
]
[Cites]
EMBO J. 1993 Dec 15;12(13):4955-67
[
8262038.001
]
[Cites]
Science. 1994 Dec 16;266(5192):1865-9
[
7997879.001
]
[Cites]
N Engl J Med. 1995 May 4;332(18):1186-91
[
7700311.001
]
[Cites]
Blood. 1995 Aug 15;86(4):1276-80
[
7632932.001
]
[Cites]
Br J Haematol. 1996 Sep;94(3):533-43
[
8790156.001
]
[Cites]
AIDS. 1996 Aug;10(9):941-9
[
8853726.001
]
[Cites]
Am J Surg Pathol. 1997 Jun;21(6):719-24
[
9199651.001
]
[Cites]
Int J Cancer. 1997 Oct 9;73(2):303-4
[
9335459.001
]
[Cites]
Int J Cancer. 1997 Nov 14;73(4):562-9
[
9389573.001
]
[Cites]
Br J Haematol. 1998 Sep;102(4):1081-9
[
9734661.001
]
[Cites]
Semin Cancer Biol. 1999 Jun;9(3):165-74
[
10343068.001
]
[Cites]
Am J Surg Pathol. 1999 Aug;23(8):992-4
[
10435572.001
]
[Cites]
Blood. 2000 Feb 15;95(4):1406-12
[
10666218.001
]
(PMID = 15681470.001).
[ISSN]
1525-1578
[Journal-full-title]
The Journal of molecular diagnostics : JMD
[ISO-abbreviation]
J Mol Diagn
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA037295; United States / NCI NIH HHS / CA / R37 CA037295; United States / NCI NIH HHS / CA / CA-37295
[Publication-type]
Case Reports; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Other-IDs]
NLM/ PMC1876263
30.
Hickman JW, Tifrea DF, Harwood CS:
A chemosensory system that regulates biofilm formation through modulation of cyclic diguanylate levels.
Proc Natl Acad Sci U S A
; 2005 Oct 4;102(40):14422-7
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[Title]
A chemosensory system that regulates biofilm formation through modulation of cyclic diguanylate
levels
.
Mutations in
a gene
called wspF, part
of a
putative chemosensory signal-transduction operon, have been shown to result in cell aggregation and altered colony morphology.
The WspF phenotypes depend on the presence of WspR, which is a member
of a
family of signal transduction proteins known as response regulators.
WspR contains a GGDEF domain known to catalyze formation
of a
cytoplasmic signaling molecule cyclic diguanylate (c-diGMP).
We observed increased cellular
levels of
c-diGMP and increased biofilm formation in a wspF mutant.
Expression
of a
protein predicted to catalyze degradation of c-diGMP reversed the phenotypes
of a
wspF mutant and inhibited biofilm initiation by wild-
type
cells, indicating that the presence of c-diGMP is necessary for biofilm formation.
A transcriptome analysis showed that expression
levels of
at least 560
genes
were affected by a wspF deletion.
The psl and
pel
operons, which are involved in exopolysaccharide production and biofilm formation, were expressed at high
levels
in a wspF mutant.
Together, the data suggest that the wsp signal transduction pathway regulates biofilm formation through modulation of cyclic diguanylate
levels
.
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[Cites]
J Bacteriol. 2004 Jul;186(14):4457-65
[
15231777.001
]
[Cites]
J Biol Chem. 2005 Sep 2;280(35):30829-37
[
15994307.001
]
[Cites]
Mol Microbiol. 2004 Aug;53(3):857-69
[
15255898.001
]
[Cites]
Microbiology. 2004 Aug;150(Pt 8):2497-502
[
15289546.001
]
[Cites]
Mol Microbiol. 2004 Aug;53(4):1123-34
[
15306016.001
]
[Cites]
Mol Microbiol. 2004 Oct;54(1):264-77
[
15458421.001
]
[Cites]
J Biol Chem. 1982 Aug 25;257(16):9759-69
[
6286632.001
]
[Cites]
Gene. 1989 Apr 15;77(1):51-9
[
2744487.001
]
[Cites]
J Bacteriol. 1989 Dec;171(12):6649-55
[
2556370.001
]
[Cites]
Microbiol Rev. 1991 Mar;55(1):35-58
[
2030672.001
]
[Cites]
Methods Enzymol. 1993;217:270-9
[
8474334.001
]
[Cites]
Biotechniques. 1993 Nov;15(5):831-4
[
8267974.001
]
[Cites]
Antimicrob Agents Chemother. 1994 May;38(5):1052-8
[
8067737.001
]
[Cites]
J Biol Chem. 1994 Dec 16;269(50):31567-72
[
7989325.001
]
[Cites]
FEBS Lett. 1997 Oct 20;416(2):207-11
[
9369216.001
]
[Cites]
Science. 1998 Apr 10;280(5361):295-8
[
9535661.001
]
[Cites]
Mol Microbiol. 1998 May;28(3):449-61
[
9632250.001
]
[Cites]
Gene. 1998 May 28;212(1):77-86
[
9661666.001
]
[Cites]
Mol Microbiol. 1998 Oct;30(2):295-304
[
9791175.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17084-9
[
15569936.001
]
[Cites]
J Bacteriol. 2005 Mar;187(5):1792-8
[
15716451.001
]
[Cites]
Microbiology. 2005 Mar;151(Pt 3):985-97
[
15758243.001
]
[Cites]
Appl Environ Microbiol. 2005 Aug;71(8):4809-21
[
16085879.001
]
[Cites]
Microbes Infect. 2000 Jul;2(9):1051-60
[
10967285.001
]
[Cites]
Proteins. 2001 Feb 1;42(2):210-6
[
11119645.001
]
[Cites]
Trends Microbiol. 2001 Jan;9(1):34-9
[
11166241.001
]
[Cites]
Lancet. 2001 Jul 14;358(9276):135-8
[
11463434.001
]
[Cites]
Microbiology. 2001 Aug;147(Pt 8):2065-75
[
11495985.001
]
[Cites]
FEMS Microbiol Lett. 2001 Oct 16;204(1):163-7
[
11682196.001
]
[Cites]
J Bacteriol. 2002 Feb;184(4):1140-54
[
11807075.001
]
[Cites]
Nature. 2002 Apr 18;416(6882):740-3
[
11961556.001
]
[Cites]
Genetics. 2002 May;161(1):33-46
[
12019221.001
]
[Cites]
Nature. 2002 May 30;417(6888):552-5
[
12037568.001
]
[Cites]
J Bacteriol. 2002 Aug;184(16):4374-83
[
12142407.001
]
[Cites]
J Bacteriol. 2002 Nov;184(21):5946-54
[
12374828.001
]
[Cites]
J Bacteriol. 2002 Dec;184(23):6481-9
[
12426335.001
]
[Cites]
J Bacteriol. 2003 Feb;185(4):1384-90
[
12562809.001
]
[Cites]
Mol Microbiol. 2003 Mar;47(6):1695-708
[
12622822.001
]
[Cites]
J Bacteriol. 2003 Apr;185(7):2066-79
[
12644476.001
]
[Cites]
J Med Microbiol. 2003 Apr;52(Pt 4):295-301
[
12676867.001
]
[Cites]
J Bacteriol. 2003 Sep;185(18):5431-41
[
12949095.001
]
[Cites]
Mol Microbiol. 2003 Oct;50(1):15-27
[
14507360.001
]
[Cites]
Nature. 2003 Nov 20;426(6964):306-10
[
14628055.001
]
[Cites]
Mol Microbiol. 2004 Feb;51(3):675-90
[
14731271.001
]
[Cites]
Mol Microbiol. 2004 Feb;51(4):973-85
[
14763974.001
]
[Cites]
Genes Dev. 2004 Mar 15;18(6):715-27
[
15075296.001
]
[Cites]
Environ Microbiol. 2004 Jun;6(6):546-51
[
15142242.001
]
[Cites]
J Bacteriol. 2004 Jul;186(14):4449-56
[
15231776.001
]
[Cites]
J Bacteriol. 2004 Jul;186(14):4466-75
[
15231778.001
]
(PMID = 16186483.001).
[ISSN]
0027-8424
[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
[Grant]
United States / NIGMS NIH HHS / GM / R01 GM056665; United States / NIGMS NIH HHS / GM / GM056665
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Bacterial Proteins; 147336-22-9 / Green Fluorescent Proteins; 61093-23-0 / bis(3',5')-cyclic diguanylic acid; H2D2X058MU / Cyclic GMP
[Other-IDs]
NLM/ PMC1234902
31.
Reinholz MM, Eckel-Passow JE, Anderson SK, Asmann YW, Zschunke MA, Oberg AL, McCullough AE, Dueck AC, Chen B, April CS, Wickham-Garcia E, Jenkins RB, Cunningham JM, Jen J, Perez EA, Fan JB, Lingle WL:
Expression profiling of formalin-fixed paraffin-embedded primary breast tumors using cancer-specific and whole genome gene panels on the DASL® platform.
BMC Med Genomics
; 2010 Dec 20;3:60
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[Title]
Expression profiling of formalin-fixed paraffin-embedded primary breast tumors using cancer-specific and whole genome
gene
panels on the DASL® platform.
BACKGROUND: The cDNA-mediated Annealing, extension, Selection and Ligation (DASL) assay has become a suitable
gene
expression profiling system for degraded RNA from paraffin-embedded tissue.
We examined assay characteristics and the performance of the DASL 502-
gene
Cancer Panel v1 (1.5K) and 24,526-
gene
panel (24K) platforms at differentiating nine human epidermal growth factor receptor 2- positive (HER2+) and 11 HER2-negative (HER2-) paraffin-embedded breast tumors.
Unequal-variance t-statistics tested for differences in expression
levels
between HER2 + and HER2 - tumors.
Inter-panel correlations of expression values for the common 498
genes
across the two panels ranged between 0.485-0.573.
In both panels,
erythroblastic
leukemia
viral oncogene homolog 2 (ERBB2) was the most differentially expressed
gene
between the HER2 + and HER2 - tumors and seven additional
genes
had p-values < 0.05 and log2 -fold changes > |0.5| in expression between HER2 + and HER2 - tumors: topoisomerase II alpha (TOP2A), cyclin a2 (CCNA2), v-fos fbj murine osteosarcoma viral oncogene homolog (FOS), wingless-
type
mmtv integration site family, member 5a (WNT5A), growth factor receptor-bound protein 7 (GRB7), cell division cycle 2 (CDC2), and baculoviral iap repeat-containing protein 5 (BIRC5).
The top 52 discriminating probes from the 24K panel are enriched with
genes
belonging to the regulatory networks centered around v-myc avian myelocytomatosis viral oncogene homolog (MYC), tumor protein p53 (TP53), and estrogen receptor α (ESR1).
Network analysis with a two-step extension also showed that the eight discriminating
genes
common to the 1.5K and 24K panels are functionally linked together through MYC, TP53, and ESR1.
CONCLUSIONS: The relative RNA abundance obtained from two highly differing density
gene
panels are correlated with eight common
genes
differentiating HER2 + and HER2 - breast tumors.
Network analyses demonstrated biological consistency between the 1.5K and 24K
gene
panels.
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[Cites]
Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15149-54
[
11742071.001
]
[Cites]
Nucleic Acids Res. 2002 Jan 1;30(1):207-10
[
11752295.001
]
[Cites]
N Engl J Med. 2002 Dec 19;347(25):1999-2009
[
12490681.001
]
[Cites]
J Natl Cancer Inst. 2003 Jan 15;95(2):142-53
[
12529347.001
]
[Cites]
Nat Genet. 2003 Jun;34(2):226-30
[
12754511.001
]
[Cites]
Cell Cycle. 2003 Sep-Oct;2(5):415-7
[
12963829.001
]
[Cites]
Hum Mol Genet. 2003 Oct 15;12 Spec No 2:R153-7
[
12928487.001
]
[Cites]
Hum Mol Genet. 2003 Dec 15;12(24):3245-58
[
14570715.001
]
[Cites]
Genome Res. 2004 May;14(5):878-85
[
15123585.001
]
[Cites]
Cancer Cell. 2004 Jun;5(6):607-16
[
15193263.001
]
[Cites]
Am J Pathol. 2004 Nov;165(5):1799-807
[
15509548.001
]
[Cites]
Cancer Res. 1990 Jul 1;50(13):3947-51
[
1972345.001
]
[Cites]
Bioinformatics. 2004 Nov 1;20(16):2778-86
[
15166021.001
]
[Cites]
Clin Chem. 2004 Dec;50(12):2384-6
[
15563488.001
]
[Cites]
N Engl J Med. 2004 Dec 30;351(27):2817-26
[
15591335.001
]
[Cites]
Am J Clin Pathol. 2005 Apr;123(4):541-6
[
15743737.001
]
[Cites]
Nat Clin Pract Oncol. 2005 May;2(5):246-54
[
16264960.001
]
[Cites]
Nature. 2006 Jan 19;439(7074):353-7
[
16273092.001
]
[Cites]
Cancer Res. 2006 Apr 15;66(8):4079-88
[
16618727.001
]
[Cites]
Hum Pathol. 2006 Sep;37(9):1217-26
[
16938528.001
]
[Cites]
Nat Biotechnol. 2006 Sep;24(9):1151-61
[
16964229.001
]
[Cites]
J Clin Oncol. 2007 Jan 1;25(1):118-45
[
17159189.001
]
[Cites]
Breast Cancer Res. 2006;8(5):214
[
17076877.001
]
[Cites]
Genomics. 2007 Jun;89(6):666-72
[
17459658.001
]
[Cites]
J Natl Cancer Inst. 2007 Nov 21;99(22):1683-94
[
18000219.001
]
[Cites]
Lab Invest. 2008 Apr;88(4):430-40
[
18305565.001
]
[Cites]
Methods Mol Biol. 2008;439:159-77
[
18370102.001
]
[Cites]
JAMA. 2008 Apr 2;299(13):1574-87
[
18387932.001
]
[Cites]
PLoS One. 2008;3(5):e2318
[
18846227.001
]
[Cites]
J Pathol. 2008 Dec;216(4):399-407
[
18810758.001
]
[Cites]
Pathology. 2009 Jan;41(1):77-88
[
19089743.001
]
[Cites]
N Engl J Med. 2009 Feb 19;360(8):790-800
[
19228622.001
]
[Cites]
Gynecol Oncol. 2009 Jul;114(1):3-11
[
19410283.001
]
[Cites]
BMC Bioinformatics. 2009;10 Suppl 11:S12
[
19811677.001
]
[Cites]
PLoS One. 2009;4(12):e8162
[
19997620.001
]
[Cites]
J Pathol. 2010 Aug;221(4):452-61
[
20593485.001
]
[Cites]
Nature. 2000 Aug 17;406(6797):747-52
[
10963602.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-74
[
11553815.001
]
[Cites]
Nature. 2002 Jan 31;415(6871):530-6
[
11823860.001
]
(PMID = 21172013.001).
[ISSN]
1755-8794
[Journal-full-title]
BMC medical genomics
[ISO-abbreviation]
BMC Med Genomics
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA129949; United States / NCI NIH HHS / CA / CA129949; United States / NCI NIH HHS / CA / CA150083
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
[Other-IDs]
NLM/ PMC3022545
32.
Choe KS, Ujhelly O, Wontakal SN, Skoultchi AI:
PU.1 directly regulates cdk6 gene expression, linking the cell proliferation and differentiation programs in erythroid cells.
J Biol Chem
; 2010 Jan 29;285(5):3044-52
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[Title]
PU.1 directly regulates cdk6
gene
expression, linking the cell proliferation and differentiation programs in
erythroid
cells.
Most
leukemia
cells are blocked from undergoing terminal differentiation and also exhibit uncontrolled proliferation.
Dysregulated expression of transcription factor PU.1 is strongly associated with Friend virus-induced
erythroleukemia
.
PU.1 inhibits
erythroid
differentiation by binding to and inhibiting GATA-1.
PU.1 also may be involved in controlling proliferation
of erythroid
cells.
We reported previously that the G(1) phase-specific cyclin-dependent kinase 6 (CDK6) also blocks
erythroid
differentiation.
We now report that PU.1 directly stimulates transcription of the cdk6
gene
in both normal
erythroid
progenitors and
erythroleukemia
cells, as well as in macrophages.
We propose that PU.1 coordinates proliferation and differentiation in immature
erythroid
cells by inhibiting the GATA-1-mediated
gene
expression program and also by regulating expression
of genes
that control progression through the G(1) phase of the cell cycle, the period during which the decision to differentiate is made.
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[Cites]
Mol Cell Biol. 2004 Aug;24(15):6560-8
[
15254224.001
]
[Cites]
Blood. 2004 May 15;103(10):3615-23
[
14739214.001
]
[Cites]
Methods Mol Med. 2005;105:323-44
[
15492405.001
]
[Cites]
Nature. 1986 Apr 24-30;320(6064):760-3
[
3458027.001
]
[Cites]
Nature. 1986 Aug 21-27;322(6081):748-50
[
3528861.001
]
[Cites]
Nature. 1986 Aug 28-Sep 3;322(6082):848-50
[
3528863.001
]
[Cites]
Proc Natl Acad Sci U S A. 1986 Sep;83(17):6480-4
[
3529085.001
]
[Cites]
Nature. 1988 Jan 21;331(6153):277-80
[
2827041.001
]
[Cites]
Cell. 1990 Apr 6;61(1):113-24
[
2180582.001
]
[Cites]
J Biol Chem. 1993 Mar 5;268(7):5014-20
[
8095266.001
]
[Cites]
Genes Dev. 1993 Oct;7(10):2006-15
[
8406004.001
]
[Cites]
Mol Cell Biol. 1994 Jul;14(7):4408-18
[
8007948.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Mar 28;92(7):2869-73
[
7708739.001
]
[Cites]
Mol Cell Biol. 1995 Oct;15(10):5830-45
[
7565736.001
]
[Cites]
J Exp Med. 1996 Jul 1;184(1):61-9
[
8691150.001
]
[Cites]
Oncogene. 1997 Jan 9;14(1):123-31
[
9010239.001
]
[Cites]
Blood. 1997 Nov 15;90(10):3984-95
[
9354667.001
]
[Cites]
Stem Cells. 1998;16(1):25-37
[
9474745.001
]
[Cites]
EMBO J. 1998 Aug 3;17(15):4456-68
[
9687512.001
]
[Cites]
Genes Dev. 1998 Aug 1;12(15):2403-12
[
9694804.001
]
[Cites]
Curr Opin Genet Dev. 1998 Oct;8(5):545-51
[
9794826.001
]
[Cites]
Genes Dev. 1999 Jun 1;13(11):1398-411
[
10364157.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8705-10
[
10411939.001
]
[Cites]
Dev Cell. 2005 Jan;8(1):97-108
[
15621533.001
]
[Cites]
Biochem Biophys Res Commun. 2005 Apr 22;329(4):1288-92
[
15766566.001
]
[Cites]
Ann N Y Acad Sci. 2005 Jun;1044:142-58
[
15958708.001
]
[Cites]
Int J Hematol. 2005 Jun;81(5):368-77
[
16158816.001
]
[Cites]
EMBO J. 2005 Nov 2;24(21):3712-23
[
16222338.001
]
[Cites]
EMBO J. 2007 May 2;26(9):2361-70
[
17431401.001
]
[Cites]
Curr Opin Hematol. 2007 Jul;14(4):307-14
[
17534154.001
]
[Cites]
Mol Cancer Res. 2007 Oct;5(10):1053-62
[
17951405.001
]
[Cites]
Int J Biochem Cell Biol. 2008;40(1):22-7
[
17374502.001
]
[Cites]
Curr Opin Cell Biol. 2007 Dec;19(6):697-704
[
18035529.001
]
[Cites]
Blood. 2000 Apr 15;95(8):2543-51
[
10753833.001
]
[Cites]
J Cell Biochem. 2000 Jun 12;78(4):519-32
[
10861849.001
]
[Cites]
Stem Cells. 1998;16 Suppl 2:79-83
[
11012179.001
]
[Cites]
Blood. 2000 Oct 15;96(8):2755-64
[
11023509.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Dec 19;97(26):14317-22
[
11114185.001
]
[Cites]
Curr Opin Genet Dev. 2001 Feb;11(1):91-7
[
11163157.001
]
[Cites]
Nat Rev Genet. 2000 Oct;1(1):57-64
[
11262875.001
]
[Cites]
Oncogene. 2002 May 13;21(21):3403-13
[
12032778.001
]
[Cites]
Acta Haematol. 2002;108(4):237-45
[
12432220.001
]
[Cites]
Eur J Immunol. 2003 Jun;33(6):1727-35
[
12778491.001
]
[Cites]
Mol Cell Biol. 2003 Jul;23(14):5031-42
[
12832487.001
]
[Cites]
Oncogene. 2003 Jul 3;22(27):4143-9
[
12833137.001
]
[Cites]
Cancer Res. 2003 Oct 1;63(19):6363-9
[
14559825.001
]
[Cites]
Mol Cell Biol. 2003 Nov;23(21):7460-74
[
14559995.001
]
[Cites]
Leuk Res. 2004 Jan;28(1):83-9
[
14630084.001
]
[Cites]
Blood. 2004 Sep 15;104(6):1873-80
[
15166028.001
]
(PMID = 19955566.001).
[ISSN]
1083-351X
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / R01 HL078381; United States / NCI NIH HHS / CA / 2P30CA13330; United States / NHLBI NIH HHS / HL / HL078381; United States / NIGMS NIH HHS / GM / 5T32GM07288; United States / NIGMS NIH HHS / GM / T32 GM007288
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / GATA1 Transcription Factor; 0 / Gata1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; EC 2.7.11.22 / Cdk6 protein, mouse; EC 2.7.11.22 / Cyclin-Dependent Kinase 6
[Other-IDs]
NLM/ PMC2823399
33.
De Filippi R, Iaccarino G, Frigeri F, Di Francia R, Crisci S, Capobianco G, Arcamone M, Becchimanzi C, Amoroso B, De Chiara A, Corazzelli G, Pinto A:
Elevation of clonal serum free light chains in patients with HIV-negative primary effusion lymphoma (PEL) and PEL-like lymphoma.
Br J Haematol
; 2009 Nov;147(3):405-8
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[Title]
Elevation of clonal serum free light chains in patients with HIV-negative primary effusion lymphoma (
PEL
) and
PEL
-like lymphoma.
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.
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consumer health - HIV
.
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(PMID = 19681885.001).
[ISSN]
1365-2141
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Case Reports; Letter; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Immunoglobulin Light Chains
34.
Uddin S, Hussain AR, Manogaran PS, Al-Hussein K, Platanias LC, Gutierrez MI, Bhatia KG:
Curcumin suppresses growth and induces apoptosis in primary effusion lymphoma.
Oncogene
; 2005 Oct 27;24(47):7022-30
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The mechanisms that regulate induction of the antiapoptotic state and mitogenic signals in primary effusion lymphoma (
PEL
) are not well known.
In efforts to identify novel approaches to block the proliferation
of PEL
cells, we found that curcumin (diferuloylmethane), a natural compound isolated from the plant Curcuma Ionga, inhibits cell proliferation and induces apoptosis in a dose dependent manner in several
PEL
cell lines.
