41 research outputs found
JAK2 V617F indeterminate results by MutaScreen can be easily resolved using MutaQuant kits
No full textAim: Janus kinase 2 (JAK2) V617F mutation testing has revolutionized the classification of myeloproliferative disorders, for which several tests have been introduced for qualitative and quantitative diagnostics including the MutaScreen and MutaQuant kits by IPSOGEN. One interesting technical observation are those values detected by MutaScreen kits, which have typically indeterminate meaning at a provided reference strand cutoff point and cannot be classified as either positive or negative for JAK2 V617F mutation. Results: We ran 10 different patients with such a finding using the MutaQuant kit and got a better resolution and interpretation into clear-cut negative or positive cases, which were also clinically followed and confirmed as being nonmyeloproliferative or myeloproliferative entities, respectively. Conclusion: We propose that it is important to not consider the indeterminate or at-the-reference strand results obtained by MutaScreen as positive but rather perform additional testing using MutaQuant kits or other JAK2 quantitative assays. For laboratories that can afford it and utilize both assays, it may be a better strategy to directly initiate diagnostic testing using the MutaQuant rather than the MutaScreen kit. © Copyright 2012, Mary Ann Liebert, Inc. 2012.Campbell PJ, 2005, LANCET, V366, P1945, DOI 10.1016-S0140-6736(05)67785-9; Cankovic M, 2009, AM J CLIN PATHOL, V132, P713, DOI 10.1309-AJCPFHUQZ9AGUEKA; Chae H, 2009, KOREAN J LAB MED, V29, P243, DOI 10.3343-kjlm.2009.29.3.243; Levine RL, 2005, BLOOD, V106, P3377, DOI 10.1182-blood-2005-05-1898; Merker JD, 2010, J MOL DIAGN, V12, P58, DOI 10.2353-jmoldx.2010.090068; Scott LM, 2005, BLOOD, V106, P2920, DOI 10.1182-blood-2005-05-2087; Steensma DP, 2005, BLOOD, V106, P1207, DOI 10.1182-blood-2005-03-1183; Veneri D, 2009, BLOOD TRANSFUS-ITALY, V7, P204, DOI 10.2450-2009.0070-08; Yamaoka K, 2004, GENOME BIOL, V5, DOI 10.1186-gb-2004-5-12-2530
Laboratory referral rates of genetic tests for thrombophilia workup in a major referral center
No full textAims: The rate of laboratory referrals for thrombophilia patients' genetic workup was assessed and compared among the medical and surgical specialties and subspecialties at a major tertiary care center in Lebanon. Methods: DNA extraction was performed using the PEL-FREEZ extraction kit (PEL-FREEZ; DYNAL) and the Factor V, prothrombin, and methylenetetrahydrofolate reductase genotypic profiles were done using the FV-PTH-MTHFR StripAssay kit (ViennaLab) that employs a polymerase chain reaction-reverse hybridization method. A total of 2238 referred cases were analyzed. Results: Around 42.23percent of all referred cases turned out to have a thrombosis-associated mutation. Referrals from medical and surgical specialties were almost equal. In the surgical