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1
b cell chronic lymphoid leukemia 2005:2010[pubdate] *count=100
5485 results
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b cell chronic lymphoid leukemia
' expanded to all its synonyms;
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Items 1 to 100 of about 5485
1.
Mathews MS, Duma CM, Brant-Zawadzki M, Hasso A, Westhout FD, Klein DJ, Vanhorn D:
Extramedullary hematopoeisis within a convexity meningioma.
Surg Neurol
; 2008 May;69(5):522-5; discussion 525
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BACKGROUND: Hematopoiesis outside the bone marrow is known to occur in patients with severe anemia,
leukemia
, polycythemia, or myelofibrosis, and in patients affected by
chronic
poisoning by marrow-toxic substances.
A hematoxylin-eosin-stained biopsy specimen showed whorls of tumor cells, diagnostic
of a
meningioma.
Flow cytometric evaluation confirmed the clinical suspicion of an underlying
chronic
lymphocytic
leukemia
.
Genetic Alliance.
consumer health - Meningioma
.
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(PMID = 17714768.001).
[ISSN]
0090-3019
[Journal-full-title]
Surgical neurology
[ISO-abbreviation]
Surg Neurol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
2.
Chipuk JE, Moldoveanu T, Llambi F, Parsons MJ, Green DR:
The BCL-2 family reunion.
Mol Cell
; 2010 Feb 12;37(3):299-310
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B cell
CLL
/
lymphoma
-2 (BCL-2) and its relatives comprise the BCL-2 family of proteins, which were originally characterized with respect to their roles in controlling outer mitochondrial membrane integrity and apoptosis.
Here we will discuss the mechanisms and functions of the BCL-2 family in the context of these pathways, highlighting the complex integration and regulation of the BCL-2 family in
cell
fate decisions.
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(PMID = 20159550.001).
[ISSN]
1097-4164
[Journal-full-title]
Molecular cell
[ISO-abbreviation]
Mol. Cell
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / F32 CA101444; United States / NIAID NIH HHS / AI / R01 AI040646; United States / NIAID NIH HHS / AI / R01 AI040646-16
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Proto-Oncogene Proteins c-bcl-2
[Number-of-references]
89
[Other-IDs]
NLM/ NIHMS337530; NLM/ PMC3222298
3.
Hogan M, Claffey J, Pampillón C, Tacke M:
Synthesis and cytotoxicity studies of new morpholino-functionalised and N-heteroaryl-substituted titanocene anticancer drugs.
Med Chem
; 2008 Mar;4(2):91-9
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When these titanocenes were tested against
LLC
-PK cells, the IC(50) values obtained were of 24, 36, and 41 microM respectively.
The most cytotoxic titanocene in this paper (5a) with an IC(50) value of 24 microM is found to be almost ten times less cytotoxic than cis-platin, which showed an IC(50) value of 3.3 microM when tested on the epithelial pig kidney
LLC
-PK
cell
line, and approximately 2 times less cytotoxic than its dimethylamino-functionalised analogue.
[MeSH-minor]
Animals. Cyclopentanes. Inhibitory Concentration 50.
LLC
-PK1 Cells. Structure-Activity Relationship. Swine
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(PMID = 18336326.001).
[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]
Netherlands
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Cyclopentanes; 0 / Morpholines; 0 / Organometallic Compounds; 1271-29-0 / titanocene; 19W699IKIE / fulvene
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4.
da Silva R, Saraiva J, de Albuquerque S, Curti C, Donate PM, Bianco TN, Bastos JK, Silva ML:
Trypanocidal structure-activity relationship for cis- and trans-methylpluviatolide.
Phytochemistry
; 2008 Jun;69(9):1890-4
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The cytotoxicity of the compounds was assessed by the MTT method using
LLC
-MK2 cells.
Trans-methylpluviatolide displayed
low
toxicity for
LLC
-MK2 cells, with an IC50 of 6.53 mM.
[MeSH-minor]
Animals.
Cell
Line. Macrophages / drug effects. Macrophages / metabolism. Mice. Molecular Structure. Nitric Oxide / biosynthesis. Structure-Activity Relationship
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(PMID = 18479721.001).
[ISSN]
0031-9422
[Journal-full-title]
Phytochemistry
[ISO-abbreviation]
Phytochemistry
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Lactones; 0 / Lignans; 0 / Trypanocidal Agents; 0 / methylpluviatolide; 31C4KY9ESH / Nitric Oxide
5.
Gross SA, Zhu X, Bao L, Ryder J, Le A, Chen Y, Wang XQ, Irons RD:
A prospective study of 728 cases of non-Hodgkin lymphoma from a single laboratory in Shanghai, China.
Int J Hematol
; 2008 Sep;88(2):165-73
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[Title]
A prospective study of 728 cases of non-Hodgkin
lymphoma
from a single laboratory in Shanghai, China.
The frequency of subtypes of
lymphoid
neoplasms was determined
in a
prospective series of 831 patients presenting at 29 Shanghai hospitals over a 4-year period.
Diagnosis
and classification was established
in a
single laboratory according to the 2001 WHO classification system.
The frequency of non-Hodgkin
lymphoma
was 87.6% (n = 728) and Hodgkin
lymphoma
was 12.4% (n = 103).
The most prevalent NHL subtypes diagnosed using WHO criteria were
diffuse
large
B cell
lymphoma
(DLBCL), precursor B
lymphoblastic
leukemia
/
lymphoma
and
chronic
lymphocytic
leukemia
/
small lymphocytic lymphoma
(
CLL
/SLL).
Although
a low
incidence has been reported in some Asian populations,
CLL
/SLL was commonly encountered, indicating that
chronic lymphoid
neoplasms are not rare in Shanghai.
Consistent with previous reports, our findings indicate a decrease in the frequency of follicular
lymphoma
and an increase in T
cell
neoplasms compared to the West.
Precursor T
lymphoblastic
leukemia
/
lymphoma
, anaplastic large T
cell
lymphoma
, aggressive NK
cell leukemia
, angioimmunoblastic T
cell
lymphoma
and peripheral T
cell
lymphoma
were prominent subtypes of T
cell
NHL.
[MeSH-major]
Asian Continental Ancestry Group / statistics & numerical data.
Lymphoma
, Non-Hodgkin / classification.
Lymphoma
, Non-Hodgkin / ethnology
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[
9704731.001
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(PMID = 18648906.001).
[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / DNA, Neoplasm
6.
Cutrona G, Colombo M, Matis S, Reverberi D, Dono M, Tarantino V, Chiorazzi N, Ferrarini M:
B lymphocytes in humans express ZAP-70 when activated in vivo.
Eur J Immunol
; 2006 Mar;36(3):558-69
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[Title]
B
lymphocytes in
humans express ZAP-70 when activated in vivo.
Recently, this important signaling element was detected in leukemic B cells from a subgroup of patients with
B cell chronic
lymphocytic
leukemia
(B-
CLL
).
The cDNA sequence of
B cell
ZAP-70 was the same as that in T cells.
Germinal center B cells and plasma cells had a substantial proportion of ZAP-70+ cells, while memory and follicular mantle B cells, which contain
low
numbers of activated B cells, expressed relatively little ZAP-70.
A
cell
fraction of IgD+, CD38+ B cells, which are comprised of many in vivo activated B cells, exhibited the highest levels of ZAP-70.
In these B cells, the expression of ZAP-70 correlated with that of CD38 and not with that of CD5, a hallmark of B-
CLL
cells.
B-
CLL
cells are activated cells and their ZAP-70 expression reflects a normal property of activated B cells populations rather than a neoplastic aberration.
[MeSH-major]
B-
Lymphocytes
/ immunology. Gene Expression Regulation, Enzymologic / immunology. Lymphocyte Activation / immunology. ZAP-70 Protein-Tyrosine Kinase / immunology
[MeSH-minor]
Antigens, CD38 / immunology. Antigens, CD5 / immunology. Cells, Cultured. Germinal Center / cytology. Germinal Center / immunology. Humans. Immunoglobulin D / immunology. Killer Cells, Natural / cytology. Killer Cells, Natural / enzymology. Killer Cells, Natural / immunology.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ enzymology.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ immunology.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ pathology. Membrane Glycoproteins / immunology. Palatine Tonsil / cytology. Palatine Tonsil / immunology. T-
Lymphocytes
/ cytology. T-
Lymphocytes
/ enzymology. T-
Lymphocytes
/ immunology
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(PMID = 16482508.001).
[ISSN]
0014-2980
[Journal-full-title]
European journal of immunology
[ISO-abbreviation]
Eur. J. Immunol.
[Language]
eng
[Grant]
United States / NCRR NIH HHS / RR / M01 RR018535; United States / NCI NIH HHS / CA / R01 CA 81554; United States / NCI NIH HHS / CA / R01 CA 87956
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, CD5; 0 / Immunoglobulin D; 0 / Membrane Glycoproteins; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
7.
Allgeier T, Garhammer S, Nössner E, Wahl U, Kronenberger K, Dreyling M, Hallek M, Mocikat R:
Dendritic cell-based immunogens for B-cell chronic lymphocytic leukemia.
Cancer Lett
; 2007 Jan 8;245(1-2):275-83
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[Title]
Dendritic
cell
-based immunogens for B-
cell chronic
lymphocytic
leukemia
.
Hybrids generated from tumor cells and dendritic cells (DC) have been proposed as tools for treating malignant
disease
.
Here, we study the underlying principles and the feasibility for the adjuvant therapy of human
B cell chronic
-
lymphocytic
leukemia
(B-
CLL
).
CLL
cells and allogeneic DC were only mixed or additionally fused.
Using a combination of FACS and fluorescence microscopic analyses, we show that DC-
CLL
hybrids can be successfully generated.
We made a systematic comparison of the immunostimulatory capacities of different stimulator
cell
populations, including DC-
CLL
fusion samples, unfused mixtures of DC and
CLL
cells as
well
as DC or tumor cells alone.
This could be explained by the capture of antigens from surrounding
leukemia
cells by DC during co-cultivation.
Although fusion frequencies were
low
, PBMC stimulation was significantly more effective when the mixtures were subjected to
cell
fusion.
The most potent stimulus was provided by DC-
CLL
fusion samples derived from mature DC, probably due to their enhanced costimulatory capacity.
In summary, DC-tumor
cell
hybrids might be feasible in the treatment of B-
CLL
.
It should be considered that FACS analysis is not sufficient to assess fusion frequencies and that interactions between unfused DC and
CLL
cells also result in PBMC activation.
[MeSH-major]
Dendritic Cells / immunology.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ immunology
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.
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(PMID = 16516377.001).
[ISSN]
0304-3835
[Journal-full-title]
Cancer letters
[ISO-abbreviation]
Cancer Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD11c; 0 / Antigens, CD19; 0 / Antigens, CD3; 0 / Antigens, CD5; 0 / Antigens, CD80; 0 / Antigens, CD86; 0 / CD83 antigen; 0 / HLA-DR Antigens; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
8.
Delgado J, Pillai S, Phillips N, Brunet S, Pratt G, Briones J, Lovell R, Martino R, Ewing J, Sureda A, Milligan DW, Sierra J:
Does reduced-intensity allogeneic transplantation confer a survival advantage to patients with poor prognosis chronic lymphocytic leukaemia? A case-control retrospective analysis.
Ann Oncol
; 2009 Dec;20(12):2007-12
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[Title]
Does reduced-intensity allogeneic transplantation confer a survival advantage to patients with poor prognosis
chronic
lymphocytic leukaemia
? A case-control retrospective analysis.
BACKGROUND: Reduced-intensity conditioning (RIC) allogeneic haemopoietic
cell
transplantation (allo-HCT) is increasingly considered as a therapeutic option for younger patients with poor-risk
chronic
lymphocytic leukaemia
(
CLL
).
In this retrospective analysis, we assessed the outcomes
of CLL
patients undergoing RIC allo-HCT compared with a group of matched controls that were candidates for transplantation but did not have a suitable donor or refused the procedure.
Haemopoietic
cell
grafts were harvested from HLA-matched siblings (27) and unrelated donors (7).
Matching variables were age at
diagnosis
and time to first
CLL
-specific therapy.
RESULTS: Both patient groups were
well
balanced in terms of cytogenetics by FISH, CD38 and ZAP-70 expression, and immunoglobulin heavy-chain variable region mutational status.
Median overall survival was 113 months for HCT patients and 85 months for controls when calculated from time
of diagnosis
(P = 0.072) and 103 and 67 months, respectively, when calculated from time of first therapy (P = 0.041).
CONCLUSION: RIC allo-HCT is a reasonable option for patients with high-risk
CLL
.
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(PMID = 19596701.001).
[ISSN]
1569-8041
[Journal-full-title]
Annals of oncology : official journal of the European Society for Medical Oncology
[ISO-abbreviation]
Ann. Oncol.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
England
9.
Omoti CE, Awodu OA, Bazuaye GN:
Chronic lymphoid leukaemia: clinico-haematological correlation and outcome in a single institution in Niger Delta region of Nigeria.
Int J Lab Hematol
; 2007 Dec;29(6):426-32
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[Title]
Chronic lymphoid
leukaemia
: clinico-haematological correlation and outcome
in a
single institution in Niger Delta region of Nigeria.
Sixty patients were prospectively studied with the aim of analyzing the clinical and laboratory features and outcome of patients diagnosed with
chronic
lymphocytic leukaemia
(
CLL
)
in a
major referral center in Niger Delta region of Nigeria for 10 years (1995-2005).
The peripheral blood, bone marrow cytology, clinical features and stage at
diagnosis
were studied.
The
CLL
incidence was 36.4% of total
leukaemias
.
There was a strong association between the blood counts at
diagnosis
and outcome of therapy.
The 2-year survival for young (&
lt
;55 years) and older (>55 years)
CLL
patients was 27.2% and 28.9%, respectively, which is still very poor because
of a
number of strong limiting factors.
CLL
is not rare in Southern Nigeria and its presentations are similar to cases seen worldwide.
[MeSH-major]
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ mortality
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(PMID = 17988297.001).
[ISSN]
1751-5521
[Journal-full-title]
International journal of laboratory hematology
[ISO-abbreviation]
Int J Lab Hematol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
10.
Zenz T, Benner A, Döhner H, Stilgenbauer S:
Chronic lymphocytic leukemia and treatment resistance in cancer: the role of the p53 pathway.
Cell Cycle
; 2008 Dec 15;7(24):3810-4
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[Title]
Chronic
lymphocytic
leukemia
and treatment resistance in cancer: the role of the p53 pathway.
The importance of studying p53 pathway defects
in CLL
has been fostered by the demonstration of the fundamentally different clinical course of patients with 17p deletion, where the clinical course is, contrary to most patients with
CLL
, very poor.
The demonstration of the resistance to chemotherapy and mutation of the remaining TP53 allele explains the clinical presentation
of CLL
with 17p deletion.
Here we review recent evidence that TP53 mutation in the absence of the deletion of 17p shows a similar clinical and biological course
in CLL
.
[MeSH-major]
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ drug therapy.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics. Tumor Suppressor Protein p53 / genetics
[MeSH-minor]
Ataxia Telangiectasia Mutated Proteins.
Cell
Cycle Proteins / genetics. Chromosomes, Human, Pair 17. DNA Damage. DNA-Binding Proteins / genetics. Drug Resistance, Neoplasm. Gene Deletion. Humans. MicroRNAs / genetics. Protein-Serine-Threonine Kinases / genetics. Survival Analysis. Tumor Suppressor Proteins / genetics
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.
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(PMID = 19098429.001).
[ISSN]
1551-4005
[Journal-full-title]
Cell cycle (Georgetown, Tex.)
[ISO-abbreviation]
Cell Cycle
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / MicroRNAs; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
[Number-of-references]
37
11.
Liu L, Yang C, Herzog C, Seth R, Kaushal GP:
Proteasome inhibitors prevent cisplatin-induced mitochondrial release of apoptosis-inducing factor and markedly ameliorate cisplatin nephrotoxicity.
Biochem Pharmacol
; 2010 Jan 15;79(2):137-46
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We demonstrate the effect of proteasome inhibitors in mitochondrial release of apoptosis-inducing factor (AIF) in cisplatin-exposed renal tubular epithelial cells (
LLC
-PK(1) cells) and
in a
model of cisplatin nephrotoxicity.
Downregulation of Mcl-1 by
small
interfering RNA promoted Bax activation and cytochrome c and AIF release, suggesting that cisplatin-induced Mcl-1 depletion and associated Bax activation are involved in the release of AIF.
[MeSH-minor]
Animals. Blotting, Western. Immunoprecipitation.
LLC
-PK1 Cells. Male. Mice. Mice, Inbred C57BL. Swine
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(PMID = 19699182.001).
[ISSN]
1873-2968
[Journal-full-title]
Biochemical pharmacology
[ISO-abbreviation]
Biochem. Pharmacol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; Q20Q21Q62J / Cisplatin
12.
Novaretti MC, Domingues AE, Manhani R, Pinto EM, Dorlhiac-Llacer PE, Chamone DA:
ABO genotyping in leukemia patients reveals new ABO variant alleles.
Genet Mol Res
; 2008;7(1):87-94
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[Title]
ABO genotyping in
leukemia
patients reveals new ABO variant alleles.
The aim of the present study was to perform ABO genotyping in patients with
leukemia
.
Blood samples were collected from 108 Brazilian patients with
chronic
myeloid
leukemia
(N = 69),
chronic lymphoid leukemia
(N = 13), acute myeloid
leukemia
(N = 15), and acute
lymphoid leukemia
(N = 11).
We identified 22 new ABO*variants in the coding region of the ABO gene in 25 individuals with
leukemia
(23.2%).
The majority of ABO variants was detected
in O
alleles (15/60.0%).
Elucidation of the diversity of this gene in
leukemia
and in other diseases is important for the determination of the effect of changes in an amino acid residue on the specificity and activity of ABO glycosyltransferases and their function.
In conclusion, this is the first report
of a
large number of patients with
leukemia
genotyped for ABO.
The findings of this study indicate that there is a high level of recombinant activity in the ABO gene in
leukemia
patients, revealing new ABO variants.
[MeSH-major]
ABO Blood-Group System / genetics. Alleles. Genetic Variation.
Leukemia
/ blood
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(PMID = 18273824.001).
[ISSN]
1676-5680
[Journal-full-title]
Genetics and molecular research : GMR
[ISO-abbreviation]
Genet. Mol. Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Brazil
[Chemical-registry-number]
0 / ABO Blood-Group System; 9007-49-2 / DNA
13.
Gintowt AA, Germer JJ, Mitchell PS, Yao JD:
Evaluation of the MagNA Pure LC used with the TRUGENE HBV Genotyping Kit.
J Clin Virol
; 2005 Oct;34(2):155-7
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BACKGROUND: The current manual sample processing method recommended for use with the TRUGENE HBV Genotyping Kit (TRUGENE HBV; Bayer HealthCare
LLC
, Tarrytown, NY) is labor-intensive and may be prone to specimen cross-contamination.
Performance of TRUGENE HBV used in conjunction with MP sample processing was evaluated further using 22 clinical serum specimens containing
low
titers of HBV DNA.
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(PMID = 16023890.001).
[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]
Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / DNA, Viral
14.
Rhyu DY, Kang KS, Sekiya M, Tanaka T, Park JC, Yokozawa T:
Active compounds isolated from traditional Chinese prescription Wen-Pi-Tang protecting against peroxynitrite-induced LLC-PK(1) cell damage.
Am J Chin Med
; 2008;36(4):761-70
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[Title]
Active compounds isolated from traditional Chinese prescription Wen-Pi-Tang protecting against peroxynitrite-induced
LLC
-PK(1)
cell
damage.
Wen-Pi-Tang, a traditional Chinese prescription, has been widely used for the treatment of patients with moderate
chronic
renal failure in China.
Although the protective effect of Wen-Pi-Tang on peroxynitrite (ONOO(-))-induced renal tubular epithelial
LLC
-PK(1)
cell
damage was elucidated in our previous research, the active components of Wen-Pi-Tang have not yet been fully clarified.
Therefore, the major bioactivity of Wen-Pi-Tang against ONOO(-)-induced cytotoxicity
in LLC
-PK(1) cells was thought to be mediated by (+)-catechin.
Although we cannot disregard the synergetic effect of various components in Wen-Pi-Tang, (+)-catechin is a major active compound protecting against ONOO(-)-induced
LLC
-PK(1)
cell
damage and may be used as an index to qualify the ONOO(-)-inhibitory activity of Wen-Pi-Tang extract.
[MeSH-minor]
Animals.
Cell
Line. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Epithelial Cells / pathology. Free Radicals / metabolism. Molsidomine / analogs & derivatives. Molsidomine / pharmacology. Nitric Oxide Donors / pharmacology. Swine
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(PMID = 18711772.001).
[ISSN]
0192-415X
[Journal-full-title]
The American journal of Chinese medicine
[ISO-abbreviation]
Am. J. Chin. Med.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Singapore
[Chemical-registry-number]
0 / Drugs, Chinese Herbal; 0 / Free Radicals; 0 / Nitric Oxide Donors; 0 / wen-pi-tang; 14691-52-2 / Peroxynitrous Acid; 5O5U71P6VQ / linsidomine; 8R1V1STN48 / Catechin; D46583G77X / Molsidomine
15.
Iglesias-Serret D, Piqué M, Barragán M, Cosialls AM, Santidrián AF, González-Gironès DM, Coll-Mulet L, de Frias M, Pons G, Gil J:
Aspirin induces apoptosis in human leukemia cells independently of NF-kappaB and MAPKs through alteration of the Mcl-1/Noxa balance.