Altogether, our findings suggest a novel function for curcumin, acting as a suppressor of JAK-1 and STAT3 activation in
PEL
cells, leading to inhibition of proliferation and induction of caspase-dependent apoptosis.
Therefore, curcumin may have a future therapeutic role in
PEL
and possibly other malignancies with constitutive activation of STAT3.
[MeSH-major]
Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Proliferation / drug effects. Curcumin / pharmacology. Lymphoma / metabolism. Pleural Effusion,
Malignant
/ metabolism. Signal Transduction / drug effects
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.
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.
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(PMID = 16044161.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Trans-Activators; 9007-43-6 / Cytochromes c; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Janus Kinase 1; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; IT942ZTH98 / Curcumin
35.
Lampronti I, Khan MT, Bianchi N, Ather A, Borgatti M, Vizziello L, Fabbri E, Gambari R:
Bangladeshi medicinal plant extracts inhibiting molecular interactions between nuclear factors and target DNA sequences mimicking NF-kappaB binding sites.
Med Chem
; 2005 Jul;1(4):327-33
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The rationale for this study is based on the observation that alteration
of gene
transcription represents a very promising approach to control the expression of selected
genes
and could be obtained using different molecules acting on the interactions between DNA and transcription factors (TFs).
Antiproliferative activity was assayed on different human cell lines, including
erythroleukemia
K562, B-lymphoid Raji, T-lymphoid Jurkat and
erythroleukemia
HEL cell lines.
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(PMID = 16789890.001).
[ISSN]
1573-4064
[Journal-full-title]
Medicinal chemistry (Shāriqah (United Arab Emirates))
[ISO-abbreviation]
Med Chem
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United Arab Emirates
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Transcription Factors; 9007-49-2 / DNA
36.
Gregory SM, West JA, Dillon PJ, Hilscher C, Dittmer DP, Damania B:
Toll-like receptor signaling controls reactivation of KSHV from latency.
Proc Natl Acad Sci U S A
; 2009 Jul 14;106(28):11725-30
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Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiological agent of Kaposi's sarcoma, primary effusion lymphoma (
PEL
), and multicentric Castleman'
s disease
.
We screened multiple TLR agonists for their ability to initiate KSHV replication in latently infected
PEL
.
Agonists specific for TLR7/8 reactivated latent KSHV and induced viral lytic
gene
transcription and replication.
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[Cites]
Science. 2004 Mar 5;303(5663):1526-9
[
14976262.001
]
[Cites]
Science. 2004 Mar 5;303(5663):1529-31
[
14976261.001
]
[Cites]
Am J Trop Med Hyg. 1966 Mar;15(2):244-6
[
4286381.001
]
[Cites]
Am J Epidemiol. 1969 Sep;90(3):255-61
[
4309413.001
]
[Cites]
Science. 1994 Dec 16;266(5192):1865-9
[
7997879.001
]
[Cites]
N Engl J Med. 1995 May 4;332(18):1186-91
[
7700311.001
]
[Cites]
J Immunol. 1995 Sep 1;155(5):2533-44
[
7650383.001
]
[Cites]
Lancet. 1995 Sep 23;346(8978):799-802
[
7674745.001
]
[Cites]
J Exp Med. 1996 Jul 1;184(1):283-8
[
8691144.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10866-71
[
9724796.001
]
[Cites]
J Biol Chem. 2005 Apr 1;280(13):12262-70
[
15664995.001
]
[Cites]
Nat Cell Biol. 2005 Jul;7(7):653-64
[
15951806.001
]
[Cites]
Immunity. 2005 Aug;23(2):165-75
[
16111635.001
]
[Cites]
Oncogene. 2005 Nov 21;24(52):7710-9
[
16299531.001
]
[Cites]
Oncogene. 2006 Jan 19;25(3):349-58
[
16186807.001
]
[Cites]
Trends Mol Med. 2006 Apr;12(4):167-76
[
16530484.001
]
[Cites]
J Immunol. 2006 Dec 1;177(11):8164-70
[
17114492.001
]
[Cites]
J Virol. 2008 Jun;82(11):5440-9
[
18367536.001
]
[Cites]
Cell Host Microbe. 2008 Nov 13;4(5):470-83
[
18996347.001
]
[Cites]
J Virol. 2009 Jan;83(1):440-53
[
18971266.001
]
[Cites]
Ann N Y Acad Sci. 2008 Nov;1143:1-20
[
19076341.001
]
[Cites]
J Virol. 2009 Feb;83(3):1474-82
[
19019960.001
]
[Cites]
J Virol. 1999 Dec;73(12):10329-38
[
10559351.001
]
[Cites]
Eur Cytokine Netw. 2000 Sep;11(3):362-71
[
11022119.001
]
[Cites]
Nat Immunol. 2002 Feb;3(2):196-200
[
11812998.001
]
[Cites]
J Virol. 2002 Jun;76(12):6213-23
[
12021355.001
]
[Cites]
J Virol. 2002 Dec;76(23):12242-9
[
12414963.001
]
[Cites]
Cancer Res. 2003 May 1;63(9):2010-5
[
12727810.001
]
[Cites]
Blood. 2003 Aug 1;102(3):956-63
[
12689944.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Apr 13;101(15):5598-603
[
15034168.001
]
(PMID = 19564611.001).
[ISSN]
1091-6490
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA109232; United States / NIDCR NIH HHS / DE / DE018281-03; United States / NIAID NIH HHS / AI / T32 AI007419; United States / NIDCR NIH HHS / DE / R01 DE018304-02; United States / NCI NIH HHS / CA / T32 CA009156; United States / NIDCR NIH HHS / DE / R01 DE018281-03; United States / NIDCR NIH HHS / DE / DE018304-01; United States / NIDCR NIH HHS / DE / R01 DE018304; United States / NIDCR NIH HHS / DE / R01 DE018304-01; United States / NIDCR NIH HHS / DE / R01 DE018304-03; United States / NIDCR NIH HHS / DE / DE018304-02; United States / NIDCR NIH HHS / DE / DE018304-03; United States / NIDCR NIH HHS / DE / R01 DE018281; United States / NIAID NIH HHS / AI / F32 AI078735; United States / NCI NIH HHS / CA / R01 CA096500
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Toll-Like Receptor 7; 0 / Toll-Like Receptor 8
[Other-IDs]
NLM/ PMC2710638
37.
Kim HH, Ahn KS, Han H, Choung SY, Choi SY, Kim IH:
Decursin and PDBu: two PKC activators distinctively acting in the megakaryocytic differentiation of K562 human erythroleukemia cells.
Leuk Res
; 2005 Dec;29(12):1407-13
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[Title]
Decursin and PDBu: two PKC activators distinctively acting in the megakaryocytic differentiation of K562 human
erythroleukemia
cells.
Phorbol 12,13-dibutyrate (PDBu) induces the megakaryocytic differentiation of K562 human
erythroleukemia
cells through PKC activation.
All these results indicate that decursin and phorbol ester are PKC activators distinctively acting in megakaryocytic differentiation and PKC modulation in K562
leukemia
cells.
[MeSH-major]
Cell Differentiation.
Leukemia
,
Erythroblastic
,
Acute
/ pathology. Megakaryocytes / pathology. Phorbol 12,13-Dibutyrate / pharmacology. Protein Kinase C / metabolism. Pyranocoumarins / pharmacology
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(PMID = 15992925.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzopyrans; 0 / Butyrates; 0 / Pyranocoumarins; 37558-16-0 / Phorbol 12,13-Dibutyrate; 5928-25-6 / decursin; EC 2.7.11.13 / Protein Kinase C
38.
Trulson A, Byström J, Engström A, Larsson R, Venge P:
The functional heterogeneity of eosinophil cationic protein is determined by a gene polymorphism and post-translational modifications.
Clin Exp Allergy
; 2007 Feb;37(2):208-18
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[Title]
The functional heterogeneity of eosinophil cationic protein is determined by
a gene
polymorphism and post-translational modifications.
A polymorphism was demonstrated in the ECP
gene
, giving rise to a substitution of arginine at position 97 with threonine.
This polymorphism is related to
disease
development.
The cytotoxic activity was determined against an
erythroleukaemia
or a small cell lung cancer cell line.
Some of this functional heterogeneity is based on the genetic polymorphism of the ECP
gene
and some on post-translational modifications.
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(PMID = 17250693.001).
[ISSN]
0954-7894
[Journal-full-title]
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
[ISO-abbreviation]
Clin. Exp. Allergy
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Blood Proteins; EC 3.1.27.- / Eosinophil Cationic Protein
39.
Keil A, Hernandez-Soto H, Noll RJ, Fico M, Gao L, Ouyang Z, Cooks RG:
Monitoring of toxic compounds in air using a handheld rectilinear ion trap mass spectrometer.
Anal Chem
; 2008 Feb 1;80(3):734-41
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Sampling, detection, identification, and quantitation of all compounds were readily achieved in times of less than 2 min, with detection
limits
ranging from 800 parts per trillion to 3 parts per million depending on the analyte.
For all but one analyte, detection
limits
were well below (3.5-130 times below)
permissible exposure limits
.
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(PMID = 18181580.001).
[ISSN]
0003-2700
[Journal-full-title]
Analytical chemistry
[ISO-abbreviation]
Anal. Chem.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
40.
Nishiwaki M, Fujimuro M, Teishikata Y, Inoue H, Sasajima H, Nakaso K, Nakashima K, Sadanari H, Yamamoto T, Fujiwara Y, Ogawa N, Yokosawa H:
Epidemiology of Epstein-Barr virus, cytomegalovirus, and Kaposi's sarcoma-associated herpesvirus infections in peripheral blood leukocytes revealed by a multiplex PCR assay.
J Med Virol
; 2006 Dec;78(12):1635-42
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Primers of multiplex PCR were designed to amplify specific regions of the EBV EBNA1, CMV IE2, and KSHV LANA
genes
.
To assess diagnostic and pre-clinical applications with this method, we utilized KSHV-positive primary effusion lymphoma (
PEL
) cells, EBV-positive Burkitt's lymphoma cells, CMV-infected fibroblast cells, and clinically prepared peripheral blood leukocytes (PBLs) that had been infected with viruses.
[MeSH-minor]
Blood Donors. Cell Line. Cytomegalovirus Infections /
diagnosis
. Cytomegalovirus Infections / epidemiology. Cytomegalovirus Infections / virology. DNA, Viral / analysis. Epstein-Barr Virus Infections /
diagnosis
. Epstein-Barr Virus Infections / epidemiology. Epstein-Barr Virus Infections / virology. Prevalence. Sarcoma, Kaposi /
diagnosis
. Sarcoma, Kaposi / epidemiology. Sarcoma, Kaposi / virology. Sensitivity and Specificity
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[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 17063511.001).
[ISSN]
0146-6615
[Journal-full-title]
Journal of medical virology
[ISO-abbreviation]
J. Med. Virol.
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Viral
41.
Liu J, Martin HJ, Liao G, Hayward SD:
The Kaposi's sarcoma-associated herpesvirus LANA protein stabilizes and activates c-Myc.
J Virol
; 2007 Oct;81(19):10451-9
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Sequencing of c-Myc coding sequences revealed that c-Myc in KSHV-positive primary effusion lymphoma (
PEL
) cell lines is wild
type
in the N-terminal region that regulates c-Myc protein stability.
Despite this, c-Myc in
PEL
cells is stabilized.
We now show that LANA increases the
level of
phosphorylated extracellular signal-regulated kinase 1 (ERK1) and increases ERK phosphorylation of c-Myc on Ser62.
LANA-mediated manipulation of c-Myc function is likely to contribute to KSHV-associated tumorigenesis through the induction of c-Myc regulated cellular
genes
, as well as by the stimulation of cell cycle progression.
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.
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[Cites]
J Virol. 2000 Sep;74(18):8532-40
[
10954554.001
]
[Cites]
J Virol. 2000 Oct;74(20):9637-45
[
11000236.001
]
[Cites]
J Biol Chem. 2006 Sep 22;281(38):28113-21
[
16861237.001
]
[Cites]
Mol Immunol. 2007 Feb;44(6):1352-60
[
16828498.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Sep 26;103(39):14554-9
[
16983096.001
]
[Cites]
J Virol. 2006 Nov;80(21):10772-86
[
16928766.001
]
[Cites]
J Virol. 2006 Nov;80(22):11178-90
[
16928741.001
]
[Cites]
PLoS Pathog. 2006 Oct;2(10):e116
[
17069461.001
]
[Cites]
Genes Dev. 2000 Oct 1;14(19):2501-14
[
11018017.001
]
[Cites]
Nat Med. 2000 Oct;6(10):1121-7
[
11017143.001
]
[Cites]
J Gen Virol. 2000 Nov;81(Pt 11):2645-52
[
11038375.001
]
[Cites]
Virology. 2001 Dec 20;291(2):241-59
[
11878894.001
]
[Cites]
Arch Biochem Biophys. 2002 Apr 15;400(2):151-61
[
12054425.001
]
[Cites]
J Biol Chem. 2002 Jul 26;277(30):27401-11
[
12015325.001
]
[Cites]
J Virol. 2002 Nov;76(22):11677-87
[
12388727.001
]
[Cites]
Science. 2002 Dec 6;298(5600):1911-2
[
12471242.001
]
[Cites]
Semin Cancer Biol. 2003 Feb;13(1):69-76
[
12507558.001
]
[Cites]
J Virol. 2003 Feb;77(4):2779-83
[
12552022.001
]
[Cites]
Nat Med. 2003 Mar;9(3):300-6
[
12592400.001
]
[Cites]
J Virol. 2003 May;77(10):5975-84
[
12719589.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5313-8
[
12702757.001
]
[Cites]
J Virol. 2003 Jun;77(11):6188-96
[
12743275.001
]
[Cites]
J Gen Virol. 2003 Jun;84(Pt 6):1451-62
[
12771414.001
]
[Cites]
J Virol. 2003 Jul;77(14):8019-30
[
12829841.001
]
[Cites]
J Virol. 2004 Jan;78(1):294-301
[
14671111.001
]
[Cites]
J Biol Chem. 2003 Dec 19;278(51):51606-12
[
14563837.001
]
[Cites]
Nat Cell Biol. 2004 Apr;6(4):308-18
[
15048125.001
]
[Cites]
J Virol. 2004 Jun;78(12):6585-94
[
15163750.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):9085-90
[
15150404.001
]
[Cites]
J Virol. 2004 Jul;78(14):7299-310
[
15220403.001
]
[Cites]
Nat Genet. 2004 Jul;36(7):687-93
[
15220918.001
]
[Cites]
J Virol. 2004 Sep;78(18):9936-46
[
15331727.001
]
[Cites]
J Virol. 2004 Oct;78(19):10348-59
[
15367601.001
]
[Cites]
Microbes Infect. 2004 Nov;6(13):1212-8
[
15488741.001
]
[Cites]
J Virol. 2004 Nov;78(22):12566-75
[
15507644.001
]
[Cites]
J Biol Chem. 1991 Dec 15;266(35):23521-4
[
1748630.001
]
[Cites]
Oncogene. 1994 Jan;9(1):59-70
[
8302604.001
]
[Cites]
Science. 1994 Dec 16;266(5192):1865-9
[
7997879.001
]
[Cites]
N Engl J Med. 1995 May 4;332(18):1186-91
[
7700311.001
]
[Cites]
Blood. 1995 Aug 15;86(4):1276-80
[
7632932.001
]
[Cites]
EMBO J. 1999 Feb 1;18(3):717-26
[
9927431.001
]
[Cites]
Mol Cell. 1999 Feb;3(2):169-79
[
10078200.001
]
[Cites]
Science. 1999 Apr 23;284(5414):641-4
[
10213686.001
]
[Cites]
EMBO Rep. 2005 Feb;6(2):177-83
[
15678160.001
]
[Cites]
J Biol Chem. 2005 Feb 4;280(5):3862-74
[
15525642.001
]
[Cites]
Mol Cell. 2005 Jul 22;19(2):159-70
[
16039586.001
]
[Cites]
J Virol. 2005 Aug;79(16):10429-41
[
16051835.001
]
[Cites]
Nature. 2005 Aug 11;436(7052):807-11
[
16094360.001
]
[Cites]
J Pathol. 2006 Jan;208(2):187-98
[
16362980.001
]
[Cites]
Science. 2006 Feb 10;311(5762):856-61
[
16469929.001
]
[Cites]
J Virol. 2006 Mar;80(5):2243-56
[
16474132.001
]
[Cites]
Mol Cell. 2006 Feb 17;21(4):509-19
[
16483932.001
]
[Cites]
J Clin Invest. 2006 Mar;116(3):735-42
[
16498502.001
]
[Cites]
Oncogene. 2006 Mar 2;25(9):1281-9
[
16247449.001
]
[Cites]
J Virol. 2006 Jun;80(11):5273-82
[
16699007.001
]
[Cites]
J Virol. 2006 Sep;80(18):8909-19
[
16940503.001
]
[Cites]
Semin Cancer Biol. 2006 Aug;16(4):253-64
[
16904903.001
]
[Cites]
Semin Cancer Biol. 2006 Aug;16(4):288-302
[
16938463.001
]
[Cites]
Semin Cancer Biol. 2006 Aug;16(4):275-87
[
16945552.001
]
[Cites]
J Virol. 2007 Apr;81(8):4021-32
[
17267510.001
]
[Cites]
J Virol. 2007 May;81(9):4722-31
[
17314169.001
]
[Cites]
Oncogene. 2007 Jul 26;26(34):4979-86
[
17310999.001
]
[Cites]
J Virol. 2002 Nov;76(22):11596-604
[
12388720.001
]
[Cites]
Nature. 1999 Dec 23-30;402(6764):889-94
[
10622254.001
]
[Cites]
Blood. 2000 Feb 15;95(4):1406-12
[
10666218.001
]
[Cites]
Am J Pathol. 2000 Mar;156(3):743-9
[
10702388.001
]
[Cites]
Blood. 2000 Mar 15;95(6):2104-10
[
10706881.001
]
[Cites]
Mol Cell Biol. 2000 Apr;20(7):2423-35
[
10713166.001
]
[Cites]
Mol Cell Biol. 2000 Jun;20(12):4309-19
[
10825194.001
]
[Cites]
Mol Cell Biol. 2000 Aug;20(16):6008-18
[
10913183.001
]
(PMID = 17634226.001).
[ISSN]
0022-538X
[Journal-full-title]
Journal of virology
[ISO-abbreviation]
J. Virol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P01 CA113239
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Viral; 0 / MYC protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Ubiquitin; 0 / latency-associated nuclear antigen; 2ZD004190S / Threonine; 452VLY9402 / Serine; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.26 / Glycogen Synthase Kinase 3
[Other-IDs]
NLM/ PMC2045471
42.
Yamamoto M, Ito T, Shimizu T, Ishida T, Semba K, Watanabe S, Yamaguchi N, Inoue J:
Epigenetic alteration of the NF-κB-inducing kinase (NIK) gene is involved in enhanced NIK expression in basal-like breast cancer.
Cancer Sci
; 2010 Nov;101(11):2391-7
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[Title]
Epigenetic alteration of the NF-κB-inducing kinase (NIK)
gene
is involved in enhanced NIK expression in basal-like breast cancer.
Basal-like breast cancers are triple-negative (estrogen receptor negative, progesterone receptor negative,
erythroblastic
leukemia
viral oncogene homolog 2 (ERBB2) negative) tumors with an aggressive clinical behavior that lacks effective molecular targets for therapy.
Here, we report that enhanced NIK expression, which is exclusively observed in the basal-like subtype rather than the luminal-like subtype or non-tumorigenic mammary epithelial cells, is caused by epigenetic alteration of the NIK
gene
.
However, histone H3 acetylation
levels
were up-regulated in the basal-like subtype.
Thus, NIK and
genes
induced by the NIK-mediated constitutive NF-κB activation could be therapeutic targets of basal-like breast cancer.
[MeSH-major]
Breast Neoplasms / genetics. Epigenesis, Genetic.
Gene
Expression Regulation, Neoplastic / genetics. Protein-Serine-Threonine Kinases / genetics
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AZACITIDINE
.
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VALPROIC ACID
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[Copyright]
© 2010 Japanese Cancer Association.
(PMID = 20735436.001).
[ISSN]
1349-7006
[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 / Enzyme Inhibitors; 0 / Histones; 0 / NF-kappa B; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 614OI1Z5WI / Valproic Acid; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.25 / NF-kappa B kinase; M801H13NRU / Azacitidine
43.
Aisaki K, Aizawa S, Fujii H, Kanno J, Kanno H:
Glycolytic inhibition by mutation of pyruvate kinase gene increases oxidative stress and causes apoptosis of a pyruvate kinase deficient cell line.
Exp Hematol
; 2007 Aug;35(8):1190-200
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[Title]
Glycolytic inhibition by mutation of pyruvate kinase
gene
increases oxidative stress and causes apoptosis
of a
pyruvate kinase deficient cell line.
OBJECTIVE: SLC3 is a Friend erythroleukemic cell line established from the Pk-1(slc) mouse, a mouse model of red blood cell
type
-pyruvate kinase (R-PK) deficiency.
DNA microarray analysis was performed to examine
gene
-expression profiles between the two transfectants and parental SLC3.
The forced expression of R-PK significantly decreased cells at the sub G0/G1 stage in an expression-
level
dependent manner.
Microarray analysis showed that proapoptotic
genes
, such as Bad, Bnip3, and Bnip3l, were downregulated in the transfectants.
In addition, peroxiredoxin 1 (Prdx1) and other antioxidant
genes
, such as Cat, Txnrd1, and Glrx1 were also downregulated.
CONCLUSION: These results indicated that glycolytic inhibition by R-PK
gene
mutation augmented oxidative stress in the Friend
erythroleukemia
cell, leading to activation of hypoxia-inducible factor-1 as well as downstream proapoptotic
gene
expression.
Thus, R-PK plays an important role as an antioxidant during
erythroid
differentiation.
[MeSH-minor]
Animals. Apoptosis. Cell Line. Cell Line, Tumor. Erythrocytes / enzymology. Flow Cytometry. Genetic Predisposition to
Disease
.
Leukemia
,
Erythroblastic
,
Acute
. Mice. Oligonucleotide Array Sequence Analysis
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(PMID = 17662887.001).
[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]
EC 2.7.1.40 / Pyruvate Kinase
44.
Gougoumas DD, Vizirianakis IS, Triviai IN, Tsiftsoglou AS:
Activation of Prn-p gene and stable transfection of Prn-p cDNA in leukemia MEL and neuroblastoma N2a cells increased production of PrP(C) but not prevented DNA fragmentation initiated by serum deprivation.
J Cell Physiol
; 2007 May;211(2):551-9
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[Title]
Activation of Prn-p
gene
and stable transfection of Prn-p cDNA in
leukemia
MEL and neuroblastoma N2a cells increased production of PrP(C) but not prevented DNA fragmentation initiated by serum deprivation.
We observed that murine
erythroleukemia
(MEL) cells arrested in phase G(1) undergo transcriptional activation of Prn-p
gene
.
Here, we explored the potential role of activation of Prn-p
gene
and cytosolic accumulation of PrP(C) in growth arrest, differentiation, and apoptotic DNA fragmentation by stably transfecting MEL and N2a cells with Prn-p cDNA.