specialty, most referrals came from the department of Obstetrics and Gynecology, while in the medical speciality, most of the workup referrals originated from the Hematology-Oncology physicians. However, low referral rates were reported from the emergency department and family medicine practitioners. Conclusion: Genetic testing for thrombophilia workup is gaining more importance among the different medical and surgical specialties and is worth being introduced into the offered test lists of all established molecular diagnostics laboratories. © 2012 Mary Ann Liebert, Inc.Ayadurai T, 2009, J OBSTET GYNAECOL RE, V35, P1061, DOI 10.1111-j.1447-0756.2009.01067.x; Cohn DM, 2010, J THROMB HAEMOST, V8, P513, DOI 10.1111-j.1538-7836.2009.03710.x; Finan RR, 2002, AM J HEMATOL, V71, P300, DOI 10.1002-ajh.10223; Hussein AS, 2010, THROMB RES, V126, pE78, DOI 10.1016-j.thromres.2010.04.017; Isma'eel H, 2006, J THROMB THROMBOLYS, V22, P121, DOI 10.1007-s11239-006-8953-3; Isma'eel H, 2006, J THROMB THROMBOLYS, V21, P267, DOI 10.1007-s11239-006-5537-1; Jadaon MM, 2010, DIAGN MOL PATHOL, V19, P180; Kfoury E, 2009, MOL BIOL REP, V36, P1041, DOI 10.1007-s11033-008-9278-4; Kosar A, 2011, BLOOD COAGUL FIBRIN, V22, P14, DOI 10.1097-MBC.0b013e32834013f2; Larciprete G, 2010, J OBSTET GYNAECOL RE, V36, P996, DOI 10.1111-j.1447-0756.2010.01262.x; Lund M, 2010, HUM REPROD, V25, P2978, DOI 10.1093-humrep-deq280; Mazoyer E, 2009, BLOOD COAGUL FIBRIN, V20, P503, DOI 10.1097-MBC.0b013e32832f5d7a; Otrock ZK, 2008, ANN HEMATOL, V87, P1013, DOI 10.1007-s00277-008-0543-3; Rahimi Z, 2010, BLOOD COAGUL FIBRIN, V21, P385, DOI 10.1097-MBC.0b013e328330e69a; Sabbagh A, 2009, MOL BIOL REP, V36, P399, DOI 10.1007-s11033-007-9193-0; Tug E, 2011, INTERNAL MED, V50, P17, DOI 10.2169-internalmedicine.50.4144; Yokus O, 2009, INT J HEMATOL, V90, P583, DOI 10.1007-s12185-009-0447-6; Zahed LF, 2006, AM J OBSTET GYNECOL, V195, P1114, DOI 10.1016-j.ajog.2006.06.08211
Kodamaea (Pichia) ohmeri fungaemia complicating acute myeloid leukaemia in a patient with haemochromatosis [11]
No full text[No abstract available]
Four primary tumors of lung, bladder, prostate, and breast in a male patient
No full textWe present a very rare case of quadruple cancers in a 65-year-old male patient. It is a case of both synchronous and metachronous primary malignant neoplasms occurring in four different organs. Immunohistochemical stains showed tumor cell nuclei to be negative for p53 over-expression. To our knowledge, this is the first documented case with this combination of primary tumors. The tumors included an adenosquamous cell carcinoma of the lung, transitional cell carcinoma of the urinary bladder, and adenocarcinomas of the prostate and the breast. We also review the medical literature for the possible causes of multiple primary malignant neoplasms. Copyright © 2005 by The Southern Medical Association.BILLROTH T, 1989, 51 VORL HDB STUD