Apoptosis
; 2010 Feb;15(2):219-29
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[Title]
Aspirin induces apoptosis in human
leukemia
cells independently of NF-kappaB and MAPKs through alteration of the Mcl-1/Noxa balance.
Aspirin and other non-steroidal anti-inflammatory drugs induce apoptosis in most
cell
types.
In this study we examined the mechanism of aspirin-induced apoptosis in human
leukemia
cells.
Our results show that aspirin induced apoptosis in
leukemia
Jurkat T cells independently of NF-kappaB.
This alteration of the Mcl-1/Noxa balance was also found in other
leukemia cell
lines and primary
chronic
lymphocytic
leukemia
cells (
CLL
).
Furthermore,
in CLL
cells aspirin induced an increase in the protein levels of Noxa.
[MeSH-major]
Apoptosis / drug effects. Aspirin / pharmacology.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ enzymology. Mitogen-Activated Protein Kinases / metabolism. NF-kappa B / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism
[MeSH-minor]
Apoptosis Regulatory Proteins / metabolism.
Cell
Line, Tumor.
Cell
Survival / drug effects. Cycloheximide / pharmacology. Cytochromes c / secretion. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. MAP Kinase Kinase Kinases / metabolism. Mitochondria / drug effects. Mitochondria / secretion. Myeloid
Cell Leukemia
Sequence 1 Protein. Proto-Oncogene Proteins / metabolism
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(PMID = 19936928.001).
[ISSN]
1573-675X
[Journal-full-title]
Apoptosis : an international journal on programmed cell death
[ISO-abbreviation]
Apoptosis
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / BBC3 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / NF-kappa B; 0 / PMAIP1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 9007-43-6 / Cytochromes c; 98600C0908 / Cycloheximide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP3K8 protein, human; R16CO5Y76E / Aspirin
16.
Mailloux AW, Clark AM, Young MR:
NK depletion results in increased CCL22 secretion and Treg levels in Lewis lung carcinoma via the accumulation of CCL22-secreting CD11b+CD11c+ cells.
Int J Cancer
; 2010 Dec 1;127(11):2598-611
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Previous studies demonstrated that NK-dependant increases in CCL22 secretion selectively recruit Tregs toward murine lungs bearing Lewis Lung Carcinoma (
LLC
).
To extend the in vitro studies, the present studies utilized in vivo depletion of NK cells to ascertain the contribution of NK-derived CCL22 toward total CCL22 and subsequent Treg levels in both normal and
LLC
-bearing lungs.
However, NK depletion had the unexpected effect of increasing both CCL22 secretion and Treg levels in the lungs of NK-depleted
LLC
-bearing mice.
Flow cytometry and a series of both immunomagnetic and FACS isolations were used to identify the CCL22-producing cellular fractions
in LLC
-bearing lungs.
A novel CD11b(+)CD11c(+)
cell
population was identified that accumulates in large numbers in NK-depleted
LLC
-bearing lung tissue.
These CD11b(+)CD11c(+) cells secreted large amounts of CCL22 that may overcompensate for the loss of NK-derived CCL22 in the lungs of NK-depleted
LLC
-bearing mice.
Taken together, these data suggest that NK cells play both a positive and negative role in the regulation of CCL22 secretion and, in turn, the recruitment of Tregs toward
LLC
-bearing lungs.
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[Cites]
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]
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]
[Cites]
Blood. 2001 Mar 15;97(6):1733-41
[
11238115.001
]
(PMID = 20198623.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01CA8566; United States / NIDCR NIH HHS / DE / R01 DE018168-02; United States / NCI NIH HHS / CA / 1R01CA128837; United States / NCI NIH HHS / CA / R01 CA085266-06; United States / NCI NIH HHS / CA / R01 CA085266; United States / NIDCR NIH HHS / DE / R01DE018168; United States / NIDCR NIH HHS / DE / R01 DE018168; United States / NCI NIH HHS / CA / CA128837-01A2; United States / NCI NIH HHS / CA / R01 CA128837; United States / NCI NIH HHS / CA / R01 CA128837-01A2; United States / NIDCR NIH HHS / DE / DE018168-02
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD11b; 0 / Antigens, CD11c; 0 / CCL22 protein, human; 0 / Chemokine CCL22; 37758-47-7 / G(M1) Ganglioside; 71012-19-6 / asialo GM1 ganglioside
[Other-IDs]
NLM/ NIHMS189166; NLM/ PMC2947555
17.
Fallah-Arani F, Schweighoffer E, Vanes L, Tybulewicz VL:
Redundant role for Zap70 in B cell development and activation.
Eur J Immunol
; 2008 Jun;38(6):1721-33
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[Title]
Redundant role for Zap70 in
B cell
development and activation.
Expression of the Syk family tyrosine kinase Zap70 is strongly correlated with poor clinical outcome in
chronic
lymphocytic
leukemia
, the most common human
leukemia
characterized by
B cell
accumulation.
The expression of Zap70 may reflect the specific
cell
of origin of the tumor or may contribute to pathology.
Thus, the normal role of Zap70 in
B cell
physiology is of great interest.
While initial studies reported that Zap70 expression in the mouse was
limited
to T and NK cells, more recent work has shown expression in early
B cell
progenitors and in splenic B cells, suggesting that the kinase may play a role in the development or activation of B cells.
In this study, we show that Zap70 is expressed in all developing subsets of B cells as
well
as in recirculating B cells, marginal zone B cells and peritoneal B1 cells.
[MeSH-major]
B-
Lymphocytes
/ metabolism.
Cell
Differentiation. ZAP-70 Protein-Tyrosine Kinase / metabolism
[MeSH-minor]
Animals. B-Lymphocyte Subsets / cytology. B-Lymphocyte Subsets / metabolism. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Calcium Signaling / physiology.
Cell
Proliferation. Flow Cytometry. Hemocyanin / immunology. Immunoblotting. Intracellular Signaling Peptides and Proteins / deficiency. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / metabolism. Lymphocyte Activation. Mice. Mice, Inbred C57BL. Mice, Inbred Strains. Mice, Knockout. Mice, Mutant Strains. Mice, Transgenic. Peritoneal Cavity / cytology. Precursor Cells, B-
Lymphoid
/ cytology. Precursor Cells, B-
Lymphoid
/ metabolism. Protein-Tyrosine Kinases / deficiency. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism. Receptors, Antigen, B-
Cell
/ physiology. Spleen / cytology. Spleen / immunology. Syk Kinase. Vaccination
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(PMID = 18465772.001).
[ISSN]
0014-2980
[Journal-full-title]
European journal of immunology
[ISO-abbreviation]
Eur. J. Immunol.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / MC/ U117527252; United Kingdom / Medical Research Council / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Intracellular Signaling Peptides and Proteins; 0 / Receptors, Antigen, B-Cell; 0 / trinitrophenyl keyhole limpet hemocyanin; 9013-72-3 / Hemocyanin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / SYK protein, human; EC 2.7.10.2 / Syk Kinase; EC 2.7.10.2 / Syk protein, mouse; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / Zap70 protein, mouse
18.
Coscia G, Vaccara E, Corvisiero R, Cavazzani P, Ruggieri FG, Taccini G:
Fractionated stereotactic radiotherapy: a method to evaluate geometric and dosimetric uncertainties using radiochromic films.
Med Phys
; 2009 Jul;36(7):2870-80
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The comparison between the dose distributions measured on films and computed by TPS, after a precise image registration procedure performed by a commercial piece of software (FILMQA, 3cognition
LLC
(Division of ISP), Wayne, NJ), allowed the authors to measure the repositioning errors, obtaining about 0.5 mm in case of central spherical PTV and about 1.5 mm in case of peripheral irregular PTV.
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(PMID = 19673186.001).
[ISSN]
0094-2405
[Journal-full-title]
Medical physics
[ISO-abbreviation]
Med Phys
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
19.
Reid-Nicholson M, Kavuri S, Ustun C, Crawford J, Nayak-Kapoor A, Ramalingam P:
Plasmablastic lymphoma: Cytologic findings in 5 cases with unusual presentation.
Cancer
; 2008 Oct 25;114(5):333-41
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[Title]
Plasmablastic
lymphoma
: Cytologic findings in 5 cases with unusual presentation.
BACKGROUND: Plasmablastic
lymphoma
(PBL) is a rare form of non-Hodgkin
lymphoma
that was once believed to occur primarily in the oral cavity of human immunodeficiency virus-positive individuals.
The presence of the following was evaluated: cellularity, plasmablastic cells, background necrosis (BN), single-
cell
necrosis (SCN), lymphoglandular bodies (LGB), tingible-body macrophages (TBM), 3-dimensional clusters/sheets, and cytoplasmic vacuoles.
Two patients had the acquired immunodeficiency syndrome and 3 had second non-PBL related malignancies including endometrial carcinoma, lung adenocarcinoma, and
small lymphocytic lymphoma
.
However, although these findings may suggest PBL, a definitive
diagnosis
requires adjunctive studies including immunohistochemistry and flow cytometry.
[MeSH-major]
Lymphoma
, Non-Hodgkin / metabolism.
Lymphoma
, Non-Hodgkin / pathology
HIV InSite.
treatment guidelines - Human Herpesvirus-8
.
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[Copyright]
(c) 2008 American Cancer Society.
(PMID = 18683216.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
20.
Amagase H, Nance DM:
A randomized, double-blind, placebo-controlled, clinical study of the general effects of a standardized Lycium barbarum (Goji) Juice, GoChi.
J Altern Complement Med
; 2008 May;14(4):403-12
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[Title]
A randomized, double-blind, placebo-controlled, clinical study of the general effects
of a
standardized Lycium barbarum (Goji) Juice, GoChi.
BACKGROUND: This randomized, double-blind, placebo-controlled clinical trial is the first study reported from outside China that has examined the general effects of the orally consumed goji berry, Lycium barbarum, as a standardized juice (GoChi; FreeLife International
LLC
, Phoenix, AZ) to healthy adults for 14 days.
METHODS: Based upon the medicinal properties of Lycium barbarum in traditional Asian medicine, we examined by questionnaire subjective ratings (0-5) of general feelings
of well
-being, neurologic/psychologic traits, gastrointestinal, musculoskeletal, and cardiovascular complaints as
well
as any adverse effects.
CONCLUSIONS: These results clearly indicate that daily consumption of GoChi for 14 days increases subjective feelings of general
well
-being, and improves neurologic/psychologic performance and gastrointestinal functions.
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.
The Lens.
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.
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(PMID = 18447631.001).
[ISSN]
1075-5535
[Journal-full-title]
Journal of alternative and complementary medicine (New York, N.Y.)
[ISO-abbreviation]
J Altern Complement Med
[Language]
eng
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Neuroprotective Agents; 0 / Plant Extracts
21.
John R, Liao K, Lietz K, Kamdar F, Colvin-Adams M, Boyle A, Miller L, Joyce L:
Experience with the Levitronix CentriMag circulatory support system as a bridge to decision in patients with refractory acute cardiogenic shock and multisystem organ failure.
J Thorac Cardiovasc Surg
; 2007 Aug;134(2):351-8
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We review our experience with the use of the CentriMag (Levitronix
LLC
, Waltham, Mass) circulatory support system in such patients whose neurologic status was uncertain.
Thus, for our 12 study patients,
long
-term survival was 75% at 1 month and 62.5% at 1 year.
By using this strategy, we avoided the urgent placement of expensive
long
-term ventricular assist devices in hemodynamically unstable patients with multisystem organ failure whose neurologic status was uncertain until end-organ recovery and excellent hemodynamic stability were achieved with the relatively inexpensive short-term CentriMag circulatory support system.
[MeSH-minor]
Acute
Disease
. Analysis of Variance. Decision Making. Heart Transplantation / statistics & numerical data. Humans. Male. Middle Aged. Survival Analysis. Treatment Outcome
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[CommentIn]
J Thorac Cardiovasc Surg. 2008 Mar;135(3):717; author reply 717-8
[
18329513.001
]
(PMID = 17662772.001).
[ISSN]
1097-685X
[Journal-full-title]
The Journal of thoracic and cardiovascular surgery
[ISO-abbreviation]
J. Thorac. Cardiovasc. Surg.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
22.
Peeters MY, Prins SA, Knibbe CA, Dejongh J, Mathôt RA, Warris C, van Schaik RH, Tibboel D, Danhof M:
Pharmacokinetics and pharmacodynamics of midazolam and metabolites in nonventilated infants after craniofacial surgery.
Anesthesiology
; 2006 Dec;105(6):1135-46
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Population pharmacokinetic and pharmacodynamic modeling was performed using NONMEM V (GloboMax
LLC
, Hanover, MD).
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.
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Midazolam
.
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(PMID = 17122576.001).
[ISSN]
0003-3022
[Journal-full-title]
Anesthesiology
[ISO-abbreviation]
Anesthesiology
[Language]
eng
[Publication-type]
Journal Article; Randomized Controlled Trial
[Publication-country]
United States
[Chemical-registry-number]
0 / Hypnotics and Sedatives; R60L0SM5BC / Midazolam
23.
Morotti A, Cilloni D, Parvis G, Guerrasio A, Saglio G:
Thalidomide-induced partial stable remission in a case of refractory progressive B Cell Chronic Lymphoid Leukemia.
Leuk Res
; 2008 Mar;32(3):506-7
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[Title]
Thalidomide-induced partial stable remission
in a
case of refractory progressive
B Cell Chronic Lymphoid Leukemia
.
[MeSH-major]
Leukemia
, B-
Cell
/ drug therapy. Thalidomide / therapeutic use
Genetic Alliance.
consumer health - Leukemia, B-cell, chronic
.
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.
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THALIDOMIDE
.
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(PMID = 17544506.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
[Chemical-registry-number]
4Z8R6ORS6L / Thalidomide
24.
Goldenberg MM:
Pharmaceutical approval update.
P T
; 2008 May;33(5):299-302
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Topics include bendamustine (Treanda) for
chronic
lymphocytic
leukemia
, hepatitis B immune globulin (HepaGam B) to prevent hepatitis B infection following liver transplantation, and a fibrin sealant (Artiss) used in skin graft surgery for burn patients.
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(PMID = 19561795.001).
[ISSN]
1052-1372
[Journal-full-title]
P & T : a peer-reviewed journal for formulary management
[ISO-abbreviation]
P T
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2683604
25.
Morrison VA:
Management of infectious complications in patients with chronic lymphocytic leukemia.
Hematology Am Soc Hematol Educ Program
; 2007;:332-8
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[Title]
Management of infectious complications in patients with
chronic
lymphocytic
leukemia
.
Infections remain a major cause of morbidity and mortality in patients with
chronic
lymphocytic
leukemia
(
CLL
).
The pathogenesis of these complications is related to immune defects inherent to the primary
disease
as
well
as to therapy-related immunosuppression.
The spectrum of infections seen has evolved with the therapeutic use of purine analogs, which induce specific cellular immune defects, as
well
as the monoclonal antibodies alemtuzumab and rituximab.
This overview will summarize the pathogenesis of infection in patients with
CLL
as
well
as the spectrum of infection and approaches to the prophylactic and therapeutic management of these complications.
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(PMID = 18024648.001).
[ISSN]
1520-4391
[Journal-full-title]
Hematology. American Society of Hematology. Education Program
[ISO-abbreviation]
Hematology Am Soc Hematol Educ Program
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
63
26.
Lamanna N, Jurcic JG, Noy A, Maslak P, Gencarelli AN, Panageas KS, Heaney ML, Brentjens RJ, Golde DW, Scheinberg DA, Zelenetz AD, Weiss MA:
Sequential therapy with fludarabine, high-dose cyclophosphamide, and rituximab in previously untreated patients with chronic lymphocytic leukemia produces high-quality responses: molecular remissions predict for durable complete responses.
J Clin Oncol
; 2009 Feb 01;27(4):491-7
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[Title]
Sequential therapy with fludarabine, high-dose cyclophosphamide, and rituximab in previously untreated patients with
chronic
lymphocytic
leukemia
produces high-quality responses: molecular remissions predict for durable complete responses.
PURPOSE: Modern combination strategies are active in
chronic
lymphocytic
leukemia
(
CLL
) but can have significant myelosuppression and immunosuppression that may require dose attenuation for safety.
In that study, cyclophosphamide consolidation improved the frequency of complete response (
CR
) four-fold.
PATIENTS AND METHODS: Thirty-six previously untreated
CLL
patients received therapy with fludarabine 25 mg/m(2) on days 1 through 5 every 4 weeks for six cycles, followed by consolidation with cyclophosphamide 3,000 mg/m(2) administered every 3 weeks for three cycles, followed by consolidation with weekly rituximab 375 mg/m(2) for four cycles.
Evaluation for minimal residual
disease
included flow cytometry and a highly sensitive clonotypic polymerase chain reaction (PCR).
The median age was 59 years (range, 37 to 71 years), 61% of patients had high-risk
disease
, and 58% had unmutated IgV(H) genes.
Twenty patients (56%) achieved flow cytometric CRs, and 12 patients (33%) achieved a molecular
CR
(PCR negative).
Patients achieving molecular CRs had an excellent prognosis with a plateau in the response duration curve, and 90% remain in clinical
CR
at 5 years.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / administration & dosage.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ drug therapy
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.
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Hazardous Substances Data Bank.
RITUXIMAB
.
Hazardous Substances Data Bank.
FLUDARABINE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
VIDARABINE
.
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[CommentIn]
J Clin Oncol. 2009 Feb 1;27(4):479-80
[
19075263.001
]
(PMID = 19075280.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA008748; United States / NIAID NIH HHS / AI / R01 AI067823; United States / NCI NIH HHS / CA / R01 CA67823
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
[Other-IDs]
NLM/ PMC2645858
27.
Kujawski L, Ouillette P, Erba H, Saddler C, Jakubowiak A, Kaminski M, Shedden K, Malek SN:
Genomic complexity identifies patients with aggressive chronic lymphocytic leukemia.
Blood
; 2008 Sep 1;112(5):1993-2003
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[Title]
Genomic complexity identifies patients with aggressive
chronic
lymphocytic
leukemia
.
Chronic
lymphocytic
leukemia
(
CLL
) has a variable clinical course.
Presence of specific genomic aberrations has been shown to impact survival outcomes and can help categorize
CLL
into clinically distinct subtypes.
We studied 178
CLL
patients enrolled
in a
prospective study at the University of Michigan, of whom 139 and 39 were previously untreated and previously treated, respectively.
Genomic complexity scores were derived and correlated with the surrogate clinical end points time to first therapy (TTFT) and time to subsequent therapy (TTST): measures
of disease
aggressiveness and/or therapy efficaciousness.
In univariate analysis, progressively increasing complexity scores in previously untreated
CLL
patients identified patients with short TTFT at high significance levels.
Similarly, TTST was significantly shorter in pretreated patients with high as opposed to
low
genomic complexity.
Finally, algorithmic subchromosomal complexity determination was developed, facilitating automation and future routine clinical application
of CLL
whole-genome analysis.
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[CommentIn]
Blood. 2008 Sep 1;112(5):1550
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18725569.001
]
(PMID = 18436738.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / R21 CA124420; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / R21 CA124420-01A1
[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 / Immunoglobulin Heavy Chains; 0 / Membrane Glycoproteins; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
[Other-IDs]
NLM/ PMC2518900
28.
Ruddy KJ, Wu D, Brown JR:
Pseudohyperkalemia in chronic lymphocytic leukemia.
J Clin Oncol
; 2008 Jun 1;26(16):2781-2
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[Title]
Pseudohyperkalemia in
chronic
lymphocytic
leukemia
.
[MeSH-major]
Hyperkalemia /
diagnosis
.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ blood
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(PMID = 18509189.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
29.
Zhang H, Luo XQ, Zhang P, Huang LB, Zheng YS, Wu J, Zhou H, Qu LH, Xu L, Chen YQ:
MicroRNA patterns associated with clinical prognostic parameters and CNS relapse prediction in pediatric acute leukemia.
PLoS One
; 2009;4(11):e7826
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[Title]
MicroRNA patterns associated with clinical prognostic parameters and CNS relapse prediction in pediatric acute
leukemia
.
BACKGROUND: Recent reports have indicated that microRNAs (miRNAs) play a critical role in malignancies, and regulations in the progress of adult
leukemia
.
The role of miRNAs in pediatric
leukemia
still needs to be established.
The purpose of this study was to investigate the aberrantly expressed miRNAs in pediatric acute
leukemia
and demonstrate miRNA patterns that are pediatric-specific and prognostic parameter-associated.
The most highly expressed miRNAs in pediatric ALL were miR-34a, miR-128a, miR-128b, and miR-146a, while the highly expressed miRNAs in pediatric AML were miR-100, miR-125b, miR-335, miR-146a, and miR-99a, which are significantly different from those reported for adult
CLL
and AML. miR-125b and miR-126 may serve as favorable prognosticators for M3 and M2 patients, respectively.
CONCLUSIONS/SIGNIFICANCE: There are existing pediatric-associated and prognostic parameter-associated miRNAs that are independent of
cell
lineage and could provide therapeutic direction for individual risk-adapted therapy for pediatric
leukemia
patients.
[MeSH-major]
Central Nervous System Neoplasms /
diagnosis
.
Leukemia
/
diagnosis
.
Leukemia
/ pathology. MicroRNAs
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[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
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United States
[Chemical-registry-number]
0 / MicroRNAs
[Other-IDs]
NLM/ PMC2773830
30.