Our results indicate that (a) Induction of terminal differentiation of stably transfected MEL cells led to growth arrest, activation of Prn-p
gene
, concomitant expression of transfected Prn-p cDNA, suppression of bax
gene
, cytosolic accumulation of PrP(C), and DNA fragmentation.
(b) similarly, serum deprivation promoted growth arrest, apoptosis/necrosis associated with DNA fragmentation in parental N2a and N2a13 cells that produced relative high
level of
PrP(C) and not PrP(SC).
These data indicate that activation of Prn-p
gene
and expression of transfected Prn-p cDNA in cells of both hematopoietic and neuronal origin occurred concomitantly, and led to cytosolic accumulation of PrP(C) and DNA damage induced by serum deprivation.
[MeSH-major]
Apoptosis. DNA Fragmentation.
Leukemia
,
Erythroblastic
,
Acute
/ metabolism. Neuroblastoma / metabolism. PrPC Proteins / biosynthesis. Prions / biosynthesis. Transcriptional Activation
[MeSH-minor]
Animals. Cell Differentiation / drug effects. Cell Line, Tumor. Cell Proliferation. Culture Media, Serum-Free / metabolism. Cytosol / metabolism. Dimethyl Sulfoxide / pharmacology. Flow Cytometry.
Gene
Expression Regulation, Neoplastic. Mice. RNA, Messenger / biosynthesis. Time Factors. Transfection. Up-Regulation. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
(PMID = 17186498.001).
[ISSN]
0021-9541
[Journal-full-title]
Journal of cellular physiology
[ISO-abbreviation]
J. Cell. Physiol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Bax protein, mouse; 0 / Culture Media, Serum-Free; 0 / PrPC Proteins; 0 / Prions; 0 / Prnp protein, mouse; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; YOW8V9698H / Dimethyl Sulfoxide
45.
Boulanger E, Duprez R, Delabesse E, Gabarre J, Macintyre E, Gessain A:
Mono/oligoclonal pattern of Kaposi Sarcoma-associated herpesvirus (KSHV/HHV-8) episomes in primary effusion lymphoma cells.
Int J Cancer
; 2005 Jul 1;115(4):511-8
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Primary effusion lymphoma (
PEL
) is a rare lymphoma of B-cell origin, developed in serous cavities.
PEL
tumor cells are latently infected with Kaposi sarcoma-associated herpesvirus (KSHV) and in most cases co-infected with Epstein-Barr virus (EBV).
In 15 primary
PEL
tumors including 10 EBV-positive cases, we analyzed the fused terminal repeat (TR) regions of KSHV episomes using pulsed-field gel electrophoresis and Southern blot.
On the same genomic DNA samples, the cellular clonality was assessed by Southern blot and PCR detection of monoclonal immunoglobulin heavy chain (IGH) VDJ
gene
rearrangements, associated in the EBV-infected cases, with Southern blot analysis of the fused termini of EBV episomes.
Monoclonal IGH
gene
rearrangements were detected in 13 tumors using Southern blot, in 11 cases using PCR, and in all cases considering both methods.
However, only 5
PEL
tumors were found to be monoclonally infected with KSHV.
We hypothesized that the apparent discrepancy between viral and cellular clonalities in
PEL
might be due to several phenomena including complex mechanisms of genomic recircularization, insertion of duplicated sequences into the TR region and simultaneous infection of tumor cells with defective KSHV variants.
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[Copyright]
Copyright 2005 Wiley-Liss, Inc.
[CommentIn]
Int J Cancer. 2006 Oct 1;119(7):1746-8; author reply 1749-50
[
16671085.001
]
(PMID = 15700304.001).
[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
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Immunoglobulin Heavy Chains
46.
Gagne S, Lesage J, Ostiguy C, Cloutier Y, Van Tra H:
Quantitative determination of hexamethylene diisocyanate (HDI), 2,4-toluene diisocyanate (2,4-TDI) and 2,6-toluene diisocyanate (2,6-TDI) monomers at ppt levels in air by alkaline adduct coordination ionspray tandem mass spectrometry.
J Environ Monit
; 2005 Feb;7(2):145-50
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[Title]
Quantitative determination of hexamethylene diisocyanate (HDI), 2,4-toluene diisocyanate (2,4-TDI) and 2,6-toluene diisocyanate (2,6-TDI) monomers at ppt
levels
in air by alkaline adduct coordination ionspray tandem mass spectrometry.
Once sensitized, some workers could react to isocyanate monomers at concentrations below 1% of the
Permissible Exposure Limit of
5 ppb in air.
Currently available methods are not sufficiently sensitive to adequately evaluate isocyanates present at these
levels
in workplace air.
The analytical method's linearity was measured for a concentration range varying from the
limit of
detection of 0.04-0.13 ng mL(-1), depending on the monomer, up to approximately 32 ng mL(-1) for every isocyanate monomer, all with correlation coefficients (R(2)) greater than 0.999.
The analytical method's lower
limit of
quantification combined with an adapted sampling strategy allow the quantification of isocyanate monomers down to 0.04 ppt for an 8 h work shift when a lithium adduct is used, which is more than 300 times lower than the most sensitive method currently available.
This novel method can be used to confirm the very low
level of
isocyanate monomers for the safe reassignment of sensitized workers and it is also useful for charting the isocyanate dispersion tail in workplace environments.
Hazardous Substances Data Bank.
2,4-TOLUENE DIISOCYANATE
.
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HEXAMETHYLENE DIISOCYANATE
.
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(PMID = 15690096.001).
[ISSN]
1464-0325
[Journal-full-title]
Journal of environmental monitoring : JEM
[ISO-abbreviation]
J Environ Monit
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Air Pollutants, Occupational; 0 / Cyanates; 0 / Isocyanates; 0I70A3I1UF / 1,6-hexamethylene diisocyanate; 17X7AFZ1GH / Toluene 2,4-Diisocyanate; 91-08-7 / 2,6-diisocyanatotoluene
47.
Cotte-Rodríguez I, Justes DR, Nanita SC, Noll RJ, Mulligan CC, Sanders NL, Cooks RG:
Analysis of gaseous toxic industrial compounds and chemical warfare agent simulants by atmospheric pressure ionization mass spectrometry.
Analyst
; 2006 Apr;131(4):579-89
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The suitability of atmospheric pressure chemical ionization mass spectrometry as sensing instrumentation for the real-time monitoring of low
levels of
toxic compounds is assessed, especially with respect to public safety applications.
Tandem MS methods were implemented in selected cases for improved selectivity, sensitivity, and
limits of
detection.
Limits of
detection in the parts-per-billion and parts-per-trillion range were achieved for this set of analytes.
In all cases detection
limits
were well below the compounds'
permissible exposure limits
(PELs), even in the presence of added complex mixtures of alkanes.
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(PMID = 16568176.001).
[ISSN]
0003-2654
[Journal-full-title]
The Analyst
[ISO-abbreviation]
Analyst
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Air Pollutants; 0 / Chemical Warfare Agents
48.
Menier C, Guillard C, Cassinat B, Carosella ED, Rouas-Freiss N:
HLA-G turns off erythropoietin receptor signaling through JAK2 and JAK2 V617F dephosphorylation: clinical relevance in polycythemia vera.
Leukemia
; 2008 Mar;22(3):578-84
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To examine this, we analyzed whether HLA-G5 affects the proliferation of UT7/EPO and HEL
erythroleukemia
cells and characterized the mechanism by which HLA-G5 influences erythropoietin receptor (EPOR) signaling.
We show that HLA-G5 inhibits the proliferation of UT7/EPO cells, the EPOR signaling of which is similar to that of normal
erythroid
progenitors.
Involvement of JAK2 in
erythroid
cell proliferation has been highlighted by the role of JAK2 V617F mutation in polycythemia vera (PV), a myeloproliferative
disorder
characterized by
erythroid
lineage overproduction.
Clinical relevance is provided by analysis of PV patients who carry JAK2 V617F mutation, showing that HLA-G5 inhibits the formation of erythropoietin-independent
erythroid
colonies.
[MeSH-minor]
Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Colony-Forming Units Assay.
Erythroid
Precursor Cells / drug effects. Erythropoietin / physiology. G1 Phase / drug effects. HLA-G Antigens. Humans. Janus Kinase 2 / antagonists & inhibitors. Janus Kinase 2 / genetics. Janus Kinase 2 / metabolism.
Leukemia
,
Erythroblastic
,
Acute
/ pathology. Microspheres. Mutation, Missense. Phosphorylation / drug effects. Point Mutation. Protein Processing, Post-Translational / drug effects. Recombinant Fusion Proteins / pharmacology. STAT3 Transcription Factor / metabolism. STAT5 Transcription Factor / metabolism
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(PMID = 18059484.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I; 0 / Receptors, Erythropoietin; 0 / Recombinant Fusion Proteins; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; 11096-26-7 / Erythropoietin; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
49.
Wu X, Murphy P, Cunnick J, Hendrich S:
Synthesis and characterization of deoxynivalenol glucuronide: its comparative immunotoxicity with deoxynivalenol.
Food Chem Toxicol
; 2007 Oct;45(10):1846-55
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The cytotoxicity of DON and DONGLU were compared in cell culture using human
erythroleukemia
cell line K562.
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METHYLTHIAZOLETETRAZOLIUM
.
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DEOXYNIVALENOL
.
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Trypan blue
.
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(PMID = 17507135.001).
[ISSN]
0278-6915
[Journal-full-title]
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
[ISO-abbreviation]
Food Chem. Toxicol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Coloring Agents; 0 / Glucuronides; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / Trichothecenes; 298-93-1 / thiazolyl blue; EC 3.2.1.31 / Glucuronidase; I2ZWO3LS3M / Trypan Blue; JT37HYP23V / deoxynivalenol
50.
Paris D, Quadros A, Patel N, DelleDonne A, Humphrey J, Mullan M:
Inhibition of angiogenesis and tumor growth by beta and gamma-secretase inhibitors.
Eur J Pharmacol
; 2005 May 2;514(1):1-15
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Interestingly, gamma-secretase cleaves several proteins including Notch, E-cadherin, CD44 and ErbB-4 (
erythroblastic
leukemia
viral oncogene homolog 4), which are important modulators of angiogenesis.
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(PMID = 15878319.001).
[ISSN]
0014-2999
[Journal-full-title]
European journal of pharmacology
[ISO-abbreviation]
Eur. J. Pharmacol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Carbamates; 0 / Dipeptides; 0 / L 685458; 0 / N-(N-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester; 0 / N-benzyloxycarbonyl-valyl-leucyl-leucinal; 0 / Oligopeptides; 0 / Protease Inhibitors; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.23.46 / Bace1 protein, mouse
51.
Joy GJ, Middendorf PJ:
Noise exposure and hearing conservation in U.S. coal mines--a surveillance report.
J Occup Environ Hyg
; 2007 Jan;4(1):26-35
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[Title]
Noise
exposure
and hearing conservation in U.S. coal mines--a surveillance report.
This study examines the patterns and trends in noise
exposure
documented in data collected by Mine Safety and Health Administration inspectors at U.S. coal mines from 1987 through 2004.
During this period, MSHA issued a new regulation on occupational noise
exposure
that changed the regulatory requirements and enforcement policies.
The
exposure
reduction was accompanied by an increase of shift length as represented by dosimeter sample duration.
For coal miners exposed above the
permissible exposure level
, use of hearing protection devices increased from 61% to 89% during this period.
Participation of miners exposed at or above the action
level
in hearing conservation programs rapidly reached 86% following the effective date of the noise rule.
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(PMID = 17162478.001).
[ISSN]
1545-9624
[Journal-full-title]
Journal of occupational and environmental hygiene
[ISO-abbreviation]
J Occup Environ Hyg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
52.
Brocco MA, Fernández ME, Frasch AC:
Filopodial protrusions induced by glycoprotein M6a exhibit high motility and aids synapse formation.
Eur J Neurosci
; 2010 Jan;31(2):195-202
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[Title]
Filopodial protrusions induced by glycoprotein
M6a
exhibit high motility and aids synapse formation.
M6a
is a neuronal membrane glycoprotein whose expression diminishes during chronic stress.
M6a
overexpression in rat primary hippocampal neurons induces the formation of filopodial protrusions that could be spine precursors.
As the filopodium and spine motility has been associated with synaptogenesis, we analysed the motility
of M6a
-induced protrusions by time-lapse imaging.
Our data demonstrate that the motile protrusions formed by the neurons overexpressing
M6a
were more abundant and moved faster than those formed in control cells.
When different putative
M6a
phosphorylation sites were mutated, the neurons transfected with a mutant lacking intracellular phosphorylation sites bore filopodia, but these protrusions did not move as fast as those formed by cells overexpressing wild-
type
M6a
.
This suggests a role for
M6a
phosphorylation state in filopodium motility.
Furthermore, we show that
M6a
-induced protrusions could be stabilized upon contact with presynaptic region.
The behavior of filopodia from
M6a
-overexpressing cells and control cells was alike.
Thus,
M6a
-induced protrusions may be spine precursors that move to reach presynaptic membrane.
We suggest that
M6a
is a key molecule for spine formation during development.
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(PMID = 20074218.001).
[ISSN]
1460-9568
[Journal-full-title]
The European journal of neuroscience
[ISO-abbreviation]
Eur. J. Neurosci.
[Language]
eng
[Grant]
United States / Howard Hughes Medical Institute / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
France
[Chemical-registry-number]
0 / Gpm6a protein, rat; 0 / Membrane Glycoproteins; 0 / Nerve Tissue Proteins; 0 / Recombinant Fusion Proteins
53.
Lan Q, Zhang L, Tang X, Shen M, Smith MT, Qiu C, Ge Y, Ji Z, Xiong J, He J, Reiss B, Hao Z, Liu S, Xie Y, Guo W, Purdue MP, Galvan N, Xin KX, Hu W, Beane Freeman LE, Blair AE, Li L, Rothman N, Vermeulen R, Huang H:
Occupational exposure to trichloroethylene is associated with a decline in lymphocyte subsets and soluble CD27 and CD30 markers.
Carcinogenesis
; 2010 Sep;31(9):1592-6
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[Title]
Occupational
exposure
to trichloroethylene is associated with a decline in
lymphocyte
subsets and soluble CD27 and CD30 markers.
Occupational cohort and case-control studies suggest that trichloroethylene (TCE)
exposure
may be associated with non-Hodgkin lymphoma (NHL) but findings are not consistent.
Personal
exposure
measurements were taken over a three-week period before blood collection.
Ninety-six percent of workers were exposed to TCE below the current US Occupational Safety and Health Administration
Permissible Exposure Limit
(100 p.p.m.
The total
lymphocyte
count and each of the major
lymphocyte
subsets including CD4+ T cells, CD8+ T cells, natural killer (NK) cells and B cells were significantly decreased among the TCE-exposed workers compared with controls (P < 0.05), with evidence
of a
dose-dependent decline.
Further, there was a striking 61% decline in sCD27 plasma
level
and a 34% decline in sCD30 plasma
level
among TCE-exposed workers compared with controls.
This is the first report that TCE
exposure
under the current Occupational Safety and Health Administration workplace standard is associated with a decline in all major
lymphocyte
subsets and sCD27 and sCD30, which play an important role in regulating cellular activity in subsets of T, B and NK cells and are associated with
lymphocyte
activation.
[MeSH-major]
Antigens, CD27 / blood. Antigens, CD30 / blood. Biomarkers / metabolism.
Lymphocyte
Subsets / drug effects. Occupational
Exposure
. Trichloroethylene / adverse effects
[MeSH-minor]
Case-Control Studies. Humans.
Lymphocyte
Count. Molecular Epidemiology
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[Cites]
Ann Rheum Dis. 2006 Jun;65(6):796-803
[
16284097.001
]
[Cites]
Exp Hematol. 2005 Dec;33(12):1500-7
[
16338493.001
]
[Cites]
Biomed Environ Sci. 2006 Oct;19(5):346-52
[
17190186.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):405-8
[
17337643.001
]
[Cites]
J Neurol Neurosurg Psychiatry. 2008 Sep;79(9):1013-5
[
18223013.001
]
[Cites]
J Occup Environ Med. 2008 Nov;50(11):1306-19
[
19001957.001
]
[Cites]
Immunol Rev. 2009 May;229(1):216-31
[
19426224.001
]
[Cites]
Toxicol Appl Pharmacol. 2009 Jun 1;237(2):188-95
[
19332086.001
]
[Cites]
Environ Health Perspect. 2009 May;117(5):696-702
[
19479009.001
]
[Cites]
J Immunol. 2009 Sep 15;183(6):3770-7
[
19710474.001
]
[Cites]
Toxicol Appl Pharmacol. 2009 Nov 1;240(3):393-400
[
19647757.001
]
[Cites]
Drug News Perspect. 2009 Sep;22(7):409-13
[
19890498.001
]
[Cites]
Transpl Immunol. 2009 Dec;22(1-2):1-4
[
19772921.001
]
[Cites]
Environ Health Perspect. 2000 May;108 Suppl 2:161-76
[
10807550.001
]
[Cites]
Environ Health Perspect. 2000 May;108 Suppl 2:359-63
[
10807565.001
]
[Cites]
Clin Exp Immunol. 2002 Mar;127(3):486-94
[
11966765.001
]
[Cites]
Transpl Int. 2002 Sep;15(8):393-6
[
12221457.001
]
[Cites]
Transpl Immunol. 2003 Oct-Nov;12(1):49-61
[
14551032.001
]
[Cites]
Am J Epidemiol. 2003 Dec 15;158(12):1182-92
[
14652303.001
]
[Cites]
J Autoimmun. 2004 Nov;23(3):211-20
[
15501392.001
]
[Cites]
J Neuroimmunol. 1991 Dec;35(1-3):211-7
[
1659587.001
]
[Cites]
Clin Rheumatol. 1995 May;14(3):293-300
[
7641505.001
]
[Cites]
Toxicol Ind Health. 1995 May-Jun;11(3):253-307
[
7482570.001
]
[Cites]
Environ Health Perspect. 1996 Oct;104 Suppl 5:871-7
[
8933028.001
]
[Cites]
IARC Monogr Eval Carcinog Risks Hum. 1995;63:33-477
[
9139128.001
]
[Cites]
Science. 2004 Dec 3;306(5702):1774-6
[
15576619.001
]
[Cites]
J Natl Cancer Inst. 2005 Mar 16;97(6):425-32
[
15770006.001
]
[Cites]
J Occup Environ Med. 2005 May;47(5):453-7
[
15891523.001
]
[Cites]
Environ Health Perspect. 2006 Sep;114(9):1471-8
[
16966107.001
]
(PMID = 20530238.001).
[ISSN]
1460-2180
[Journal-full-title]
Carcinogenesis
[ISO-abbreviation]
Carcinogenesis
[Language]
eng
[Grant]
United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P30ES01896; United States / NIEHS NIH HHS / ES / P42ES04705
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD27; 0 / Antigens, CD30; 0 / Biomarkers; 290YE8AR51 / Trichloroethylene
[Other-IDs]
NLM/ PMC2930801
54.
Monni R, Haddaoui L, Naba A, Gallais I, Arpin M, Mayeux P, Moreau-Gachelin F:
Ezrin is a target for oncogenic Kit mutants in murine erythroleukemia.
Blood
; 2008 Mar 15;111(6):3163-72
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[Title]
Ezrin is a target for oncogenic Kit mutants in murine
erythroleukemia
.
The model
of erythroleukemia
caused by Spi-1/PU.1 transgenesis in mice is a multistage
disease
.
A preleukemic step is characterized by an
acute
proliferation of proerythroblasts due to the arrest of differentiation provoked by Spi-1/PU.1.
To gain insights into the mechanisms of the leukemic progression, we performed proteomic profiling analyses of proerythroblasts isolated at the 2 stages of the
disease
.
Our results indicate that the
level of
ezrin, a membrane cytoskeletal crosslinker, is increased in the leukemic cells.
Another recurrent oncogenic form of tyrosine kinases (Flt3) most frequently involved in human
myeloid leukemia
was also able to phosphorylate ezrin.
These findings point to a new role for ezrin as signaling player in the development of
leukemia
, being a downstream effector of oncogenic tyrosine kinases in leukemic blasts.
[MeSH-major]
Cytoskeletal Proteins / metabolism.
Leukemia
,
Erythroblastic
,
Acute
/ metabolism. Proto-Oncogene Proteins c-kit / metabolism
[MeSH-minor]
Animals. Cell Line. Cell Proliferation. Erythroblasts / cytology. Erythroblasts / metabolism.
Gene
Expression Regulation, Neoplastic. Mice. Mice, Transgenic. Mutation / genetics. Peptides / genetics. Peptides / metabolism. Phosphotyrosine / metabolism. Protein-Tyrosine Kinases / metabolism
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(PMID = 18182570.001).
[ISSN]
0006-4971
[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 / Cytoskeletal Proteins; 0 / Peptides; 0 / ezrin; 129712-62-5 / lambda Spi-1; 21820-51-9 / Phosphotyrosine; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
55.
Ades S, Maxfield LF, Gould CJ, Jones GK, Levy SB:
Selection of non-P-glycoprotein mediated high-level etoposide resistant cell lines by adriamycin with P-gp inhibitors.
Int J Oncol
; 2006 Mar;28(3):747-53
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[Title]
Selection of non-P-glycoprotein mediated high-
level
etoposide resistant cell lines by adriamycin with P-gp inhibitors.
In murine
erythroleukemia
(MEL) A20 cells (grown in 20 ng/ml adriamycin), mutation(s) producing 10-fold adriamycin (doxorubicin) resistance emerged via an unknown mechanism.
Exposure of
A20 cells to further stepwise increasing concentrations of ADR in combination with MDR modulators (PSC833 and verapamil) aimed to amplify the undetermined A20 mechanism while controlling P-glycoprotein (P-gp) overexpression.
Resistance to vincristine was unchanged, but resistance to etoposide (VP-16) was 3.7-fold higher in A40P than A20 (itself 97-fold higher than wild-
type
).
No mutations in the coding sequence of topoisomerase IIalpha could be located to account for the high etoposide resistance
levels
.
[MeSH-minor]
ATP Binding Cassette Transporter, Sub-Family B / antagonists & inhibitors. ATP Binding Cassette Transporter, Sub-Family B / genetics. ATP Binding Cassette Transporter, Sub-Family B / metabolism. ATP-Binding Cassette Transporters / genetics. ATP-Binding Cassette Transporters / metabolism. Animals. Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Antineoplastic Agents / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Cyclosporins / pharmacology. DNA Topoisomerases,
Type
II / genetics. DNA Topoisomerases,
Type
II / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Daunorubicin / pharmacology. Dose-Response Relationship, Drug. Drug Resistance, Multiple / genetics.
Gene
Expression Regulation, Neoplastic / drug effects. Mice. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Verapamil / pharmacology
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(PMID = 16465381.001).
[ISSN]
1019-6439
[Journal-full-title]
International journal of oncology
[ISO-abbreviation]
Int. J. Oncol.
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / P-30 DK 34928
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / ATP Binding Cassette Transporter, Sub-Family B; 0 / ATP-Binding Cassette Transporters; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Cyclosporins; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / multidrug resistance protein 3; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; CJ0O37KU29 / Verapamil; EC 5.99.1.3 / DNA Topoisomerases, Type II; Q7ZP55KF3X / valspodar; ZS7284E0ZP / Daunorubicin
56.