ART, P14; CASELNOV.DA, 1968, OBSTET GYNECOL, V32, P826; CLEARY JB, 1975, AM J SURG, V129, P686, DOI 10.1016-0002-9610(75)90346-3; CULOTTA E, 1994, SCIENCE, V264, P16; Demandante CGN, 2003, AM J CLIN ONCOL-CANC, V26, P79, DOI 10.1097-00000421-200302000-00015; DoussisAnagnostopoulou I, 1996, J PATHOL, V178, P170, DOI 10.1002-(SICI)1096-9896(199602)178:2170::AID-PATH4483.0.CO;2-Z; FADHLI HA, 1963, JAMA-J AM MED ASSOC, V185, P757; Gao JP, 2000, INT J ONCOL, V16, P469; Horwich A, 2004, BRIT J CANCER, V90, P294, DOI 10.1038-sj.bjc.6601499; Ireland AP, 1997, ANN SURG, V225, P17, DOI 10.1097-00000658-199701000-00003; Kony SJ, 1997, LANCET, V350, P91, DOI 10.1016-S0140-6736(97)01116-1; Luciani A, 2004, SEMIN ONCOL, V31, P264, DOI 10.1053-j.seminocol.2003.12.035; Merimsky O, 2001, CANCER, V91, P1363, DOI 10.1002-1097-0142(20010401)91:71363::AID-CNCR11403.0.CO;2-F; Mitchell ME, 1996, J CLIN GASTROENTEROL, V23, P284, DOI 10.1097-00004836-199612000-00009; MOERTEL CG, 1961, CANCER, V14, P221, DOI 10.1002-1097-0142(196103-04)14:2221::AID-CNCR28201402023.0.CO;2-6; PICKREN JW, 1963, NEW YORK STATE J MED, V63, P95; Ries L. A. G., 1994, SEER CANC STAT REV 1; Sasco AJ, 2004, LUNG CANCER-J IASLC, V45, pS3, DOI 10.1016-j.lungcan.2004.07.000; SPRATT JS, 1966, ANN SURG, V164, P775, DOI 10.1097-00000658-196611000-00001; TSUKADA Y, 1964, CANCER, V17, P1229, DOI 10.1002-1097-0142(196410)17:101229::AID-CNCR28201710023.0.CO;2-I; Warren S, 1932, AM J CANCER, V16, P1358; Weiss JR, 2005, CANCER EPIDEM BIOMAR, V14, P20; Yancik R, 2000, HEMATOL ONCOL CLIN N, V14, P17, DOI 10.1016-S0889-8588(05)70275-684
Should we screen Eastern Mediterranean sickle beta-thalassemia patients for inherited thrombophilia? [7]
No full text[No abstract available]Almawi WY, 2004, AM J HEMATOL, V76, P85, DOI 10.1002-ajh.20047; Ataga KI, 2003, AM J MED, V115, P721, DOI 10.1016-j.amjmed.2003.07.011; DAHLBACK B, 1995, BLOOD, V85, P607; Eldor A, 2002, BLOOD, V99, P36, DOI 10.1182-blood.V99.1.36; Graham IM, 1997, JAMA-J AM MED ASSOC, V277, P1775, DOI 10.1001-jama.277.22.1775; Irani-Hakime N, 2000, AM J HEMATOL, V65, P45, DOI 10.1002-1096-8652(200009)65:145::AID-AJH83.0.CO;2-V; Rosen SB, 1997, EUR J CLIN CHEM CLIN, V35, P501; Taher A, 2001, THROMB HAEMOSTASIS, V86, P72344
Prevalence of factor V R2 (H1299R) polymorphism in the Lebanese population
No full textAims: A recently identified polymorphism in factor V gene (His1299Arg; also named HR2) has been reported to be a possible risk factor for the development of venous thromboembolism (VTE), with a high prevalence of 9.5-15.2percent in patients of different ethnic groups in different parts of the world. The aim of this study is to assess the prevalence of HR2 haplotype in Lebanon. Methods: We randomly selected 125 samples from unrelated donors logged into our HLA registry; these represent healthy Lebanese individuals originating from different provinces and religious communities of the