Dennison JB, Ayres ML, Kaluarachchi K, Plunkett W, Gandhi V:
Intracellular succinylation of 8-chloroadenosine and its effect on fumarate levels.
J Biol Chem
; 2010 Mar 12;285(11):8022-30
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8-Chloroadenosine (8-Cl-Ado) is a ribosyl nucleoside analog currently in phase I testing for the treatment of
chronic
lymphocytic
leukemia
(
CLL
).
In the current study with four mantle
cell
lymphoma
cell
lines, we report a new major metabolic pathway for 8-Cl-Ado intracellular metabolism, the formation of succinyl-8-chloro-adenosine (S-8-Cl-Ado) and its monophosphate (S-8-Cl-AMP).
Consistent with fumarate as a required substrate for formation of succinyl-8-Cl-adenylate metabolites, the S-8-Cl-adenylate concentrations in multiple
cell
lines were associated with fumarate loss.
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]
[Cites]
Cancer Res. 2007 Oct 15;67(20):9913-20
[
17942923.001
]
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Mol Cell Proteomics. 2009 Jan;8(1):70-85
[
18723843.001
]
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Mol Cancer Ther. 2009 Mar;8(3):626-35
[
19276158.001
]
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Diabetes Obes Metab. 2009 May;11 Suppl 2:3-8
[
19385978.001
]
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Science. 2009 May 22;324(5930):1029-33
[
19460998.001
]
[Cites]
J Clin Oncol. 2009 Jul 10;27(20):3297-302
[
19487376.001
]
[Cites]
Mol Cell Biol. 2009 Aug;29(15):4080-90
[
19470762.001
]
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[
19477165.001
]
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[
19709085.001
]
[Cites]
J Inherit Metab Dis. 2000 Jun;23(4):371-4
[
10896297.001
]
(PMID = 20064937.001).
[ISSN]
1083-351X
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA085915; United States / NCI NIH HHS / CA / CA 85915; United States / NCI NIH HHS / CA / CA136411; United States / NCI NIH HHS / CA / P50 CA136411
[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 / Antineoplastic Agents; 0 / Fumarates; 0 / Hypoglycemic Agents; 0 / Oligomycins; 0 / Purines; 0 / Uncoupling Agents; 146-77-0 / 2-Chloroadenosine; 23583-48-4 / 8-Bromo Cyclic Adenosine Monophosphate; 34408-14-5 / 8-chloroadenosine; 41941-56-4 / 8-chloro-cyclic adenosine monophosphate; 9100L32L2N / Metformin; AB6MNQ6J6L / Succinic Acid
[Other-IDs]
NLM/ PMC2832953
31.
Sweeney N, Gallagher WM, Müller-Bunz H, Pampillón C, Strohfeldt K, Tacke M:
Heteroaryl substituted titanocenes as potential anti-cancer drugs.
J Inorg Biochem
; 2006 Sep;100(9):1479-86
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When titanocenes 3a-c were tested against pig kidney (
LLC
-PK) cells inhibitory concentrations (IC(50)) of 1.6x10(-4)M, 1.5x10(-4)M and 9.1x10(-4)M, respectively, were observed.
These values represent improved cytotoxicity against
LLC
-PK, when compared to their corresponding ansa substituted analogues and also in comparison to unsubstituted titanocene dichloride.
[MeSH-minor]
Animals.
Cell
Line.
Cell
Survival. Drug Evaluation, Preclinical. Molecular Conformation. Molecular Structure. Swine
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(PMID = 16764931.001).
[ISSN]
0162-0134
[Journal-full-title]
Journal of inorganic biochemistry
[ISO-abbreviation]
J. Inorg. Biochem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Organometallic Compounds; 1271-29-0 / titanocene
32.
Yu Z, Sun B, Kantarjian HM, Keating MJ, Amin HM, Sun X:
Protein expression profiling of cytokines and cytokine receptors on purified chronic lymphocytic leukemia cells from patients with favourable prognostic indicators.
Leuk Lymphoma
; 2008 Apr;49(4):751-6
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[Title]
Protein expression profiling of cytokines and cytokine receptors on purified
chronic
lymphocytic
leukemia
cells from patients with favourable prognostic indicators.
Chronic
lymphocytic
leukemia
(
CLL
) cells rapidly undergo apoptosis when cultured in vitro, which contrasts with their prolonged survival in vivo.
Multiple cytokines and cytokine receptors are believed to work together to regulate the survival
of CLL
cells.
The aim of the current study was to measure the endogenous expression and secretion of cytokines and cytokine receptors
in CLL
cells when exogenous cytokines are minimized.
We demonstrated that the intracellular and secreted levels of 174 cytokines and cytokine receptors of purified
CLL
B-cells were not significantly different from those of normal B-cells except for the secreted levels of IL-6 and eotaxin.
IL-6 was 3.0 times lower (p = 0.038) whereas eotaxin was 2.2 times higher (p = 0.027)
in CLL
conditioned medium than in normal B-
cell
conditioned medium.
Our results suggest that, except for IL-6 and eotaxin,
CLL
B-cells and their normal counterparts produce and secrete similar amounts of cytokines and cytokine receptors in vitro.
[MeSH-major]
Cytokines / analysis.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ pathology. Receptors, Cytokine / analysis
[MeSH-minor]
Adult. Aged. B-
Lymphocytes
/ secretion. Case-Control Studies. Cells, Cultured. Chemokine CCL11 / analysis. Chemokine CCL11 / secretion. Female. Humans. Interleukin-6 / analysis. Interleukin-6 / secretion. Male. Middle Aged. Prognosis. Proteomics / methods
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(PMID = 18398743.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / CCL11 protein, human; 0 / Chemokine CCL11; 0 / Cytokines; 0 / Interleukin-6; 0 / Receptors, Cytokine
33.
Lundin J, Karlsson C, Celsing F:
Alemtuzumab therapy for severe autoimmune hemolysis in a patient with B-cell chronic lymphocytic leukemia.
Med Oncol
; 2006;23(1):137-9
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[Title]
Alemtuzumab therapy for severe autoimmune hemolysis
in a
patient with B-
cell chronic
lymphocytic
leukemia
.
B-
cell chronic
lymphocytic
leukemia
(B-
CLL
) is the most common cause of autoimmune hemolytic anemia (AIHA), and a subgroup of these patients who develop both these conditions fail to respond to corticosteroids, cytotoxic drugs, splenectomy, and iv immunoglobulins.
Alemtuzumab is a humanized anti-CD52 monoclonal antibody that is an effective therapy for B-
CLL
, mycosis fungoides, and T-
cell
prolymphocytic
leukemia
.
Here we present a case report
of a
78-yr-old woman with B-
CLL
and progressive life-threatening AIHA with hemoglobin count 5.5 g/dL following fludarabine treatment, who was treated successfully with alemtuzumab.
We conclude that alemtuzumab may be indicated for the treatment of AIHA in B-
CLL
patients who have failed other treatments.
[MeSH-major]
Anemia, Hemolytic, Autoimmune / drug therapy. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ complications
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.
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consumer health - Leukemia, B-cell, chronic
.
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(PMID = 16645240.001).
[ISSN]
1357-0560
[Journal-full-title]
Medical oncology (Northwood, London, England)
[ISO-abbreviation]
Med. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
34.
Hus I, Roliński J, Tabarkiewicz J, Wojas K, Bojarska-Junak A, Greiner J, Giannopoulos K, Dmoszyńska A, Schmitt M:
Allogeneic dendritic cells pulsed with tumor lysates or apoptotic bodies as immunotherapy for patients with early-stage B-cell chronic lymphocytic leukemia.
Leukemia
; 2005 Sep;19(9):1621-7
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[Title]
Allogeneic dendritic cells pulsed with tumor lysates or apoptotic bodies as immunotherapy for patients with early-stage B-
cell chronic
lymphocytic
leukemia
.
Recently, immunotherapies with allogeneic dendritic cells (DCs) pulsed with tumor antigens to generate specific T-
cell
responses have been tested in clinical trials for patients with solid tumors.
This is the first report on a clinical vaccination study with DCs for patients with B-
cell chronic
lymphocytic
leukemia
(B-
CLL
).
The potential of allogeneic DCs pulsed ex vivo with tumor
cell
lysates or apoptotic bodies to stimulate antitumor immunity in patients with B-
CLL in
early stages was evaluated.
In one patient, a significant increase of specific cytotoxic T
lymphocytes
against RHAMM/CD168, a recently characterized
leukemia
-associated antigen, could be detected after DC vaccination.
Taken together, the study demonstrated that DC vaccination
in CLL
patients is feasible and safe.
[MeSH-major]
Apoptosis / immunology. Cancer Vaccines / therapeutic use. Dendritic Cells / immunology. Immunotherapy / methods.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ therapy. Neoplasm Proteins / immunology
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(PMID = 15990861.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD44; 0 / Cancer Vaccines; 0 / Extracellular Matrix Proteins; 0 / Neoplasm Proteins; 0 / hyaluronan-mediated motility receptor
35.
Zhou R, Gray NA, Yuan P, Li X, Chen J, Chen G, Damschroder-Williams P, Du J, Zhang L, Manji HK:
The anti-apoptotic, glucocorticoid receptor cochaperone protein BAG-1 is a long-term target for the actions of mood stabilizers.
J Neurosci
; 2005 May 4;25(18):4493-502
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[Title]
The anti-apoptotic, glucocorticoid receptor cochaperone protein BAG-1 is
a long
-term target for the actions of mood stabilizers.
Increasing data suggest that impairments of cellular plasticity/resilience underlie the pathophysiology of bipolar
disorder
.
A series of microarray studies with validating criteria have recently revealed a common, novel target for the
long
-term actions of the structurally highly dissimilar mood stabilizers lithium and valproate: BAG-1 [BCL-2 (B-
cell
CLL
/
lymphoma
2)-associated athanogene].
Chronic
administration of both agents at therapeutic doses increased the expression of BAG-1 in rat hippocampus.
Furthermore, these findings were validated at the protein level, and the effects were seen
in a
time frame consistent with therapeutic effects and were specific for mood stabilizers.
Furthermore,
small
interfering RNA studies showed that these inhibitory effects on GR activity were mediated, at least in part, through BAG-1.
The observation that BAG-1 inhibits glucocorticoid activation suggests that mood stabilizers may counteract the deleterious effects of hypercortisolemia seen in bipolar
disorder
by upregulating BAG-1.
Additionally, these studies suggest that regulation of GR-mediated plasticity may play a role in the treatment of bipolar
disorder
and raise the possibility that agents affecting BAG-1 more directly may represent novel therapies for this devastating illness.
[MeSH-minor]
Alkaline Phosphatase / genetics. Alkaline Phosphatase / metabolism. Animals. Behavior, Animal. Blotting, Western / methods.
Cell
Line, Tumor. Dexamethasone / pharmacology. Dose-Response Relationship, Drug. Drug Interactions. Gene Expression / drug effects. Humans. Immunohistochemistry / methods. Indoles / metabolism. Male. Molecular Weight. Neuroblastoma. RNA,
Small
Interfering / pharmacology. Rats. Rats, Wistar. Receptors, Glucocorticoid / metabolism. Time Factors. Transfection / methods
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gene/protein/disease-specific - Gene Ontology annotations from this paper
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(PMID = 15872096.001).
[ISSN]
1529-2401
[Journal-full-title]
The Journal of neuroscience : the official journal of the Society for Neuroscience
[ISO-abbreviation]
J. Neurosci.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimanic Agents; 0 / BCL2-associated athanogene 1 protein; 0 / DNA-Binding Proteins; 0 / Indoles; 0 / RNA, Small Interfering; 0 / Receptors, Glucocorticoid; 0 / Transcription Factors; 47165-04-8 / DAPI; 614OI1Z5WI / Valproic Acid; 7S5I7G3JQL / Dexamethasone; 9FN79X2M3F / Lithium; EC 3.1.3.1 / Alkaline Phosphatase
36.
Nunes P, Hasler U, McKee M, Lu HA, Bouley R, Brown D:
A fluorimetry-based ssYFP secretion assay to monitor vasopressin-induced exocytosis in LLC-PK1 cells expressing aquaporin-2.
Am J Physiol Cell Physiol
; 2008 Dec;295(6):C1476-87
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[Title]
A fluorimetry-based ssYFP secretion assay to monitor vasopressin-induced exocytosis
in LLC
-PK1 cells expressing aquaporin-2.
Vasopressin (VP)-induced exocytosis was dissected in native and aquaporin-2 (AQP2)-expressing renal
LLC
-PK(1) cells by a fluorimetric exocytosis assay based on soluble secreted yellow fluorescent protein (ssYFP).
Fluorimetry and Western blot analysis demonstrated similar constitutive ssYFP secretion in native
LLC
-PK(1) and AQP2-expressing cells.
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.
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[
18695390.001
]
[Cites]
J Cell Biol. 2008 Aug 11;182(3):587-601
[
18678705.001
]
[Cites]
J Am Soc Nephrol. 2005 Jun;16(6):1571-82
[
15843469.001
]
(PMID = 18799651.001).
[ISSN]
0363-6143
[Journal-full-title]
American journal of physiology. Cell physiology
[ISO-abbreviation]
Am. J. Physiol., Cell Physiol.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK-38452; United States / NIDDK NIH HHS / DK / DK-43341; United States / NIDDK NIH HHS / DK / DK-57521; United States / NIDDK NIH HHS / DK / K08 DK-075940-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Aquaporin 2; 0 / Luminescent Proteins; 11000-17-2 / Vasopressins
[Other-IDs]
NLM/ PMC2603565
37.
Montillo M, Tedeschi A, Miqueleiz S, Veronese S, Cairoli R, Intropido L, Ricci F, Colosimo A, Scarpati B, Montagna M, Nichelatti M, Regazzi M, Morra E:
Alemtuzumab as consolidation after a response to fludarabine is effective in purging residual disease in patients with chronic lymphocytic leukemia.
J Clin Oncol
; 2006 May 20;24(15):2337-42
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[Title]
Alemtuzumab as consolidation after a response to fludarabine is effective in purging residual
disease in
patients with
chronic
lymphocytic
leukemia
.
PURPOSE: Treatment with alemtuzumab has resulted in negative responses for minimal residual
disease
(MRD) in patients with
chronic
lymphocytic
leukemia
(
CLL
).
In a
prior analysis we demonstrated that it is possible to achieved MRD negativity, as assessed by polyclonality of immunoglobulin heavy chain after consolidation with alemtuzumab.
This phase II study evaluated 34 patients with
CLL
who received alemtuzumab consolidation in an effort to improve the quality of their response to fludarabine-based induction.
Subsequent peripheral blood stem-
cell
(PBSC) collection and transplantation, tolerability, and pharmacokinetics also were assessed.
CONCLUSION: Subcutaneously administered alemtuzumab was effective, safe, and
well
tolerated as consolidation therapy in patients with
CLL
who responded to fludarabine induction therapy.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ drug therapy. Peripheral Blood Stem
Cell
Transplantation
Genetic Alliance.
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.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
Hazardous Substances Data Bank.
FLUDARABINE
.
Hazardous Substances Data Bank.
VIDARABINE
.
Hazardous Substances Data Bank.
GANCICLOVIR
.
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(PMID = 16618945.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Antiviral Agents; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; P9G3CKZ4P5 / Ganciclovir
38.
Borthakur G, O'Brien S, Wierda WG, Thomas DA, Cortes JE, Giles FJ, Kantarjian HM, Lerner S, Keating MJ:
Immune anaemias in patients with chronic lymphocytic leukaemia treated with fludarabine, cyclophosphamide and rituximab--incidence and predictors.
Br J Haematol
; 2007 Mar;136(6):800-5
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[Title]
Immune anaemias in patients with
chronic
lymphocytic leukaemia
treated with fludarabine, cyclophosphamide and rituximab--incidence and predictors.
Immune anaemias (IA) [auto-immune haemolytic anaemia (AIHA) and pure red
cell
aplasia (PRCA)] are complications of
chronic
lymphocytic leukaemia
(
CLL
).
Additional markers of haemolysis (indirect hyperbilirubinaemia, reticulocytosis,
low
haptoglobin and elevated lactate dehydrogenase levels) confirmed the presence of AIHA in these patients.
Thus, the incidence of IA among
CLL
patients treated with FCR was comparable with historical rates.
The
diagnosis of
AIHA can be considered even if the DAT is negative.
[MeSH-major]
Anemia, Hemolytic, Autoimmune / etiology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ drug therapy. Red-
Cell
Aplasia, Pure / etiology
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
RITUXIMAB
.
Hazardous Substances Data Bank.
FLUDARABINE
.
Hazardous Substances Data Bank.
CYCLOPHOSPHAMIDE
.
Hazardous Substances Data Bank.
VIDARABINE
.
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[CommentIn]
Br J Haematol. 2007 Nov;139(4):622-3
[
17979948.001
]
(PMID = 17341265.001).
[ISSN]
0007-1048
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Glucocorticoids; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
39.
Sliwinski T, Czechowska A, Szemraj J, Morawiec Z, Skorski T, Blasiak J:
STI571 reduces NER activity in BCR/ABL-expressing cells.
Mutat Res
; 2008 Jul 31;654(2):162-7
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STI571 is used mostly in the treatment of
chronic
myeloid
leukemia
and inhibits activity of the BCR/ABL oncogenic tyrosine kinase, which is a hallmark of this
disease
.
NER activity was examined in the BCR/ABL-expressing
cell
lines K562 and BV173 of myeloid and
lymphoid
origin, respectively, as
well
as in CCRF-CEM cells, which do not express BCR/ABL.
A murine myeloid parental 32D
cell
line and its counterpart transfected with the BCR/ABL gene were also tested.
NER activity was assessed in the
cell
extracts by use of an UV-irradiated plasmid as a substrate and by a modified single-
cell
gel electrophoresis (comet) assay on UV-treated nucleoids.
Therefore, STI571 may overcome the drug resistance associated with increased DNA repair in BCR/ABL-positive
leukemias
.
[MeSH-major]
DNA Repair.
Leukemia
, Myelogenous,
Chronic
, BCR-ABL Positive / genetics. Piperazines / pharmacology. Pyrimidines / pharmacology
[MeSH-minor]
Animals. Benzamides.
Cell
Line, Tumor.
Cell
Survival / drug effects.
Cell
Survival / radiation effects. Comet Assay. Humans. Imatinib Mesylate. Mice. Polymerase Chain Reaction
MedlinePlus Health Information.
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.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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(PMID = 18602021.001).
[ISSN]
0027-5107
[Journal-full-title]
Mutation research
[ISO-abbreviation]
Mutat. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
40.
Paydas S, Tanriverdi K, Yavuz S, Seydaoglu G:
PRAME mRNA levels in cases with chronic leukemia: Clinical importance and review of the literature.
Leuk Res
; 2007 Mar;31(3):365-9
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[Title]
PRAME mRNA levels in cases with
chronic leukemia
: Clinical importance and review of the literature.
The aim of this study is to determine the frequency and the clinical importance of PRAME expression in
chronic
myeloid
leukemia
(CML)/
chronic
myeloproliferative disorders (CMPD) and
chronic
lymphocytic
leukemia
(
CLL
).
PRAME mRNA was measured by real time RT-PCR in 88 cases with
chronic leukemia
(CL) and 42 controls.
Seventy cases had CML/CMPD (56 had
chronic
phase (CP)-14 had accelerated/blastic phase
disease
(AP/BP) and 18 cases had
CLL
(11 had early stage (Rai 0-I-II) and 7 had late stage (Rai III-IV).
Twenty-four of 70 (34%) cases with CML/CMPD and 5 of 18 (28%) cases with
CLL
showed PRAME expression.
PRAME (+) and PRAME (-) cases were not different for age, Hb, Hct, WBC count, platelet count, stage of the
disease
and response to therapy.
PRAME was monitorised in eight cases during follow-up: in three cases PRAME was negative at CP and expression developed at the AP/BP
disease
.
PRAME mRNA may be a useful marker to detect the minimal residual
disease
(MRD) and to determine the response to therapy in CLs.
[MeSH-major]
Antigens, Neoplasm / genetics. Biomarkers, Tumor / genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics.
Leukemia
, Myelogenous,
Chronic
, BCR-ABL Positive / genetics. Myeloproliferative Disorders / genetics. RNA, Messenger / genetics
[MeSH-minor]
Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Chronic
Disease
.
Disease
Progression. Female. Follow-Up Studies. Gene Expression Profiling. Humans. Male. Middle Aged. Neoplasm Staging. Reverse Transcriptase Polymerase Chain Reaction / methods. Treatment Outcome
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(PMID = 16914202.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / PRAME protein, human; 0 / RNA, Messenger
41.
Kuramochi K, Matsui R, Matsubara Y, Nakai J, Sunoki T, Arai S, Nagata S, Nagahara Y, Mizushina Y, Ikekita M, Kobayashi S:
Apoptosis-inducing effect of epolactaene derivatives on BALL-1 cells.
Bioorg Med Chem
; 2006 Apr 1;14(7):2151-61
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Epolactaene, a neuritogenic compound in human neuroblastoma SH-SY5Y, induces apoptosis
in a
human
leukemia B
-
cell
line, BALL-1.
The alpha-acyl-alpha,beta-epoxy-gamma-lactam moiety as
well
as the hydrophobicity derived from the
long
alkyl side chain are both important for activity.
[MeSH-major]
Apoptosis / drug effects.
Leukemia
, B-
Cell
/ drug therapy
[MeSH-minor]
Cell
Line, Tumor.
