1
|
Nagata S: Apoptosis regulated by a death
factor and its receptor: Fas ligand and Fas. Philos Trans R Soc
Lond B Biol Sci. 345:281–287. 1994. View Article : Google Scholar : PubMed/NCBI
|
2
|
Nagata S: Apoptosis by death factor. Cell.
88:355–365. 1997. View Article : Google Scholar : PubMed/NCBI
|
3
|
Itoh N, Yonehara S, Ishii A, Yonehara M,
Mizushima S, Sameshima M, Hase A, Seto Y and Nagata S: The
polypeptide encoded by the cDNA for human cell surface antigen Fas
can mediate apoptosis. Cell. 66:233–243. 1991. View Article : Google Scholar : PubMed/NCBI
|
4
|
Zornig M, Hueber A, Baum W and Evan G:
Apoptosis regulators and their role in tumorigenesis. Biochim
Biophys Acta. 1551:F1–F37. 2001.PubMed/NCBI
|
5
|
Li Y, Hao YL, Kang S, Zhou RM, Wang N and
Qi BL: Genetic polymorphisms in the Fas and FasL genes are
associated with epithelial ovarian cancer risk and clinical
outcomes. Gynecol Oncol. 128:584–589. 2013. View Article : Google Scholar : PubMed/NCBI
|
6
|
Wang W, Zheng Z, Yu W, Lin H, Cui B and
Cao F: Polymorphisms of the FAS and FASL genes and risk of breast
cancer. Oncol Lett. 3:625–628. 2012.PubMed/NCBI
|
7
|
Han W, Zhou Y, Zhong R, Wu C, Song R, Liu
L, Zou L, Qiao Y, Zhai K, Chang J, et al: Functional polymorphisms
in FAS/FASL system increase the risk of neuroblastoma in Chinese
population. PloS One. 8:e716562013. View Article : Google Scholar : PubMed/NCBI
|
8
|
Westendorf JJ, Lammert JM and Jelinek DF:
Expression and function of Fas (APO-1/CD95) in patient myeloma
cells and myeloma cell lines. Blood. 85:3566–3576. 1995.PubMed/NCBI
|
9
|
Shima Y, Nishimoto N, Ogata A, Fujii Y,
Yoshizaki K and Kishimoto T: Myeloma cells express Fas
antigen/APO-1 (CD95) but only some are sensitive to anti-Fas
antibody resulting in apoptosis. Blood. 85:757–764. 1995.PubMed/NCBI
|
10
|
Gutierrez MI, Cherney B, Hussain A,
Mostowski H, Tosato G, Magrath I and Bhatia K: Bax is frequently
compromised in Burkitt's lymphomas with irreversible resistance to
Fas-induced apoptosis. Cancer Res. 59:696–703. 1999.PubMed/NCBI
|
11
|
Pordzik S, Petrovici K, Schmid C, Kroell
T, Schweiger C, Köhne CH and Schmetzer H: Expression and prognostic
value of FAS receptor/FAS ligand and TrailR1/TrailR2 in acute
myeloid leukemia. Hematology. 16:341–350. 2011. View Article : Google Scholar : PubMed/NCBI
|
12
|
Chongli Y and Xiaobo Z: Anemia CESGoLaA:
Incidence Survey of Leukemia in China in 1986. Chinese Journal of
Hematology. 10:618–621. 1986.
|
13
|
Kasim K, Levallois P, Abdous B, Auger P
and Johnson KC: Lifestyle factors and the risk of adult leukemia in
Canada. Cancer Causes Control. 16:489–500. 2005. View Article : Google Scholar : PubMed/NCBI
|
14
|
Wong O, Harris F, Yiying W and Hua F: A
hospital-based case-control study of acute myeloid leukemia in
Shanghai: Analysis of personal characteristics, lifestyle and
environmental risk factors by subtypes of the WHO classification.
Regul Toxicol Pharmacol. 55:340–352. 2009. View Article : Google Scholar : PubMed/NCBI
|
15
|
Filippini T, Heck JE, Malagoli C, Del
Giovane C and Vinceti M: A review and meta-analysis of outdoor air
pollution and risk of childhood leukemia. J Environ Sci Health C
Environ Carcinog Ecotoxicol Rev. 33:36–66. 2015. View Article : Google Scholar : PubMed/NCBI
|
16
|
Min YJ, Lee JH, Choi SJ, Chi HS, Lee JS,
Kim WK and Lee KH: Prognostic significance of Fas (CD95) and TRAIL
receptors (DR4/DR5) expression in acute myelogenous leukemia. Leuk
Res. 28:359–365. 2004. View Article : Google Scholar : PubMed/NCBI
|
17
|
Iijima N, Miyamura K, Itou T, Tanimoto M,
Sobue R and Saito H: Functional expression of Fas (CD95) in acute
myeloid leukemia cells in the context of CD34 and CD38 expression:
Possible correlation with sensitivity to chemotherapy. Blood.