country. Their DNA was extracted using the Pel-Freez extraction kit and stored at -80°C for later use. The CVD StripAssay was used for PCR and reverse hybridisation. It screens for several gene mutations including factor V H1299R. Results: A total of 125 controls were studied: 72 males and 53 females with a median age 42 years. Thirteen (10.4percent) had the HR2 haplotype; 11 (8.8percent) were heterozygous (R1-R2), and two (1.6percent) were homozygous (R2-R2), with an allelic frequency of 0.06. Conclusions: Our study is the first report from Lebanon that describes the prevalence of HR2 haplotype and the frequency of its alleles. We are reporting a high prevalence of the HR2 in our population (10.4percent). The hypothesis that A4070G polymorphism might contribute to the expression of a thrombotic phenotype deserves to be tested in our population through larger studies. © 2006 Royal College of Pathologists of Australasia.Akar N, 2000, HAEMOSTASIS, V30, P118; Alhenc-Gelas M, 1999, THROMB HAEMOSTASIS, V81, P193; Benson JM, 2001, THROMB HAEMOSTASIS, V86, P1188; Bernardi F, 1997, BLOOD, V90, P1552; BERTINA RM, 1995, THROMB HAEMOSTASIS, V74, P449; BERTINA RM, 1994, NATURE, V369, P64, DOI 10.1038-369064a0; Castaman G, 1997, BRIT J HAEMATOL, V99, P257, DOI 10.1046-j.1365-2141.1997.3993213.x; Castoldi E, 2000, THROMB HAEMOSTASIS, V83, P362; DeStefano V, 1996, BLOOD, V87, P3531; de Visser MCH, 2000, THROMB HAEMOSTASIS, V83, P577; Doggen CJM, 2000, THROMB HAEMOSTASIS, V84, P815; Faioni EM, 1999, BLOOD, V94, P3062; Faioni EM, 2004, HAEMATOLOGICA, V89, P195; Herrmann FH, 2001, THROMB HAEMOSTASIS, V85, P1120; Jadaon MM, 2005, J THROMB HAEMOST, V3, P1467, DOI 10.1111-j.1538-7836.2005.01326.x; Kostka H, 2003, BLOOD COAGUL FIBRIN, V14, P49, DOI 10.1097-01.mbc.0000046197.72384.42; Lecumberri R, 2003, HAEMATOLOGICA, V88, P236; Luddington R, 2000, THROMB HAEMOSTASIS, V83, P204; Lunghi B, 1996, THROMB HAEMOSTASIS, V75, P45; Margaglione M, 2002, THROMB HAEMOSTASIS, V87, P32; Pecheniuk NM, 2001, BLOOD COAGUL FIBRIN, V12, P201, DOI 10.1097-00001721-200104000-00006; PITTMAN DD, 1994, J BIOL CHEM, V269, P17329; ROSING J, 1980, J BIOL CHEM, V255, P274; Yanqing Hu, 2003, Thrombosis and Haemostasis, V89, P44616141
Angiotensin-converting enzyme gene polymorphism and allele frequencies in the lebanese population: Prevalence and review of the literature
No full textWe studied the distribution of the D-D, I-D, and I-I genotypes of the angiotensin-converting enzyme (ACE) in a sample of healthy Lebanese individuals to assess their prevalence and compare them with other populations. ACE genotypes were determined using the Cardiovascular Disease (CVD) StripAssay, which is based on a Polymerase Chain Reaction-Reverse hybridization technique. DNA from 133 unrelated healthy donors from our HLA-bank was used. The prevalence of D-D, I-D, and I-I genotypes was found to be 39.1, 45.1, and 15.8percent respectively, with