Cell
Survival / drug effects. Drug Screening Assays, Antitumor. Epoxy Compounds / chemical synthesis. Epoxy Compounds / chemistry. Epoxy Compounds / pharmacology. Humans. Hydrolysis. Molecular Structure. Polyenes / chemical synthesis. Polyenes / chemistry. Polyenes / pharmacology. Stereoisomerism. Structure-Activity Relationship
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(PMID = 16298530.001).
[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 / Epoxy Compounds; 0 / Polyenes; 0 / epolactaene
42.
Gutiérrez NC, Ocio EM, de Las Rivas J, Maiso P, Delgado M, Fermiñán E, Arcos MJ, Sánchez ML, Hernández JM, San Miguel JF:
Gene expression profiling of B lymphocytes and plasma cells from Waldenström's macroglobulinemia: comparison with expression patterns of the same cell counterparts from chronic lymphocytic leukemia, multiple myeloma and normal individuals.
Leukemia
; 2007 Mar;21(3):541-9
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[Title]
Gene expression profiling of B
lymphocytes
and plasma cells from Waldenström's macroglobulinemia: comparison with expression patterns of the same
cell
counterparts from
chronic
lymphocytic
leukemia
, multiple myeloma and normal individuals.
The tumoral clone of Waldenström's macroglobulinemia (WM) shows a wide morphological heterogeneity, which ranges from B
lymphocytes
(BL) to plasma cells (PC).
By means of genome-wide expression profiling we have been able to identify genes exclusively deregulated in BL and PC from WM, but with a similar expression pattern in their corresponding
cell
counterparts from
chronic
lymphocytic
leukemia
(
CLL
) and multiple myeloma (MM), as
well
as normal individuals.
The differentially expressed genes have important functions in B-
cell
differentiation and oncogenesis.
Thus, two of the genes downregulated in WM-BL were IL4R, which plays a relevant role
in CLL
B-
cell
survival, and BACH2, which participates in the development of class-switched PC.
A set of four genes was able to discriminate clonal BL from WM and
CLL
: LEF1 (WNT/beta-catenin pathway), MARCKS, ATXN1 and FMOD.
We also found deregulation of genes involved in plasma
cell
differentiation such as PAX5, which was overexpressed in WM-PC, and IRF4 and BLIMP1, which were underexpressed.
In summary, these results indicate that both PC and BL from WM are genetically different from the MM and
CLL
cell
counterpart.
[MeSH-major]
B-
Lymphocytes
/ metabolism.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ pathology. Multiple Myeloma / pathology. Plasma Cells / metabolism. Waldenstrom Macroglobulinemia / pathology
Genetic Alliance.
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.
Genetic Alliance.
consumer health - Multiple myeloma
.
Genetic Alliance.
consumer health - Plasma cell leukemia
.
MedlinePlus Health Information.
consumer health - Multiple Myeloma
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
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(PMID = 17252022.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Neoplasm Proteins
43.
Buhl AM, Jurlander J, Geisler CH, Pedersen LB, Andersen MK, Josefsson P, Petersen JH, Leffers H:
CLLU1 expression levels predict time to initiation of therapy and overall survival in chronic lymphocytic leukemia.
Eur J Haematol
; 2006 Jun;76(6):455-64
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[Title]
CLLU1 expression levels predict time to initiation of therapy and overall survival in
chronic
lymphocytic
leukemia
.
OBJECTIVES:
Chronic
lymphocytic
leukemia
(
CLL
) is an incurable
disease
with a highly variable clinical course.
IgV(H) mutational status, chromosomal aberrations, CD38 expression and ZAP-70 expression are prognostic markers
in CLL
, however, they are not exclusively confined to this
disease
.
We recently identified a novel
CLL
-specific gene (
CLL
upregulated gene1, CLLU1) that is exclusively upregulated
in CLL
cells.
Here we describe our evaluation of the prognostic significance of CLLU1
in CLL
.
METHODS: A cohort of 59 previously untreated
CLL
patients was studied.
RESULTS: Analyzed as a continuous, quantitative parameter CLLU1 levels significantly predicted time from
diagnosis
to initiation of therapy (P &
lt
; or = 0.0003) Analyzed as a categorical parameter, by segregation of the patients into groups with cDNA1 or CDS expression above or below the median, the CLLU1 levels significantly predicted time from
diagnosis
to initiation of therapy (P = 0.001) and predicted overall survival with borderline significance (P &
lt
; or = 0.05).
Patient stratification according to clinical stage, cytogenetics, IgV(H) mutational status, ZAP-70 and CD38, demonstrated significantly increased CLLU1 expression in all investigated
CLL
poor risk groups.
CONCLUSIONS: CLLU1 is the first identified
CLL
specific gene.
The CLLU1 mRNA expression level can predict time to initiation of treatment and survival
in CLL
patients.
[MeSH-major]
Biomarkers, Tumor / biosynthesis.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics. Neoplasm Proteins / biosynthesis
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[CommentIn]
Eur J Haematol. 2006 Aug;77(2):177; author reply 178
[
16856913.001
]
(PMID = 16529606.001).
[ISSN]
0902-4441
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / CLLU1 protein, human; 0 / DNA, Complementary; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38
44.
Chae HW, Kim IW, Jin HE, Kim DD, Chung SJ, Shim CK:
Effect of ion-pair formation with bile salts on the in vitro cellular transport of berberine.
Arch Pharm Res
; 2008 Jan;31(1):103-10
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The objective of this study was to examine the effect of ion-pair complexation with endogenous bile salts on the transport
of a
quarternary ammonium organic cationic (OC) drug, berberine, across the Caco-2 and
LLC
-PK1
cell
monolayers.
Similar results were observed for the transport of berberine across the
LLC
-PK1 cells.
These results suggest that an efflux transporter, probably P-gp, is involved in the Caco-2
cell
transport.
The apparent partition coefficient (APC) of berberine between n-octanol and a phosphate buffer (pH 7.4) was increased by the presence of an organic anion (OA), taurodeoxycholate (TDC, a bile salt), suggesting the formation
of a
lipophilic ion-pair complex between an OC (berberine) and an OA (TDC).
Despite the ion-pair complexation, however, the BL-AP transport of berberine across the Caco-2 and
LLC
-PK1 cells was not altered by the cis-presence of bile salts or the rat bile juice.
This is consistent with the reportedly unaltered secretory transport
of a
quarternary ammonium compound, tributylmethylammonium (TBuMA), across the Caco-2
cell
monolayers in the cis-presence of bile salts or the rat bile juice, but not with our previous report in which the secretory transport of TBuMA across the
LLC
-PK1
cell
was increased in the cis-presence of TDC.
Therefore, the effect of ion-pair formation with the bile components or bile salts on the secretory transport of OCs appears to depend on the molecular properties of OCs (e.g., molecular weight, lipophilicity and affinity to relevant transporters) and the characteristics of
cell
strains (e.g., expression and contribution of responsible transporters to the transport).
[MeSH-minor]
Animals. Biological Transport, Active. Caco-2 Cells.
Cell
Membrane / metabolism. Chemistry, Physical. Chromatography, High Pressure Liquid. Data Interpretation, Statistical. Humans.
LLC
-PK1 Cells. P-Glycoprotein / antagonists & inhibitors. P-Glycoprotein / metabolism. Physicochemical Phenomena. Solubility. Swine. Taurodeoxycholic Acid / chemistry
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(PMID = 18277615.001).
[ISSN]
0253-6269
[Journal-full-title]
Archives of pharmacal research
[ISO-abbreviation]
Arch. Pharm. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Bile Acids and Salts; 0 / P-Glycoprotein; 0I8Y3P32UF / Berberine; 516-50-7 / Taurodeoxycholic Acid
45.
Moore DA, Fuller B, Hazzan M, Jones JW:
Development of a security vulnerability assessment process for the RAMCAP chemical sector.
J Hazard Mater
; 2007 Apr 11;142(3):689-94
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[Title]
Development
of a
security vulnerability assessment process for the RAMCAP chemical sector.
The Department of Homeland Security (DHS), Directorate of Information Analysis & Infrastructure Protection (IAIP), Protective Services Division (PSD), contracted the American Society of Mechanical Engineers Innovative Technologies Institute,
LLC
(ASME ITI,
LLC
) to develop guidance on Risk Analysis and Management for Critical Asset Protection (RAMCAP).
AcuTech Consulting Group (AcuTech) has been contracted by ASME ITI,
LLC
, to provide assistance by facilitating the development of sector-specific guidance on vulnerability analysis and management for critical asset protection for the chemical manufacturing, petroleum refining, and liquefied natural gas (LNG) sectors.
This activity involves two key tasks for these three sectors: Development
of a
screening to supplement DHS understanding of the assets that are important to protect against terrorist attack and to prioritize the activities.
Development
of a
standard security vulnerability analysis (SVA) framework for the analysis of consequences, vulnerabilities, and threats.
This project involves the cooperative effort of numerous leading industrial
companies
, industry trade associations, professional societies, and security and safety consultants representative of those sectors.
Jones is the chief technology officer for ASME-ITI,
LLC
for RAMCAP.
MedlinePlus Health Information.
consumer health - Disaster Preparation and Recovery
.
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(PMID = 16920260.001).
[ISSN]
0304-3894
[Journal-full-title]
Journal of hazardous materials
[ISO-abbreviation]
J. Hazard. Mater.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Hazardous Substances
46.
Fernàndez V, Jares P, Salaverria I, Giné E, Beà S, Aymerich M, Colomer D, Villamor N, Bosch F, Montserrat E, Campo E:
Gene expression profile and genomic changes in disease progression of early-stage chronic lymphocytic leukemia.
Haematologica
; 2008 Jan;93(1):132-6
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[Title]
Gene expression profile and genomic changes
in disease
progression of early-stage
chronic
lymphocytic
leukemia
.
The biologic mechanisms involved in the clinical progression from early stages of patients with
chronic
lymphocytic
leukemia
(
CLL
) are not
well
known.
We investigated sequential samples from 16 untreated
CLL
patients obtained at
diagnosis in
early stage and after progression before treatment.
One patient had a p16 (INK4a) homozygous deletion at
diagnosis
and progression, and 3 patients acquired a p53 mutation, gains of 5q21-q23 and 11pter-p14, and a gain of chromosome 12 respectively, during the progression of the
disease
.
Gene expression profile analysis showed a significant modulation of 58 genes with a particular downregulation of genes that are inhibitors of
cell
adhesion and motility.
[MeSH-major]
Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genome.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/
diagnosis
.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ pathology
[MeSH-minor]
Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p16 / metabolism.
Disease
Progression. Female. Genes, p53 / genetics. Humans. Male. Middle Aged. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis
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(PMID = 18166798.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / Cyclin-Dependent Kinase Inhibitor p16
47.
Zenz T, Mohr J, Edelmann J, Sarno A, Hoth P, Heuberger M, Helfrich H, Mertens D, Dohner H, Stilgenbauer S:
Treatment resistance in chronic lymphocytic leukemia: the role of the p53 pathway.
Leuk Lymphoma
; 2009 Mar;50(3):510-3
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[Title]
Treatment resistance in
chronic
lymphocytic
leukemia
: the role of the p53 pathway.
The importance of studying p53 pathway defects in
chronic
lymphocytic
leukemia
(
CLL
) has been promoted by the demonstration of the fundamentally different clinical course of patients with 17p deletion.
The observation of resistance to chemotherapy and mutation of the remaining TP53 allele explain the clinical presentation
of CLL
with 17p deletion.
In addition, other principal components of the DNA damage pathway reportedly are
de
-regulated by mutation (ATM), deletion (ATM) or potentially more complex down-regulation (miR-34a)
in CLL
.
Nonetheless, challenges remain because we can only explain resistance
in a
proportion of the cases that are resistant to first line treatment.
[MeSH-major]
Drug Resistance, Neoplasm / genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics. Tumor Suppressor Protein p53 / genetics
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(PMID = 19347737.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Tumor Suppressor Protein p53
[Number-of-references]
12
48.
Sureda NC, Bosch MP, Kurpis M, Ruiz Lascano A:
[Leukaemia cutis: clinical manifestation of chronic lymphocytic leukaemia relapse].
Rev Fac Cien Med Univ Nac Cordoba
; 2007;64(1):42-4
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[Title]
[
Leukaemia
cutis: clinical manifestation of
chronic
lymphocytic leukaemia
relapse].
[Transliterated title]
Leucemia
cutis: expresión clínica
de
recaída
de leucemia
linfocítica crónica.
We present a 71 year old male patient with previous records of
Chronic
Lymphocytic Leukaemia
who presented with a tumoral skin lesion.
Histological and immunohistochemical studies confirmed the
Leukaemia
Cutis
diagnosis
.
[MeSH-major]
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ pathology. Leukemic Infiltration / pathology. Skin / pathology
Hazardous Substances Data Bank.
CHLORAMBUCIL
.
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(PMID = 18426096.001).
[ISSN]
0014-6722
[Journal-full-title]
Revista de la Facultad de Ciencias Médicas (Córdoba, Argentina)
[ISO-abbreviation]
Rev Fac Cien Med Univ Nac Cordoba
[Language]
spa
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Argentina
[Chemical-registry-number]
0 / Antineoplastic Agents, Alkylating; 18D0SL7309 / Chlorambucil
49.
Wilhelm C, Neubauer A, Brendel C:
Discordant results of flow cytometric ZAP-70 expression status in B-CLL samples if different gating strategies are applied.
Cytometry B Clin Cytom
; 2006 Jul 15;70(4):242-50
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[Title]
Discordant results of flow cytometric ZAP-70 expression status in B-
CLL
samples if different gating strategies are applied.
BACKGROUND: Recent studies have identified ZAP-70 expression status as an excellent prognostic parameter in
chronic
lymphocytic
leukemia
(
CLL
).
METHODS: One hundred and one patients with B-
CLL
were analyzed employing a directly labeled alexa-fluor-488-ZAP-70-antibody.
RESULTS: Applying either T-/NK-
cell
isotype or healthy control analysis strategies on patient samples that were processed in parallel revealed discrepant results in 48% (12/25) of all cases.
Taken together with the 74 B-
CLL
patients, who were analyzed with regard to average reference values, disconcordant results were obtained in 58% of the samples.
We demonstrate that high variances in ZAP-70 T-/NK-
cell
staining within B-
CLL
patients, paired with a close proximity of ZAP-70 B-
cell
values to the suggested cut-off levels, may lead to interpretation difficulties of ZAP-70 status.
Further standardization is required before ZAP-70 can be used as a reliable prognostic parameter in immunophenotyping of B-
CLL
.
[MeSH-major]
Flow Cytometry / methods.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/
diagnosis
. ZAP-70 Protein-Tyrosine Kinase / analysis
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / immunology. Humans. Immunophenotyping. Kaplan-Meier Estimate. Killer Cells, Natural / immunology. Middle Aged. Reference Values. Reproducibility of Results. Survival Rate. T-
Lymphocytes
/ immunology
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[Copyright]
(c) 2006 International Society for Analytical Cytology.
(PMID = 16906574.001).
[ISSN]
1552-4949
[Journal-full-title]
Cytometry. Part B, Clinical cytometry
[ISO-abbreviation]
Cytometry B Clin Cytom
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
50.
Agrawal SG, Liu FT, Wiseman C, Shirali S, Liu H, Lillington D, Du MQ, Syndercombe-Court D, Newland AC, Gribben JG, Jia L:
Increased proteasomal degradation of Bax is a common feature of poor prognosis chronic lymphocytic leukemia.
Blood
; 2008 Mar 1;111(5):2790-6
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[Title]
Increased proteasomal degradation of Bax is a common feature of poor prognosis
chronic
lymphocytic
leukemia
.
Many biologic markers are associated with poor prognosis in
chronic
lymphocytic
leukemia
(
CLL
), but their mechanistic role remains unclear.
Using a Bax degradation activity (BDA) assay,
CLL
cells were found to show variable Bax instability.
However, BDA did not correlate with Bax protein levels: BDA positive and negative cases had high and
low
baseline Bax levels.
Patients with BDA positive cells had a shorter median overall survival (
OS
; 126 months vs not reached, P = .011) and time to first treatment (16 vs 156 months, P = .029) than BDA negative cases.
Dual BDA and ZAP-70 positivity had a median
OS of
84 months (P = .012).
The BDA assay measures the intrinsic ubiquitin/proteasome activity
of CLL
cells and dynamic changes in Bax protein levels over time.
Mechanistically, Bax instability may represent a final common pathway for disparate prognostic markers, as
well
as being itself an indicator of poor prognosis.
[MeSH-major]
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/
diagnosis
.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ metabolism. Proteasome Endopeptidase Complex / metabolism. Protein Processing, Post-Translational. bcl-2-Associated X Protein / metabolism
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(PMID = 18160666.001).
[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 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / bcl-2-Associated X Protein; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human; EC 3.4.25.1 / Proteasome Endopeptidase Complex
51.
Kiran S, Cocco P, Mannetje A, Satta G, D'Andrea I, Becker N, de Sanjosé S, Foretova L, Staines A, Kleefeld S, Maynadié M, Nieters A, Brennan P, Boffetta P:
Occupational exposure to ethylene oxide and risk of lymphoma.
Epidemiology
; 2010 Nov;21(6):905-10
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[Title]
Occupational exposure to ethylene oxide and risk
of lymphoma
.
BACKGROUND: Ethylene oxide, a high-volume commodity, is an established human carcinogen, although the relevant epidemiologic evidence is
limited
.
METHODS: We explored the association between occupational exposure to ethylene oxide and risk
of lymphoma in a
case-control study, including 2347
lymphoma
cases first diagnosed in 1998-2004 and 2463 controls, from 6 European countries.
The
diagnosis of lymphoma
was based on the 2001 World Health Organization Classification
of lymphoma
.
We modeled risk
of lymphoma
with unconditional logistic regression analysis as a function of various exposure measures, adjusting for age, sex, and participating center.
Lymphoma
risk showed a 4.3-fold increase associated with medium-high frequency of exposure to ethylene oxide (95% CI = 1.4-13).
Among major subtypes,
chronic
lymphocytic
leukemia
was consistently associated with ethylene oxide exposure, related
in a
dose-response manner to probability, frequency, and duration of exposure, as
well
as to cumulative exposure and (less definitively) with exposure intensity.
[MeSH-major]
Carcinogens / toxicity. Ethylene Oxide / toxicity.
Lymphoma
/ chemically induced. Occupational Exposure
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ETHYLENE OXIDE
.
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(PMID = 20811284.001).
[ISSN]
1531-5487
[Journal-full-title]
Epidemiology (Cambridge, Mass.)
[ISO-abbreviation]
Epidemiology
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Carcinogens; JJH7GNN18P / Ethylene Oxide
52.
Vasilatou D, Papageorgiou S, Pappa V, Papageorgiou E, Dervenoulas J:
The role of microRNAs in normal and malignant hematopoiesis.
Eur J Haematol
; 2010 Jan 1;84(1):1-16
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MicroRNAs are
small
non-coding RNAs that act at the post-transcriptional level, regulating protein expression by repressing translation or destabilizing mRNA target.
Because of their discovery, microRNAs have been associated with almost every normal
cell
function, including proliferation, differentiation and apoptosis.
Several lines of evidence suggest that they have an important role in normal hematopoiesis as exemplified by the role of mir-155 and mir-150 in the differentiation of B and T
lymphocytes
, the suppressive role of mir-221 and mir-222 in erythroid differentiation, the inhibitory effect of mir-181 on hematopoietic differentiation and the induction of myeloid differentiation by mir-223.
Their aberrant expression has been associated with solid tumors and hematopoietic malignancies as suggested by the frequent deletion of mir-15a and mir-16-1 in
chronic
lymphocytic
leukemia
, the increased levels of mir-155
in diffuse
large B-
cell
lymphomas
and the increased levels of mir-181 in acute myeloid
leukemia
M1 and M2.
[MeSH-minor]
Animals.
Cell
Transformation, Neoplastic / genetics. Down-Regulation. Erythroid Precursor Cells / cytology. Gene Expression Regulation, Neoplastic / genetics. Genes, Tumor Suppressor. Humans. Invertebrates / genetics.
Lymphocytes
/ cytology. Mice. Myeloid Cells / cytology. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Oncogenes. RNA, Neoplasm / antagonists & inhibitors. RNA, Neoplasm / genetics
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(PMID = 19744129.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm
[Number-of-references]
110
53.
Bogner C, Sandherr M, Perker M, Weick K, Ringshausen I, Peschel C, Decker T:
Cyclin E but not bcl-2, bax or mcl-1 is differentially expressed in ZAP 70-positive and ZAP 70-negative B-CLL cells.
Ann Hematol
; 2006 Jul;85(7):458-62
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[Title]
Cyclin E but not bcl-2, bax or mcl-1 is differentially expressed in ZAP 70-positive and ZAP 70-negative B-
CLL
cells.
The clinical course of
chronic
lymphocytic
leukemia
is variable.
While some patients have indolent
disease
, others require aggressive treatment within a short time after
diagnosis
.
Differences in the expression of proteins regulating
cell
cycle and apoptosis may be responsible for the heterogeneous course of the
disease
.
Recently, protein ZAP 70 [zeta-chain (T-
cell
receptor) associated protein kinase 70 kDa] has been found to be differentially expressed within two biologic subgroups, characterized by the presence or absence of somatic mutations in specific immunoglobulin heavy-chain variable region genes.