90:4901–4909. 1997.PubMed/NCBI
|
18
|
Komada Y, Zhou YW, Zhang XL, Xue HL, Sakai
H, Tanaka S, Sakatoku H and Sakurai M: Fas receptor (CD95)-mediated
apoptosis is induced in leukemic cells entering G1B compartment of
the cell cycle. Blood. 86:3848–3860. 1995.PubMed/NCBI
|
19
|
Nunobiki O, Ueda M, Toji E, Yamamoto M,
Akashi K, Sato N, Izuma S, Torii K, Tanaka I, Okamoto Y and Noda S:
Genetic polymorphism of cancer susceptibility genes and HPV
infection in cervical carcinogenesis. Patholog Res Int.
2011:3640692011.PubMed/NCBI
|
20
|
Huang QR, Morris D and Manolios N:
Identification and characterization of polymorphisms in the
promoter region of the human Apo-1/Fas (CD95) gene. Mol Immunol.
34:577–582. 1997. View Article : Google Scholar : PubMed/NCBI
|
21
|
Sibley K, Rollinson S, Allan JM, Smith AG,
Law GR, Roddam PL, Skibola CF, Smith MT and Morgan GJ: Functional
FAS promoter polymorphisms are associated with increased risk of
acute myeloid leukemia. Cancer Res. 63:4327–4330. 2003.PubMed/NCBI
|
22
|
Sun T, Zhou Y, Li H, Han X, Shi Y, Wang L,
Miao X, Tan W, Zhao D, Zhang X, et al: FASL-844C polymorphism is
associated with increased activation-induced T cell death and risk
of cervical cancer. J Exp Med. 202:967–974. 2005. View Article : Google Scholar : PubMed/NCBI
|
23
|
Kordi Tamandani DM, Sobti RC and Shekari
M: Association of Fas-670 gene polymorphism with risk of cervical
cancer in North Indian population. Clin Exp Obstet Gynecol.
35:183–186. 2008.PubMed/NCBI
|
24
|
Kim HJ, Jin XM, Kim HN, Lee IK, Park KS,
Park MR, Jo DY, Won JH, Kwak JY, Kim HJ, et al: Fas and FasL
polymorphisms are not associated with acute myeloid leukemia risk
in Koreans. DNA Cell Biol. 29:619–624. 2010. View Article : Google Scholar : PubMed/NCBI
|
25
|
Lai HC, Lin WY, Lin YW, Chang CC, Yu MH,
Chen CC and Chu TY: Genetic polymorphisms of FAS and FASL
(CD95/CD95L) genes in cervical carcinogenesis: An analysis of
haplotype and gene-gene interaction. Gynecol Oncol. 99:113–118.
2005. View Article : Google Scholar : PubMed/NCBI
|
26
|
Park SH, Choi JE, Kim EJ, Jang JS, Lee WK,
Cha SI, Kim CH, Kam S, Kim DS, Park RW, et al: Polymorphisms in the
FAS and FASL genes and risk of lung cancer in a Korean population.
Lung Cancer. 54:303–308. 2006. View Article : Google Scholar : PubMed/NCBI
|
27
|
Tan A, Gao Y, Yang X, Zhang H, Qin X, Mo
L, Peng T, Xia N and Mo Z: Low serum osteocalcin level is a
potential marker for metabolic syndrome: Results from a Chinese
male population survey. Metabolism. 60:1186–1192. 2011. View Article : Google Scholar : PubMed/NCBI
|
28
|
Yang X, Sun J, Gao Y, Tan A, Zhang H, Hu
Y, Feng J, Qin X, Tao S, Chen Z, et al: Genome-wide association
study for serum complement C3 and C4 levels in healthy Chinese
subjects. PLoS Genet. 8:e10029162012. View Article : Google Scholar : PubMed/NCBI
|
29
|
Tian J, Pan F, Li J, Ma Y, Cen H, Pan HF,
Pan YY and Ye DQ: Association between the FAS/FASL polymorphisms
and gastric cancer risk: A meta-analysis. Asian Pac J Cancer Prev.