D and I allelic frequency of 61.7 and 38.3percent, respectively. The sampled Lebanese population showed ACE genotypic distributions similar to Caucasians; however, with tendency towards harboring high D allele frequency together with a low I allele frequency just like the Spanish population. This first report from Lebanon will serve as a baseline statistical data for future investigations of the prevalence of ACE genotypes in association with various clinical entities notably cardiovascular diseases. The medical literature was also reviewed in this context. © 2006 Springer Science+Business Media, Inc.Abbud ZA, 1998, AM J CARDIOL, V81, P244, DOI 10.1016-S0002-9149(97)00876-X; AgerholmLarsen B, 1997, CIRCULATION, V95, P2358; Agerholm-Larsen B, 2000, ARTERIOSCL THROM VAS, V20, P484; Al-Eisa A, 2001, SCAND J UROL NEPHROL, V35, P239; Alvarez R, 1998, CARDIOVASC RES, V40, P375, DOI 10.1016-S0008-6363(98)00179-5; Bautista LE, 2004, MED SCI MONITOR, V10, P473; Bouba I, 2003, EUR J OBSTET GYN R B, V110, P8, DOI 10.1016-S0301-2115(03)00046-0; CAMBIEN F, 1988, AM J HUM GENET, V43, P774; Cicoira M, 2001, J AM COLL CARDIOL, V37, P1808, DOI 10.1016-S0735-1097(01)01237-2; Della Valle C J, 2001, BMC Musculoskelet Disord, V2, P1, DOI 10.1186-1471-2474-2-1; Dilley A, 1998, AM J EPIDEMIOL, V147, P30; DURU K, 1994, AM J HYPERTENS, V7, P759; DZAU VJ, 1991, HYPERTENSION, V18, P100; Fatini C, 2003, EUR J CLIN INVEST, V33, P642, DOI 10.1046-j.1365-2362.2003.01185.x; Ferrieres J, 1999, ATHEROSCLEROSIS, V142, P211, DOI 10.1016-S0021-9150(98)00204-4; Gonzalez Ordonez A. J., 2000, Blood Coagulation and Fibrinolysis, V11, P485, DOI 10.1097-00001721-200007000-00011; HIGASHIMORI K, 1993, BIOCHEM BIOPH RES CO, V191, P399, DOI 10.1006-bbrc.1993.1231; Hooper WC, 2002, AM J HEMATOL, V70, P1, DOI 10.1002-ajh.10078; Jackson A, 2000, BRIT J HAEMATOL, V111, P562, DOI 10.1046-j.1365-2141.2000.02408.x; Kim DK, 1997, ARTERIOSCL THROM VAS, V17, P3242; LEATHAM E, 1994, J HUM HYPERTENS, V8, P635; LINDPAINTNER K, 1995, NEW ENGL J MED, V332, P706, DOI 10.1056-NEJM199503163321103; Margaglione M, 1998, ARTERIOSCL THROM VAS, V18, P562; MARIAN AJ, 1993, LANCET, V342, P1085, DOI 10.1016-0140-6736(93)92064-Z; MATTU RK, 1995, CIRCULATION, V91, P270; Murphey LJ, 2000, CIRCULATION, V102, P829; NAKAI K, 1994, CIRCULATION, V90, P2199; O'Donnell CJ, 1998, CIRCULATION, V97, P1766; Philipp CS, 1998, THROMB HAEMOSTASIS, V80, P869; Pinto YM, 1999, CARDIOVASC RES, V43, P23, DOI 10.1016-S0008-6363(99)00090-5; RAKUGI H, 1994, J CLIN INVEST, V93, P339, DOI 10.1172-JCI116965; RAYNOLDS MV, 1993, LANCET, V342, P1073, DOI 10.1016-0140-6736(93)92061-W; Rice GI, 1999, CARDIOVASC RES, V41, P746, DOI 10.1016-S0008-6363(98)00246-6; RIDKER PM, 1993, CIRCULATION, V87, P1969; RIGAT B, 1990, J CLIN INVEST, V86, P1343, DOI 10.1172-JCI114844; Saeed M, 2005, HYPERTENS RES, V28, P345, DOI 10.1291-hypres.28.345; Samani NJ, 1996, CIRCULATION, V94, P708; SCHELLING