Won JH, Han SH, Bae SB, Kim CK, Lee NS, Lee KT, Park SK, Hong DS, Lee DW, Park HS:
Successful eradication of relapsed primary effusion lymphoma with high-dose chemotherapy and autologous stem cell transplantation in a patient seronegative for human immunodeficiency virus.
Int J Hematol
; 2006 May;83(4):328-30
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Primary effusion lymphoma (
PEL
) is a recently recognized
disease
that occurs most often in immunosuppressed patients, either with human immunodeficiency virus (HIV) or in the posttransplantation setting, and it occasionally occurs in nonimmunosuppressed patients.
PEL
rarely responds to systemic chemotherapy, and the prognosis is poor, with a median survival time of less than 6 months for most cohorts.
A standard treatment for
PEL
has not yet been identified.
We describe a patient with HIV-seronegative
PEL
who relapsed after combination chemotherapy and then underwent successful treatment with high-dose chemotherapy (HDC) and autologous stem cell transplantation (ASCT).
The treatment was well tolerated, and the patient has been in
remission
for 12 months after HDC and ASCT.
[MeSH-minor]
Disease
-Free Survival. HIV Seropositivity. Humans. Male. Middle Aged. Prognosis. Recurrence. Transplantation, Autologous
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[Cites]
Am J Hematol. 2003 Jul;73(3):143-8
[
12827649.001
]
[Cites]
Leuk Lymphoma. 2002 Mar;43(3):595-601
[
12002764.001
]
[Cites]
J Pathol. 1999 Oct;189(2):288-93
[
10547588.001
]
[Cites]
AIDS Patient Care STDS. 2004 Feb;18(2):67-73
[
15006181.001
]
[Cites]
Blood. 1989 Feb 15;73(3):792-9
[
2537119.001
]
[Cites]
Blood. 1996 Jul 15;88(2):645-56
[
8695812.001
]
[Cites]
N Engl J Med. 1995 May 4;332(18):1186-91
[
7700311.001
]
[Cites]
Lab Invest. 1998 Dec;78(12):1637-42
[
9881964.001
]
[Cites]
Cancer Genet Cytogenet. 2005 Jan 1;156(1):49-53
[
15588855.001
]
[Cites]
Leuk Lymphoma. 2001 Apr;41(3-4):439-43
[
11378560.001
]
[Cites]
Blood. 2001 Dec 15;98(13):3857-9
[
11739198.001
]
[Cites]
Leukemia. 1997 Feb;11(2):266-72
[
9009091.001
]
[Cites]
Blood. 2002 Jan 15;99(2):698-701
[
11781257.001
]
[Cites]
Blood. 1995 Oct 1;86(7):2708-14
[
7670109.001
]
[Cites]
Ann Intern Med. 1996 Nov 15;125(10):822-5
[
8928989.001
]
[Cites]
Blood. 1996 Oct 15;88(8):3124-8
[
8874212.001
]
[Cites]
Mayo Clin Proc. 2002 Sep;77(9):941-9
[
12233927.001
]
[Cites]
J Clin Oncol. 2003 Dec 1;21(23):4423-7
[
14581441.001
]
[Cites]
Am J Clin Pathol. 1996 Feb;105(2):221-9
[
8607449.001
]
[Cites]
Hematol J. 2001;2(3):172-9
[
11920242.001
]
(PMID = 16757433.001).
[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
57.
Dei S, Budriesi R, Sudwan P, Ferraroni M, Chiarini A, Garnier-Suillerot A, Manetti D, Martelli C, Scapecchi S, Teodori E:
Diphenylcyclohexylamine derivatives as new potent multidrug resistance (MDR) modulators.
Bioorg Med Chem
; 2005 Feb 15;13(4):985-98
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A series of compounds with a diphenylmethyl cyclohexyl skeleton, loosely related to verapamil, has been synthesized and tested as MDR modulators on anthracycline-resistant
erythroleukemia
K 562 cells.
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(PMID = 15670906.001).
[ISSN]
0968-0896
[Journal-full-title]
Bioorganic & medicinal chemistry
[ISO-abbreviation]
Bioorg. Med. Chem.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Cyclohexylamines
58.
Vorobiev DS, Kiselevskii MV, Chikileva IO, Semenova IB:
Effect of recombinant heat shock protein 70 of mycobacterial origin on cytotoxic activity and immunophenotype of human peripheral blood mononuclear leukocytes.
Bull Exp Biol Med
; 2009 Jul;148(1):64-7
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Recombinant heat shock protein of mycobacterial origin with a molecular weight 70 kDa in concentration 0.1 microg/ml in vitro activates cytotoxic activity of mononuclear
lymphocytes
from peripheral blood of healthy donors against K-562 human
erythroblastic
leukemia
cells sensitive to natural killers.
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(PMID = 19902099.001).
[ISSN]
1573-8221
[Journal-full-title]
Bulletin of experimental biology and medicine
[ISO-abbreviation]
Bull. Exp. Biol. Med.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Heat-Shock Proteins; 0 / Recombinant Proteins
59.
Rush M, Appanah R, Lee S, Lam LL, Goyal P, Lorincz MC:
Targeting of EZH2 to a defined genomic site is sufficient for recruitment of Dnmt3a but not de novo DNA methylation.
Epigenetics
; 2009 Aug 16;4(6):404-14
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[Title]
Targeting of EZH2 to a defined genomic site is sufficient for recruitment of Dnmt3a but not
de
novo DNA methylation.
Polycomb-mediated
gene
silencing and DNA methylation underlie many epigenetic processes important in normal development as well as in cancer.
Interestingly, however, the majority of H3K27me3 marked
genes
lack DNA methylation in ES cells, indicating that EZH2 recruitment may not be sufficient to promote DNA methylation.
Here, we employed a Gal4DBD/gal4UAS-based system to directly test if EZH2 binding at a defined genomic site is sufficient to promote
de
novo DNA methylation in a murine
erythroleukaemia
cell line.
Targeting
of a
Gal4DBD-EZH2 fusion to an intergenic transgene bearing a gal4 binding-site array promoted localized recruitment of Suz12 and Bmi1, subunits of PRC2 and PRC1, respectively, and deposition of H3K27me3.
Strikingly, while Dnmt3a was also recruited in an EZH2-dependent manner,
de
novo DNA methylation of the transgene was not observed.
Thus, while targeting of EZH2 to a specific genomic site is sufficient for recruitment of Dnmt3a, additional events are required for
de
novo DNA methylation.
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(PMID = 19717977.001).
[ISSN]
1559-2308
[Journal-full-title]
Epigenetics
[ISO-abbreviation]
Epigenetics
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Histones; 0 / Polycomb-Group Proteins; 0 / Recombinant Fusion Proteins; 0 / Repressor Proteins; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3A; EC 2.1.1.43 / Ezh2 protein, mouse; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Polycomb Repressive Complex 2; K3Z4F929H6 / Lysine
60.
Karikó K, Buckstein M, Ni H, Weissman D:
Suppression of RNA recognition by Toll-like receptors: the impact of nucleoside modification and the evolutionary origin of RNA.
Immunity
; 2005 Aug;23(2):165-75
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We show that RNA signals through human TLR3, TLR7, and TLR8, but incorporation of modified nucleosides m5C,
m6A
, m5U, s2U, or pseudouridine ablates activity.
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[CommentIn]
Immunity. 2005 Aug;23(2):111-3
[
16111629.001
]
(PMID = 16111635.001).
[ISSN]
1074-7613
[Journal-full-title]
Immunity
[ISO-abbreviation]
Immunity
[Language]
eng
[Grant]
United States / NIAID NIH HHS / AI / AI060505; United States / NIAID NIH HHS / AI / AI50484; United States / NIDCR NIH HHS / DE / DE14825
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Biomarkers; 0 / CD83 antigen; 0 / Cytokines; 0 / HLA-DR Antigens; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 0 / Nucleosides; 0 / Phosphatidylethanolamines; 0 / Receptors, Cell Surface; 0 / TLR3 protein, human; 0 / TLR7 protein, human; 0 / TLR8 protein, human; 0 / Toll-Like Receptor 3; 0 / Toll-Like Receptor 7; 0 / Toll-Like Receptor 8; 0 / Toll-Like Receptors; 63231-63-0 / RNA; 76391-83-8 / 1,2-dielaidoylphosphatidylethanolamine
61.
Liao J, Gallas M, Pegram M, Slingerland J:
Lapatinib: new opportunities for management of breast cancer.
Breast Cancer (Dove Med Press)
; 2010;2:79-91
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Approximately 20% of new diagnosed breast cancers overexpress the human epidermal growth factor receptor 2 (EGFR2), also known as
erythroblastic
leukemia
viral oncogene homolog 2 (ERBB2) protein, as a consequence of ERBB2
gene
amplification, resulting in a poor prognosis.
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(PMID = 24367169.001).
[ISSN]
1179-1314
[Journal-full-title]
Breast cancer (Dove Medical Press)
[ISO-abbreviation]
Breast Cancer (Dove Med Press)
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
New Zealand
[Other-IDs]
NLM/ PMC3846530
[Keywords]
NOTNLM ; ERBB family / ERBB2 / breast cancer / capecitabine / lapatinib / letrozole / trastuzumab
62.
Kishimoto S, Nakamura S, Hattori H, Nakamura S, Oonuma F, Kanatani Y, Tanaka Y, Mori Y, Harada Y, Tagawa M, Ishihara M:
Human stem cell factor (SCF) is a heparin-binding cytokine.
J Biochem
; 2009 Mar;145(3):275-8
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Furthermore, pre-immobilized SCF on F/P MP-coated plates significantly stimulated proliferation
of a
human
erythroleukemia
cell line.
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(PMID = 19074504.001).
[ISSN]
1756-2651
[Journal-full-title]
Journal of biochemistry
[ISO-abbreviation]
J. Biochem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Disaccharides; 0 / Stem Cell Factor; 9005-49-6 / Heparin
63.
Glaister BC, Orendurff MS, Schoen JA, Klute GK:
Rotating horizontal ground reaction forces to the body path of progression.
J Biomech
; 2007;40(15):3527-32
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When studying the biomechanics
of a
transient turn, the orientation of the body will change relative to the orientation of the force plates over the progression of the turn.
Body reference frames were chosen whose origins were the center of mass (COM) and the pelvis origin (
PEL
).
A finite-difference method was used to align the axes of the reference frames according to the horizontal paths of the COM and
PEL
.
The ground reaction impulses (GRIs) were calculated relative to the COM and
PEL
reference frames.
GRI differences were small between the
PEL
and COM frames, suggesting that either is acceptable for turning studies.
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(PMID = 17597134.001).
[ISSN]
0021-9290
[Journal-full-title]
Journal of biomechanics
[ISO-abbreviation]
J Biomech
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
64.
Léger DY, Battu S, Liagre B, Cardot PJ, Beneytout JL:
Sedimentation field flow fractionation to study human erythroleukemia cell megakaryocytic differentiation after short period diosgenin induction.
J Chromatogr A
; 2007 Jul 20;1157(1-2):309-20
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[Title]
Sedimentation field flow fractionation to study human
erythroleukemia
cell megakaryocytic differentiation after short period diosgenin induction.
It concerns the study of megakaryocytic differentiation processes after a short
exposure
to an inducting agent (diosgenin).
A short
exposure
to diosgenin was able to induce complete differentiation leading to maximal maturation which ended naturally after 192h incubation without the influence
of a
secondary effect of diosgenin.
[MeSH-major]
Cell Differentiation. Diosgenin / metabolism.
Leukemia
,
Erythroblastic
,
Acute
/ pathology. Megakaryocytes / pathology
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(PMID = 17499257.001).
[ISSN]
0021-9673
[Journal-full-title]
Journal of chromatography. A
[ISO-abbreviation]
J Chromatogr A
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / DNA Primers; 0 / RNA, Neoplasm; K49P2K8WLX / Diosgenin
65.
Régnier-Rosencher E, Barrou B, Marcelin AG, Jacobzone-Leveque C, Cadranel J, Leblond V, Francès C:
[Primary effusion lymphoma in two kidney transplant recipients].
Ann Dermatol Venereol
; 2010 Apr;137(4):285-9
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BACKGROUND: Primary effusion lymphoma (
PEL
) is a highly
malignant
non-Hodgkin lymphoma associated with Kaposi's sarcoma-associated herpesvirus/human herpesvirus-8 infection (KSHV/HHV-8).
OBSERVATION: We describe two male kidney transplant recipients, aged 47 and 51 years, followed for Kaposi's sarcoma in skin, lymph nodes, gastrointestinal (GI) tract and lung whose
disease
was poorly controlled by sirolimus and chemotherapy.
CONCLUSION: The contrast between a very low KHSV viral load in plasma and a very high viral load pleural effusion should alert physicians and prompt suspicion
of PEL
in Kaposi's sarcoma patients with recurrent serous effusion.
The potential inhibitory role of sirolimus on
PEL
progression is discussed.
[MeSH-minor]
Digestive System Neoplasms / drug therapy. Digestive System Neoplasms / secondary. Digestive System Neoplasms / virology. Fatal Outcome. Giant Lymph Node Hyperplasia / complications. Giant Lymph Node Hyperplasia / virology. Humans. Immunocompromised Host. Kidney Failure, Chronic / etiology. Kidney Failure, Chronic / surgery. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Lung Neoplasms / virology. Lymphatic Metastasis. Male. Middle Aged. Pleural Effusion,
Malignant
/ cytology. Pleural Effusion,
Malignant
/ virology. Sarcoma, Kaposi / drug therapy. Sarcoma, Kaposi / etiology. Sarcoma, Kaposi / virology. Skin Neoplasms / drug therapy. Skin Neoplasms / etiology. Skin Neoplasms / virology. Viral Load
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[Copyright]
2010 Elsevier Masson SAS. All rights reserved.
(PMID = 20417362.001).
[ISSN]
0151-9638
[Journal-full-title]
Annales de dermatologie et de vénéréologie
[ISO-abbreviation]
Ann Dermatol Venereol
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Immunosuppressive Agents
66.
Liao CH, Fett W, Tzean SS, Hoffman G:
Detection and sequence analysis of an altered pectate lyase gene in Pseudomonas syringae pv. glycinea and related bacteria.
Can J Microbiol
; 2006 Nov;52(11):1051-9
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[Title]
Detection and sequence analysis of an altered
pectate lyase gene
in Pseudomonas syringae pv. glycinea and related bacteria.
Pectate lyase
(PL) is a potent cell wall-degrading enzyme known to play a role in the microbial infection of plants.
However, the PL
gene
(
pel
) was detected by Southern hybridization in four out of four P. syringae pv. glycinea strains examined.
A P. syringae pv. glycinea
pel gene
was cloned, sequenced, and predicted to encode a protein sharing 70%-90% identity in amino acid sequence with PLs produced by pectolytic pseudomonads and xanthomonads.
A series of amino acid and nucleotide sequence analyses reveal that (i) the predicted P. syringae pv. glycinea PL contains two regions in the amino acid sequence that may affect the formation
of a
beta-helix structure important for the enzyme activity, and (ii) the P. syringae pv. glycinea
pel gene
contains a single-base insertion, a double-base insertion, and an 18-bp deletion, which can lead to the synthesis of an inactive PL protein.
The altered
pel
sequence was also detected by polymerase chain reaction and nucleotide sequencing in the genomes of other pathovars of P. syringae, including phaseolicola and tagetis.
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(PMID = 17215896.001).
[ISSN]
0008-4166
[Journal-full-title]
Canadian journal of microbiology
[ISO-abbreviation]
Can. J. Microbiol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Canada
[Chemical-registry-number]
EC 4.2.2.- / Polysaccharide-Lyases; EC 4.2.2.2 / pectate lyase
67.
Comelli M, Genero N, Mavelli I:
Caspase-independent apoptosis in Friend's erythroleukemia cells: role of mitochondrial ATP synthesis impairment in relocation of apoptosis-inducing factor and endonuclease G.
J Bioenerg Biomembr
; 2009 Feb;41(1):49-59
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[Title]
Caspase-independent apoptosis in Friend'
s erythroleukemia
cells: role of mitochondrial ATP synthesis impairment in relocation of apoptosis-inducing factor and endonuclease G.
We previously documented that parental and differentiated Friend'
s erythroleukemia
cells were induced to apoptosis by oligomycin and H(2)O(2)
exposure
, showing that the energy impairment occurring in both cases as a consequence
of a
severe mitochondrial F(0)F(1)ATPsynthase inactivation was a common early feature.
No detectable change in mitochondrial transmembrane potential and no variation in mitochondrial
levels of
Bcl-2 and Bax are observed.
These results point to the osmotic rupture of the mitochondrial outer membrane as occurring in response to cell
exposure
to the two energy-impairing treatments under conditions preserving the mitochondrial inner membrane.
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[Cites]
Science. 1997 Feb 21;275(5303):1129-32
[
9027314.001
]
[Cites]
Cell Mol Life Sci. 2001 Mar;58(3):356-70
[
11315185.001
]
[Cites]
EMBO J. 1998 Jan 2;17(1):37-49
[
9427739.001
]
[Cites]
J Neurosci. 1999 Sep 1;19(17):7394-404
[
10460246.001
]
[Cites]
J Exp Med. 1998 Apr 20;187(8):1261-71
[
9547337.001
]
[Cites]
Nature. 1999 Jun 3;399(6735):483-7
[
10365962.001
]
[Cites]
FEBS Lett. 1998 Apr 10;426(1):111-6
[
9598989.001
]
[Cites]
Biochimie. 2002 Feb-Mar;84(2-3):131-41
[
12022944.001
]
[Cites]
Biochem Biophys Res Commun. 1985 Mar 29;127(3):1039-44
[
3985951.001
]
[Cites]
Biophys J. 1988 May;53(5):785-94
[
3390520.001
]
[Cites]
Trends Cell Biol. 2000 Sep;10(9):369-77
[
10932094.001
]
[Cites]
Biol Pharm Bull. 2007 Aug;30(8):1516-22
[
17666813.001
]
[Cites]
Nat Med. 2005 Jul;11(7):725-30
[
16015365.001
]
[Cites]
J Neurosci. 1999 Aug 1;19(15):6235-47
[
10414953.001
]
[Cites]
EMBO J. 2003 Sep 1;22(17):4385-99
[
12941691.001
]
[Cites]
Cell. 2004 Jun 11;117(6):773-86
[
15186778.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3668-72
[
9108035.001
]
[Cites]
Free Radic Biol Med. 2003 May 1;34(9):1190-9
[
12706499.001
]
[Cites]
Biochem Biophys Res Commun. 2004 Sep 17;322(2):355-63
[
15325238.001
]
[Cites]
Cell. 1993 Oct 22;75(2):241-51
[
7503812.001
]
[Cites]
Trends Biochem Sci. 2001 Feb;26(2):112-7
[
11166569.001
]
[Cites]
Science. 2004 Jul 30;305(5684):626-9
[
15286356.001
]
[Cites]
Blood. 1996 May 1;87(9):3837-43
[
8611710.001
]
[Cites]
Biochemistry. 1991 May 7;30(18):4480-6
[
2021638.001
]
[Cites]
Cell. 1997 Nov 28;91(5):627-37
[
9393856.001
]
[Cites]
Physiol Rev. 2007 Jan;87(1):99-163
[
17237344.001
]
[Cites]
Am J Physiol Cell Physiol. 2003 Dec;285(6):C1483-93
[
12930708.001
]
[Cites]
J Clin Invest. 2005 Oct;115(10):2640-7
[
16200197.001
]
[Cites]
Cell. 1997 Nov 14;91(4):479-89
[
9390557.001
]
[Cites]
J Biol Chem. 1998 Nov 6;273(45):29540-4
[
9792662.001
]
[Cites]
Biochim Biophys Acta. 1995 Jul 17;1241(2):139-76
[
7640294.001
]
[Cites]
Nat Chem Biol. 2005 Sep;1(4):188-9
[
16408030.001
]
[Cites]
Genes Dev. 2001 Nov 15;15(22):2922-33
[
11711427.001
]
[Cites]
Science. 1997 Feb 21;275(5303):1132-6
[
9027315.001
]
[Cites]
FEBS Lett. 2001 Jul 6;500(3):114-8
[
11445067.001
]
[Cites]
J Biol Chem. 2008 Feb 29;283(9):5622-31
[
18167347.001
]
[Cites]
Acta Pharmacol Sin. 2004 Jan;25(1):83-9
[
14704127.001
]
[Cites]
EMBO J. 2005 Apr 6;24(7):1375-86
[
15775970.001
]
[Cites]
Free Radic Biol Med. 2005 Jan 1;38(1):12-23
[
15589367.001
]
[Cites]
Nature. 2000 Aug 24;406(6798):855-62
[
10972280.001
]
[Cites]
EMBO J. 1998 Jul 15;17(14):3878-85
[
9670005.001
]
[Cites]
FEBS Lett. 1996 Jan 8;378(2):107-10
[
8549813.001
]
[Cites]
Apoptosis. 2005 Oct;10(5):997-1007
[
16151635.001
]
[Cites]
Cell Death Differ. 2000 Mar;7(3):282-91
[
10745273.001
]
[Cites]
Mol Biol Cell. 2007 Jan;18(1):84-93
[
17079734.001
]
[Cites]
Cell Death Differ. 2006 Aug;13(8):1396-402
[
16710362.001
]
[Cites]
Nature. 2001 Mar 29;410(6828):549-54
[
11279485.001
]
[Cites]
J Mol Biol. 2004 Apr 23;338(2):217-28
[
15066427.001
]
[Cites]
J Biol Chem. 1951 Nov;193(1):265-75
[
14907713.001
]
[Cites]
Free Radic Biol Med. 1998 Apr;24(6):924-32
[
9607602.001
]
[Cites]
Anal Biochem. 1989 May 15;179(1):1-7
[
2667390.001
]
[Cites]
Biochem Soc Trans. 2000 Feb;28(2):170-7
[
10816121.001
]
[Cites]
Cell Death Differ. 2005 Nov;12 Suppl 2:1478-80
[
16247494.001
]
[Cites]
Dev Cell. 2002 Jan;2(1):55-67
[
11782314.001
]
[Cites]
Trends Cell Biol. 2006 May;16(5):264-72
[
16621561.001
]
[Cites]
J Cell Physiol. 2002 Aug;192(2):131-7
[
12115719.001
]
[Cites]
FEBS Lett. 2004 Jan 16;557(1-3):14-20
[
14741334.001
]
[Cites]
Nature. 1999 Feb 4;397(6718):441-6
[
9989411.001
]
[Cites]
Cell Death Differ. 2001 Dec;8(12):1136-42
[
11753562.001
]
[Cites]
FEBS Lett. 1994 Sep 19;352(1):71-5
[
7925947.001
]
[Cites]
Science. 1993 Nov 19;262(5137):1274-7
[
8235659.001
]
[Cites]
J Neurochem. 1996 Sep;67(3):1259-67
[
8752134.001
]
(PMID = 19184384.001).