In the present work, we analyzed highly purified B-
CLL
cells from 60 patients for ZAP 70 expression and the expression of cyclin E, bcl-2, bax, and mcl-1 as
well
as the ratios of bcl-2/bax and mcl-1/bax.
We conclude that higher cyclin E expression in samples of ZAP 70-positive patients may reflect a larger proliferating compartment in vivo compared to ZAP 70-negative patients and that cyclin E may add prognostic information in this context for patients with B-
CLL
.
[MeSH-major]
Cyclin E / genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics. Neoplasm Proteins / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics. ZAP-70 Protein-Tyrosine Kinase / metabolism. bcl-2-Associated X Protein / genetics
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal. Gene Expression Regulation, Neoplastic. Humans. Middle Aged. Myeloid
Cell Leukemia
Sequence 1 Protein. Neoplasm Staging. Tumor Cells, Cultured
NCI CPTC Antibody Characterization Program.
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(PMID = 16538501.001).
[ISSN]
0939-5555
[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 / Antibodies, Monoclonal; 0 / Cyclin E; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
54.
Obermann EC, Eward KL, Dogan A, Paul EA, Loddo M, Munson P, Williams GH, Stoeber K:
DNA replication licensing in peripheral B-cell lymphoma.
J Pathol
; 2005 Feb;205(3):318-28
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[Title]
DNA replication licensing in peripheral B-
cell
lymphoma
.
Peripheral B-
cell
lymphomas
representing 90% of
lymphoid
neoplasms are divided into
low
- and high-growth fraction
lymphomas
.
Here we investigate regulation of DNA replication licensing during B-
cell
lymphomagenesis.
Combined analysis of origin licensing factors Mcm2 and geminin with the proliferation marker Ki67 in SLL/
CLL
, MCL, DLBCL and Burkitt
lymphoma
reveals for the first time the precise
cell
cycle state of these entities.
Given that tight Mcm2 downregulation defines the quiescent state (G0) and that both high- and
low
-growth fraction
lymphomas
express Mcm2, the data demonstrate that neoplastic
lymphocytes of
SLL/
CLL
and MCL reside in an "in-cycle" G1 state and not in G0 as previously thought.
Absence of the S/G2/M phase marker geminin in SLL/
CLL
and MCL further indicates failure of
cell
cycle progression in these tumours.
In contrast, the high-growth fraction
lymphomas
DLBCL and Burkitt
lymphoma
exhibit differential expression of geminin, with the geminin/Ki67 ratio increasing for more aggressive neoplasms in keeping with a shortened G1 phase and thus representing an important discriminator for differential
diagnosis
.
These data provide new insights into abrogation of
cell
cycle control during
B cell
lymphomagenesis and suggest that combined analysis of origin licensing factors may contribute to improved treatment decisions and prognosis in haematopoietic malignancies.
[MeSH-major]
DNA Replication. DNA, Neoplasm / genetics.
Lymphoma
, B-
Cell
/ pathology
[MeSH-minor]
Biomarkers, Tumor / metabolism.
Cell
Cycle.
Cell
Cycle Proteins / metabolism.
Cell
Transformation, Neoplastic / pathology.
Diagnosis
, Differential. Flow Cytometry / methods. Geminin. Humans. Ki-67 Antigen / metabolism.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ metabolism. Minichromosome Maintenance Complex Component 2. Mitosis. Neoplasm Proteins / metabolism. Nuclear Proteins / metabolism. Tumor Cells, Cultured
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(PMID = 15682442.001).
[ISSN]
0022-3417
[Journal-full-title]
The Journal of pathology
[ISO-abbreviation]
J. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / GMNN protein, human; 0 / Geminin; 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; EC 3.6.4.12 / MCM2 protein, human; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2
55.
Deaglio S, Vaisitti T, Zucchetto A, Gattei V, Malavasi F:
CD38 as a molecular compass guiding topographical decisions of chronic lymphocytic leukemia cells.
Semin Cancer Biol
; 2010 Dec;20(6):416-23
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[Title]
CD38 as a molecular compass guiding topographical decisions of
chronic
lymphocytic
leukemia
cells.
CLL
is characterized by a dynamic balance between cells proliferating in the
lymphoid
organs and circulating cells resisting programmed
cell
death.
Regulating this equilibrium entails complex interactions between tumor and host, modulated by a set of surface molecules expressed by the
CLL
cell
according to environmental conditions.
The CD38 surface molecule is an independent negative prognostic factor expressed by approximately one-third
of CLL
patients.
CD38(+)
CLL
cells can proliferate in vitro in the presence of anti-CD38 mAbs and IL-2 and are more sensitive to the effects of the CXCL12 chemokine.
Blockage of CD38 signals impairs
CLL
cell
movement from blood to
lymphoid
organs, as confirmed using animal models.
One model to be explored considers CD38 a key component of the
CLL
invadosome, a still hypothetical membrane domain containing adhesion molecules, chemokine receptors and matrix metalloproteases.
In addition to driving the clinical outcome of the
disease
, CD38 is thus an excellent candidate therapeutic target for a significant subset
of CLL
patients.
[MeSH-major]
Antigens, CD38 / immunology.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ immunology.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ metabolism
[MeSH-minor]
Animals.
Cell
Movement.
Cell
Proliferation.
Cell
Transformation, Neoplastic / genetics. Humans. Signal Transduction
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[Copyright]
Copyright © 2010 Elsevier Ltd. All rights reserved.
(PMID = 20817095.001).
[ISSN]
1096-3650
[Journal-full-title]
Seminars in cancer biology
[ISO-abbreviation]
Semin. Cancer Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
EC 3.2.2.5 / Antigens, CD38
56.
Li HX, Yan FH, Lei L:
[Effects of Porphyromonas gingivalis lipopolysaccharide on apoptotic genes in foam cells].
Zhonghua Kou Qiang Yi Xue Za Zhi
; 2010 May;45(5):274-8
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METHODS: Macrophages from THP-1 monocytes and foam cells from macrophages by oxLDL inducement were treated with oxidized
low
density lipoprotein (oxLDL) or oxLDL+ Pg-LPS.
Cell
apoptosis was detected by acridine orange-ethidium bromide (AO-EB) staining.
RESULTS: Pg-LPS enhanced
cell
apoptosis rate during and after foam cells formation [(5.47+/-0.93)% vs. (7.50+/-0.54)%].
PCR array demonstrated that it increased B-
cell
CLL
-
lymphoma
2 (BCL2) related protein A1 (BCL2A1) transcription during foam cells formation (>2 fold), and promoted BCL2 and BCL2A1 transcription after foam cells formation (>2 fold).
CONCLUSIONS: Pg-LPS affected apoptotic gene transcription during and after foam cells formation and enhanced
cell
apoptosis.
[MeSH-minor]
Caspase 3 / metabolism.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Gene Expression. Humans. Lipoproteins, LDL / pharmacology. Macrophages / physiology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Proto-Oncogene Proteins c-myc / metabolism. Tumor Suppressor Protein p53 / metabolism
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(PMID = 20654241.001).
[ISSN]
1002-0098
[Journal-full-title]
Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology
[ISO-abbreviation]
Zhonghua Kou Qiang Yi Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / BCL2-related protein A1; 0 / Lipopolysaccharides; 0 / Lipoproteins, LDL; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / Tumor Suppressor Protein p53; 0 / oxidized low density lipoprotein; EC 3.4.22.- / Caspase 3
57.
Brickner AG, Evans AM, Mito JK, Xuereb SM, Feng X, Nishida T, Fairfull L, Ferrell RE, Foon KA, Hunt DF, Shabanowitz J, Engelhard VH, Riddell SR, Warren EH:
The PANE1 gene encodes a novel human minor histocompatibility antigen that is selectively expressed in B-lymphoid cells and B-CLL.
Blood
; 2006 May 1;107(9):3779-86
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[Title]
The PANE1 gene encodes a novel human minor histocompatibility antigen that is selectively expressed in B-
lymphoid
cells and B-
CLL
.
Minor histocompatibility antigens (mHAg's) are peptides encoded by polymorphic genes that are presented by major histocompatibility complex (MHC) molecules and recognized by T cells in recipients of allogeneic hematopoietic
cell
transplants.
Here we report that an alternative transcript of the proliferation-associated nuclear element 1 (PANE1) gene encodes a novel human leukocyte antigen (HLA)-A(*)0301-restricted mHAg that is selectively expressed in B-
lymphoid
cells.
Sequencing of PANE1 alleles in mHAg-positive and mHAg-negative cells demonstrates that differential T-
cell
recognition is due to a single nucleotide polymorphism within the variant exon that replaces an arginine codon with a translation termination codon.
The PANE1 transcript that encodes the mHAg is expressed at high levels in resting CD19(+) B cells and B-lineage
chronic
lymphocytic
leukemia
(B-
CLL
) cells, and at significantly lower levels in activated B cells.
Activation of B-
CLL
cells through CD40 ligand (CD40L) stimulation decreases expression of the mHAg-encoding PANE1 transcript and reciprocally increases expression of PANE1 transcripts lacking the mHAg-encoding exon.
These studies suggest distinct roles for different PANE1 isoforms in resting compared with activated CD19(+) cells, and identify PANE1 as a potential therapeutic target in B-
CLL
.
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Immunogenetics. 2002 Nov;54(8):562-9
[
12439619.001
]
(PMID = 16391015.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA18029; United States / NIAID NIH HHS / AI / AI339933; United States / NIAID NIH HHS / AI / AI44134; United States / NIAID NIH HHS / AI / AI20963; United States / NCI NIH HHS / CA / CA106512
[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 / Antigens, CD19; 0 / Epitopes; 0 / HLA-A Antigens; 0 / HLA-A*03:01 antigen; 0 / HLA-A3 Antigen; 0 / Minor Histocompatibility Antigens; 0 / Nuclear Proteins; 0 / proliferation associated nuclear element protein 1, human; 9007-49-2 / DNA
[Other-IDs]
NLM/ PMC1895781
58.
Escolar E, García-Vela J, Aladro Y, Martínez-Menéndez B, Martín A:
[Mononeuropathy in chronic lymphatic leukaemia].
Rev Neurol
; 2007 Aug 16-31;45(4):233-5
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[Title]
[Mononeuropathy in
chronic
lymphatic leukaemia
].
[Transliterated title]
Mononeuropatía en la
leucemia
linfática crónica.
INTRODUCTION:
Chronic
lymphatic leukaemia
(
CLL
) is the most frequent form
of leukaemia
in the adult population in western countries.
Only 7.2% of the complications
of CLL
are neurological and most of them are secondary to an infection by herpes zoster virus.
CASE REPORT: We report the case
of a
71-year-old female with B-
type CLL
in stage IV or
type C
that was progressing and becoming
diffuse
large B-
cell
lymphoma
(Richter's syndrome), who developed an incomplete axonotmesis of the left peroneal nerve and numerous violet-coloured nodules under the skin in the left knee.
Magnetic resonance imaging showed signs
of diffuse
infiltration into the subcutaneous tissue and the muscles of the left
leg
; a biopsy study of one of the subcutaneous nodules revealed a
lymphoid
infiltration by large B-cells.
In this patient, the injury to the left peroneal nerve was probably secondary to a
lymphoid
infiltration of the nerve from adjacent infiltrated soft tissues.
CONCLUSION: Peripheral neuropathy due to direct infiltration can be a neurological complication
of CLL
that has not be reported to date, but which is known to occur in other lymphoproliferative processes.
[MeSH-major]
Leukemia
,
Lymphoid
/ complications. Nervous System Diseases / etiology
[MeSH-minor]
Adult. Aged.
Chronic
Disease
. Female. Humans. Karyotyping
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.
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.
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(PMID = 17668406.001).
[ISSN]
0210-0010
[Journal-full-title]
Revista de neurologia
[ISO-abbreviation]
Rev Neurol
[Language]
spa
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Spain
59.
Burton BJ, Cunningham ET Jr, Cree IA, Pavesio CE:
Eye involvement mimicking scleritis in a patient with chronic lymphocytic leukaemia.
Br J Ophthalmol
; 2005 Jun;89(6):775-6
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[Title]
Eye involvement mimicking scleritis
in a
patient with
chronic
lymphocytic leukaemia
.
[MeSH-major]
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ pathology. Leukemic Infiltration /
diagnosis
. Sclera / pathology. Scleritis /
diagnosis
[MeSH-minor]
Aged. Aged, 80 and over.
Diagnosis
, Differential. Humans. Male
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[Cites]
Eye (Lond). 2003 Jan;17(1):27-30
[
12579166.001
]
[Cites]
Arch Ophthalmol. 1961 Oct;66:490-508
[
13860566.001
]
[Cites]
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[
6342189.001
]
[Cites]
Br J Ophthalmol. 1968 Oct;52(10):781-5
[
5686969.001
]
(PMID = 15923522.001).
[ISSN]
0007-1161
[Journal-full-title]
The British journal of ophthalmology
[ISO-abbreviation]
Br J Ophthalmol
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
[Other-IDs]
NLM/ PMC1772664
60.
Gao Y, Kristinsson SY, Goldin LR, Björkholm M, Caporaso NE, Landgren O:
Increased risk for non-Hodgkin lymphoma in individuals with celiac disease and a potential familial association.
Gastroenterology
; 2009 Jan;136(1):91-8
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[Title]
Increased risk for non-Hodgkin
lymphoma in
individuals with celiac
disease
and a potential familial association.
BACKGROUND & AIMS: Celiac
disease
(CD), a common digestive
disease
, is
well
known to be associated with excess non-Hodgkin
lymphoma
(NHL) risk.
However, there are only
limited
data on risk in the current era of serologic testing and human leukocytes antigen typing to screen for CD.
There is also no information on the role of family history of CD in relation to
lymphoma
risk.
METHODS: We identified 37,869 NHL, 8323 Hodgkin
lymphoma
(HL), and 13,842
chronic
lymphocytic
leukemia
patients diagnosed in Sweden between 1965 and 2004, as
well
as 236,408 matched controls and 613,961 first-degree relatives.
RESULTS: Overall we found persons with a hospital discharge
diagnosis of
CD to have a 5.35-fold (95% CI, 3.56-8.06) increased NHL risk.
Risk of HL was borderline increased (OR=2.54, 95% CI, 0.99-6.56); however, there was no excess
chronic
lymphocytic
leukemia
risk.
Persons diagnosed with CD in 1975-1984, 1985-1994, and 1995-2004 had a 13.2-fold (95% CI, 3.63-48.0), 7.90-fold (95% CI, 3.38-18.5), and 3.84-fold (95% CI, 2.28-6.45) increased risk of NHL, respectively (P(trend)&
lt
; .0001).
Future studies are needed to explore the roles of gluten intake, secondary intestinal inflammation, and susceptibility genes in relation to subsequent risk of developing
lymphoma
.
[MeSH-major]
Celiac
Disease
/ complications. Celiac
Disease
/ genetics.
Lymphoma
, Non-Hodgkin / etiology
[MeSH-minor]
Adult. Aged. Female. Humans.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ etiology. Male. Middle Aged. Risk
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.
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.
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.
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.
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.
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[CommentIn]
Gastroenterology. 2009 Jan;136(1):32-4
[
19041868.001
]
(PMID = 18950631.001).
[ISSN]
1528-0012
[Journal-full-title]
Gastroenterology
[ISO-abbreviation]
Gastroenterology
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z01 CP004410-31
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS339011; NLM/ PMC3227529
61.
Crespo M, Villamor N, Giné E, Muntañola A, Colomer D, Marafioti T, Jones M, Camós M, Campo E, Montserrat E, Bosch F:
ZAP-70 expression in normal pro/pre B cells, mature B cells, and in B-cell acute lymphoblastic leukemia.
Clin Cancer Res
; 2006 Feb 1;12(3 Pt 1):726-34
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[Title]
ZAP-70 expression in normal pro/pre B cells, mature B cells, and in B-
cell
acute
lymphoblastic
leukemia
.
PURPOSE: The ZAP-70 gene is normally expressed in T and natural killer cells, where it is required for the T-
cell
receptor (TCR) signaling.
More recently, it has been described that ZAP-70 contributes to the B-
cell
development at early stages of B-
cell
differentiation in mice.
The purpose was to investigate the presence of ZAP-70 in normal pro/pre B cells and mature B cells and in tumoral cells from B-acute
lymphoblastic leukemias
(B-ALL).
Among tumoral cells, ZAP-70 was expressed in 56% of B-ALLs with pro/pre B-
cell
phenotype and in 4 of 6 Burkitt/ALL
lymphomas
.
CONCLUSIONS: Among normal B-
cell
subsets, ZAP-70 was found expressed in normal pro/pre B cells but not
in a
significant proportion of normal B cells with mature phenotype.
The lack of ZAP-70 expression in normal mature B cells suggests that its expression in mature-derived neoplasms with different cellular origin, such as Burkitt'
s lymphoma
and
chronic
lymphocytic
leukemia
, might be due to an aberrant phenomenon.
[MeSH-major]
B-
Lymphocytes
/ metabolism. Burkitt
Lymphoma
/ genetics. Gene Expression Regulation. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / metabolism. ZAP-70 Protein-Tyrosine Kinase / genetics
[MeSH-minor]
Adolescent. Adult. Aged. Child. DNA Mutational Analysis. Humans. Middle Aged. Phenotype. Phosphorylation. Receptors, Antigen, T-
Cell
/ metabolism
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(PMID = 16467082.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Receptors, Antigen, T-Cell; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
62.
Molica S, Digiesi G, Battaglia C, Cutrona G, Antenucci A, Molica M, Giannarelli D, Sperduti I, Gentile M, Morabito F, Ferrarini M:
Baff serum level predicts time to first treatment in early chronic lymphocytic leukemia.
Eur J Haematol
; 2010 Oct;85(4):314-20
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[Title]
Baff serum level predicts time to first treatment in early
chronic
lymphocytic
leukemia
.
We analyzed the correlation between
well
-established biological parameters of prognostic relevance in B-
cell chronic
lymphocytic
leukemia
(
CLL
) [i.e. mutational status of the immunoglobulin heavy chain variable region (IgVH), ZAP-70 and CD38 expression] and serum levels of
B cell
-activating factor (BAFF of the TNF family) by evaluating the impact of these variables on the time to first treatment (TFT)
in a
series of 169 previously untreated
CLL
patients in Binet stage A.
Higher levels of BAFF were more frequently associated with female gender (P=0.02), younger age (P=0.01), Rai stage 0 (P=0.002), higher platelet count (P=0.005), mutated IgVH
disease
(P=0.002), higher occurrence of normal cytogenetic profile or presence of 13q deletion (P=0.02),
low
ZAP-70- (P=0.003), and CD38-expression (P=0.02).
Maximally selected log-rank statistic plot identified a serum BAFF concentration of 0.313 ng/mL as the best cut-off (P&
lt
;0.0001).
This threshold recognized two subsets of patients with different TFT (P&
lt
;0.0001).
Because in multivariate analysis soluble BAFF [Hazard ratio (HR), 8.23; confidence Interval (CI) 95%,3.0-22.6, P&
lt
;0.0001] and mutational status of IgVH (HR=2.60; CI 95% 1.10-6.14, P=0.03) maintained the discriminating power their combined effect on clinical outcome was assessed.
(1)
low
-risk (n=93), patients with concordant IgVH(mut) and higher soluble BAFF;.
(2) intermediate-risk (n=50), patients with IgVH(mut) and
low
BAFF levels or IgVH(unmut) and soluble higher BAFF;(3) high-risk (n=26), patients with concordant IgVH (unmut) and
low
soluble BAFF, the 2-yr TFTs were, respectively, 95%, 85%, and 41% (P&
lt
;0.0001).
In conclusion, our results indicate that in early B-
cell
CLL
, the biological profile including among other parameters soluble BAFF may provide a useful insight into the complex interrelationship of prognostic variables.
[MeSH-major]
B-
Cell
Activating Factor / blood. Biomarkers, Tumor / blood.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ blood
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[Copyright]
© 2010 John Wiley & Sons A/S.
(PMID = 20546021.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / B-Cell Activating Factor; 0 / Biomarkers, Tumor; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38
63.
Caldas LA, Attias M, de Souza W:
Dynamin inhibitor impairs Toxoplasma gondii invasion.
FEMS Microbiol Lett
; 2009 Nov;301(1):103-8
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We found that previous incubation of the host cells, but not the parasites, with Dynasore,
a small
molecule that inhibits dynamin GTPase activity, markedly reduced the penetration of T. gondii tachyzoites into
LLC
-MK2 cells.
In contrast, parasite adhesion to the host
cell
surface increased, as observed both by light and electron microscopy.
Intriguingly, the few parasites internalized by Dynasore-treated cells remained in vacuoles located at the periphery of the
cell
, in contrast to the perinuclear localization seen in the control.
[MeSH-minor]
Animals.
Cell
Adhesion.
Cell
Line. Dose-Response Relationship, Drug. Host-Parasite Interactions. Humans. Hydrazones / administration & dosage. Macaca mulatta. Mice. Microscopy, Electron, Scanning. Microscopy, Electron, Transmission. Vacuoles / metabolism. Vacuoles / parasitology
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(PMID = 19817867.001).
[ISSN]
1574-6968
[Journal-full-title]
FEMS microbiology letters
[ISO-abbreviation]
FEMS Microbiol. Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Hydrazones; 0 / N'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide; EC 3.6.5.5 / Dynamins
64.
Guggisberg K, Jordan RC:
Mantle cell lymphoma of the oral cavity: case series and comprehensive review of the literature.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
; 2010 Jan;109(1):98-104
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[Title]
Mantle
cell
lymphoma of
the oral cavity: case series and comprehensive review of the literature.