P, 1991, J HYPERTENS, V9, P3; Schieffer B, 2000, ARTERIOSCL THROM VAS, V20, P281; SCHMIDT S, 1993, J HYPERTENS, V11, P345, DOI 10.1097-00004872-199304000-00003; SCHUNKERT H, 1994, NEW ENGL J MED, V330, P1634, DOI 10.1056-NEJM199406093302302; TIRET L, 1994, LANCET, V344, P910, DOI 10.1016-S0140-6736(94)92268-3; Uhm WS, 2002, LUPUS, V11, P227, DOI 10.1191-0961203302lu174oa; Vaughan DE, 1998, EUR HEART J, V19, P9; VAUGHAN DE, 1995, J CLIN INVEST, V95, P995, DOI 10.1172-JCI117809; von Depka M, 2003, THROMB HAEMOSTASIS, V89, P847; Wells PS, 2003, THROMB HAEMOSTASIS, V90, P829, DOI 10.1160-TH03-03-0170; Winkelmann BR, 1996, ANN INTERN MED, V125, P1921222
Compound heterozygosity for factor V and methylenetetrahydrofolate reductase mutations in a patient with Budd-Chiari syndrome [2]
No full text[No abstract available]DAHLBACK B, 1995, BLOOD, V85, P607; Deltenre P, 2001, GUT, V48, P264, DOI 10.1136-gut.48.2.264; Graham IM, 1997, JAMA-J AM MED ASSOC, V277, P1775, DOI 10.1001-jama.277.22.1775; Karasu Z, 2003, TRANSPLANT P, V35, P3008, DOI 10.1016-j.transproceed.2003.10.038; Li XM, 2002, AM J HEMATOL, V71, P11, DOI 10.1002-ajh.10149; Mahmoud AEA, 1997, GUT, V40, P798; Menon KVN, 2004, NEW ENGL J MED, V350, P578, DOI 10.1056-NEJMra020282; Rosen SB, 1997, EUR J CLIN CHEM CLIN, V35, P5010
Human leukocyte antigen-DQA1 gene allelic distribution: Experience of a major tertiary care center in Lebanon
No full textAims: DQA1 is a human leukocyte antigen (HLA) class II molecule that is similar to the other class II molecules DR and DP. This study is the first of its kind to describe the distribution of HLA-DQA1 alleles in Lebanon. Methods: HLA-DQA1 typing was detected using the polymerase chain reaction-sequence- specific priming method in 111 Lebanese individuals referred for HLA typing and possible bone marrow donation. Results: Our data was compared to that of several populations. Some similarities were found between the Lebanese, Tunisian, Spanish, and Kuwaiti populations. Conclusion: This very first report from Lebanon will be of great help for later research to study the association of DQA1 alleles with major diseases in the Lebanese population and will add to the published international literature related to this important histocompatibility locus. Copyright 2011, Mary Ann Liebert, Inc.Alsaeid K, 2006, RHEUMATOL INT, V26, P224, DOI 10.1007-s00296-004-0553-y; Amirzargar A, 2001, HUM IMMUNOL, V62, P1234, DOI 10.1016-S0198-8859(01)00320-2; Ayed K, 2004, TISSUE ANTIGENS, V64, P520, DOI 10.1111-j.1399-0039.2004.00313.x; BEGOVICH AB, 1992, J IMMUNOL, V148, P249; BOWCOCK AM, 1991, P NATL ACAD SCI USA, V88, P839, DOI 10.1073-pnas.88.3.839; CHAKRABORTY R, 1991, SCIENCE, V254, P1735, DOI 10.1126-science.1763323; Cortes LM, 2004, TISSUE ANTIGENS, V63, P458, DOI 10.1111-j.0001-2815.2004.00202.x; Kapustin S, 1999, TISSUE ANTIGENS, V54, P517, DOI 10.1034-j.1399-0039.1999.540509.x; KAUFMAN JF, 