13:945–951. 2012. View Article : Google Scholar : PubMed/NCBI
|
30
|
Higgins JP, Thompson SG, Deeks JJ and
Altman DG: Measuring inconsistency in meta-analyses. BMJ.
327:557–560. 2003. View Article : Google Scholar : PubMed/NCBI
|
31
|
William GC: The combination of estimates
from different experiments. Biometrics. 10:101–129. 1954.
View Article : Google Scholar
|
32
|
DerSimonian R and Laird N: Meta-analysis
in clinical trials. Control Clin Trials. 7:177–188. 1986.
View Article : Google Scholar : PubMed/NCBI
|
33
|
Mantel N and Haenszel W: Statistical
aspects of the analysis of data from retrospective studies of
disease. J Natl Cancer Inst. 22:719–748. 1959.PubMed/NCBI
|
34
|
Begg CB and Mazumdar M: Operating
characteristics of a rank correlation test for publication bias.
Biometrics. 50:1088–1101. 1994. View
Article : Google Scholar : PubMed/NCBI
|
35
|
Behrmann I, Walczak H and Krammer PH:
Structure of the human APO-1 gene. Eur J Immunol. 24:3057–3062.
1994. View Article : Google Scholar : PubMed/NCBI
|
36
|
Wang J, Gao J, Li Y, Zhao X, Gao W, Peng
L, Yan D, Liu L, Li D, Wei L, et al: Functional polymorphisms in
FAS and FASL contribute to risk of squamous cell carcinoma of the
larynx and hypopharynx in a Chinese population. Gene. 524:193–196.
2013. View Article : Google Scholar : PubMed/NCBI
|
37
|
Xu Y, He B, Li R, Pan Y, Gao T, Deng Q,
Sun H, Song G and Wang S: Association of the polymorphisms in the
Fas/FasL promoter regions with cancer susceptibility: A systematic
review and meta-analysis of 52 studies. PloS One. 9:e900902014.
View Article : Google Scholar : PubMed/NCBI
|
38
|
Chen Y, He Y, Lu X, Zeng Z, Tang C, Xue T
and Li Y: Association between Fas/FasL polymorphism and
susceptibility to leukemia: A meta-analysis. Int J Clin Exp Med.
8:3817–3824. 2015.PubMed/NCBI
|
39
|
Gianni M, Terao M, Fortino I, LiCalzi M,
Viggiano V, Barbui T, Rambaldi A and Garattini E: Stat1 is induced
and activated by all-trans retinoic acid in acute promyelocytic
leukemia cells. Blood. 89:1001–1012. 1997.PubMed/NCBI
|
40
|
Battle TE and Frank DA: STAT1 mediates
differentiation of chronic lymphocytic leukemia cells in response
to Bryostatin 1. Blood. 102:3016–3024. 2003. View Article : Google Scholar : PubMed/NCBI
|
41
|
Kanemitsu S, Ihara K, Saifddin A, Otsuka
T, Takeuchi T, Nagayama J, Kuwano M and Hara T: A functional
polymorphism in fas (CD95/APO-1) gene promoter associated with
systemic lupus erythematosus. J Rheumatol. 29:1183–1188.
2002.PubMed/NCBI
|
42
|
Farre L, Bittencourt AL, Silva-Santos G,
Almeida A, Silva AC, Decanine D, Soares GM, Alcantara LC Jr, Van
Dooren S, Galvão-Castro B, et al: Fas 670 promoter polymorphism is
associated to susceptibility, clinical presentation and survival in
adult T cell leukemia. J Leukoc Biol. 83:220–222. 2008. View Article : Google Scholar : PubMed/NCBI
|
43
|
Fang Y, Zhong L, Lin M, Zhou X, Jing H,
Ying M, Luo P, Yang B and He Q: MEK/ERK dependent activation of
STAT1 mediates dasatinib-induced differentiation of acute myeloid
leukemia. PloS One. 8:e669152013. View Article : Google Scholar : PubMed/NCBI
|
44
|
Wu J, Wilson J, He J, Xiang L, Schur PH
and Mountz JD: Fas ligand mutation in a patient with systemic lupus
erythematosus and lymphoproliferative disease. J Clin Invest.