[ISSN]
1573-6881
[Journal-full-title]
Journal of bioenergetics and biomembranes
[ISO-abbreviation]
J. Bioenerg. Biomembr.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Apoptosis Inducing Factor; 8L70Q75FXE / Adenosine Triphosphate; EC 3.1.- / Endodeoxyribonucleases; EC 3.1.21.- / endonuclease G; EC 3.6.3.14 / Proton-Translocating ATPases
68.
Baniushin BF:
[Methylation of adenine residues in DNA of eukaryotes].
Mol Biol (Mosk)
; 2005 Jul-Aug;39(4):557-66
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In plants
m6A
was detected in total, mitochondrial and nuclear DNAs; in plants one and the same
gene
(DRM2) can be methylated both at adenine and cytosine residues.
First N6-adenine DNA-methyltransferase (wadmtase) of higher eukaryotes was isolated from vacuolar fraction of vesicles obtained from aging wheat coleoptiles; in the presence
of S
-adenosyl-L-methionine this Mg2+ -, Ca2+ -dependent enzyme
de
novo methylates first adenine residue in TGATCA sequence in single- and double-stranded DNA but it prefers single-stranded DNA structures.
Adenine DNA methylation in eukaryotes seems to be involved in regulation of both
gene
expression and DNA replication including replication of mitochondrial DNA.
Thus, in eukaryotic cell there are, at least, two different systems of the enzymatic DNA methylations (adenine and cytosine ones) and a special
type
of regulation
of gene
functioning based on the combinatory hierarchy of these interdependent genome modifications.
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(PMID = 16083005.001).
[ISSN]
0026-8984
[Journal-full-title]
Molekuliarnaia biologiia
[ISO-abbreviation]
Mol. Biol. (Mosk.)
[Language]
rus
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Russia (Federation)
[Chemical-registry-number]
0 / DNA, Mitochondrial; EC 2.1.1.- / DNA Modification Methylases; JAC85A2161 / Adenine
[Number-of-references]
94
69.
Di Pietro R, di Giacomo V, Caravatta L, Sancilio S, Rana RA, Cataldi A:
Cyclic nucleotide response element binding (CREB) protein activation is involved in K562 erythroleukemia cells differentiation.
J Cell Biochem
; 2007 Mar 1;100(4):1070-9
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[Title]
Cyclic nucleotide response element binding (CREB) protein activation is involved in K562
erythroleukemia
cells differentiation.
K562 are human
erythroleukemia
cells inducible to differentiate into megakaryocytic or
erythroid
lineage by different agents.
Cyclic nucleotide Response Element Binding (CREB) protein, a nuclear transcription factor which mediates c-AMP signaling, is a potential candidate involved in the occurrence
of erythroid
differentiation and adaptive response.
Here we investigated signaling events in K562 cells induced with 30 microM hemin to undergo
erythroid
differentiation.
All in all these results document a novel relationship between CREB activation and differentiation-related apoptotic cell death and assign a role to p38 MAP kinase pathway in determining these events in K562
erythroleukemia
cells.
[MeSH-minor]
Apoptosis / drug effects. Blotting, Western. Hemin / pharmacology. Humans. Imidazoles / pharmacology. K562 Cells.
Leukemia
,
Erythroblastic
,
Acute
/ metabolism.
Leukemia
,
Erythroblastic
,
Acute
/ pathology. Microscopy, Fluorescence. Phosphorylation / drug effects. Pyridines / pharmacology. Serine / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism
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L-SERINE
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(PMID = 17063485.001).
[ISSN]
0730-2312
[Journal-full-title]
Journal of cellular biochemistry
[ISO-abbreviation]
J. Cell. Biochem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cyclic AMP Response Element-Binding Protein; 0 / Imidazoles; 0 / Pyridines; 0 / SB 203580; 452VLY9402 / Serine; 743LRP9S7N / Hemin; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
70.
Karim N, Jones JT, Okada H, Kikuchi T:
Analysis of expressed sequence tags and identification of genes encoding cell-wall-degrading enzymes from the fungivorous nematode Aphelenchus avenae.
BMC Genomics
; 2009;10:525
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[Title]
Analysis of expressed sequence tags and identification
of genes
encoding cell-wall-degrading enzymes from the fungivorous nematode Aphelenchus avenae.
This nematode is also found in association with plants but its ability to cause plant
disease
remains largely undetermined.
The taxonomic position and intermediate lifestyle
of A
. avenae make it an important model for studying the evolution of plant parasitism within the Nematoda.
Expressed sequence tag (EST) analysis may therefore be useful in providing an initial insight into the poorly understood genetic background
of A
. avenae.
In addition, 1,100 (40.7%) of the sequences were functionally classified using
Gene
Ontology (GO) hierarchy.
Similarity searches of the cluster sequences identified a set
of genes
with significant homology to
genes
encoding enzymes that degrade plant or fungal cell walls.
The full length sequences of two
genes
encoding glycosyl hydrolase family 5 (GHF5) cellulases and two
pectate lyase genes
encoding polysaccharide
lyase
family 3 (PL3) proteins were identified and characterized.
CONCLUSION: We have described at least 2,214 putative
genes
from A. avenae and identified a set
of genes
encoding a range of cell-wall-degrading enzymes.
The presence
of genes
encoding a battery of cell-wall-degrading enzymes in A. avenae and their similarities with
genes
from other plant parasitic nematodes suggest that this nematode can act not only as a fungal feeder but also a plant parasite.
Further studies on
genes
encoding cell-wall-degrading enzymes in A. avenae will accelerate our understanding of the complex evolutionary histories of plant parasitism and the use
of genes
obtained by horizontal
gene
transfer from prokaryotes.
[MeSH-minor]
Amino Acid Sequence. Animals. Base Sequence. Cellulase / genetics. Cluster Analysis. Databases, Protein. Desiccation.
Gene
Expression Regulation.
Gene
Library. Molecular Sequence Data. Phylogeny. Polysaccharide-Lyases / chemistry. Polysaccharide-Lyases / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Stress, Physiological / genetics
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[Cites]
J Mol Biol. 2004 Jul 16;340(4):783-95
[
15223320.001
]
[Cites]
Bioinformatics. 2004 Jun 12;20(9):1398-404
[
14988115.001
]
[Cites]
FEBS Lett. 2004 Aug 13;572(1-3):201-5
[
15304348.001
]
[Cites]
Mol Biochem Parasitol. 1985 Oct;17(1):93-104
[
3932852.001
]
[Cites]
Mol Biochem Parasitol. 1987 Oct;25(3):267-72
[
3696175.001
]
[Cites]
Mol Biochem Parasitol. 1992 Feb;50(2):285-94
[
1741016.001
]
[Cites]
Mol Biochem Parasitol. 1993 Apr;58(2):317-23
[
8479456.001
]
[Cites]
Exp Parasitol. 1993 Sep;77(2):155-61
[
8375484.001
]
[Cites]
J Biol Chem. 1996 Jan 19;271(3):1441-7
[
8576136.001
]
[Cites]
Genome Res. 1997 Oct;7(10):986-95
[
9331369.001
]
[Cites]
J Bacteriol. 1997 Dec;179(23):7321-30
[
9393696.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):4906-11
[
9560201.001
]
[Cites]
Gene. 1998 Oct 5;220(1-2):61-70
[
9767113.001
]
[Cites]
Science. 1998 Dec 11;282(5396):2012-8
[
9851916.001
]
[Cites]
Mol Plant Microbe Interact. 1999 Jul;12(7):585-91
[
10478479.001
]
[Cites]
FEBS Lett. 2005 Apr 25;579(11):2451-7
[
15848187.001
]
[Cites]
Int J Parasitol. 2005 May;35(6):685-92
[
15862581.001
]
[Cites]
Biochem J. 2005 May 15;388(Pt 1):151-7
[
15631617.001
]
[Cites]
Biochem J. 2005 Jul 1;389(Pt 1):117-25
[
15727561.001
]
[Cites]
Bioinformatics. 2005 Sep 15;21(18):3674-6
[
16081474.001
]
[Cites]
J Biol Chem. 2005 Dec 9;280(49):40845-56
[
16186127.001
]
[Cites]
Nucleic Acids Res. 2006 Jan 1;34(Database issue):D16-20
[
16381837.001
]
[Cites]
Parasitology. 2004;128 Suppl 1:S49-70
[
16454899.001
]
[Cites]
Mol Plant Microbe Interact. 2006 Mar;19(3):280-7
[
16570658.001
]
[Cites]
Mol Biol Evol. 2006 Sep;23(9):1792-800
[
16790472.001
]
[Cites]
Gene. 2006 Nov 1;382:121-8
[
16962258.001
]
[Cites]
Mol Phylogenet Evol. 2007 Mar;42(3):622-36
[
17084644.001
]
[Cites]
Mol Biochem Parasitol. 2007 Sep;155(1):9-17
[
17560668.001
]
[Cites]
WormBook. 2006;:1-10
[
18023127.001
]
[Cites]
Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W465-9
[
18424797.001
]
[Cites]
Nat Biotechnol. 2008 Aug;26(8):909-15
[
18660804.001
]
[Cites]
Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):14802-7
[
18809916.001
]
[Cites]
BMC Evol Biol. 2008;8:305
[
18980666.001
]
[Cites]
BMC Genomics. 2009;10:69
[
19203352.001
]
[Cites]
Mol Plant Microbe Interact. 2002 Jun;15(6):549-56
[
12059103.001
]
[Cites]
Genome Res. 1999 Nov;9(11):1026-39
[
10568743.001
]
[Cites]
Nat Genet. 2000 May;25(1):25-9
[
10802651.001
]
[Cites]
Nature. 2000 Jul 6;406(6791):36-7
[
10894530.001
]
[Cites]
Mol Plant Microbe Interact. 2001 Jan;14(1):63-71
[
11194873.001
]
[Cites]
Parasitology. 2001 Jul;123(Pt 1):77-83
[
11467786.001
]
[Cites]
Nature. 2002 Mar 7;416(6876):38
[
11882885.001
]
[Cites]
Nucleic Acids Res. 2002 Apr 1;30(7):e32
[
11917038.001
]
[Cites]
FEBS Lett. 2002 Jul 3;522(1-3):109-12
[
12095628.001
]
[Cites]
Int J Parasitol. 2002 Sep;32(10):1293-300
[
12204229.001
]
[Cites]
Bioinformatics. 2003 Feb 12;19(3):390-5
[
12584125.001
]
[Cites]
Genome Biol. 2003;4(6):R39
[
12801413.001
]
[Cites]
J Parasitol. 2003 Aug;89(4):761-6
[
14533688.001
]
[Cites]
BMC Bioinformatics. 2002 Oct 25;3:31
[
12398795.001
]
[Cites]
Nature. 2004 Jan 1;427(6969):30
[
14702076.001
]
[Cites]
Genome Res. 2004 Feb;14(2):209-20
[
14762059.001
]
[Cites]
Eukaryot Cell. 2004 Aug;3(4):966-75
[
15302829.001
]
(PMID = 19917084.001).
[ISSN]
1471-2164
[Journal-full-title]
BMC genomics
[ISO-abbreviation]
BMC Genomics
[Language]
eng
[Databank-accession-numbers]
GENBANK/ AB495300/ AB495301/ AB495302/ AB495303/ AB495304/ AB495305/ AB495306/ AB495307/ GO479265/ GO484340
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / RNA, Messenger; EC 3.2.1.4 / Cellulase; EC 4.2.2.- / Polysaccharide-Lyases; EC 4.2.2.2 / pectate lyase
[Other-IDs]
NLM/ PMC2784482
71.
Fuchs R, Stelzer I, Haas HS, Leitinger G, Schauenstein K, Sadjak A:
The alpha1-adrenergic receptor antagonists, benoxathian and prazosin, induce apoptosis and a switch towards megakaryocytic differentiation in human erythroleukemia cells.
Ann Hematol
; 2009 Oct;88(10):989-97
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[Title]
The alpha1-adrenergic receptor antagonists, benoxathian and prazosin, induce apoptosis and a switch towards megakaryocytic differentiation in human
erythroleukemia
cells.
The
erythroleukemia
cell lines K562 and human
erythroleukemia
(HEL) are established models to study
erythroid
and megakaryocytic differentiation in vitro.
Furthermore, both tested substances induced the expression of the megakaryocytic marker CD41a, whereas the expression of the
erythroid
marker glycophorin-a was decreased or unchanged.
Even though the expression of differentiation markers was similar after benoxathian and prazosin treatment in both cell lines, endomitosis
of erythroleukemia
cells was observed only after prazosin treatment.
In summary, these results indicate a possible role of alpha1-adrenergic receptor signaling in the regulation
of erythroid
and megakaryocytic differentiation, even though the receptor dependence of the observed effects needs further investigation.
[MeSH-major]
Apoptosis / drug effects. Cell Differentiation / drug effects.
Leukemia
,
Erythroblastic
,
Acute
/ drug therapy. Megakaryocytes / cytology. Oxathiins / pharmacology. Prazosin / pharmacology. Receptors, Adrenergic, alpha-1 / metabolism
[MeSH-minor]
Adrenergic alpha-Antagonists / pharmacology. Cell Line, Tumor.
Erythroid
Cells. Humans. K562 Cells
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.
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(PMID = 19241077.001).
[ISSN]
1432-0584
[Journal-full-title]
Annals of hematology
[ISO-abbreviation]
Ann. Hematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Adrenergic alpha-Antagonists; 0 / Oxathiins; 0 / Receptors, Adrenergic, alpha-1; 92642-94-9 / benoxathian; XM03YJ541D / Prazosin
72.
Zoet YM, Eijsink C, Kardol MJ, Franke-van Dijk ME, Wilson GL, de Paus R, Mickelson E, Heemskerk M, van den Elsen PJ, Claas FH, Mulder A, Doxiadis II:
The single antigen expressing lines (SALs) concept: an excellent tool for screening for HLA-specific antibodies.
Hum Immunol
; 2005 May;66(5):519-25
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Definition of the antibody specificity in the serum of patients waiting for a renal transplant or in need for platelet transfusion is a crucial step for
finding
adequate donors.
Confounding factors are the complexity of the serum antibodies and the expression of several, up to six, different human leukocyte antigens (HLA) on peripheral blood
lymphocytes
used as target cells in the antibody screening.
Single antigen-expressing (SAL) cell lines were generated by transfecting human major histocompatibility complex (MHC) class I sequences into K562, an
erythroleukemia
-derived cell line lacking MHC class I and II expression.
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(PMID = 15935889.001).
[ISSN]
0198-8859
[Journal-full-title]
Human immunology
[ISO-abbreviation]
Hum. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies; 0 / Antibodies, Monoclonal; 0 / HLA Antigens; 0 / HLA-A2 Antigen; 0 / HLA-A3 Antigen; 0 / HLA-B7 Antigen; 0 / Histocompatibility Antigens Class I; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 9007-36-7 / Complement System Proteins
73.
Murakami Y, Yamagoe S, Noguchi K, Takebe Y, Takahashi N, Uehara Y, Fukazawa H:
Ets-1-dependent expression of vascular endothelial growth factor receptors is activated by latency-associated nuclear antigen of Kaposi's sarcoma-associated herpesvirus through interaction with Daxx.
J Biol Chem
; 2006 Sep 22;281(38):28113-21
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LANA associated with Daxx in
a PEL
cell line infected with KSHV.
To address the physiological significance of this interaction, we focused on a Daxx-mediated VEGF receptor
gene
regulation.
We found that Daxx repressed Ets-1-dependent Flt-1/VEGF receptor-1
gene
expression, and that LANA inhibited the repression by Daxx in a reporter assay.
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(PMID = 16861237.001).
[ISSN]
0021-9258
[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 / Adaptor Proteins, Signal Transducing; 0 / Antigens, Viral; 0 / Carrier Proteins; 0 / DAXX protein, human; 0 / ETS1 protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Protein c-ets-1; 0 / latency-associated nuclear antigen; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
74.
Ng PP, Helguera G, Daniels TR, Lomas SZ, Rodriguez JA, Schiller G, Bonavida B, Morrison SL, Penichet ML:
Molecular events contributing to cell death in malignant human hematopoietic cells elicited by an IgG3-avidin fusion protein targeting the transferrin receptor.
Blood
; 2006 Oct 15;108(8):2745-54
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[Title]
Molecular events contributing to cell death in
malignant
human hematopoietic cells elicited by an IgG3-avidin fusion protein targeting the transferrin receptor.
We have previously reported that an anti-human transferrin receptor IgG3-avidin fusion protein (anti-hTfR IgG3-Av) inhibits the proliferation of an
erythroleukemia
-cell line.
We have now found that anti-hTfR IgG3-Av also inhibits the proliferation of additional human
malignant
B and plasma cells.
[MeSH-minor]
Amino Acid Chloromethyl Ketones / pharmacology. Apoptosis / drug effects. Caspase Inhibitors. Cell Line, Tumor. Cell Proliferation / drug effects. Cross-Linking Reagents. Deferoxamine / pharmacology. Humans. Iron / pharmacology.
Leukemia
, Plasma Cell / metabolism.
Leukemia
, Plasma Cell / pathology.
Leukemia
, Plasma Cell / therapy. Multiple Myeloma / metabolism. Multiple Myeloma / pathology. Multiple Myeloma / therapy. Recombinant Fusion Proteins / pharmacology. Siderophores / pharmacology
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.
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Cited by Patents in
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[Cites]
Leukemia. 1993 Dec;7(12):2019-25
[
8255102.001
]
[Cites]
Blood. 1997 Jul 15;90(2):754-65
[
9226176.001
]
[Cites]
Neurosurgery. 1997 Nov;41(5):1039-49; discussion 1049-51
[
9361057.001
]
[Cites]
Eur J Haematol. 1997 Nov;59(5):318-26
[
9414644.001
]
[Cites]
Clin Immunol Immunopathol. 1994 Jan;70(1):10-8
[
7505211.001
]
[Cites]
Mol Immunol. 1994 Oct;31(15):1201-10
[
7935507.001
]
[Cites]
J Immunol. 1995 Feb 15;154(4):1675-83
[
7836751.001
]
[Cites]
Biochem J. 1996 Jun 15;316 ( Pt 3):777-86
[
8670152.001
]
[Cites]
J Immunol. 1997 May 15;158(10):4797-804
[
9144494.001
]
[Cites]
Int J Oncol. 1998 Oct;13(4):871-5
[
9735419.001
]
[Cites]
Clin Cancer Res. 1995 Nov;1(11):1259-65
[
9815920.001
]
[Cites]
Int J Oncol. 2000 Oct;17(4):643-51
[
10995873.001
]
[Cites]
Haematologica. 2001 Mar;86(3):227-36
[
11255268.001
]
[Cites]
Exp Hematol. 2001 Apr;29(4):441-7
[
11301184.001
]
[Cites]
J Cell Biochem. 2001 Apr 2-27;82(1):171-86
[
11400174.001
]
[Cites]
Blood. 2001 Aug 1;98(3):795-804
[
11468181.001
]
[Cites]
Rev Clin Exp Hematol. 2001 Mar;5(1):3-14
[
11486731.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):2264-9
[
11854522.001
]
[Cites]
Nat Rev Cancer. 2001 Nov;1(2):118-29
[
11905803.001
]
[Cites]
Curr Treat Options Oncol. 2001 Jun;2(3):205-16
[
12057120.001
]
[Cites]
J Biol Chem. 2002 Jul 12;277(28):25568-75
[
11980894.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10706-11
[
12149472.001
]
[Cites]
Biochem Pharmacol. 2003 Jan 15;65(2):161-72
[
12504792.001
]
[Cites]
Int J Cancer. 2003 Apr 20;104(4):400-8
[
12584735.001
]
[Cites]
Biochim Biophys Acta. 2003 Mar 17;1620(1-3):225-34
[
12595093.001
]
[Cites]
Cell Immunol. 2002 Dec;220(2):96-106
[
12657244.001
]
[Cites]
Immunol Rev. 2003 Jun;193:10-21
[
12752666.001
]
[Cites]
Free Radic Biol Med. 2003 Nov 15;35(10):1171-84
[
14607516.001
]
[Cites]
J Neurooncol. 2003 Oct;65(1):3-13
[
14649881.001
]
[Cites]
Blood. 2004 Mar 1;103(5):1838-45
[
14592824.001
]
[Cites]
Science. 2004 Jul 30;305(5684):626-9
[
15286356.001
]
[Cites]
Lancet. 1980 Aug 23;2(8191):390-2
[
6105517.001
]
[Cites]
Nature. 1980 Aug 28;286(5776):888-91
[
7412870.001
]
[Cites]
Int J Cancer. 1981 Mar 15;27(3):329-34
[
6270015.001
]
[Cites]
Nature. 1981 Nov 12;294(5837):171-3
[
6272120.001
]
[Cites]
Proc Natl Acad Sci U S A. 1982 Feb;79(4):1175-9
[
6280171.001
]
[Cites]
Blood. 1982 Sep;60(3):703-13
[
6286014.001
]
[Cites]
J Cell Physiol. 1982 Sep;112(3):403-10
[
6290505.001
]
[Cites]
Biochem Biophys Res Commun. 1982 Oct 29;108(4):1495-501
[
7181903.001
]
[Cites]
Int J Biochem Cell Biol. 1999 Oct;31(10):1111-37
[
10582342.001
]
[Cites]
Lancet. 1983 Mar 5;1(8323):498-501
[
6131211.001
]
[Cites]
Proc Natl Acad Sci U S A. 1983 Jun;80(11):3494-8
[
6304712.001
]
[Cites]
Blood. 1983 Oct;62(4):821-6
[
6309286.001
]
[Cites]
Int J Cancer. 1983 Sep 15;32(3):343-9
[
6309680.001
]
[Cites]
Cell Death Differ. 1999 Jun;6(6):516-24
[
10381654.001
]
[Cites]
Cell Death Differ. 1999 Apr;6(4):362-9
[
10381624.001
]
[Cites]
Cancer Res. 2000 Jul 1;60(13):3384-8
[
10910043.001
]
[Cites]
J Cell Biol. 1983 Aug;97(2):508-21
[
6309862.001
]
[Cites]
Cell Immunol. 1984 Jan;83(1):14-25
[
6319033.001
]
[Cites]
Exp Cell Res. 1984 Feb;150(2):400-7
[
6319165.001
]
[Cites]
Vox Sang. 1984;46(4):217-23
[
6324490.001
]
[Cites]
J Biol Chem. 1984 Aug 25;259(16):10053-9
[
6432778.001
]
[Cites]
Mol Cell Biol. 1984 Sep;4(9):1675-81
[
6092931.001
]
[Cites]
Immunology. 1985 Feb;54(2):333-41
[
2981766.001
]
[Cites]
J Clin Invest. 1985 Mar;75(3):1061-7
[
2984253.001
]
[Cites]
J Immunol. 1985 Sep;135(3):1987-97
[
2991374.001
]
[Cites]
Cancer Res. 1986 Apr;46(4 Pt 1):1759-63
[
3004704.001
]
[Cites]
J Cell Biol. 1986 Mar;102(3):951-8
[
3005341.001
]
[Cites]
Mol Cell Biol. 1985 Aug;5(8):1814-21
[
3018527.001
]
[Cites]
Immunogenetics. 1986;24(3):163-70
[
3489674.001
]
[Cites]
J Immunol. 1987 Apr 15;138(8):2422-6
[
2951439.001
]
[Cites]
Ann N Y Acad Sci. 1987;507:187-98
[
3327412.001
]
[Cites]
Prog Allergy. 1988;45:121-46
[
3064093.001
]
[Cites]
Exp Cell Res. 1989 May;182(1):215-33
[
2653853.001
]
[Cites]
J Oral Pathol Med. 1989 Dec;18(10):582-5
[
2559980.001
]
[Cites]
Cancer Res. 1990 Oct 1;50(19):6295-301
[
2400993.001
]
[Cites]
J Exp Med. 1992 Jun 1;175(6):1501-9
[
1375263.001
]
(PMID = 16804109.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / K01 CA086915; United States / NCI NIH HHS / CA / R01 CA107023; United States / NCI NIH HHS / CA / CA 107023; United States / NCI NIH HHS / CA / CA 86915
[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 / Amino Acid Chloromethyl Ketones; 0 / Caspase Inhibitors; 0 / Cross-Linking Reagents; 0 / Immunoglobulin G; 0 / Receptors, Transferrin; 0 / Recombinant Fusion Proteins; 0 / Siderophores; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 1405-69-2 / Avidin; E1UOL152H7 / Iron; J06Y7MXW4D / Deferoxamine
[Other-IDs]
NLM/ PMC1895578
75.