1984, CELL, V36, P1, DOI 10.1016-0092-8674(84)90068-0; KWOK WW, 1993, J IMMUNOL, V150, P2263; LINCH DC, 1984, J IMMUNOL, V132, P2324; Maciel LMZ, 2001, THYROID, V11, P31; Marrosu MG, 1998, HUM MOL GENET, V7, P1235, DOI 10.1093-hmg-7.8.1235; Moustakas AK, 2002, AM J MED GENET, V115, P37, DOI 10.1002-ajmg.10342; Papassavas EC, 2000, HUM IMMUNOL, V61, P615, DOI 10.1016-S0198-8859(00)00115-4; Planelles D, 2006, BRIT J DERMATOL, V154, P261, DOI 10.1111-j.1365-2133.2005.06896.x; Price P, 1999, IMMUNOL REV, V167, P257, DOI 10.1111-j.1600-065X.1999.tb01398.x; Yang S, 2005, INT J DERMATOL, V44, P1022, DOI 10.1111-j.1365-4632.2004.02389.x; Zubillaga P, 2002, J PEDIATR GASTR NUTR, V34, P548, DOI 10.1097-00005176-200205000-000140
High prevalence of MTHFR gene A1298C polymorphism in Lebanon
No full textBackground: Mutations in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene could reduce the enzyme activity and lead to hyperhomocysteinemia, a condition that has been associated with several vascular conditions, in particular, coronary artery disease and deep vein thrombosis. Aim: The aim of this study was to assess the prevalence of the two most common polymorphisms, C677T and A1298C, which have not been well studied in the Lebanese population. Methods: We randomly selected 205 healthy individuals originating from different Lebanese provinces and religious communities. The CVD StripAssay was used to test for MTHFR gene polymorphisms. Results: We found that for C677T, the prevalence of C-C, C-T, and T-T genotypes was 65.3percent, 30.8percent, and 3.9percent, respectively, with an overall carrier rate of 34.6percent and allelic frequency of 0.19. However, the A1298C genotypic prevalence of A-C, A-A, and C-C was 50.2percent, 25.9percent, and 23.9percent, respectively, with an overall carrier rate of 74.14percent and an allelic frequency of 0.49. Conclusions: Compared to all other populations reported so far, the Lebanese population harbors the highest prevalence of the MTHFR A1298C polymorphism. This is an important finding to be followed in terms of clinical significance and sheds light on an additional unique genetic feature in this community. © Copyright 2008, Mary Ann Liebert, Inc.Al-Habboubi H, 2003, J THROMB HAEMOST, V1, P2246, DOI 10.1046-j.1538-7836.2003.00390.x; Al-Habboubi HH, 2004, THROMB HAEMOSTASIS, V91, P843; Almawi WY, 2004, AM J HEMATOL, V76, P85, DOI 10.1002-ajh.20047; Angeline T, 2004, EXP MOL PATHOL, V77, P85, DOI 10.1016-j.yexmp.2004.04.006; Antoniadi T, 1999, AM J HEMATOL, V61, P265, DOI 10.1002-(SICI)1096-8652(199908)61:4265::AID-AJH83.0.CO;2-#; Arruda VR, 1998, AM J MED GENET, V78, P332, DOI 10.1002-(SICI)1096-8628(19980724)78:4332::AID-AJMG53.0.CO;2-N; Chango A, 2000, BRIT J NUTR, V84, P891; Chiusolo P, 2004, HAEMATOLOGICA, V89, P139; DAngelo A, 1997, HAEMATOLOGICA, V82, P211; DeFranchis R, 1996, AM J HUM GENET, V59, P262; De Marco P, 2002, J HUM GENET, V47, P319, DOI 