98:1107–1113. 1996. View Article : Google Scholar : PubMed/NCBI
|
45
|
Wang J, Zheng L, Lobito A, Chan FK, Dale
J, Sneller M, Yao X, Puck JM, Straus SE and Lenardo MJ: Inherited
human caspase 10 mutations underlie defective lymphocyte and
dendritic cell apoptosis in autoimmune lymphoproliferative syndrome
type II. Cell. 98:47–58. 1999. View Article : Google Scholar : PubMed/NCBI
|
46
|
Chun HJ, Zheng L, Ahmad M, Wang J, Speirs
CK, Siegel RM, Dale JK, Puck J, Davis J, Hall CG, et al:
Pleiotropic defects in lymphocyte activation caused by caspase-8
mutations lead to human immunodeficiency. Nature. 419:395–399.
2002. View Article : Google Scholar : PubMed/NCBI
|
47
|
Kennedy NJ, Kataoka T, Tschopp J and Budd
RC: Caspase activation is required for T cell proliferation. J Exp
Med. 190:1891–1896. 1999. View Article : Google Scholar : PubMed/NCBI
|
48
|
Alam A, Cohen LY, Aouad S and Sékaly RP:
Early activation of caspases during T lymphocyte stimulation
results in selective substrate cleavage in nonapoptotic cells. J
Exp Med. 190:1879–1890. 1999. View Article : Google Scholar : PubMed/NCBI
|
49
|
Su H, Bidère N, Zheng L, Cubre A, Sakai K,
Dale J, Salmena L, Hakem R, Straus S and Lenardo M: Requirement for
caspase-8 in NF-kappaB activation by antigen receptor. Science.
307:1465–1468. 2005. View Article : Google Scholar : PubMed/NCBI
|
50
|
Newton K, Harris AW, Bath ML, Smith KG and
Strasser A: A dominant interfering mutant of FADD/MORT1 enhances
deletion of autoreactive thymocytes and inhibits proliferation of
mature T lymphocytes. EMBO J. 17:706–718. 1998. View Article : Google Scholar : PubMed/NCBI
|
51
|
Rouvier E, Luciani MF and Golstein P: Fas
involvement in Ca(2+)-independent T cell-mediated cytotoxicity. J
Exp Med. 177:195–200. 1993. View Article : Google Scholar : PubMed/NCBI
|
52
|
Suda T and Nagata S: Purification and
characterization of the Fas-ligand that induces apoptosis. J Exp
Med. 179:873–879. 1994. View Article : Google Scholar : PubMed/NCBI
|
53
|
Kagi D, Vignaux F, Ledermann B, Bürki K,
Depraetere V, Nagata S, Hengartner H and Golstein P: Fas and
perforin pathways as major mechanisms of T cell-mediated
cytotoxicity. Science. 265:528–530. 1994. View Article : Google Scholar : PubMed/NCBI
|
54
|
Szczepanski MJ, Szajnik M, Czystowska M,
Mandapathil M, Strauss L, Welsh A, Foon KA, Whiteside TL and
Boyiadzis M: Increased frequency and suppression by regulatory T
cells in patients with acute myelogenous leukemia. Clin Cancer Res.
15:3325–3332. 2009. View Article : Google Scholar : PubMed/NCBI
|
55
|
Ustun C, Miller JS, Munn DH, Weisdorf DJ
and Blazar BR: Regulatory T cells in acute myelogenous leukemia: Is
it time for immunomodulation? Blood. 118:5084–5095. 2011.
View Article : Google Scholar : PubMed/NCBI
|
56
|
Yang W and Xu Y: Clinical significance of
Treg cell frequency in acute myeloid leukemia. Int J Hematol.
98:558–562. 2013. View Article : Google Scholar : PubMed/NCBI
|
57
|
Zhou Q, Munger ME, Highfill SL, Tolar J,
Weigel BJ, Riddle M, Sharpe AH, Vallera DA, Azuma M, Levine BL, et
al: Program death-1 signaling and regulatory T cells collaborate to
resist the function of adoptively transferred cytotoxic T
lymphocytes in advanced acute myeloid leukemia. Blood.
116:2484–2493. 2010. View Article : Google Scholar : PubMed/NCBI
|
58
|
Look DC, Pelletier MR, Tidwell RM, Roswit
WT and Holtzman MJ: Stat1 depends on transcriptional synergy with
Sp1. J Biol Chem. 270:30264–30267. 1995. View Article : Google Scholar : PubMed/NCBI
|