OBJECTIVE: Mantle
cell
lymphoma
(MCL) is a rare B-
cell
neoplasm that has only recently been defined as a distinct entity.
Because of its rarity and histologic similarities to other
small
cell
lymphomas
, the microscopic
diagnosis of
MCL may be challenging.
This is particularly true within the oral cavity, where other
lymphomas
are more frequent.
Historical cases were reviewed, and available data regarding
morphology
, special stains, demographics, clinical presentation, radiographic findings, management, and outcome were extracted.
CONCLUSION: We conclude that MCL of the oral cavity is an uncommon
diagnosis
.
The microscopic
diagnosis
can be challenging, given its similar appearance to other
small
cell
lymphomas
, requiring a comprehensive immunohistochemical panel for the accurate
diagnosis
.
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[Copyright]
Copyright 2010 Mosby, Inc. All rights reserved.
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Tumori. 2005 Nov-Dec;91(6):456-62
[
16457141.001
]
(PMID = 19880332.001).
[ISSN]
1528-395X
[Journal-full-title]
Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
[ISO-abbreviation]
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
[Language]
ENG
[Grant]
United States / NIDCR NIH HHS / DE / T32 DE017249; United States / NIDCR NIH HHS / DE / T32 DE017249-04; United States / NIDCR NIH HHS / DE / T32 DE017249-05; United States / NIDCR NIH HHS / DE / DE017249-04; United States / NIDCR NIH HHS / DE / T32 DE019096-02; United States / NIDCR NIH HHS / DE / DE017249-01; United States / NCI NIH HHS / CA / R21 CA095231; United States / NIDCR NIH HHS / DE / DE019096-02; United States / NIDCR NIH HHS / DE / T32 DE017249-03; United States / NCI NIH HHS / CA / R33 CA095231; United States / NIDCR NIH HHS / DE / T32 DE019096; United States / NIDCR NIH HHS / DE / T32DE017249; United States / NIDCR NIH HHS / DE / DE019096-01; United States / NIDCR NIH HHS / DE / T32 DE017249-02; United States / NIDCR NIH HHS / DE / DE017249-02; United States / NIDCR NIH HHS / DE / T32 DE019096-01; United States / NIDCR NIH HHS / DE / DE017249-03; United States / NIDCR NIH HHS / DE / T32 DE017249-01; United States / NIDCR NIH HHS / DE / DE017249-05; United States / NIDCR NIH HHS / DE / T32DE019096; United States / NCI NIH HHS / CA / CA095231
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
United States
[Chemical-registry-number]
136601-57-5 / Cyclin D1
[Number-of-references]
29
[Other-IDs]
NLM/ NIHMS156688; NLM/ PMC2818374
65.
de Sanjosé S, Benavente Y, Nieters A, Foretova L, Maynadié M, Cocco PL, Staines A, Vornanen M, Boffetta P, Becker N, Alvaro T, Brennan P:
Association between personal use of hair dyes and lymphoid neoplasms in Europe.
Am J Epidemiol
; 2006 Jul 1;164(1):47-55
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[Title]
Association between personal use of hair dyes and
lymphoid
neoplasms in Europe.
The authors evaluated the risk of
lymphoid
malignancies associated with personal use of hair dyes.
The analysis included 2,302 incident cases of
lymphoid
neoplasms and 2,417 hospital- or population-based controls from the Czech Republic, France, Germany, Ireland, Italy, and Spain (1998-2003).
Lymphoma
risk among dye users was significantly increased by 19% in comparison with never use (odds ratio (OR) = 1.19, 95% confidence interval (CI): 1.00, 1.41) and by 26% among persons who used hair dyes 12 or more times per year (OR = 1.26, 95% CI: 1.00, 1.60; p for linear trend = 0.414).
Lymphoma
risk was significantly higher among persons who had started coloring their hair before 1980 (OR = 1.37, 95% CI: 1.09, 1.72) and persons who had used hair dyes only before 1980 (OR = 1.62, 95% CI: 1.10, 2.40).
Personal use of hair dyes is associated with a moderate increase
in lymphoma
risk, particularly among women and persons who used dyes before 1980.
[MeSH-major]
Hair Dyes / toxicity.
Lymphoma
/ chemically induced.
Lymphoma
/ epidemiology
[MeSH-minor]
Adult. Aged. Case-Control Studies. Confidence Intervals. Europe / epidemiology. Female. Hodgkin
Disease
/ chemically induced. Hodgkin
Disease
/ epidemiology. Humans.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ chemically induced.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ epidemiology.
Lymphoma
, Follicular / chemically induced.
Lymphoma
, Follicular / epidemiology. Lymphoproliferative Disorders / chemically induced. Lymphoproliferative Disorders / epidemiology. Male. Middle Aged. Odds Ratio. Risk Assessment. Risk Factors
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(PMID = 16731576.001).
[ISSN]
0002-9262
[Journal-full-title]
American journal of epidemiology
[ISO-abbreviation]
Am. J. Epidemiol.
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Hair Dyes
66.
Wei J, Zhou S, Bachem MG, Debatin KM, Beltinger C:
Infiltration of blood outgrowth endothelial cells into tumor spheroids: role of matrix metalloproteinases and irradiation.
Anticancer Res
; 2007 May-Jun;27(3B):1415-21
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MATERIALS AND METHODS: Infiltration of BOECs into spheroids made of tumor cells and fibroblasts was determined in the presence
of low
-dose EDTA, a potent inhibitor of MMPs.
RESULTS: Infiltration of BOECs into spheroids was blocked by
low
-dose EDTA.
Irradiation enhanced secretion of MMP-2 and, less so, of MMP-9 by tumor-stromal cells and tumor cells, and increased the amount of MMP-2 and -9 in subcutaneous
LLC
tumors.
[MeSH-major]
Blood Cells / physiology.
Cell
Movement. Endothelial Cells / physiology. Matrix Metalloproteinase 2 / physiology. Matrix Metalloproteinase 9 / physiology. Spheroids, Cellular / physiology
Hazardous Substances Data Bank.
Disodium EDTA
.
Hazardous Substances Data Bank.
ETHYLENEDIAMINE TETRAACETIC ACID
.
Hazardous Substances Data Bank.
DISODIUM CALCIUM EDTA
.
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(PMID = 17595756.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Matrix Metalloproteinase Inhibitors; 9G34HU7RV0 / Edetic Acid; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
67.
Rankin JS, Orozco RE, Rodgers TL, Alfery DD, Glower DD:
"Adjustable" artificial chordal replacement for repair of mitral valve prolapse.
Ann Thorac Surg
; 2006 Apr;81(4):1526-8
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Gore & Associates Inc, Flagstaff, AZ) artificial chordal replacement and Carpentier ring annuloplasty (Edwards Lifesciences
LLC
, Irvine, CA), without leaflet resection.
Only 1 of 52 patients (1.9%) experienced late failure, and this patient was
re
-repaired with artificial chords.
Thus, "adjustable" artificial chordal replacement facilitates uniform repair of mitral valve prolapse with
a low
late failure rate.
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(PMID = 16564319.001).
[ISSN]
1552-6259
[Journal-full-title]
The Annals of thoracic surgery
[ISO-abbreviation]
Ann. Thorac. Surg.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
68.
Suresh K, Rodriguez-Lecompte JC, Gauldie J, Foley R:
Recent advances in immunotherapy of B-CLL using ex vivo modified dendritic cells.
Hematology
; 2005 Jun;10(3):189-203
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[Title]
Recent advances in immunotherapy of B-
CLL
using ex vivo modified dendritic cells.
Chronic
lymphocytic
leukemia
(
CLL
) results from the relentless accumulation
of small
mature, slowly dividing, monoclonal B-
lymphocytes
.
The clinical course is heterogeneous, some patients with aggressive form of the
disease
progressing rapidly with early death while others exhibit a more stable, possibly, non-progressing indolent
type of
the
disease
lasting many years.
Despite progress in modern treatment modalities, relapse invariably occurs and
disease
still remains incurable.
The clinical management
of CLL
is therefore challenging and considerable effort has been directed towards novel therapeutic strategies aimed at reducing minimal residual
disease
which can increase remission duration.
Ex-vivo modified and monocyte-derived DCs represents a promising approach within the context
of CLL
.
After a brief survey of general properties of DCs, this review focuses on the different approaches exploiting monocyte-derived DCs
in CLL
, which may help to design novel strategies for phase-I clinical trials.
[MeSH-major]
Dendritic Cells / transplantation. Immunotherapy, Adoptive.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ therapy. Monocytes / transplantation
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(PMID = 16019468.001).
[ISSN]
1024-5332
[Journal-full-title]
Hematology (Amsterdam, Netherlands)
[ISO-abbreviation]
Hematology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
109
69.
Hwang HS, Min YS, Lee SC, Sun MK, Lim HS:
Change of lip-line cant after 1-jaw orthognathic surgery in patients with mandibular asymmetry.
Am J Orthod Dentofacial Orthop
; 2009 Oct;136(4):564-9
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INTRODUCTION: The purpose of this study was to investigate the change of lip-line cant (
LLC
) after 1-jaw orthognathic surgery in mandibular asymmetry patients.
LLC
was measured in the preoperative and postoperative frontal photographs, and its change was correlated with various craniofacial measurements obtained from preoperative and postoperative frontal cephalograms and maxillofacial 3-dimensional computed tomography images.
RESULTS: Although these subjects had 2.4 degrees
of LLC
on average before surgery,
LLC
improved to 0.5 degrees after surgery, and the change (1.9 degrees ) was statistically significant.
In the correlation analysis, preoperative
LLC
showed positive correlations with menton deviation and mandibular anterior occlusal plane cant.
In the correlation analysis
of LLC
change, it had positive correlations with preoperative
LLC
and mandibular anterior occlusal plane cant and preoperative and postoperative change of menton deviation.
CONCLUSIONS: These results suggest that
LLC
is present with chin deviation, even without significant maxillary canting, and can be improved considerably by 1-jaw surgery alone.
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(PMID = 19815160.001).
[ISSN]
1097-6752
[Journal-full-title]
American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics
[ISO-abbreviation]
Am J Orthod Dentofacial Orthop
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
70.
Collins SA, Buhles A, Scallan MF, Harrison PT, O'Hanlon DM, O'Sullivan GC, Tangney M:
AAV2-mediated in vivo immune gene therapy of solid tumours.
Genet Vaccines Ther
; 2010;8:8
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METHODS: Immune-competent Balb/C or C57 mice bearing subcutaneous JBS fibrosarcoma or Lewis Lung Carcinoma (
LLC
) tumour xenografts respectively were treated by intra-tumoural administration of AAV2 vector encoding the immune up-regulating cytokine granulocyte macrophage-colony stimulating factor (GM-CSF) and the co-stimulatory molecule B7-1 to subcutaneous tumours, either alone or in combination with intra-muscular (IM) delivery of AAV2 vector encoding Nk4 14 days prior to tumour induction.
Cured animals were
re
-challenged with tumourigenic doses of the original tumour
type
.
In vivo cytotoxicity assays were used to investigate establishment of
cell
-mediated responses in treated animals.
RESULTS: AAV2-mediated GM-CSF, B7-1 treatment resulted
in a
significant reduction in tumour growth and an increase in survival in both tumour models.
Cured animals were resistant to
re
-challenge, and induction of T
cell
mediated anti-tumour responses were demonstrated.
CONCLUSIONS: Overall, this study demonstrates the potential for in vivo AAV2 mediated immune gene therapy, and provides data on the inter-relationship between tumour vasculature and immune
cell
recruitment.
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(PMID = 21172020.001).
[ISSN]
1479-0556
[Journal-full-title]
Genetic vaccines and therapy
[ISO-abbreviation]
Genet Vaccines Ther
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC3016353
71.
Küçköztaş MF, Ozgünes N, Yazici S:
[Investigation of the relationship between hepatitis c virus (HCV) genotypes with HCV-RNA and alanine aminotransferase levels in chronic hepatitis c patients].
Mikrobiyol Bul
; 2010 Jan;44(1):111-5
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[Title]
[Investigation of the relationship between hepatitis c virus (HCV) genotypes with HCV-RNA and alanine aminotransferase levels in
chronic
hepatitis c patients].
The objective of this retrospective study was to determine the distribution of HCV genotypes in patients with
chronic
hepatitis C infection at our region and to investigate the relation between genotypes and serum alanine aminotransferase (ALT) and HCV-RNA levels.
Serum samples from 52 patients (26 females, 26 males; mean age: 51.07 +/- 13.13 years) with
chronic
HCV infection were analyzed in this study.
Viral genotypes were determined by using the Versant HCV genotype assay (LiPA) 2.0 system (Bayer HealthCare
LLC
, USA) according to the manufacturer's instructions.
The mean age of the patients infected with genotype 1 (51.4 +/- 12.6 years) we e statistically significantly higher than the mean age of the patients infected with
type
2 and 3 (37.8 +/- 12.3 years), (p = 0.023).
[MeSH-major]
Alanine Transaminase / blood. Hepacivirus / genetics. Hepatitis C,
Chronic
/ enzymology. Hepatitis C,
Chronic
/ virology. RNA, Viral / blood
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(PMID = 20455406.001).
[ISSN]
0374-9096
[Journal-full-title]
Mikrobiyoloji bülteni
[ISO-abbreviation]
Mikrobiyol Bul
[Language]
tur
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Turkey
[Chemical-registry-number]
0 / RNA, Viral; EC 2.6.1.2 / Alanine Transaminase
72.
Kano R, Sato E, Okamura T, Watanabe S, Hasegawa A:
Expression of Bcl-2 in feline lymphoma cell lines.
Vet Clin Pathol
; 2008 Mar;37(1):57-60
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[Title]
Expression of Bcl-2 in feline
lymphoma
cell
lines.
Bcl-2 has been shown to repress
cell
death triggered by a diverse array of stimuli, including chemotherapy and gamma irradiation.
OBJECTIVE: The purpose of this study was to determine feline Bcl-2 expression level in feline
lymphoma
cells using an immunoblot assay with anti-human and anti-canine Bcl-2 monoclonal antibodies.
An immunoblot assay using the monoclonal antibodies was carried out to determine the level of feline Bcl-2 expression
in lymphoma
and
lymphocytic
leukemia cell
lines.
RESULTS: The recombinant feline Bcl-2 protein produced
in E
. coli had a molecular weight of about 26 kDa and was detected by immunoblot assay by using anti-human Bcl-2 mouse monoclonal antibody.
Feline Bcl-2 expression was high
in lymphoma
cell
lines (FL-74-UDC-1 and FT-1) and
low in
the
cell
line from peripheral blood mononuclear cells from a healthy cat (FeTJ-1) but not
low in
freshly isolated peripheral blood mononuclear cells from a healthy cat.
CONCLUSIONS: These results confirm the expression of Bcl-2 in T-
cell
lymphoma
cell
lines and indicate that it is suitable to detect feline Bcl-2 using an immunoblot assay.
Pending further evaluation, Bcl-2 expression might be useful in the differential
diagnosis of
feline tumors.
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(PMID = 18366545.001).
[ISSN]
0275-6382
[Journal-full-title]
Veterinary clinical pathology
[ISO-abbreviation]
Vet Clin Pathol
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Proto-Oncogene Proteins c-bcl-2
73.
Edwards TB, Gartsman GM, O'Connor DP, Sarin VK:
Safety and utility of computer-aided shoulder arthroplasty.
J Shoulder Elbow Surg
; 2008 May-Jun;17(3):503-8
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This study evaluated the safety and utility
of a
novel, image-free, shoulder navigation system
in a
cadaver and in an initial cohort of shoulder arthroplasty patients.
Shoulder arthroplasty was performed on a cadaver and 27 patients using an image-free navigation system (NaviProtrade mark; Kinamed Navigation Systems
LLC
, Camarillo, CA).
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(PMID = 18262802.001).
[ISSN]
1532-6500
[Journal-full-title]
Journal of shoulder and elbow surgery
[ISO-abbreviation]
J Shoulder Elbow Surg
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
74.
Yang C, Kaushal V, Shah SV, Kaushal GP:
Mcl-1 is downregulated in cisplatin-induced apoptosis, and proteasome inhibitors restore Mcl-1 and promote survival in renal tubular epithelial cells.
Am J Physiol Renal Physiol
; 2007 Jun;292(6):F1710-7
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Mcl-1 is an antiapoptotic member of the Bcl-2 family that plays an important role in
cell
survival.
We demonstrate that proteasome-dependent regulation of Mcl-1 plays a critical role in renal tubular epithelial
cell
injury from cisplatin.
Protein levels of Mcl-1 rapidly declined
in a
time-dependent manner following cisplatin treatment
of LLC
-PK(1) cells.
[MeSH-minor]
Animals. Caspase 3 / metabolism.
Cell
Survival / drug effects. Fluorescent Antibody Technique.
LLC
-PK1 Cells. Myeloid
Cell Leukemia
Sequence 1 Protein. Reverse Transcriptase Polymerase Chain Reaction. Swine
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(PMID = 17311906.001).
[ISSN]
1931-857X
[Journal-full-title]
American journal of physiology. Renal physiology
[ISO-abbreviation]
Am. J. Physiol. Renal Physiol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; EC 3.4.22.- / Caspase 3; Q20Q21Q62J / Cisplatin
75.
Saygili EI, Aksoy N, Pehlivan M, Sever T, Yilmaz M, Cimenci IG, Pehlivan S:
Enzyme levels and G-463A polymorphism of myeloperoxidase in chronic lymphocytic leukemia and multiple myeloma.
Leuk Lymphoma
; 2009 Dec;50(12):2030-7
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[Title]
Enzyme levels and G-463A polymorphism of myeloperoxidase in
chronic
lymphocytic
leukemia
and multiple myeloma.
The aim of this study was to investigate how myeloperoxidase (MPO) G-463A gene polymorphism and enzyme levels varied among patients with
chronic
lymphocytic
leukemia
(
CLL
) and multiple myeloma (MM) and to find the relationship between the MPO gene, enzyme levels, and clinical parameters.
We studied the sera from 40 healthy volunteers, patients with
CLL
(n = 34) and MM (n = 28).
In subjects with homozygote GG genotype, MPO levels were higher in the patients with both
CLL
and MM than in the control group.
This difference was statistically significant in patients with
CLL
.
In accordance with the results of the study, we assess that the increase in the MPO enzyme level in the patient groups with
CLL
and MM generated bactericidal effects as
well
as the increased formation of ROP, thus setting off a pro-
cell
death pathway and playing a role on the pathogenesis of lymphoproliferative malignancies through this mechanism.
[MeSH-major]
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics. Multiple Myeloma / genetics. Peroxidase / genetics
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(PMID = 19814685.001).
[ISSN]
1029-2403
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
EC 1.11.1.7 / Peroxidase
76.
Horie R, Watanabe M, Okamura T, Taira M, Shoda M, Motoji T, Utsunomiya A, Watanabe T, Higashihara M, Umezawa K:
DHMEQ, a new NF-kappaB inhibitor, induces apoptosis and enhances fludarabine effects on chronic lymphocytic leukemia cells.
Leukemia
; 2006 May;20(5):800-6
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[Title]
DHMEQ, a new NF-kappaB inhibitor, induces apoptosis and enhances fludarabine effects on
chronic
lymphocytic
leukemia
cells.
Chronic
lymphocytic
leukemia
(
CLL
) is
a low
-
grade
lymphoid
malignancy
incurable with conventional modalities of chemotherapy.
Strong and constitutive nuclear factor kappa B (NF-kappaB) activation is a characteristic
of CLL
cells.
We examined the effects
of a
new NF-kappaB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on
CLL
cells.
Dehydroxymethylepoxyquinomicin completely abrogated constitutive NF-kappaB activity and induced apoptosis
of CLL
cells.
Dehydroxymethylepoxyquinomicin also inhibited NF-kappaB induced by CD40 and enhanced fludarabine-mediated apoptosis
of CLL
cells.
Results of this study suggest that inhibition of constitutive and inducible NF-kappaB by DHMEQ in combination with fludarabine is a promising strategy for the treatment
of CLL
.
[MeSH-major]
Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Benzamides / pharmacology. Cyclohexanones / pharmacology.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ drug therapy. NF-kappa B / antagonists & inhibitors. Vidarabine / analogs & derivatives
[MeSH-minor]
Aged. Aged, 80 and over. Antigens, CD40 / drug effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. CASP8 and FADD-Like Apoptosis Regulating Protein. Caspases / drug effects. Caspases / metabolism.
Cell
Line, Tumor.
Cell
Survival / drug effects. Down-Regulation. Drug Synergism. Female. Humans. Inhibitor of Apoptosis Proteins / drug effects. Inhibitor of Apoptosis Proteins / metabolism. Intracellular Signaling Peptides and Proteins / drug effects. Intracellular Signaling Peptides and Proteins / metabolism. Male. Middle Aged. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Cells, Cultured. bcl-X Protein / drug effects. bcl-X Protein / metabolism
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(PMID = 16525497.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD40; 0 / Antineoplastic Agents; 0 / BCL2-related protein A1; 0 / Benzamides; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Cyclohexanones; 0 / Inhibitor of Apoptosis Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; 0 / dehydroxymethylepoxyquinomicin; EC 3.4.22.- / Caspases; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
77.