10.1007-s100380200043; denHeijer M, 1996, NEW ENGL J MED, V334, P759, DOI 10.1056-NEJM199603213341203; Eid Suhair S, 2004, Clin Lab Sci, V17, P200; Esfahani ST, 2003, J AM DIET ASSOC, V103, P200, DOI 10.1053-jada.2003.50030; Falchi A, 2005, EXP MOL PATHOL, V79, P210, DOI 10.1016-j.yexmp.2005.09.005; Franco RF, 1998, THROMB HAEMOSTASIS, V79, P119; Friedman G, 1999, J NUTR, V129, P1656; FROSST P, 1995, NAT GENET, V10, P111, DOI 10.1038-ng0595-111; Gibson CS, 2005, PATHOLOGY, V37, P160, DOI 10.1080-00313020500058250; Graham IM, 1997, JAMA-J AM MED ASSOC, V277, P1775, DOI 10.1001-jama.277.22.1775; Gudnason V, 1998, ATHEROSCLEROSIS, V136, P347, DOI 10.1016-S0021-9150(97)00237-2; Hanson NQ, 2001, CLIN CHEM, V47, P661; Hiraoka M, 2004, BIOCHEM BIOPH RES CO, V316, P1210, DOI 10.1016-j.bbrc.2004.02.174; Kahleova R, 2002, AM J HYPERTENS, V15, P857, DOI 10.1016-S0895-7061(02)02984-9; KANG SS, 1991, AM J HUM GENET, V48, P536; Kiffmeyer WR, 2004, CANCER, V100, P411, DOI 10.1002-cncr.11913; Koch MC, 1998, EUR J PEDIATR, V157, P487, DOI 10.1007-s004310050860; Kostulas K, 1998, EUR J CLIN INVEST, V28, P285; Lu YH, 2002, THROMB RES, V106, P7, DOI 10.1016-S0049-3848(02)00064-6; Mahfouz RAR, 2006, MOL BIOL REP, V33, P145, DOI 10.1007-s11033-006-6260-x; Markan S, 2007, MOL CELL BIOCHEM, V302, P125, DOI 10.1007-s11010-007-9434-5; Mornet E, 1997, HUM GENET, V100, P512, DOI 10.1007-s004390050544; Mutchinick OM, 1999, MOL GENET METAB, V68, P461, DOI 10.1006-mgme.1999.2939; Nishio H, 1996, JPN J HUM GENET, V41, P247, DOI 10.1007-BF01875985; Ou CY, 1996, AM J MED GENET, V63, P610, DOI 10.1002-(SICI)1096-8628(19960628)63:4610::AID-AJMG153.3.CO;2-Y; Peng FY, 2001, INT J MOL MED, V8, P509; Pepe G, 1998, AM J HUM GENET, V63, P917, DOI 10.1086-302015; Perez ABA, 2003, AM J MED GENET A, V119A, P20, DOI 10.1002-ajmg.a.10059; Rady PL, 1999, AM J MED GENET, V86, P380, DOI 10.1002-(SICI)1096-8628(19991008)86:4380::AID-AJMG133.0.CO;2-9; Rosenberg N, 2002, AM J HUM GENET, V70, P758, DOI 10.1086-338932; Rozen R, 1997, THROMB HAEMOSTASIS, V78, P523; SABBAGH AS, 2006, MOL BIOL REP, V34, P47; Sacchi E, 1997, THROMB HAEMOSTASIS, V78, P963; Sazci A, 2005, CELL BIOCHEM FUNCT, V23, P51, DOI 10.1027-cbf.1132; Shrubsole MJ, 2004, CANCER EPIDEM BIOMAR, V13, P190, DOI 10.1158-1055-9965.EPI-03-0273; Stevenson RE, 1997, AM J HUM GENET, V60, P229; Taher A, 2001, THROMB HAEMOSTASIS, V86, P723; van der Put NMJ, 1998, AM J HUM GENET, V62, P1044, DOI 10.1086-301825; Vanegas OC, 1998, THROMB HAEMOSTASIS, V79, P883; Viel A, 1997, BRIT J CANCER, V75, P1105, DOI 10.1038-bjc.1997.191; Weisberg I, 1998, MOL GENET METAB, V64, P169, DOI 10.1006-mgme.1998.2714; Wilcken DEL, 1996, ARTERIOSCL THROM VAS, V16, P878; Yoo JH, 2000, THROMB RES, V97, P77, DOI 10.1016-S0049-3848(99)00127-9; Zaatari GS, 2006, PATHOLOGY, V38, P442, DOI 10.1080-00313020600922934; Zetterberg H, 2002, THROMB RES, V108, P127, DOI 10.1016-S0049-3848(03)00004-519191