Greene W, Kuhne K, Ye F, Chen J, Zhou F, Lei X, Gao SJ:
Molecular biology of KSHV in relation to AIDS-associated oncogenesis.
Cancer Treat Res
; 2007;133:69-127
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KSHV has been established as the causative agent of KS,
PEL
, and MCD, malignancies occurring more frequently in AIDS patients.
KSHV latent infection and lytic reactivation are characterized by distinct
gene
expression profiles, and both latency and lytic reactivation seem to be required for
malignant
progression.
As a sophisticated oncogenic virus, KSHV has evolved to possess a formidable repertoire of potent mechanisms that enable it to target and manipulate host cell pathways, leading to increased cell proliferation, increased cell survival, dysregulated angiogenesis, evasion of immunity, and
malignant
progression in the immunocompromised host.
The complex interplay between the two viruses dramatically elevates the risk for development of KSHV-induced malignancies, KS,
PEL
, and MCD.
Genetic Alliance.
consumer health - AIDS-HIV
.
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consumer health - HIV/AIDS
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[Cites]
Semin Cancer Biol. 1999 Jun;9(3):201-9
[
10343071.001
]
[Cites]
Blood. 1999 Jun 15;93(12):4034-43
[
10361100.001
]
[Cites]
J Virol. 1999 Jul;73(7):5556-67
[
10364304.001
]
[Cites]
J Virol. 1999 Jul;73(7):5722-30
[
10364323.001
]
[Cites]
J Virol. 1999 Aug;73(8):6892-902
[
10400787.001
]
[Cites]
J Virol. 1999 Aug;73(8):6953-63
[
10400794.001
]
[Cites]
J Acquir Immune Defic Syndr. 1999 Aug 1;21 Suppl 1:S58-65
[
10430220.001
]
[Cites]
J Virol. 1999 Sep;73(9):7334-42
[
10438822.001
]
[Cites]
Science. 1999 Aug 13;285(5430):1028-32
[
10446041.001
]
[Cites]
J Gen Virol. 1999 Aug;80 ( Pt 8):2205-9
[
10466820.001
]
[Cites]
J Infect Dis. 1999 Oct;180(4):1010-7
[
10479125.001
]
[Cites]
J Virol. 1999 Oct;73(10):8268-78
[
10482577.001
]
[Cites]
J Exp Med. 1999 Sep 20;190(6):827-40
[
10499921.001
]
[Cites]
J Exp Med. 1999 Oct 4;190(7):1025-32
[
10510092.001
]
[Cites]
AIDS. 1999 Oct 1;13(14):1851-5
[
10513642.001
]
[Cites]
J Infect Dis. 1999 Nov;180(5):1466-76
[
10515805.001
]
[Cites]
J Virol. 1999 Nov;73(11):9348-61
[
10516043.001
]
[Cites]
Cancer Res. 1999 Oct 1;59(19):4984-9
[
10519412.001
]
[Cites]
Oncogene. 1999 Oct 14;18(42):5738-46
[
10523854.001
]
[Cites]
Acta Unio Int Contra Cancrum. 1962;18:330-63
[
14481196.001
]
[Cites]
Blood. 2004 Nov 15;104(10):3349-54
[
15271792.001
]
[Cites]
J Biol Chem. 2004 Dec 10;279(50):51793-803
[
15258150.001
]
[Cites]
Cancer Invest. 2004;22(5):774-86
[
15581058.001
]
[Cites]
J Virol. 2005 Jan;79(2):800-11
[
15613308.001
]
[Cites]
J Virol. 2005 Jan;79(2):1191-206
[
15613346.001
]
[Cites]
J Virol. 2005 Feb;79(3):1397-408
[
15650166.001
]
[Cites]
Blood. 2005 Feb 1;105(3):1310-8
[
15471957.001
]
[Cites]
Immunity. 2005 Jan;22(1):59-70
[
15664159.001
]
[Cites]
J Virol. 2005 Feb;79(4):2420-31
[
15681443.001
]
[Cites]
Science. 2005 Feb 4;307(5710):739-41
[
15692053.001
]
[Cites]
J Virol. 2005 Mar;79(6):3468-78
[
15731241.001
]
[Cites]
J Virol. 2005 Mar;79(6):3479-87
[
15731242.001
]
[Cites]
J Immunol. 2005 Mar 15;174(6):3686-94
[
15749907.001
]
[Cites]
Chest. 2005 Mar;127(3):762-7
[
15764755.001
]
[Cites]
J Virol. 2005 Apr;79(8):4651-63
[
15795251.001
]
[Cites]
J Virol. 2005 May;79(9):5640-52
[
15827179.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Apr 12;102(15):5570-5
[
15800047.001
]
[Cites]
J Clin Invest. 2005 May;115(5):1369-78
[
15864354.001
]
[Cites]
Blood. 2005 May 15;105(10):3987-94
[
15665117.001
]
[Cites]
Nat Methods. 2005 Apr;2(4):269-76
[
15782219.001
]
[Cites]
J Virol. 2005 Jun;79(12):7453-65
[
15919901.001
]
[Cites]
J Virol. 2005 Jul;79(14):8750-63
[
15994769.001
]
[Cites]
J Virol. 2005 Jul;79(14):9301-5
[
15994824.001
]
[Cites]
J Biol Chem. 2005 Jul 15;280(28):26216-24
[
15878864.001
]
[Cites]
Int J Cancer. 1998 Aug 12;77(4):543-8
[
9679756.001
]
[Cites]
Nature. 1998 Aug 6;394(6693):588-92
[
9707121.001
]
[Cites]
Lab Invest. 1998 Aug;78(8):949-55
[
9714182.001
]
[Cites]
Cytokine Growth Factor Rev. 1998 Mar;9(1):63-83
[
9720757.001
]
[Cites]
Transplant Proc. 1998 Aug;30(5):2095-6
[
9723403.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10866-71
[
9724796.001
]
[Cites]
Br J Haematol. 1998 Sep;102(4):1081-9
[
9734661.001
]
[Cites]
J Virol. 1998 Oct;72(10):8309-15
[
9733875.001
]
[Cites]
Virology. 1998 Sep 15;249(1):140-9
[
9740785.001
]
[Cites]
Curr Clin Top Infect Dis. 1998;18:237-51
[
9779358.001
]
[Cites]
Blood. 2006 Jan 1;107(1):277-84
[
16150942.001
]
[Cites]
J Pathol. 2006 Jan;208(2):187-98
[
16362980.001
]
[Cites]
EMBO Rep. 2006 Jan;7(1):114-9
[
16311516.001
]
[Cites]
FASEB J. 2006 Jan;20(1):9-22
[
16394262.001
]
[Cites]
Blood. 2006 Jan 15;107(2):725-32
[
16160006.001
]
[Cites]
Annu Rev Med. 2006;57:1-18
[
16409133.001
]
[Cites]
J Virol. 2006 Feb;80(3):1385-92
[
16415016.001
]
[Cites]
J Immunol. 2006 Feb 1;176(3):1741-9
[
16424204.001
]
[Cites]
Science. 2006 Feb 10;311(5762):856-61
[
16469929.001
]
[Cites]
J Virol. 2006 Mar;80(5):2234-42
[
16474131.001
]
[Cites]
J Virol. 2006 Mar;80(5):2243-56
[
16474132.001
]
[Cites]
J Virol. 2006 Mar;80(5):2257-66
[
16474133.001
]
[Cites]
J Virol. 2006 Mar;80(6):3062-70
[
16501115.001
]
[Cites]
J Clin Invest. 2006 Mar;116(3):735-42
[
16498502.001
]
[Cites]
J Gen Virol. 2006 Apr;87(Pt 4):795-802
[
16528027.001
]
[Cites]
J Virol. 2006 Apr;80(7):3445-58
[
16537612.001
]
[Cites]
Cancer Res. 2006 Mar 15;66(6):3051-61
[
16540654.001
]
[Cites]
J Virol. 2006 Apr;80(8):4068-78
[
16571823.001
]
[Cites]
Science. 2006 Mar 31;311(5769):1921-4
[
16574866.001
]
[Cites]
Cancer Res. 2006 Apr 1;66(7):3658-66
[
16585191.001
]
[Cites]
Blood. 2006 Apr 15;107(8):3295-302
[
16380446.001
]
[Cites]
Trends Microbiol. 2006 Apr;14(4):169-75
[
16531046.001
]
[Cites]
RNA. 2006 May;12(5):733-50
[
16540699.001
]
[Cites]
Wkly Epidemiol Rec. 2006 Jan 27;81(4):40
[
16671237.001
]
[Cites]
J Clin Invest. 2006 May;116(5):1264-73
[
16604194.001
]
[Cites]
J Virol. 2006 Jun;80(11):5251-60
[
16699005.001
]
[Cites]
J Virol. 2006 Jun;80(11):5371-82
[
16699017.001
]
[Cites]
Virology. 2006 May 10;348(2):309-27
[
16546233.001
]
[Cites]
Virology. 2006 Jun 20;350(1):192-205
[
16616289.001
]
[Cites]
Blood. 2006 Jul 1;108(1):141-51
[
16543476.001
]
[Cites]
Int J Cancer. 2006 Sep 15;119(6):1262-7
[
16615115.001
]
[Cites]
J Virol. 2005 Dec;79(24):15027-37
[
16306573.001
]
[Cites]
J Biol Chem. 1999 Nov 5;274(45):31863-7
[
10542211.001
]
[Cites]
AIDS. 1999 Oct 22;13(15):2105-11
[
10546864.001
]
[Cites]
Virology. 1999 Oct 25;263(2):436-49
[
10544116.001
]
[Cites]
J Natl Cancer Inst. 1999 Oct 20;91(20):1725-33
[
10528022.001
]
[Cites]
Adv Cancer Res. 2000;77:1-24
[
10549354.001
]
[Cites]
Hum Immunol. 1999 Oct;60(10):921-7
[
10566591.001
]
[Cites]
Virology. 1999 Nov 25;264(2):254-64
[
10562490.001
]
[Cites]
J Gen Virol. 1999 Nov;80 ( Pt 11):2889-900
[
10580050.001
]
[Cites]
Eur Cytokine Netw. 1999 Dec;10(4):501-8
[
10586116.001
]
[Cites]
Blood. 1999 Dec 15;94(12):4247-54
[
10590069.001
]
[Cites]
N Engl J Med. 1998 Nov 5;339(19):1358-63
[
9801396.001
]
[Cites]
Int J STD AIDS. 1998 Dec;9(12):751-5
[
9874123.001
]
[Cites]
AIDS. 1998 Dec 24;12(18):2481-8
[
9875587.001
]
[Cites]
Virology. 1998 Dec 20;252(2):304-12
[
9878608.001
]
[Cites]
J Virol. 1999 Feb;73(2):1341-9
[
9882339.001
]
[Cites]
Ann Biol Clin (Paris). 1999 Jan-Feb;57(1):19-28
[
9920963.001
]
[Cites]
J Acquir Immune Defic Syndr Hum Retrovirol. 1999 Jan 1;20(1):34-8
[
9928727.001
]
[Cites]
EMBO J. 1999 Feb 1;18(3):644-53
[
9927424.001
]
[Cites]
EMBO J. 1999 Feb 1;18(3):654-63
[
9927425.001
]
[Cites]
Crit Rev Oncog. 1998;9(2):107-24
[
9973245.001
]
[Cites]
J Virol. 1999 Mar;73(3):2232-42
[
9971806.001
]
[Cites]
Lab Invest. 1999 Feb;79(2):243-51
[
10068212.001
]
[Cites]
Curr Opin Genet Dev. 1999 Feb;9(1):40-8
[
10072350.001
]
[Cites]
Annu Rev Med. 1999;50:425-40
[
10073287.001
]
[Cites]
J Virol. 1999 Apr;73(4):3040-53
[
10074154.001
]
[Cites]
J Hum Virol. 1999 Jan-Feb;2(1):19-32
[
10200596.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4546-51
[
10200299.001
]
[Cites]
Virology. 1999 Apr 25;257(1):84-94
[
10208923.001
]
[Cites]
Science. 1999 Apr 23;284(5414):641-4
[
10213686.001
]
[Cites]
Leukemia. 1999 Apr;13 Suppl 1:S110-2
[
10232382.001
]
[Cites]
J Virol. 2000 Jun;74(11):5300-9
[
10799607.001
]
[Cites]
Blood. 2000 May 15;95(10):3032-43
[
10807766.001
]
[Cites]
J Virol. 2000 Jul;74(13):6207-12
[
10846108.001
]
[Cites]
Am J Pathol. 2000 Jun;156(6):1961-71
[
10854219.001
]
[Cites]
Am J Pathol. 2000 Jun;156(6):2179-83
[
10854238.001
]
[Cites]
J Med Virol. 2000 Jul;61(3):332-5
[
10861641.001
]
[Cites]
Mol Pathol. 2000 Feb;53(1):43-7
[
10884921.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Jul 5;97(14):8051-6
[
10859362.001
]
[Cites]
J Biol Chem. 2000 Jul 21;275(29):21785-8
[
10801897.001
]
[Cites]
Leukemia. 2000 Jul;14(7):1301-9
[
10914556.001
]
[Cites]
J Gen Virol. 2000 Aug;81(Pt 8):2049-58
[
10900044.001
]
[Cites]
J Immunol. 2000 Aug 15;165(4):2077-83
[
10925292.001
]
[Cites]
J Virol. 2000 Sep;74(17):8194-201
[
10933732.001
]
[Cites]
Semin Oncol. 2000 Aug;27(4):390-401
[
10950365.001
]
[Cites]
J Virol. 2000 Sep;74(18):8532-40
[
10954554.001
]
[Cites]
J Virol. 2000 Sep;74(18):8623-34
[
10954564.001
]
[Cites]
Cancer Res. 2000 Sep 1;60(17):4873-80
[
10987301.001
]
[Cites]
J Virol. 2000 Oct;74(20):9637-45
[
11000236.001
]
[Cites]
J Virol. 2000 Oct;74(20):9646-54
[
11000237.001
]
[Cites]
Blood. 2000 Oct 1;96(7):2537-42
[
11001908.001
]
[Cites]
Immunity. 2000 Sep;13(3):365-74
[
11021534.001
]
[Cites]
Nat Med. 2000 Oct;6(10):1121-7
[
11017143.001
]
[Cites]
Mol Cell Biol. 2000 Nov;20(21):8254-63
[
11027294.001
]
[Cites]
Adv Cancer Res. 2001;80:115-46
[
11034542.001
]
[Cites]
J Gen Virol. 2000 Nov;81(Pt 11):2645-52
[
11038375.001
]
[Cites]
Nat Cell Biol. 2000 Nov;2(11):819-25
[
11056537.001
]
[Cites]
AIDS. 2000 Sep 29;14(14):2217-8
[
11061672.001
]
[Cites]
Exp Cell Res. 2000 Nov 25;261(1):25-36
[
11082272.001
]
[Cites]
J Gen Virol. 2000 Dec;81(Pt 12):3043-8
[
11086135.001
]
[Cites]
J Virol. 2001 Jan;75(1):429-38
[
11119611.001
]
[Cites]
J Virol. 2001 Jan;75(2):891-902
[
11134302.001
]
[Cites]
J Virol. 2001 Feb;75(3):1378-86
[
11152511.001
]
[Cites]
Cancer Genet Cytogenet. 2001 Jan 1;124(1):16-9
[
11165317.001
]
[Cites]
J Virol. 2001 Feb;75(4):1857-63
[
11160684.001
]
[Cites]
J Virol. 2001 Feb;75(4):1864-9
[
11160685.001
]
[Cites]
J Virol. 2001 Feb;75(4):1909-17
[
11160690.001
]
[Cites]
J Virol. 2001 Mar;75(5):2345-52
[
11160738.001
]
[Cites]
J Virol. 2001 Mar;75(5):2435-43
[
11160746.001
]
[Cites]
J Virol. 2001 Mar;75(6):2866-78
[
11222712.001
]
[Cites]
J Virol. 2001 Mar;75(6):2938-45
[
11222719.001
]
[Cites]
Nat Rev Mol Cell Biol. 2000 Dec;1(3):187-98
[
11252894.001
]
[Cites]
Science. 2001 Mar 16;291(5511):2150-5
[
11251120.001
]
[Cites]
N Engl J Med. 2005 Jul 14;353(2):156-63
[
16014885.001
]
[Cites]
J Virol. 2005 Aug;79(16):10308-29
[
16051824.001
]
[Cites]
J Virol. 2005 Aug;79(16):10429-41
[
16051835.001
]
[Cites]
J Virol. 2005 Sep;79(17):10952-67
[
16103147.001
]
[Cites]
Trends Immunol. 2005 Sep;26(9):469-76
[
16006187.001
]
[Cites]
J Clin Microbiol. 2005 Sep;43(9):4840-3
[
16145154.001
]
[Cites]
J Virol. 2005 Oct;79(19):12173-84
[
16160144.001
]
[Cites]
Blood. 2005 Oct 15;106(8):2790-7
[
15976177.001
]
[Cites]
Int J Epidemiol. 2005 Oct;34(5):1110-7
[
16043440.001
]
[Cites]
Eur J Histochem. 2005 Jul-Sep;49(3):273-84
[
16216813.001
]
[Cites]
AIDS Res Hum Retroviruses. 2005 Oct;21(10):869-75
[
16225414.001
]
[Cites]
J Virol. 2005 Nov;79(21):13618-29
[
16227282.001
]
[Cites]
J Virol. 2005 Nov;79(22):14371-82
[
16254371.001
]
[Cites]
J Virol. 2005 Nov;79(22):14457-64
[
16254382.001
]
[Cites]
Virology. 2005 Dec 5;343(1):47-64
[
16154170.001
]
[Cites]
J Exp Med. 1998 Jul 6;188(1):193-8
[
9653095.001
]
[Cites]
Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S4-11
[
16341240.001
]
[Cites]
Cell Res. 2005 Nov-Dec;15(11-12):947-52
[
16354573.001
]
[Cites]
Nature. 2005 Dec 15;438(7070):932-6
[
16355210.001
]
[Cites]
Hum Pathol. 2006 Jan;37(1):23-31
[
16360412.001
]
[Cites]
Traffic. 2001 Jun;2(6):375-84
[
11389765.001
]
[Cites]
J Clin Invest. 2001 Jun;107(12):1599-606
[
11413168.001
]
[Cites]
J Virol. 2006 Jan;80(2):697-709
[
16378973.001
]
[Cites]
FEBS Lett. 2006 Jan 9;580(1):93-8
[
16364321.001
]
[Cites]
Oncogene. 2001 Jun 7;20(26):3311-22
[
11423981.001
]
[Cites]
Adv Cancer Res. 2001;81:125-59
[
11430594.001
]
[Cites]
Adv Cancer Res. 2001;81:161-200
[
11430595.001
]
[Cites]
J Virol. 2001 Aug;75(15):6894-900
[
11435569.001
]
[Cites]
J Virol. 2001 Aug;75(15):7161-74
[
11435597.001
]
[Cites]
J Hum Virol. 2001 Mar-Apr;4(2):62-73
[
11437316.001
]
[Cites]
J Gen Virol. 2001 Aug;82(Pt 8):1965-70
[
11458004.001
]
[Cites]
J Virol. 2001 Aug;75(16):7517-27
[
11462024.001
]
[Cites]
J Virol. 2001 Aug;75(16):7572-82
[
11462029.001
]
[Cites]
Biochim Biophys Acta. 2001 Jul 25;1540(1):1-21
[
11476890.001
]
[Cites]
J Virol. 2001 Sep;75(17):7882-92
[
11483733.001
]
[Cites]
J Biol Chem. 2001 Aug 17;276(33):31016-22
[
11425857.001
]
[Cites]
J Virol. 2001 Sep;75(18):8660-73
[
11507211.001
]
[Cites]
J Virol. 2001 Sep;75(18):8761-71
[
11507221.001
]
[Cites]
J Biol Chem. 2001 Sep 7;276(36):33805-11
[
11448967.001
]
[Cites]
J Virol. 2001 Oct;75(19):9509-16
[
11533213.001
]
[Cites]
J Clin Oncol. 2001 Sep 15;19(18):3848-51
[
11559722.001
]
[Cites]
J Virol. 2001 Nov;75(22):10933-40
[
11602733.001
]
[Cites]
J Virol. 2001 Dec;75(23):11583-93
[
11689640.001
]
[Cites]
J Virol. 2001 Dec;75(24):11961-73
[
11711586.001
]
[Cites]
J Biol Chem. 2001 Dec 7;276(49):45979-87
[
11590141.001
]
[Cites]
Mol Biol Cell. 2001 Dec;12(12):3987-99
[
11739795.001
]
[Cites]
J Pathol. 2001 Dec;195(5):586-92
[
11745695.001
]
[Cites]
Biotechniques. 2001 Dec;31(6):1286, 1288, 1290, passim
[
11768657.001
]
[Cites]
Cancer. 2001 Dec 15;92(12):3076-84
[
11753987.001
]
[Cites]
J Gen Virol. 2002 Jan;83(Pt 1):179-88
[
11752715.001
]
[Cites]
J Virol. 2002 Jan;76(2):802-16
[
11752170.001
]
[Cites]
Blood. 2002 Jan 15;99(2):649-54
[
11781250.001
]
[Cites]
Recent Results Cancer Res. 2002;159:27-37
[
11785841.001
]
[Cites]
Am J Pathol. 2002 Jan;160(1):23-9
[
11786394.001
]
[Cites]
J Virol. 2002 Feb;76(4):1744-52
[
11799169.001
]
[Cites]
J Immunol. 2002 Feb 1;168(3):1226-34
[
11801659.001
]
[Cites]
Front Biosci. 2002 Feb 1;7:d358-75
[
11815281.001
]
[Cites]
J Virol. 2002 Mar;76(5):2440-8
[
11836422.001
]
[Cites]
J Virol. 2002 Mar;76(5):2551-6
[
11836434.001
]
[Cites]
Cell. 2002 Feb 8;108(3):407-19
[
11853674.001
]
[Cites]
Int J Cancer. 2002 Feb 20;97(6):791-5
[
11857356.001
]
[Cites]
J Leukoc Biol. 2002 Mar;71(3):445-57
[
11867682.001
]
[Cites]
J Immunol. 2002 Mar 15;168(6):2634-43
[
11884427.001
]
[Cites]
J Virol. 2002 Apr;76(7):3168-78
[
11884541.001
]
[Cites]
J Virol. 2000 Jan;74(1):436-46
[
10590133.001
]
[Cites]
J Exp Med. 1999 Dec 20;190(12):1857-68
[
10601360.001
]
[Cites]
Virology. 2000 Jan 5;266(1):17-25
[
10612656.001
]
[Cites]
Nature. 1999 Dec 23-30;402(6764):889-94
[
10622254.001
]
[Cites]
Blood. 2000 Feb 15;95(4):1151-7
[
10666184.001
]
[Cites]
Blood. 2000 Feb 15;95(4):1406-12
[
10666218.001
]
[Cites]
J Exp Med. 2000 Feb 7;191(3):445-54
[
10662790.001
]
[Cites]
J Virol. 2000 Mar;74(6):2867-75
[
10684303.001
]
[Cites]
Am J Pathol. 2000 Mar;156(3):743-9
[
10702388.001
]
[Cites]
J Virol. 2000 Apr;74(7):3388-98
[
10708456.001
]
[Cites]
J Vasc Res. 2000 Jan-Feb;37(1):1-7
[
10720880.001
]
[Cites]
J Virol. 2000 Apr;74(8):3659-67
[
10729142.001
]
[Cites]
Biochem Biophys Res Commun. 2000 Apr 2;270(1):23-7
[
10733899.001
]
[Cites]
Clin Cancer Res. 2000 Mar;6(3):1180-9
[
10741750.001
]
[Cites]
J Clin Virol. 2000 May;16(3):203-13
[
10738139.001
]
[Cites]
Virology. 2000 Apr 10;269(2):335-44
[
10753712.001
]
[Cites]
Mol Med. 1998 Jun;4(6):402-12
[
10780883.001
]
[Cites]
J Immunol. 2000 May 1;164(9):4672-7
[
10779772.001
]
[Cites]
J Natl Cancer Inst. 2000 May 3;92(9):729-36
[
10793109.001
]
[Cites]
J Virol. 2000 Jun;74(11):5024-31