Kojima M, Sato E, Oshimi K, Murase T, Koike T, Tsunoda S, Matsumoto T, Marutsuka K, Ogiya D, Moriuchi M, Tokunaka M, Yara Kikuti Y, Kikuchi T, Nakamura N, Ando K:
Characteristics of CD5-positive splenic marginal zone lymphoma with leukemic manifestation ; clinical, flow cytometry, and histopathological findings of 11 cases.
J Clin Exp Hematop
; 2010;50(2):107-12
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[Title]
Characteristics of CD5-positive splenic marginal zone
lymphoma
with leukemic manifestation ; clinical, flow cytometry, and histopathological findings of 11 cases.
Splenic marginal zone
lymphoma
(SP-MZL) is a rare
low
-
grade
B-
cell
neoplasm that often shows leukemic manifestation.
The clinical characteristics of these cases did not
differ
from those of CD5-negative SP-MZL.
Flow cytometry revealed positive results as follows : CD3, 0/9 ; CD5, 11/11 ; CD10, 0/11 ; CD11c, 4/10, CD13, 5/11 ; CD19, 11/11 ; CD20, 10/11 ; CD21, 4/4 ; CD22, 7/7 ; CD23, 5/10 ; CD25, 8/11 ; FMC7, 5/7 ; κ
type
6/9, and λ
type
2/9.
Immunohistochemistry showed that the
lymphoma
cells were positive for CD5, CD20, and BCL-2 and negative for CD3, CD10, cyclin D1, BCL-6, and MUM-1 in all 11 cases.
These results suggest that CD5-positive SP-MZL differs from B-
cell chronic
lymphocytic
leukemia
, that CD13 expression is found in about half of CD5-positive SP-MZL cases, and that CD5-positive SP-MZL may be related to memory B-
cell
neoplasm or plasma
cell
differentiation.
[MeSH-major]
Antigens, CD5 / metabolism.
Lymphoma
, B-
Cell
, Marginal Zone / metabolism.
Lymphoma
, B-
Cell
, Marginal Zone / pathology. Splenic Neoplasms / metabolism. Splenic Neoplasms / pathology
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(PMID = 21123968.001).
[ISSN]
1880-9952
[Journal-full-title]
Journal of clinical and experimental hematopathology : JCEH
[ISO-abbreviation]
J Clin Exp Hematop
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antigens, CD5; 0 / Biomarkers, Tumor
78.
Kreitman RJ, Pastan I:
Immunotoxins in the treatment of hematologic malignancies.
Curr Drug Targets
; 2006 Oct;7(10):1301-11
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Immunotoxins, composed of protein toxins connected to
cell
binding ligands including monoclonal antibodies and growth factors, have been developed for several decades to target hematologic malignancies.
Plant toxins, particularly ricin, are useful for chemically conjugating to monoclonal antibodies, and have shown clinical activity in several types
of lymphoma
and
leukemia
.
Their dose is generally
limited
by vascular leak syndrome.
Denileukin diftitox has shown efficacy in cutaneous T-
cell
lymphoma
,
chronic
lymphocytic
leukemia
, and non-Hodgkin'
s lymphoma
.
Recombinant immunotoxin BL22 is an anti-CD22 Fv fragment fused to truncated Pseudomonas exotoxin; it induces complete remissions
in a
high percentage of patients with chemoresistant hairy
cell leukemia
.
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(PMID = 17073592.001).
[ISSN]
1873-5592
[Journal-full-title]
Current drug targets
[ISO-abbreviation]
Curr Drug Targets
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Immunotoxins
[Number-of-references]
235
79.
Marina O, Hainz U, Biernacki MA, Zhang W, Cai A, Duke-Cohan JS, Liu F, Brusic V, Neuberg D, Kutok JL, Alyea EP, Canning CM, Soiffer RJ, Ritz J, Wu CJ:
Serologic markers of effective tumor immunity against chronic lymphocytic leukemia include nonmutated B-cell antigens.
Cancer Res
; 2010 Feb 15;70(4):1344-55
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[Title]
Serologic markers of effective tumor immunity against
chronic
lymphocytic
leukemia
include nonmutated B-
cell
antigens.
Patients with
chronic
lymphocytic
leukemia
(
CLL
) who relapse after allogeneic transplant may achieve durable remission following donor lymphocyte infusion (DLI), showing the potency of donor-derived immunity in eradicating tumors.
We sought to elucidate the antigenic basis of the effective graft-versus-
leukemia
(GvL) responses associated with DLI for the treatment
of CLL
by analyzing the specificity of plasma antibody responses developing in two DLI-treated patients who achieved
long
-term remission without graft-versus-host
disease
.
Along with additional candidate antigens DAPK3, SERBP1, and OGFOD1, these proteins showed higher transcript and protein expression in B cells and
CLL
cells compared with normal peripheral blood mononuclear cells.
Although ZFYVE19, DAPK3, and OGFOD1 elicited minimal antibody reactivity in 12 normal subjects and 12 chemotherapy-treated
CLL
patients, 5 of 12
CLL
patients with clinical GvL responses were serologically reactive to these antigens.
Moreover, antibody reactivity against these antigens was temporally correlated with clinical
disease
regression.
These B-
cell
antigens represent promising biomarkers of effective anti-
CLL
immunity.
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Blood. 2005 Dec 15;106(13):4389-96
[
16131571.001
]
(PMID = 20124481.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / 5R21CA115043-2; United States / NCI NIH HHS / CA / R21 CA132232-02; United States / NCI NIH HHS / CA / P01 CA078378; United States / NCI NIH HHS / CA / P01 CA155258; United States / NCI NIH HHS / CA / CA132232-02; United States / NCI NIH HHS / CA / R21 CA132232; United States / NCI NIH HHS / CA / R21 CA115043; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / P50 CA100707
[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.; Validation Studies
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Surface; 0 / Biomarkers, Tumor; 0 / Immunodominant Epitopes
[Other-IDs]
NLM/ NIHMS167268; NLM/ PMC2852266
80.
Kokhaei P, Palma M, Mellstedt H, Choudhury A:
Biology and treatment of chronic lymphocytic leukemia.
Ann Oncol
; 2005;16 Suppl 2:ii113-23
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[Title]
Biology and treatment of
chronic
lymphocytic
leukemia
.
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(PMID = 15958440.001).
[ISSN]
0923-7534
[Journal-full-title]
Annals of oncology : official journal of the European Society for Medical Oncology
[ISO-abbreviation]
Ann. Oncol.
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Genetic Markers
[Number-of-references]
90
81.
Majumder D, Banerjee D, Chandra S, Banerjee S, Chakrabarti A:
Red cell morphology in leukemia, hypoplastic anemia and myelodysplastic syndrome.
Pathophysiology
; 2006 Dec;13(4):217-25
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[Title]
Red
cell
morphology in
leukemia
, hypoplastic anemia and myelodysplastic syndrome.
In the present work, we have studied the overall
morphology of
intact red cells in different leukemic patients along with patients of hypoplastic anemia (HPA) by scanning electron microscopy.
We have also studied the ultrastructure of the red
cell
surface membranes by transmission electron microscopy.
We have shown direct evidence of the altered red
cell
(RBC) membrane
morphology
irrespective of the hemoglobin status of the patients which includes (1) presence of large central holes in RBCs of acute myeloid
leukemia
(AML), (2) presence of thorn- and horn-like structure in RBCs of acute
lymphoblastic
leukemia
(ALL) and
chronic
myeloid
leukemia
(CML) and (3) flaccid appearance of RBCs in
chronic
lymphocytic
leukemia
(
CLL
) patients.
TEM studies revealed presence of pores with diameters ranging from 100 to 200nm on the RBC membrane surface of myeloid
leukemia
with AML being the most prominent among others.
Such pathophysiological alterations of the RBC
morphology in
leukemic patients could be identified as characteristic signature of the onset of anemia associated with the
disease
.
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(PMID = 16876391.001).
[ISSN]
0928-4680
[Journal-full-title]
Pathophysiology : the official journal of the International Society for Pathophysiology
[ISO-abbreviation]
Pathophysiology
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
Netherlands
82.
Trachootham D, Zhang H, Zhang W, Feng L, Du M, Zhou Y, Chen Z, Pelicano H, Plunkett W, Wierda WG, Keating MJ, Huang P:
Effective elimination of fludarabine-resistant CLL cells by PEITC through a redox-mediated mechanism.
Blood
; 2008 Sep 1;112(5):1912-22
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[Title]
Effective elimination of fludarabine-resistant
CLL
cells by PEITC through a redox-mediated mechanism.
Chronic
lymphocytic
leukemia
(
CLL
) is the most common adult
leukemia
, and resistance to fludarabine-based therapies is a major challenge
in CLL
treatment.
Because
CLL
cells are known to have elevated levels of reactive oxygen species (ROS), we aimed to test a novel ROS-mediated strategy to eliminate fludarabine-resistant
CLL
cells based on this redox alteration.
Using primary
CLL
cells and normal
lymphocytes
from patients (n = 58) and healthy subjects (n = 12), we showed that both fludarabine-resistant and -sensitive
CLL
cells were highly sensitive to beta-phenylethyl isothiocyanate (PEITC) with mean IC(50) values of 5.4 microM and 5.1 microM, respectively.
Normal
lymphocytes
were significantly less sensitive to PEITC (IC(50) = 27 microM, P &
lt
; .001).
CLL
cells exhibited intrinsically higher ROS level and lower cellular glutathione, which were shown to be the critical determinants
of CLL
sensitivity to PEITC.
Exposure
of CLL
cells to PEITC induced severe glutathione depletion, ROS accumulation, and oxidation of mitochondrial cardiolipin leading to massive
cell
death.
Such ROS stress also caused deglutathionylation of MCL1, followed by a rapid degradation of this
cell
survival molecule.
Our study demonstrated that the natural compound PEITC is effective in eliminating fludarabine-resistant
CLL
cells through a redox-mediated mechanism with
low
toxicity to normal
lymphocytes
, and warrants further clinical evaluation.
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Cell Death Differ. 2004 Jul;11 Suppl 1:S73-85
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(PMID = 18574029.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA100428; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA085563; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA109041; United States / NCI NIH HHS / CA / R01 CA109041; United States / NCI NIH HHS / CA / CA100428; United States / NCI NIH HHS / CA / CA085563
[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 / Antineoplastic Agents; 0 / Isothiocyanates; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Reactive Oxygen Species; 6U7TFK75KV / phenethyl isothiocyanate; 9007-43-6 / Cytochromes c; EC 1.11.1.9 / Glutathione Peroxidase; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; FA2DM6879K / Vidarabine; GAN16C9B8O / Glutathione; P2K93U8740 / fludarabine
[Other-IDs]
NLM/ PMC2518893
83.
Reuters I, Weber M, Schulze-Lohoff E:
Rho/Rho kinase pathway regulates maintenance of the differentiated tubular epithelial cell phenotype on laminin-1.
Nephron Physiol
; 2006;104(2):p95-p106
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[Title]
Rho/Rho kinase pathway regulates maintenance of the
differentiated
tubular epithelial
cell
phenotype on laminin-1.
BACKGROUND: Maintenance
of a
polarized tubular epithelium by appropriate intracellular signaling and extracellular matrix is critical both in normal renal function as
well
as in acute and
chronic
tubular injury.
We examined the hypothesis that maintenance
of a differentiated
epithelial phenotype on the basement membrane glycoprotein laminin-1 is controlled by the Rho/Rho kinase pathway.
METHODS: Using the tubular epithelial
cell
lines
LLC
-PK1 and MDCK which were cultured on laminin-1 vs. collagen IV, we analyzed
cell
morphology
and motility (cohort migration assay) as
well
as expression of differentiation and dedifferentiation markers (immunofluorescence microscopy).
RESULTS: Cohort migration
of LLC
-PK1 cells was significantly slowed down on laminin-1 (10.7 +/- 2.2 m.u. (migratory units)) compared with collagen IV (16.6 +/- 2.3 m.u.
In parallel to the increased migratory activity, inhibition of the Rho/Rho kinase pathway resulted
in a
more mesenchymal phenotype
of LLC
-PK1 cells on laminin-1 with increased formation of lamellopodia and filopodia, distinct loss of focal contacts and stress fibers, upregulation of the dedifferentiation marker vimentin, and loss of
cell
-
cell
contacts with translocation of beta-catenin from the adherens junctions to the cytosol and nucleus.
Similarly, cohort migration of MDCK cells was retarded on laminin-1 when compared with collagen IV, and addition of the Rho kinase inhibitor Y27632 resulted in enhanced motility and a change in
cell
morphology
.
CONCLUSION: The study demonstrates that the Rho/Rho kinase pathway is required to maintain a non-migratory epithelial phenotype of cultured renal tubular
LLC
-PK1 and MDCK cells on the basement membrane glycoprotein laminin-1.
[MeSH-minor]
Animals.
Cell
Differentiation.
Cell
Line.
Cell
Movement. Dogs. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Phenotype. Signal Transduction / drug effects. Signal Transduction / physiology. Swine. rho-Associated Kinases
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[Copyright]
Copyright 2006 S. Karger AG, Basel.
(PMID = 16847378.001).
[ISSN]
1660-2137
[Journal-full-title]
Nephron. Physiology
[ISO-abbreviation]
Nephron Physiol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Intracellular Signaling Peptides and Proteins; 0 / Laminin; 0 / laminin 1; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / rho-Associated Kinases; EC 3.6.5.2 / rho GTP-Binding Proteins
84.
Virgin F, Zhang S, Schuster D, Azbell C, Fortenberry J, Sorscher EJ, Woodworth BA:
The bioflavonoid compound, sinupret, stimulates transepithelial chloride transport in vitro and in vivo.
Laryngoscope
; 2010 May;120(5):1051-6
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OBJECTIVES/HYPOTHESIS: Dehydration of airway surface liquid (ASL) disrupts normal mucociliary clearance in sinonasal epithelium leading to
chronic
rhinosinusitis.
Abnormal chloride (Cl(-)) transport is one mechanism that contributes to this
disorder
, as demonstrated by the
disease
cystic fibrosis.
Sinupret (Bionorica,
LLC
, San Clemente, CA), a combination of naturally occurring bioflavonoids, is a widely used treatment for respiratory ailments in Europe.
METHODS:
Well
characterized murine nasal septal epithelial (MNSE) cultures, and murine nasal potential difference (NPD) techniques were used to evaluate the effects of Sinupret on Cl(-) secretion.
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(PMID = 20422703.001).
[ISSN]
1531-4995
[Journal-full-title]
The Laryngoscope
[ISO-abbreviation]
Laryngoscope
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Chloride Channels; 0 / Chlorides; 0 / Flavonoids; 0 / Plant Extracts; 1F7A44V6OU / Colforsin; 77321-52-9 / Sinupret
85.
Biebinger R, Zimmermann MB, Al-Hooti SN, Al-Hamed N, Al-Salem E, Zafar T, Kabir Y, Al-Obaid I, Petry N, Hurrell RF:
Efficacy of wheat-based biscuits fortified with microcapsules containing ferrous sulfate and potassium iodate or a new hydrogen-reduced elemental iron: a randomised, double-blind, controlled trial in Kuwaiti women.
Br J Nutr
; 2009 Nov;102(9):1362-9
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The first objective of the study was to measure the efficacy in wheat flour of two newly developed Fe compounds, an H-reduced Fe powder (NutraFine RS; North America Höganäs High Alloys
LLC
, Johnstown, PA, USA) and
small
particle-sized (40 microm) encapsulated FeSO4.
A randomised, double-blind controlled intervention trial was conducted in Kuwaiti women (n 279; aged 18-35 years) with
low
body Fe stores (serum ferritin (SF) &
lt
; 25 microg/l) randomly assigned to one of three groups (20 mg Fe as NutraFine RS, 10 mg Fe as encapsulated FeSO4 and 150 microg iodine, or no fortification Fe) who consumed wheat-based biscuits 5 d per week.
Relative to control, mean SF in the encapsulated FeSO4 group increased by 88 % (P &
lt
; 0.001) and body Fe stores increased from - 0.96 to 2.24 mg/kg body weight (P &
lt
; 0.001), while NutraFine RS did not significantly increase SF or body Fe stores.
The median urinary iodine concentration increased from 140 to 213 microg/l (P &
lt
; 0.01).
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IRON, ELEMENTAL
.
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FERROUS SULFATE
.
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.
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(PMID = 19653920.001).
[ISSN]
1475-2662
[Journal-full-title]
The British journal of nutrition
[ISO-abbreviation]
Br. J. Nutr.
[Language]
eng
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Capsules; 0 / Ferrous Compounds; 0 / Hemoglobins; 0 / Iodates; 0 / Iron, Dietary; 0 / Potassium Compounds; 0 / Transferrin; 39R4TAN1VT / ferrous sulfate; E1UOL152H7 / Iron; I139E44NHL / potassium iodate
86.
Chen Z, Wang Y, Ratia K, Mesecar AD, Wilkinson KD, Baker SC:
Proteolytic processing and deubiquitinating activity of papain-like proteases of human coronavirus NL63.
J Virol
; 2007 Jun;81(11):6007-18
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Human coronavirus NL63 (HCoV-NL63), a common human respiratory pathogen, is associated with both upper and lower respiratory tract
disease in
children and adults.
We generated polyclonal antisera directed against two of the predicted replicase nonstructural proteins (nsp3 and nsp4) and detected replicase proteins from HCoV-NL63-infected
LLC
-MK2 cells by immunofluorescence, immunoprecipitation, and Western blot assays.
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(PMID = 17392370.001).
[ISSN]
0022-538X
[Journal-full-title]
Journal of virology
[ISO-abbreviation]
J. Virol.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / P01 AI060915; United States / NIAID NIH HHS / AI / P01-AI060915; United States / PHS HHS / / R01-A1045798
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Ubiquitin; 0 / Viral Envelope Proteins; EC 3.4.22.- / 3C-like proteinase, Coronavirus; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.2 / Papain
[Other-IDs]
NLM/ PMC1900296
87.
Mowery YM, Weinberg JB, Kennedy MN, Bond KM, Moore JO, Lanasa MC, Gockerman JP, Diehl LF, Pizzo SV, Cianciolo GJ, Friedman DR:
LMP-420: a novel purine nucleoside analog with potent cytotoxic effects for CLL cells and minimal toxicity for normal hematopoietic cells.
Leukemia
; 2010 Sep;24(9):1580-7
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[Title]
LMP-420: a novel purine nucleoside analog with potent cytotoxic effects for
CLL
cells and minimal toxicity for normal hematopoietic cells.
B-
cell chronic
lymphocytic
leukemia
(
CLL
) is characterized by slow accumulation of malignant cells, which are supported in the microenvironment by
cell
-
cell
interactions and soluble cytokines such as tumor necrosis factor (TNF).
We evaluated the effect of the
small
molecule TNF inhibitor LMP-420 on primary
CLL
cells.
CLL
cells from patients with poor prognostic indicators showed LMP-420 sensitivity equal to that for cells from patients with favorable characteristics.
In addition, LMP-420 potentiated the cytotoxic effect of fludarabine and inhibited in vitro proliferation of stimulated
CLL
cells.
Gene expression profiling indicated that the mechanism of action of LMP-420 may involve suppression of nuclear factor-kappaB and immune response pathways
in CLL
cells.
LMP-420 had minimal effects on normal peripheral blood mononuclear
cell
, B- and T-
cell
function, and hematopoietic colony formation.
Our data suggest that LMP-420 may be a useful treatment for
CLL
with negligible hematologic toxicities.
[MeSH-major]
Antineoplastic Agents / pharmacology. Boron Compounds / pharmacology.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ pathology. Purines / pharmacology. Tumor Necrosis Factor-alpha / antagonists & inhibitors
[MeSH-minor]
Apoptosis / drug effects.
Cell
Line, Tumor. Dose-Response Relationship, Drug. Drug Synergism. Female. Flow Cytometry. Gene Expression Profiling. Humans. Male. Prognosis. Vidarabine / analogs & derivatives. Vidarabine / pharmacology
Hazardous Substances Data Bank.
BORON COMPOUNDS
.
Hazardous Substances Data Bank.
FLUDARABINE
.
Hazardous Substances Data Bank.
VIDARABINE
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 20613784.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[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.
[Publication-country]
England
[Chemical-registry-number]
0 / 2-amino-6-chloro-9-((5-dihydroxyboryl)pentyl)purine; 0 / Antineoplastic Agents; 0 / Boron Compounds; 0 / Purines; 0 / Tumor Necrosis Factor-alpha; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
88.
Rezvany MR, Kazemi A, Hajifathali A, Kaviani S, Mellstedt H:
Analysis of HLA-G gene expression in B-lymphocytes from chronic lymphocytic leukemia patients.
Iran Biomed J
; 2007 Apr;11(2):125-9
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[Title]
Analysis of HLA-G gene expression in B-
lymphocytes
from
chronic
lymphocytic
leukemia
patients.
BACKGROUND: The human leukocyte antigen G (HLA-G) molecule exhibits
limited
tissue distribution,
low
polymorphism and alternative splicings that generate seven HLA-G isoforms.
This study it is an effort to clarify the presence of HLA-
G in
B-
cell chronic
lymphocytic
leukemia
(B-
CLL
) patients.
METHODS: HLA-G mRNA expression was studied
in a
pilot study in circulating B-
CLL
and also healthy controls by reverse transcription (RT)-PCR using a set of pan-HLA-G primers.
RESULTS: RT-PCR was performed on B-cells from 74 B-
CLL
patients and 12 healthy controls.
The data showed HLA-G gene expression in 20% of the B-
CLL
patients.
CONCLUSION: These data suggest that HLA-G is expressed at the gene level in B cells from B-
CLL
patients but not in B cells from healthy controls.