[
10799576.001
]
[Cites]
Genes Dev. 2002 Aug 1;16(15):1977-89
[
12154127.001
]
[Cites]
J Virol. 2002 Sep;76(17):8797-807
[
12163600.001
]
[Cites]
J Infect Dis. 2000 Jun;181(6):1940-9
[
10837173.001
]
[Cites]
J Acquir Immune Defic Syndr. 1999 Oct 1;22(2):209-10
[
10843538.001
]
[Cites]
Cell Growth Differ. 2002 Aug;13(8):387-95
[
12193477.001
]
[Cites]
J Med Virol. 2002 Nov;68(3):404-11
[
12226829.001
]
[Cites]
Cancer Cell. 2002 Sep;2(3):229-41
[
12242155.001
]
[Cites]
Nat Immunol. 2002 Oct;3(10):975-83
[
12352970.001
]
[Cites]
Virology. 2002 Sep 30;301(2):293-304
[
12359431.001
]
[Cites]
J Virol. 2002 Nov;76(22):11491-504
[
12388711.001
]
[Cites]
J Virol. 2002 Nov;76(22):11596-604
[
12388720.001
]
[Cites]
J Virol. 2002 Nov;76(22):11677-87
[
12388727.001
]
[Cites]
J Virol. 2002 Dec;76(23):11880-8
[
12414930.001
]
[Cites]
J Virol. 2002 Dec;76(23):12044-54
[
12414946.001
]
[Cites]
J Pathol. 2002 Dec;198(4):511-6
[
12434421.001
]
[Cites]
Science. 2002 Nov 15;298(5597):1432-5
[
12434062.001
]
[Cites]
J Biol Chem. 2002 Nov 22;277(47):44765-71
[
12235164.001
]
[Cites]
J Virol. 2002 Dec;76(24):12574-83
[
12438583.001
]
[Cites]
J Virol. 2002 Dec;76(24):12917-24
[
12438617.001
]
[Cites]
J Virol. 2003 Jan;77(1):592-9
[
12477863.001
]
[Cites]
J Virol. 2003 Jan;77(1):600-23
[
12477864.001
]
[Cites]
Am J Surg Pathol. 2003 Jan;27(1):91-100
[
12502931.001
]
[Cites]
J Virol. 2003 Jan;77(2):1524-39
[
12502866.001
]
[Cites]
Annu Rev Med. 2003;54:285-303
[
12525676.001
]
[Cites]
J Virol. 2003 Feb;77(4):2779-83
[
12552022.001
]
[Cites]
Br J Cancer. 2003 Jan 13;88(1):1-3
[
12556950.001
]
[Cites]
J Gen Virol. 2003 Feb;84(Pt 2):329-36
[
12560564.001
]
[Cites]
J Virol. 2003 Mar;77(5):3131-47
[
12584338.001
]
[Cites]
J Virol. 2003 Mar;77(6):3878-81
[
12610165.001
]
[Cites]
Mol Cell Biol. 2003 Mar;23(6):2055-67
[
12612078.001
]
[Cites]
Nat Med. 2003 Mar;9(3):300-6
[
12592400.001
]
[Cites]
Cancer Cell. 2003 Feb;3(2):131-43
[
12620408.001
]
[Cites]
J Virol. 2003 Apr;77(7):4205-20
[
12634378.001
]
[Cites]
J Virol. 2003 Apr;77(7):4221-30
[
12634379.001
]
[Cites]
J Biol Chem. 2003 Mar 14;278(11):9283-9
[
12645526.001
]
[Cites]
J Gen Virol. 2003 May;84(Pt 5):1123-31
[
12692277.001
]
[Cites]
J Virol. 2003 May;77(10):5975-84
[
12719589.001
]
[Cites]
Cancer Res. 2003 May 1;63(9):2010-5
[
12727810.001
]
[Cites]
J Virol. 2003 Jun;77(11):6188-96
[
12743275.001
]
[Cites]
J Virol. 2003 Jun;77(11):6474-81
[
12743304.001
]
[Cites]
Curr Drug Targets Infect Disord. 2003 Jun;3(2):129-35
[
12769790.001
]
[Cites]
J Gen Virol. 2003 Jun;84(Pt 6):1485-91
[
12771417.001
]
[Cites]
Oncogene. 2003 May 29;22(22):3371-85
[
12776188.001
]
[Cites]
Microbiol Mol Biol Rev. 2003 Jun;67(2):175-212, table of contents
[
12794189.001
]
[Cites]
J Virol. 2001 Apr;75(8):3948-59
[
11264383.001
]
[Cites]
J Virol. 2001 Apr;75(8):4008-13
[
11264393.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):4119-24
[
11274437.001
]
[Cites]
Cancer Res. 2001 Mar 15;61(6):2641-8
[
11289142.001
]
[Cites]
Blood. 2001 Apr 15;97(8):2374-80
[
11290600.001
]
[Cites]
Virology. 2001 Apr 10;282(2):245-55
[
11289807.001
]
[Cites]
J Biol Chem. 2001 Apr 20;276(16):13427-32
[
11154704.001
]
[Cites]
Oncogene. 2001 Jan 25;20(4):523-30
[
11313983.001
]
[Cites]
Oncogene. 2001 Feb 15;20(7):800-11
[
11314014.001
]
[Cites]
Philos Trans R Soc Lond B Biol Sci. 2001 Apr 29;356(1408):499-516
[
11313008.001
]
[Cites]
Philos Trans R Soc Lond B Biol Sci. 2001 Apr 29;356(1408):545-67
[
11313011.001
]
[Cites]
Cytokine Growth Factor Rev. 2001 Jun-Sep;12(2-3):245-57
[
11325605.001
]
[Cites]
Mol Cell. 2001 Apr;7(4):833-43
[
11336706.001
]
[Cites]
Blood. 2001 May 15;97(10):3244-50
[
11342455.001
]
[Cites]
J Virol. 2001 Jun;75(12):5614-26
[
11356969.001
]
[Cites]
Arch Pathol Lab Med. 2001 Jun;125(6):785-9
[
11371231.001
]
[Cites]
Virology. 2001 Jun 5;284(2):235-49
[
11384223.001
]
[Cites]
J Dermatol Sci. 2001 Jul;26(3):182-93
[
11390203.001
]
[Cites]
J Virol. 2001 Jul;75(13):6193-8
[
11390621.001
]
[Cites]
J Virol. 2001 Jul;75(13):6245-8
[
11390631.001
]
[Cites]
J Virol. 2004 Jan;78(1):294-301
[
14671111.001
]
[Cites]
Blood. 2004 Jan 1;103(1):222-8
[
12969971.001
]
[Cites]
J Immunol. 2001 Jul 1;167(1):505-13
[
11418689.001
]
[Cites]
Eur J Cancer. 2001 Jul;37(10):1251-69
[
11423257.001
]
[Cites]
Cancer Res. 2004 Jan 1;64(1):72-84
[
14729610.001
]
[Cites]
Cell. 2004 Jan 23;116(2):281-97
[
14744438.001
]
[Cites]
Herpes. 2003 Dec;10(3):72-7
[
14759339.001
]
[Cites]
Virology. 2004 Jan 20;318(2):542-55
[
14972523.001
]
[Cites]
Virology. 2004 Feb 20;319(2):225-36
[
14980483.001
]
[Cites]
FASEB J. 2004 Mar;18(3):422-7
[
15003988.001
]
[Cites]
J Virol. 2004 Apr;78(7):3601-20
[
15016882.001
]
[Cites]
Ann N Y Acad Sci. 2003 Dec;1010:237-48
[
15033728.001
]
[Cites]
J Virol. 2004 Apr;78(8):4207-23
[
15047836.001
]
[Cites]
J Virol. 2004 Apr;78(8):4248-67
[
15047839.001
]
[Cites]
J Med Primatol. 2004 Feb;33(1):1-9
[
15061726.001
]
[Cites]
J Exp Med. 2004 Apr 5;199(7):993-1003
[
15067035.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4821-6
[
15047889.001
]
[Cites]
J Biol Chem. 2004 Apr 16;279(16):16822-31
[
14742422.001
]
[Cites]
Cancer Res. 2004 Apr 15;64(8):2774-81
[
15087393.001
]
[Cites]
Blood. 2004 May 1;103(9):3465-73
[
14726403.001
]
[Cites]
J Virol. 2004 May;78(10):5491-9
[
15113928.001
]
[Cites]
J Virol. 2004 Jun;78(12):6389-98
[
15163732.001
]
[Cites]
J Virol. 2004 Jun;78(12):6585-94
[
15163750.001
]
[Cites]
J Gen Virol. 2004 Jun;85(Pt 6):1347-61
[
15166416.001
]
[Cites]
Cancer Res. 2004 Jun 15;64(12):4064-8
[
15205312.001
]
[Cites]
J Biol Chem. 2004 Jun 25;279(26):27088-97
[
15102829.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Jun 22;101(25):9399-404
[
15190178.001
]
[Cites]
J Virol. 2004 Jul;78(14):7299-310
[
15220403.001
]
[Cites]
Nat Genet. 2004 Jul;36(7):687-93
[
15220918.001
]
[Cites]
Front Biosci. 1997 Mar 1;2:d126-46
[
9159220.001
]
[Cites]
Blood. 2004 Aug 1;104(3):810-4
[
15073028.001
]
[Cites]
Oncogene. 2004 Jul 29;23(34):5770-80
[
15235582.001
]
[Cites]
Virus Genes. 2004 Oct;29(2):175-82
[
15284477.001
]
[Cites]
Semin Cancer Biol. 2004 Oct;14(5):387-96
[
15288264.001
]
[Cites]
J Virol. 2004 Sep;78(17):9336-42
[
15308728.001
]
[Cites]
J Interferon Cytokine Res. 2004 Aug;24(8):439-54
[
15320958.001
]
[Cites]
Invest Ophthalmol Vis Sci. 2004 Sep;45(9):2906-14
[
15326101.001
]
[Cites]
J Virol. 2004 Sep;78(18):10187-92
[
15331751.001
]
[Cites]
Front Biosci. 2004 Sep 1;9:2245-72
[
15353285.001
]
[Cites]
J Virol. 2004 Oct;78(19):10348-59
[
15367601.001
]
[Cites]
Virology. 2004 Oct 10;328(1):7-18
[
15380353.001
]
[Cites]
J Med Virol. 2004 Nov;74(3):390-6
[
15368522.001
]
[Cites]
J Virol. 2004 Oct;78(20):11108-20
[
15452231.001
]
[Cites]
J Virol. 2004 Oct;78(20):11121-9
[
15452232.001
]
[Cites]
J Virol. 2002 Apr;76(7):3421-39
[
11884567.001
]
[Cites]
J Biol Chem. 2002 Apr 5;277(14):12023-31
[
11821384.001
]
[Cites]
J Virol. 2002 May;76(9):4390-400
[
11932406.001
]
[Cites]
Biol Chem. 2002 Feb;383(2):255-61
[
11934263.001
]
[Cites]
J Biol Chem. 2002 Apr 19;277(16):13745-51
[
11830587.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Apr 16;99(8):5573-8
[
11943871.001
]
[Cites]
J Biol Chem. 2002 Apr 26;277(17):14547-56
[
11832484.001
]
[Cites]
J Virol. 2002 May;76(10):4688-98
[
11967286.001
]
[Cites]
J Virol. 2002 May;76(10):5000-13
[
11967316.001
]
[Cites]
AIDS. 2002 May 24;16(8):F9-18
[
12004288.001
]
[Cites]
DNA Cell Biol. 2002 Mar;21(3):151-62
[
12015894.001
]
[Cites]
J Virol. 2002 Jun;76(12):6185-96
[
12021352.001
]
[Cites]
EMBO J. 2002 Jun 3;21(11):2602-15
[
12032073.001
]
[Cites]
Lancet Infect Dis. 2002 May;2(5):281-92
[
12062994.001
]
[Cites]
J Gen Virol. 2002 Jul;83(Pt 7):1535-45
[
12075072.001
]
[Cites]
Clin Microbiol Rev. 2002 Jul;15(3):439-64
[
12097251.001
]
[Cites]
Blood. 2002 Aug 1;100(3):888-96
[
12130499.001
]
[Cites]
Virology. 2002 Jul 5;298(2):181-8
[
12127781.001
]
[Cites]
J Cutan Pathol. 2002 Feb;29(2):72-8
[
12150136.001
]
[Cites]
Hum Pathol. 2002 Jun;33(6):652-9
[
12152166.001
]
[Cites]
Science. 1993 Feb 12;259(5097):971-4
[
8438157.001
]
[Cites]
Medicine (Baltimore). 1993 Jul;72(4):245-61
[
8341141.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10683-8
[
12145325.001
]
[Cites]
Blood. 2002 Sep 1;100(5):1919-21
[
12176919.001
]
[Cites]
Arch Dermatol. 1993 Oct;129(10):1291-6
[
7692824.001
]
[Cites]
J Virol. 1994 Mar;68(3):1886-902
[
8107249.001
]
[Cites]
Cancer Lett. 1994 Aug 15;83(1-2):191-6
[
8062214.001
]
[Cites]
Blood. 1994 Oct 15;84(8):2711-20
[
7522639.001
]
[Cites]
Cell. 1994 Oct 7;79(1):119-30
[
7923370.001
]
[Cites]
J Pathol. 1994 May;173(1):23-31
[
7523640.001
]
[Cites]
Int Immunol. 1994 Aug;6(8):1125-31
[
7526889.001
]
[Cites]
Science. 1994 Dec 16;266(5192):1865-9
[
7997879.001
]
[Cites]
Res Virol. 1994 May-Aug;145(3-4):251-9
[
7528440.001
]
[Cites]
Science. 1995 Feb 24;267(5201):1078-9
[
7855583.001
]
[Cites]
Lancet. 1995 Mar 25;345(8952):761-2
[
7891488.001
]
[Cites]
J Immunol. 1995 Apr 1;154(7):3582-92
[
7897237.001
]
[Cites]
N Engl J Med. 1995 May 4;332(18):1181-5
[
7700310.001
]
[Cites]
N Engl J Med. 1995 May 4;332(18):1186-91
[
7700311.001
]
[Cites]
Lancet. 1995 Apr 22;345(8956):1043-4
[
7723505.001
]
[Cites]
Lancet. 1995 May 6;345(8958):1180
[
7723569.001
]
[Cites]
Blood. 1995 Aug 15;86(4):1276-80
[
7632932.001
]
[Cites]
Nature. 1995 Aug 17;376(6541):596-9
[
7637809.001
]
[Cites]
N Engl J Med. 1995 Sep 21;333(12):798; author reply 798-9
[
7643891.001
]
[Cites]
J Cell Sci. 1995 Jun;108 ( Pt 6):2511-23
[
7673365.001
]
[Cites]
Gene Ther. 1994 May;1(3):208-16
[
7584083.001
]
[Cites]
Nat Med. 1995 Jul;1(7):707-8
[
7585156.001
]
[Cites]
J Emerg Med. 1995 Sep-Oct;13(5):671-4
[
8530789.001
]
[Cites]
Nat Med. 1995 Dec;1(12):1274-8
[
7489408.001
]
[Cites]
J Virol. 1996 Jan;70(1):549-58
[
8523568.001
]
[Cites]
Arch Intern Med. 1996 Jan 22;156(2):202-4
[
8546554.001
]
[Cites]
J Natl Cancer Inst. 1996 Apr 3;88(7):450-5
[
8618237.001
]
[Cites]
EMBO J. 1996 Feb 15;15(4):799-809
[
8631301.001
]
[Cites]
J Infect Dis. 1996 Mar;173(3):542-9
[
8627015.001
]
[Cites]
Nat Med. 1996 Mar;2(3):342-6
[
8612236.001
]
[Cites]
N Engl J Med. 1996 Jul 25;335(4):233-41
[
8657239.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6641-6
[
8692871.001
]
[Cites]
Leukemia. 1996 Jul;10(7):1237-40
[
8684008.001
]
[Cites]
Annu Rev Immunol. 1996;14:649-83
[
8717528.001
]
[Cites]
Nature. 1996 Aug 1;382(6590):410
[
8684480.001
]
[Cites]
Nat Med. 1996 Aug;2(8):918-24
[
8705863.001
]
[Cites]
Nat Med. 1996 Aug;2(8):925-8
[
8705864.001
]
[Cites]
Nature. 1996 Aug 29;382(6594):816-8
[
8752276.001
]
[Cites]
Clin Infect Dis. 1996 Jun;22(6):1120-1
[
8783733.001
]
[Cites]
AIDS. 1996 Feb;10(2):175-80
[
8838705.001
]
[Cites]
J Virol. 2003 Jul;77(14):7978-90
[
12829837.001
]
[Cites]
J Virol. 2003 Jul;77(14):8019-30
[
12829841.001
]
[Cites]
J Virol. 2003 Jul;77(14):8147-52
[
12829853.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8490-5
[
12832621.001
]
[Cites]
Clin Infect Dis. 2003 Jul 15;37(2):285-91
[
12856221.001
]
[Cites]
J Virol. 2003 Aug;77(15):8532-40
[
12857922.001
]
[Cites]
Intervirology. 2003;46(3):141-9
[
12867751.001
]
[Cites]
Oncogene. 2003 Aug 11;22(33):5150-63
[
12910252.001
]
[Cites]
J Virol. 2003 Sep;77(17):9346-58
[
12915550.001
]
[Cites]
J Virol. 2003 Sep;77(17):9399-411
[
12915555.001
]
[Cites]
J Virol. 2003 Sep;77(17):9451-62
[
12915560.001
]
[Cites]
J Cell Sci. 2003 Sep 15;116(Pt 18):3721-8
[
12890756.001
]
[Cites]
J Virol. 2003 Sep;77(18):9738-49
[
12941882.001
]
[Cites]
J Virol. 2003 Sep;77(18):9758-68
[
12941884.001
]
[Cites]
J Virol. 2003 Oct;77(19):10179-85
[
12970403.001
]
[Cites]
APMIS. 2003 Jul-Aug;111(7-8):698-714
[
12974773.001
]
[Cites]
N Engl J Med. 2003 Sep 18;349(12):1113-22
[
13679525.001
]
[Cites]
J Virol. 2003 Nov;77(21):11425-35
[
14557628.001
]
[Cites]
Mol Cell Biol. 2003 Nov;23(22):8282-94
[
14585985.001
]
[Cites]
J Leukoc Biol. 2003 Nov;74(5):757-63
[
12960240.001
]
[Cites]
Cell. 1996 Oct 4;87(1):13-20
[
8858144.001
]
[Cites]
AIDS. 1996 Sep;10(10):1101-5
[
8874626.001
]
[Cites]
J Biol Chem. 2003 Dec 26;278(52):52437-45
[
14563855.001
]
[Cites]
Oncogene. 2004 Jan 15;23(2):514-23
[
14724579.001
]
[Cites]
Lancet. 1996 Oct 26;348(9035):1133-8
[
8888167.001
]
[Cites]
Science. 1996 Dec 6;274(5293):1739-44
[
8939871.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14862-7
[
8962146.001
]
[Cites]
N Engl J Med. 1997 Jan 16;336(3):163-71
[
8988896.001
]
[Cites]
J Virol. 1997 Jan;71(1):314-24
[
8985352.001
]
[Cites]
J Virol. 1997 Jan;71(1):715-9
[
8985403.001
]
[Cites]
Nature. 1997 Jan 23;385(6614):347-50
[
9002520.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):690-4
[
9012846.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Feb 4;94(3):979-84
[
9023368.001
]
[Cites]
J Virol. 1997 Mar;71(3):1984-91
[
9032330.001
]
[Cites]
Lancet. 1997 Feb 15;349(9050):490-5
[
9040590.001
]
[Cites]
Nat Med. 1997 Mar;3(3):287-92
[
9055855.001
]
[Cites]
Nat Med. 1997 Mar;3(3):293-8
[
9055856.001
]
[Cites]
Lancet. 1997 Mar 15;349(9054):774-5
[
9074581.001
]
[Cites]
J Virol. 1997 May;71(5):4138-44
[
9094697.001
]
[Cites]
J Infect Dis. 1997 May;175(5):1193-7
[
9129084.001
]
[Cites]
AIDS. 1997 May;11(6):713-21
[
9143602.001
]
[Cites]
J Virol. 1997 Jun;71(6):4193-8
[
9151805.001
]
[Cites]
Hum Pathol. 1997 Jun;28(6):748-50
[
9191012.001
]
[Cites]
Br J Haematol. 1997 Jun;97(3):515-22
[
9207392.001
]
[Cites]
Lymphology. 1997 Jun;30(2):63-76
[
9215976.001
]
[Cites]
J Virol. 1997 Aug;71(8):5915-21
[
9223481.001
]
[Cites]
J Biol Chem. 1997 Aug 1;272(31):19625-31
[
9235971.001
]
[Cites]
Science. 1997 Sep 12;277(5332):1656-9
[
9287217.001
]
[Cites]
AIDS. 1997 Sep;11(11):1333-40
[
9302442.001
]
[Cites]
Blood. 1997 Oct 1;90(7):2826-9
[
9326251.001
]
[Cites]
Science. 1997 Oct 10;278(5336):290-4
[
9323208.001
]
[Cites]
J Pathol. 1997 Jul;182(3):262-5
[
9349227.001
]
[Cites]
Oncogene. 1997 Oct 16;15(16):1979-85
[
9365244.001
]
[Cites]
Nature. 1997 Nov 13;390(6656):184-7
[
9367157.001
]
[Cites]
Virology. 1997 Nov 10;238(1):22-9
[
9375005.001
]
[Cites]
Int J Cancer. 1997 Nov 14;73(4):562-9
[
9389573.001
]
[Cites]
J Virol. 1998 Jan;72(1):701-7
[
9420276.001
]
[Cites]
Nature. 1998 Jan 1;391(6662):86-9
[
9422510.001
]
[Cites]
J Virol. 1998 Feb;72(2):1005-12
[
9444993.001
]
[Cites]
Blood. 1998 Mar 1;91(5):1671-9
[
9473233.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3537-42
[
9520401.001
]
[Cites]
Nat Med. 1998 Apr;4(4):435-40
[
9546789.001
]
[Cites]
J Virol. 1998 Jun;72(6):4980-8
[
9573267.001
]
[Cites]
J Virol. 1998 Jun;72(6):5182-8
[
9573290.001
]
[Cites]
J Virol. 1998 Jul;72(7):5433-40
[
9620998.001
]
[Cites]
Lancet. 1998 Jun 20;351(9119):1833-9
[
9652666.001
]
[Cites]
J Virol. 2004 Nov;78(21):11926-38
[
15479833.001
]
[Cites]
Blood. 2004 Nov 1;104(9):2903-11
[
15231571.001
]
[Cites]
Blood. 2004 Nov 1;104(9):2736-8
[
15238422.001
]
[Cites]
J Virol. 2004 Nov;78(22):12566-75
[
15507644.001
]
[Cites]
J Natl Cancer Inst. 1972 Dec;49(6):1509-26
[
4647841.001
]
[Cites]
Am J Dermatopathol. 1981 Summer;3(2):111-4
[
7270808.001
]
[Cites]
Lancet. 1981 Sep 19;2(8247):598-600
[
6116083.001
]
[Cites]
J Am Acad Dermatol. 1981 Oct;5(4):468-71
[
7287964.001
]
[Cites]
N Engl J Med. 1981 Dec 10;305(24):1439-44
[
6272110.001
]
[Cites]
Ariz Med. 1981 Dec;38(12):902-4
[
7332494.001
]
[Cites]
JAMA. 1986 Jul 4;256(1):20-1, 24-5
[
3012133.001
]
[Cites]
Cancer Res. 1986 Dec;46(12 Pt 1):6333-8
[
3022918.001
]
[Cites]
Cell. 1989 Aug 25;58(4):729-39
[
2475256.001
]
[Cites]
Lancet. 1990 Jan 20;335(8682):123-8
[
1967430.001
]
[Cites]
Mol Cell Biol. 1990 Jun;10(6):2448-57
[
2342456.001
]
[Cites]
Cell. 1991 Sep 20;66(6):1071-4
[
1833062.001
]
[Cites]
Biochem Biophys Res Commun. 1992 Mar 31;183(3):1167-74
[
1567395.001
]
[Cites]
Cancer Surv. 1991;10:5-22
[
1821323.001
]
[Cites]
J Biol Chem. 1992 Dec 15;267(35):25589-96
[
1460054.001
]
[Cites]
Gene Expr. 1992;2(4):329-37
[
1472868.001
]
[Cites]
Am J Pathol. 1993 Aug;143(2):528-37
[
8342600.001
]
[Cites]
Mol Cell Biol. 1993 Oct;13(10):6501-8
[
8413249.001
]
(PMID = 17672038.001).
[ISSN]
0927-3042
[Journal-full-title]
Cancer treatment and research
[ISO-abbreviation]
Cancer Treat. Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA096512; United States / NCI NIH HHS / CA / R01 CA124332-03; United States / NCI NIH HHS / CA / R01 CA096512-02; United States / NIDCR NIH HHS / DE / R01 DE017333-03; United States / NCI NIH HHS / CA / R01 CA096512-03; United States / NIDCR NIH HHS / DE / DE017333-02; United States / NCI NIH HHS / CA / R01 CA124332; United States / NCI NIH HHS / CA / CA096512-01A2; United States / NIDCR NIH HHS / DE / R01 DE017333-02; United States / NCI NIH HHS / CA / R01 CA096512-05; United States / NCI NIH HHS / CA / R01 CA132637-02; United States / NIDCR NIH HHS / DE / DE017333-01; United States / NCI NIH HHS / CA / CA096512-02; United States / NIDCR NIH HHS / DE / DE017333-03; United States / NIDCR NIH HHS / DE / R01 DE017333; United States / NCI NIH HHS / CA / R01 CA096512-01A2; United States / NCI NIH HHS / CA / R01 CA096512-04; United States / NIDCR NIH HHS / DE / R01 DE017333-01; United States / NCI NIH HHS / CA / R01 CA132637; United States / NCI NIH HHS / CA / R01 CA132637-01A1; United States / NCI NIH HHS / CA / R01 CA124332-02
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
504
[Other-IDs]
NLM/ NIHMS165766; NLM/ PMC2798888
76.
Ohtawa M, Ichikawa S, Teishikata Y, Fujimuro M, Yokosawa H, Matsuda A:
9-(2-C-Cyano-2-deoxy-beta-D-arabino-pentofuranosyl)guanine, a potential antitumor agent against B-lymphoma infected with Kaposi's sarcoma-associated herpesvirus.
J Med Chem
; 2007 May 3;50(9):2007-10
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Several 9-(2-C-cyano-2-deoxy-l-beta-d-arabino-pentofuranosyl)purine derivatives were tested against Kaposi's sarcoma-associated herpesvirus (KSHV)-infected primary effusion lymphoma (
PEL
) cells.
Therefore, it was found that compounds 3, 4, 5, and 6 showed selective cytotoxicity against
PEL
cells infected with KSHV.
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(PMID = 17402726.001).
[ISSN]
0022-2623
[Journal-full-title]
Journal of medicinal chemistry
[ISO-abbreviation]
J. Med. Chem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / 9-(2-C-cyano-2-deoxy-arabino-pentofuranosyl)guanine; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 12133JR80S / Guanosine; 63231-63-0 / RNA; 9007-49-2 / DNA
77.
Maeder M, Spieler P, Krapf R, Diethelm M:
Cytologically malignant lymphoid pericardial effusion with benign clinical outcome.
Swiss Med Wkly
; 2005 Jun 25;135(25-26):377-81
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[Title]
Cytologically
malignant
lymphoid pericardial effusion with benign clinical outcome.
BACKGROUND: Isolated
malignant
pericardial effusion is a manifestation of primary cardiac lymphoma (PCL) and primary effusion lymphoma (
PEL
), rare types of non-Hodgkin's lymphoma (NHL).
The
diagnosis
is based on different cytological methods and analyses including DNA-image cytometry (ICM-DNA).
CONCLUSIONS: Despite the highly atypical cytomorphology including unequivocal DNA aneuploidy, long-term survival in both patients strongly suggests that pronounced reactive lymphocytic changes are probably due to viral pericarditis rather than PCL or
PEL
as underlying conditions.
It seems that DNA-aneuploidy may be not absolutely specific for the detection
of malignant
lymphoid cells in pericardial fluid.
[MeSH-major]
Heart Neoplasms /
diagnosis
. Lymphoma, Non-Hodgkin /
diagnosis
. Pericardial Effusion /
diagnosis
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consumer health - Pericardial Disorders
.
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(PMID = 16106328.001).
[ISSN]
1424-7860
[Journal-full-title]
Swiss medical weekly
[ISO-abbreviation]
Swiss Med Wkly
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
78.
Boulanger E, Meignin V, Afonso PV, Duprez R, Oksenhendler E, Agbalika F, Gessain A:
Extracavitary tumor after primary effusion lymphoma: relapse or second distinct lymphoma?
Haematologica
; 2007 Sep;92(9):1275-6
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HHV-8-associated solid lymphomas which develop in extracavitary sites during the course of primary effusion lymphoma (
PEL
) could represent the relapse of original
PEL
tumors in different anatomical sites, or newly occurring distinct HHV-8-associated lymphomas, such as multicentric Castleman
disease
-related microlymphomas.
[MeSH-major]
Herpesviridae Infections / complications. Herpesvirus 8, Human / isolation & purification. Lymphoma / complications. Lymphoma, AIDS-Related / complications. Neoplasm Recurrence, Local / complications. Pleural Effusion,
Malignant
/ complications
Genetic Alliance.
consumer health - Primary effusion lymphoma
.
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consumer health - Lymphoma
.
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(PMID = 17768127.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Letter; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
79.
Meeker JD, Susi P, Flynn MR:
Hexavalent chromium exposure and control in welding tasks.
J Occup Environ Hyg
; 2010 Nov;7(11):607-15
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[Title]
Hexavalent chromium
exposure
and control in welding tasks.
Studies
of exposure
to the lung carcinogen hexavalent chromium (CrVI) from welding tasks are limited, especially within the construction industry where overexposure may be common.
In addition, despite the OSHA requirement that the use of engineering controls such as local exhaust ventilation (LEV) first be considered before relying on other strategies to reduce worker
exposure
to CrVI, data on the effectiveness of LEV to reduce CrVI exposures from welding are lacking.
(3) field survey data of construction welders collected by the Center for Construction Research and Training (CPWR); and (4) controlled welding trials conducted by CPWR to assess the effectiveness
of a
portable LEV unit to reduce CrVI
exposure
.
In the OSHA (n = 181) and TWI (n = 124) datasets, which included very few samples from the construction industry, the OSHA
permissible exposure level
(
PEL
) for CrVI (5 μg/m(3)) was exceeded in 9% and 13% of samples, respectively.
CrVI concentrations measured in the CPWR field surveys (n = 43) were considerably higher, and 25% of samples exceeded the
PEL
.
Only weak-to-moderate correlations were found between total particulate matter and CrVI, suggesting that total particulate matter concentrations are not a good surrogate for CrVI
exposure
in retrospective studies.
However,
exposure
could be substantially reduced with proper use of LEV.
[MeSH-major]
Air Pollutants, Occupational. Chromium. Occupational
Exposure
/ prevention & control. Occupational
Exposure
/ statistics & numerical data. Welding / statistics & numerical data
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CHROMIUM, ELEMENTAL
.
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(PMID = 20845207.001).
[ISSN]
1545-9632
[Journal-full-title]
Journal of occupational and environmental hygiene
[ISO-abbreviation]
J Occup Environ Hyg
[Language]
eng
[Grant]
United States / PHS HHS / / 0H008307
[Publication-type]
Journal Article; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Air Pollutants, Occupational; 0 / Particulate Matter; 0R0008Q3JB / Chromium; 12597-68-1 / Stainless Steel; 18540-29-9 / chromium hexavalent ion
80.
Zhuge B, Du GC, Shen W, Zhuge J, Chen J:
Efficient secretory expression of an alkaline pectate lyase gene from Bacillus subtilis in E. coli and the purification and characterization of the protein.
Biotechnol Lett
; 2007 Mar;29(3):405-10
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[Title]
Efficient secretory expression of an alkaline
pectate lyase gene
from Bacillus subtilis in E. coli and the purification and characterization of the protein.
The
gene
encoding
pectate lyase
(PL) from Bacillus subtilis WSHB04-02 was amplified by PCR, fused with a periplasmic secretion signal peptide sequence, pelB, from pET22b(+), cloned and expressed in Escherichia coli cells using a temperature control vector, pHsh.
[MeSH-minor]
Enzyme Activation. Enzyme Stability.
Gene
Expression Regulation, Bacterial / physiology.
Gene
Expression Regulation, Enzymologic / physiology. Genetic Enhancement / methods. Recombinant Proteins / biosynthesis. Recombinant Proteins / chemistry
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(PMID = 17237974.001).
[ISSN]
1573-6776
[Journal-full-title]
Biotechnology letters
[ISO-abbreviation]
Biotechnol. Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Recombinant Proteins; EC 4.2.2.- / Polysaccharide-Lyases; EC 4.2.2.2 / pectate lyase
81.
Nemunaitis MC, Schussler JM, Shiller SM, Sloan LM, Mennel RG:
Primary effusion lymphoma diagnosed by pericardiocentesis.
Proc (Bayl Univ Med Cent)
; 2009 Jan;22(1):77-80
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Primary effusion lymphoma (
PEL
), formerly known as body cavity-based lymphoma, is a high-grade B-cell non-Hodgkin's lymphoma associated with Kaposi's sarcoma and human herpesvirus 8 infection.
PEL
is often diagnosed in patients with HIV infection and carries a poor prognosis, with median survival near 6 months.
We describe a patient who presented with symptomatic pericardial effusion, secondary to newly diagnosed
PEL
, and no prior history of HIV infection.
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[Cites]
Curr Opin Oncol. 2005 Sep;17(5):447-55
[
16093794.001
]
[Cites]
Ann Hematol. 2005 Aug;84(8):551-2
[
15800785.001
]
[Cites]
J Clin Oncol. 2005 Jul 1;23(19):4372-80
[
15994147.001
]
[Cites]
Cancer Biol Ther. 2005 Jan;4(1):77-82
[
15662128.001
]
[Cites]
Clin Cancer Res. 2005 Apr 15;11(8):3102-8
[
15837766.001
]
[Cites]
Leukemia. 2005 Mar;19(3):473-6
[
15674353.001
]
[Cites]
Blood. 2005 Mar 15;105(6):2510-8
[
15572586.001
]
[Cites]
Leukemia. 1999 May;13(5):664-70
[
10374868.001
]
[Cites]
Am J Hematol. 1998 Mar;57(3):266
[
9495391.001
]
[Cites]
Blood. 1997 Dec 15;90(12):4894-900
[
9389706.001
]
[Cites]
N Engl J Med. 1995 May 4;332(18):1186-91
[
7700311.001
]
[Cites]
Blood. 1989 Feb 15;73(3):792-9
[
2537119.001
]
[Cites]
MMWR Morb Mortal Wkly Rep. 1985 Jun 28;34(25):373-5
[
2989677.001
]
[Cites]
Clin Pharmacol Ther. 1978 Jan;23(1):68-72
[
618710.001
]
[Cites]
Leukemia. 2004 Oct;18(10):1699-704
[
15343345.001
]
[Cites]
AIDS Patient Care STDS. 2004 Feb;18(2):67-73
[
15006181.001
]
[Cites]
J Clin Oncol. 2003 Nov 1;21(21):3948-54
[
14581418.001
]
[Cites]
Leuk Lymphoma. 2001 Apr;41(3-4):439-43
[
11378560.001
]
[Cites]
JAMA. 2001 Apr 11;285(14):1880-5
[
11308402.001
]
[Cites]
Blood. 2001 Feb 1;97(3):744-51
[
11157493.001
]
[Cites]
AIDS. 2001 Jan 26;15(2):280-2
[
11216942.001
]
[Cites]
J Natl Cancer Inst. 2000 May 3;92(9):729-36
[
10793109.001
]
[Cites]
Cancer. 2007 Aug 25;111(4):224-33
[
17554754.001
]
[Cites]
Leukemia. 2007 Aug;21(8):1792-801
[
17568816.001
]
[Cites]
Oncologist. 2007 May;12(5):569-76
[
17522245.001
]
[Cites]
J Cardiol. 2007 Apr;49(4):205-10
[
17460882.001
]
[Cites]
Ann Oncol. 2006 Dec;17(12):1849-50
[
16766593.001
]
[Cites]
Int J Hematol. 2006 May;83(4):328-30
[
16757433.001
]
[Cites]
Blood. 2006 Jan 1;107(1):13-20
[
16099881.001
]
(PMID = 19169406.001).
[ISSN]
0899-8280
[Journal-full-title]
Proceedings (Baylor University. Medical Center)
[ISO-abbreviation]
Proc (Bayl Univ Med Cent)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2626366
82.
Bakare AA, Pandey AK, Bajpayee M, Bhargav D, Chowdhuri DK, Singh KP, Murthy RC, Dhawan A:
DNA damage induced in human peripheral blood lymphocytes by industrial solid waste and municipal sludge leachates.
Environ Mol Mutagen
; 2007 Jan;48(1):30-7
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[Title]
DNA damage induced in human peripheral blood
lymphocytes
by industrial solid waste and municipal sludge leachates.
Exposure of
humans to toxic compounds occurs mostly in the form of complex mixtures.
In the present study, leachates of solid wastes from a polyfiber factory (PFL), an aeronautical plant (
AEL
), and a municipal sludge leachate (MSL) were assessed for their ability to induce DNA damage in human peripheral blood
lymphocytes
using the alkaline Comet assay.
Lymphocytes
were incubated with 0.5-15.0% concentrations (pH range 7.1-7.4) of the test leachates for 3 hr at 37 degrees C, and treatment with 1 mM ethyl methanesulfonate served as a positive control.
Our data indicate that the ever-increasing amounts of leachates from waste landfill sites have the potential to induce DNA damage and suggest that the
exposure of
human populations to these leachates may lead to adverse health effects.
[MeSH-major]
Industrial Waste.
Lymphocytes
/ drug effects. Water Pollutants, Chemical / pharmacology
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(PMID = 17163505.001).
[ISSN]
0893-6692
[Journal-full-title]
Environmental and molecular mutagenesis
[ISO-abbreviation]
Environ. Mol. Mutagen.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Industrial Waste; 0 / Metals, Heavy; 0 / Water Pollutants, Chemical
83.
Deloose ST, Smit LA, Pals FT, Kersten MJ, van Noesel CJ, Pals ST:
High incidence of Kaposi sarcoma-associated herpesvirus infection in HIV-related solid immunoblastic/plasmablastic diffuse large B-cell lymphoma.
Leukemia
; 2005 May;19(5):851-5
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Kaposi sarcoma-associated herpesvirus (KSHV) is known to be associated with two distinct lymphoproliferative disorders: primary effusion lymphoma (
PEL
) and multicentric Castleman
disease
(MCD)/MCD-associated plasmablastic lymphoma.
Our results indicate that KSHV infection is not restricted to
PEL
and MCD; it is also common (38%) in HIV-related solid immunoblastic/plasmablastic lymphomas.
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consumer health - HIV/AIDS
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consumer health - HIV/AIDS in Women
.
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consumer health - Kaposi's Sarcoma
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(PMID = 15744337.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
84.
Lefort S, Flamand L:
Kaposi's sarcoma-associated herpesvirus K-bZIP protein is necessary for lytic viral gene expression, DNA replication, and virion production in primary effusion lymphoma cell lines.
J Virol
; 2009 Jun;83(11):5869-80
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[Title]
Kaposi's sarcoma-associated herpesvirus K-bZIP protein is necessary for lytic viral
gene
expression, DNA replication, and virion production in primary effusion lymphoma cell lines.
Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of three human proliferative disorders, namely, Kaposi's sarcoma, primary effusion lymphomas (
PEL
), and multicentric Castleman'
s disease
.
To evaluate the physiological roles of K-bZIP in the context
of PEL
, we generated BCBL-1 cells with a tetracycline (Tet)-inducible small hairpin RNA (shRNA) directed against the K8 mRNA to knock down K-bZIP expression at different points during KSHV's life cycle.
Similar effects were seen at the protein
level
for RTA (immediate-early protein) and K8.1 (late protein) expression.
Interestingly, a direct correlation between K-bZIP
levels
and viral lytic mRNAs was noticed.
The same effects were observed following knockdown of K-bZIP in another
PEL
cell line, BC3.
Finally, using shRNA-K8-inducible 293 cells, we report that
de
novo synthesis of K-bZIP is not necessary for initiation of infection and latency establishment.
These data support the concept that K-bZIP is essential for lytic viral
gene
expression, viral DNA replication, and virus propagation in
PEL
cells.
[MeSH-major]
Basic-Leucine Zipper Transcription Factors / metabolism. DNA Replication / genetics.
Gene
Expression Regulation, Viral / genetics. Herpesvirus 8, Human / metabolism. Lymphoma, Primary Effusion / virology. Repressor Proteins / metabolism. Viral Proteins / metabolism. Virion / growth & development. Virus Assembly
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[Cites]
Blood. 1995 Aug 15;86(4):1276-80
[
7632932.001
]
[Cites]
J Virol. 1995 May;69(5):2998-3006
[
7707526.001
]
[Cites]
Nat Med. 1996 Mar;2(3):342-6
[
8612236.001
]
[Cites]
N Engl J Med. 1996 May 16;334(20):1292-7
[
8609946.001
]
[Cites]
Blood. 1996 Oct 1;88(7):2648-54
[
8839859.001
]
[Cites]
J Virol. 1996 Dec;70(12):8340-7
[
8970953.001
]
[Cites]
J Virol. 1997 Jan;71(1):314-24
[
8985352.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10866-71
[
9724796.001
]
[Cites]
J Virol. 1999 Mar;73(3):1909-17
[
9971770.001
]
[Cites]
J Virol. 1999 Mar;73(3):2232-42
[
9971806.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4546-51
[
10200299.001
]
[Cites]
J Virol. 1999 Nov;73(11):9348-61
[
10516043.001
]
[Cites]
J Virol. 2005 Mar;79(6):3479-87
[
15731242.001
]
[Cites]
J Virol. 2005 Apr;79(8):4952-64
[
15795281.001
]
[Cites]
J Virol. 2005 Aug;79(15):9912-25
[
16014952.001
]
[Cites]
J Virol. 2006 Dec;80(24):12171-86
[
17020951.001
]
[Cites]
J Virol. 2007 Oct;81(20):10950-60
[
17652396.001
]
[Cites]
J Virol. 2007 Dec;81(24):13519-32
[
17913803.001
]
[Cites]
J Virol. 2000 Jul;74(13):6207-12
[
10846108.001
]
[Cites]
J Virol. 2000 Dec;74(24):11977-82
[
11090200.001
]
[Cites]
J Virol. 2001 Feb;75(3):1487-506
[
11152521.001
]
[Cites]
J Gen Virol. 2001 Mar;82(Pt 3):507-12
[
11172091.001
]
[Cites]
J Virol. 2001 Aug;75(15):6786-99
[
11435557.001
]
[Cites]
J Virol. 2001 Oct;75(19):9509-16
[
11533213.001
]
[Cites]
J Virol. 2003 Jan;77(2):1441-51
[
12502859.001
]
[Cites]
J Virol. 2003 Mar;77(6):3809-15
[
12610155.001
]
[Cites]
J Virol. 2003 Apr;77(7):4205-20
[
12634378.001
]
[Cites]
EMBO Rep. 2003 Jun;4(6):609-15
[
12776180.001
]
[Cites]
Virology. 2004 Jan 20;318(2):542-55
[
14972523.001
]
[Cites]
J Virol. 2004 Apr;78(7):3601-20
[
15016882.001
]
[Cites]
Virology. 2004 Aug 1;325(2):225-40
[