Further study is required to clarify the role of HLA-G as a regulatory factor that could affect immune response in B-
CLL
patients.
[MeSH-major]
B-
Lymphocytes
/ immunology. Gene Expression Regulation / immunology. HLA Antigens / genetics. Histocompatibility Antigens Class I / genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ immunology
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(PMID = 18051955.001).
[ISSN]
1028-852X
[Journal-full-title]
Iranian biomedical journal
[ISO-abbreviation]
Iran. Biomed. J.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Iran
[Chemical-registry-number]
0 / DNA Primers; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I
89.
Lu CM, Murata-Collins JL, Wang E, Siddiqi I, Lawrence H:
Concurrent acute myeloid leukemia with inv(16)(p13.1q22) and chronic lymphocytic leukemia: molecular evidence of two separate diseases.
Am J Hematol
; 2006 Dec;81(12):963-8
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[Title]
Concurrent acute myeloid
leukemia
with inv(16)(p13.1q22) and
chronic
lymphocytic
leukemia
: molecular evidence of two separate diseases.
Acute myeloid
leukemia
(AML) occurring concurrently with or after untreated
chronic
lymphocytic
leukemia
(
CLL
) is rare.
We report a case
of a
59-year-old man who was evaluated for anemia, thrombocytopenia, and leukocytosis with circulating blasts.
On the basis of the
morphology
and immunophenotyping results, a preliminary
diagnosis of
chronic
myelomonocytic
leukemia
with concurrent
CLL
was considered.
Subsequently, cytogenetic analysis of the leukemic blood specimen revealed inv(16)(p13.1q22) with secondary trisomy 22
in a
sideline clone.
Fluorescence in situ hybridization confirmed the CBFbeta rearrangement associated with inv(16) in myeloblasts and myelomonocytic cells, but not
in CLL
cells.
Therefore, a final
diagnosis of
AML with inv(16) with concurrent
CLL
was made.
After standard chemotherapy for AML, the patient achieved complete remission for both his AML and
CLL
.
The unique aspects of this case include concomitant AML and
CLL
, which do not share clonality, complex cytogenetic abnormalities with trisomy 22 as a secondary
abnormality
associated with inv(16), and achievement of remission for both AML and
CLL
by AML chemotherapy regimen.
This case also represents one of the rare instances where
a diagnosis
of AML can be established even when the blast percentage in the marrow and blood is less than 20%.
[MeSH-major]
Chromosome Inversion / genetics. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 22 / genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics.
Leukemia
, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics. Trisomy / genetics
[MeSH-minor]
Blast Crisis /
diagnosis
. Blast Crisis / drug therapy. Blast Crisis / genetics. Blast Crisis / pathology. Bone Marrow / pathology. Humans. In Situ Hybridization, Fluorescence / methods. Male. Middle Aged. Remission Induction
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.
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(PMID = 16917916.001).
[ISSN]
0361-8609
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
90.
Caraway NP, Thomas E, Khanna A, Payne L, Zhang HZ, Lin E, Keating MJ, Katz RL:
Chromosomal abnormalities detected by multicolor fluorescence in situ hybridization in fine-needle aspirates from patients with small lymphocytic lymphoma are useful for predicting survival.
Cancer
; 2008 Oct 25;114(5):315-22
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[Title]
Chromosomal abnormalities detected by multicolor fluorescence in situ hybridization in fine-needle aspirates from patients with
small lymphocytic lymphoma
are useful for predicting survival.
BACKGROUND: Fine-needle aspiration (FNA) of lymph nodes is commonly used to assess
disease
progression in patients with
small lymphocytic lymphoma
(SLL).
Although cytologic features are helpful for diagnosing typical SLL and transformed large-
cell
lymphoma
(tLCL), SLL in accelerated phase (SLLacc) is more difficult to diagnose.
Additional tests are needed to identify those patients who are transforming to a higher-
grade lymphoma
.
This study evaluated the use
of a
multicolor fluorescence in situ hybridization (FISH) probe panel specifically designed for
chronic
lymphocytic
leukemia
(
CLL
)/SLL and assessed the association between FISH findings and cytologic
diagnosis
, proliferation index, and risk of death.
METHODS: FNA specimens from 50 patients (32 men and 18 women; mean age, 57 years [range, 36-77 years]) with histologically confirmed
CLL
and/or SLL were evaluated in this study for chromosomal abnormalities of 11q22 (ATM), 12, 13q14.3, 13q34.3 (LAMP1), and 17p13.1 (p53) by using a multiprobe FISH kit.
CONCLUSIONS: FISH can be performed on FNA specimens from patients with a history of SLL/
CLL
.
[MeSH-major]
Biopsy, Fine-Needle. Chromosome Aberrations. In Situ Hybridization, Fluorescence.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ mortality
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[Copyright]
(c) 2008 American Cancer Society.
(PMID = 18683215.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672
[Publication-type]
Journal Article
[Publication-country]
United States
91.
Storey R, Gatt M, Bradford I:
Mucosa associated lymphoid tissue lymphoma presenting within a solitary anti-mesenteric dilated segment of ileum: a case report.
J Med Case Rep
; 2009;3:6
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[Title]
Mucosa associated
lymphoid
tissue
lymphoma
presenting within a solitary anti-mesenteric dilated segment of ileum: a case report.
INTRODUCTION: Mucosa associated
lymphoid
tissue (MALT)
lymphoma
is the third most common non-Hodgkin'
s lymphoma
subtype.
Clinical presentation is often insidious as
a low
-
grade
lesion and
disease
tends to remain localised for
a long
period of time.
Histology of this segment demonstrated MALT
lymphoma of
the
small
bowel.
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[Cites]
Scand J Gastroenterol. 2008;43(4):497-505
[
18365916.001
]
[Cites]
Ann Surg. 2005 Mar;241(3):529-33
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Blood. 1994 Sep 1;84(5):1361-92
[
8068936.001
]
(PMID = 19126231.001).
[ISSN]
1752-1947
[Journal-full-title]
Journal of medical case reports
[ISO-abbreviation]
J Med Case Rep
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2627909
92.
Stilgenbauer S, Zenz T, Winkler D, Bühler A, Schlenk RF, Groner S, Busch R, Hensel M, Dührsen U, Finke J, Dreger P, Jäger U, Lengfelder E, Hohloch K, Söling U, Schlag R, Kneba M, Hallek M, Döhner H, German Chronic Lymphocytic Leukemia Study Group:
Subcutaneous alemtuzumab in fludarabine-refractory chronic lymphocytic leukemia: clinical results and prognostic marker analyses from the CLL2H study of the German Chronic Lymphocytic Leukemia Study Group.
J Clin Oncol
; 2009 Aug 20;27(24):3994-4001
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[Title]
Subcutaneous alemtuzumab in fludarabine-refractory
chronic
lymphocytic
leukemia
: clinical results and prognostic marker analyses from the CLL2H study of the German
Chronic
Lymphocytic
Leukemia
Study Group.
PURPOSE: The phase II CLL2H trial evaluated safety and efficacy of subcutaneous alemtuzumab in patients with fludarabine-refractory
chronic
lymphocytic
leukemia
(
CLL
).
The median progression-free survival was 7.7 months, and the median overall survival (
OS
) was 19.1 months.
In multivariate analysis of clinical and biologic variables, age, performance status, beta2-MG, and TK were independent prognostic factors for
OS
.
CONCLUSION: Subcutaneous alemtuzumab appears as effective and safe as intravenous alemtuzumab in fludarabine-refractory
CLL
.
[MeSH-major]
Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ drug therapy. Vidarabine / analogs & derivatives
Genetic Alliance.
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.
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ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
Hazardous Substances Data Bank.
FLUDARABINE
.
Hazardous Substances Data Bank.
VIDARABINE
.
NCI CPTAC Assay Portal.
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.
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(PMID = 19597025.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
93.
Giannopoulos K, Schmitt M, Własiuk P, Chen J, Bojarska-Junak A, Kowal M, Roliñski J, Dmoszyñska A:
The high frequency of T regulatory cells in patients with B-cell chronic lymphocytic leukemia is diminished through treatment with thalidomide.
Leukemia
; 2008 Jan;22(1):222-4
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[Title]
The high frequency of T regulatory cells in patients with B-
cell chronic
lymphocytic
leukemia
is diminished through treatment with thalidomide.
[MeSH-major]
Immunosuppressive Agents / therapeutic use.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ drug therapy.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ immunology. T-
Lymphocytes
, Regulatory / immunology. Thalidomide / therapeutic use
[MeSH-minor]
Adult. Aged. CD4-Positive T-
Lymphocytes
/ metabolism. Female. Forkhead Transcription Factors / metabolism. Humans. Interleukin-2 Receptor alpha Subunit / metabolism. Male. Middle Aged
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THALIDOMIDE
.
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(PMID = 17657216.001).
[ISSN]
1476-5551
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Letter
[Publication-country]
England
[Chemical-registry-number]
0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Immunosuppressive Agents; 0 / Interleukin-2 Receptor alpha Subunit; 4Z8R6ORS6L / Thalidomide
94.
Morrison VA:
Infectious complications of chronic lymphocytic leukaemia: pathogenesis, spectrum of infection, preventive approaches.
Best Pract Res Clin Haematol
; 2010 Mar;23(1):145-53
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[Title]
Infectious complications of
chronic
lymphocytic leukaemia
: pathogenesis, spectrum of infection, preventive approaches.
Infectious complications continue to be a major cause of morbidity and mortality in patients with
chronic
lymphocytic leukaemia
(
CLL
).
This review focuses on the pathogenesis and risk factors for infections in patients with
CLL
, the spectrum of infectious complications and preventive approaches to infection in these patients, using antimicrobial and immunoglobulin prophylaxis and vaccination strategies.
[MeSH-major]
Infection / etiology.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ complications
The Lens.
Cited by Patents in
.
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[Copyright]
Published by Elsevier Ltd.
(PMID = 20620978.001).
[ISSN]
1532-1924
[Journal-full-title]
Best practice & research. Clinical haematology
[ISO-abbreviation]
Best Pract Res Clin Haematol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antibodies, Monoclonal
[Number-of-references]
70
95.
Goldin LR, Lanasa MC, Slager SL, Cerhan JR, Vachon CM, Strom SS, Camp NJ, Spector LG, Leis JF, Morrison VA, Glenn M, Rabe KG, Achenbach SJ, Algood SD, Abbasi F, Fontaine L, Yau M, Rassenti LZ, Kay NE, Call TG, Hanson CA, Weinberg JB, Marti GE, Caporaso NE:
Common occurrence of monoclonal B-cell lymphocytosis among members of high-risk CLL families.
Br J Haematol
; 2010 Oct;151(2):152-8
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[Title]
Common occurrence of monoclonal B-
cell
lymphocytosis among members of high-risk
CLL
families.
Monoclonal B-
cell
lymphocytosis (MBL) is an asymptomatic haematological condition characterized by
low
absolute levels of B-
cell
clones with a surface immunophenotype similar to that of
chronic
lymphocytic leukaemia
(
CLL
).
It has been reported to be higher among first-degree relatives from
CLL
families.
We report results of multi-parameter flow cytometry among 505 first-degree relatives with no personal history of lymphoproliferative
disease
from 140 families having at least two cases
of CLL
.
MBL clustered in certain families but clustering was independent of the number of known
CLL
cases
in a
family.
As is the case with
CLL
, males had a significantly higher risk for MBL than did females (P = 0·04).
MBL patients had significantly higher mean absolute lymphocyte counts (2·4 × 10(9) /l) and B-
cell
counts (0·53 × 10(9) /l) than those with a normal B-
cell
immuno-phenotype.
Our findings show that MBL occurs at a very high rate in high risk
CLL
families.
Both the age and gender distribution of MBL are parallel to
CLL
, implying a shared inherited risk.
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[Copyright]
Published 2010. This article is a US Government work and is in the public domain in the USA.
[Cites]
Br J Haematol. 2009 Nov;147(3):339-46
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]
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Leukemia. 2010 Jan;24(1):133-40
[
19946263.001
]
(PMID = 20738309.001).
[ISSN]
1365-2141
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA118444; United States / NCI NIH HHS / PC / N01-PC-35141; United States / NCI NIH HHS / CA / N01PC35141; United States / NIAID NIH HHS / AI / P30 AI051445; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R43 CA137941; United States / NCI NIH HHS / CA / CA137941; United States / NIAID NIH HHS / AI / AI-51445; United States / NCI NIH HHS / CA / CA116237; United States / NCI NIH HHS / CA / U01 CA118444; United States / NCI NIH HHS / CA / R01 CA116237
[Publication-type]
Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Other-IDs]
NLM/ NIHMS230867; NLM/ PMC2966536
96.
Dreger P, Corradini P, Kimby E, Michallet M, Milligan D, Schetelig J, Wiktor-Jedrzejczak W, Niederwieser D, Hallek M, Montserrat E, Chronic Leukemia Working Party of the EBMT:
Indications for allogeneic stem cell transplantation in chronic lymphocytic leukemia: the EBMT transplant consensus.
Leukemia
; 2007 Jan;21(1):12-7
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[Title]
Indications for allogeneic stem
cell
transplantation in
chronic
lymphocytic
leukemia
: the EBMT transplant consensus.
The aim of this project was to identify situations where allogeneic stem
cell
transplantation (allo-SCT) might be considered as a preferred treatment option for patients with B-
cell chronic
lymphocytic
leukemia
(
CLL
).
Key elements of the consensus are (1) allo-SCT is a procedure with evidence-based efficacy in poor-risk
CLL
;.
(2) although definition of 'poor-risk
CLL
' requires further investigation, allo-SCT is a reasonable treatment option for younger patients with (i) non-response or early relapse (within 12 months) after purine analogues, (ii) relapse within 24 months after having achieved a response with purine-analogue-based combination therapy or autologous transplantation, and (iii) patients with p53 abnormalities requiring treatment; and (3) optimum transplant strategies may vary according to distinct clinical situations and should be defined in prospective trials.
This is the first attempt to define standard indications for allo-SCT
in CLL
.
Nevertheless, whenever possible, allo-SCT should be performed within
disease
-specific prospective clinical protocols in order to continuously refine transplant indications according to new developments in risk assessment and treatment
of CLL
.
[MeSH-major]
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ therapy. Stem
Cell
Transplantation
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(PMID = 17109028.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Consensus Development Conference; Journal Article; Multicenter Study
[Publication-country]
England
[Number-of-references]
43
97.
Hamblin TJ:
Chronic lymphocytic leukaemia: clinical translations of biological features.
Curr Top Microbiol Immunol
; 2005;294:165-85
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[Title]
Chronic
lymphocytic leukaemia
: clinical translations of biological features.
The
chronic
lymphatic leukaemia
(
CLL
) world was surprised to find that the
disease
split so neatly down the middle into those patients with unmutated immunoglobulin genes who were mainly men, had aggressive
disease
and were destined to die from their
disease
, on average at about 8 years from
diagnosis
, and those with mutated immunoglobulin genes who were equally distributed between the sexes, had indolent
disease
and usually died of something else a quarter
of a
century later.
This discovery gave fresh impetus to the investigation into the biology
of CLL
.
We now know more about, though we are still not certain of, the
cell
of origin of the
disease
and how it functions and fails to function.
[MeSH-major]
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ immunology
[MeSH-minor]
B-
Lymphocytes
/ immunology. Biomarkers, Tumor. Female. Genes, Immunoglobulin. Germinal Center / immunology. Humans. Immunologic Memory. Male. Mutation. Prognosis
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(PMID = 16323432.001).
[ISSN]
0070-217X
[Journal-full-title]
Current topics in microbiology and immunology
[ISO-abbreviation]
Curr. Top. Microbiol. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Biomarkers, Tumor
[Number-of-references]
77
98.
Masago M, Takaai M, Sakata J, Horie A, Ito T, Ishida K, Taguchi M, Hashimoto Y:
Membrane transport mechanisms of quinidine and procainamide in renal LLC-PK1 and intestinal LS180 cells.
Biol Pharm Bull
; 2010;33(8):1407-12
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[Title]
Membrane transport mechanisms of quinidine and procainamide in renal
LLC
-PK1 and intestinal LS180 cells.
The aim of the present study was to compare the membrane transport mechanisms of procainamide with those of quinidine using renal epithelial
LLC
-PK(1) and intestinal epithelial LS180 cells.
In LLC
-PK(1) cells, the transcellular transport of 10 microM quinidine in the basolateral-to-apical direction was similar to that in the opposite direction, and 1 mM tetraethylammonium (TEA) did not affect the transcellular transport of the drug.
On the other hand, the transcellular transport of 10 microM TEA and procainamide
in LLC
-PK(1) cells was directional from the basolateral side to the apical side.
[MeSH-major]
Anti-Arrhythmia Agents / pharmacokinetics.
Cell
Membrane / metabolism. Intestines / metabolism. Kidney / metabolism. Procainamide / pharmacokinetics. Quinidine / pharmacokinetics
[MeSH-minor]
Animals. Biological Transport, Active. Caco-2 Cells. Cation Transport Proteins / metabolism. Drug Interactions. Epithelial Cells / metabolism. Humans. Hydrogen-Ion Concentration.
LLC
-PK1 Cells. Swine. Temperature. Tetraethylammonium / pharmacology
Hazardous Substances Data Bank.
PROCAINAMIDE
.
Hazardous Substances Data Bank.
QUINIDINE
.
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(PMID = 20686239.001).
[ISSN]
1347-5215
[Journal-full-title]
Biological & pharmaceutical bulletin
[ISO-abbreviation]
Biol. Pharm. Bull.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Anti-Arrhythmia Agents; 0 / Cation Transport Proteins; 66-40-0 / Tetraethylammonium; ITX08688JL / Quinidine; L39WTC366D / Procainamide
99.
Cerezo M, Bandelt HJ, Martín-Guerrero I, Ardanaz M, Vega A, Carracedo A, García-Orad A, Salas A:
High mitochondrial DNA stability in B-cell chronic lymphocytic leukemia.
PLoS One
; 2009;4(11):e7902
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[Title]
High mitochondrial DNA stability in B-
cell chronic
lymphocytic
leukemia
.
BACKGROUND:
Chronic
Lymphocytic
Leukemia
(
CLL
) leads to progressive accumulation
of lymphocytes
in the blood, bone marrow, and
lymphatic
tissues.
Previous findings have suggested that the mtDNA could play an important role
in CLL
.
METHODOLOGY/PRINCIPAL FINDINGS: The mitochondrial DNA (mtDNA) control-region was analyzed in lymphocyte
cell
DNA extracts and compared with their granulocyte counterpart extract of 146 patients suffering from B-
Cell
CLL
; B-
CLL
(all recruited from the Basque country).
Only twenty instabilities were finally confirmed, most of them affecting the homopolymeric stretch located in the second hypervariable segment (HVS-II) around position 310, which is
well
known to constitute an extreme mutational hotspot of length polymorphism, as these mutations are frequently observed in the general human population.
A critical revision of the findings in previous studies indicates a lack of proper methodological standards, which eventually led to an overinterpretation of the role of the mtDNA
in CLL
tumorigenesis.
CONCLUSIONS/SIGNIFICANCE: Our results suggest that mtDNA instability is not the primary causal factor in B-
CLL
.
[MeSH-major]
DNA, Mitochondrial / genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ genetics.
Leukemia
,
Lymphocytic
,
Chronic
, B-
Cell
/ metabolism
[MeSH-minor]
Base Sequence. DNA Primers / genetics. Databases, Genetic. Granulocytes / cytology. Haplotypes. Humans.
Lymphocytes
/ cytology. Models, Statistical. Molecular Sequence Data. Mutation. Phylogeny. Sequence Analysis, DNA
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.
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[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; 0 / DNA, Mitochondrial
[Other-IDs]
NLM/ PMC2775629
100.
Wang J, Zhang B, Guo Y, Li G, Xie Q, Zhu B, Gao J, Chen Z:
Artemisinin inhibits tumor lymphangiogenesis by suppression of vascular endothelial growth factor C.
Pharmacology
; 2008;82(2):148-55
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We have previously reported that dihydroartemisinin is found to have a potent ability in influencing
lymphatic
endothelial
cell
migration and tube formation.
In this study, we investigated the effect of artemisinin on tumor growth, lymphangiogenesis, metastasis and survival in mouse Lewis lung carcinoma (
LLC
) models.
Furthermore, IL-1beta-induced p38 mitogen-activated protein kinase (MAPK) activation and upregulation of VEGF-C mRNA and protein
in LLC
cells was also suppressed by artemisinin or by the p38 MAPK inhibitor SB-203580, suggesting that p38 MAPK could serve as a mediator of proinflammatory cytokine-induced VEGF-C expression.
[MeSH-minor]
Administration, Oral. Animals. Female. Gene Expression Regulation, Neoplastic / drug effects. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Lymphangiogenesis / drug effects.
Lymphatic
Metastasis / prevention & control. Mice. Mice, Inbred C57BL. Neoplasm Metastasis / prevention & control. Survival Rate. p38 Mitogen-Activated Protein Kinases / drug effects. p38 Mitogen-Activated Protein Kinases / metabolism
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.
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[Copyright]
Copyright 2008 S. Karger AG, Basel.
(PMID = 18667841.001).
[ISSN]
1423-0313
[Journal-full-title]
Pharmacology
[ISO-abbreviation]
Pharmacology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; 0 / Artemisinins; 0 / Vascular Endothelial Growth Factor C; 9RMU91N5K2 / artemisinine; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases