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National Cancer Institute®
Ultima Vez Modificado: 1 de agosto del 2002
UI - 11721435
AU - Fu G; Lu C; Zhang R
TI - [Deletions and aberrant transcription of p16 and p15 genes in childhood acute lymphoblastic leukemia]
SO - Zhonghua Xue Ye Xue Za Zhi 1999 Jul;20(7):366-8
AD - Department of Immunology, China Medical University, Shenyang 110001.
OBJECTIVE: To explore the role of p16(MTS1) and p15(MTS2) genes in the pathogenesis of childhood acute lymphoblastic leukemia(ALL). METHODS: PCR and Southern blot were used to analyse p16 and p15 gene deletions, RT-PCR was used to analyse p15 gene transcription. RESULTS: Exon 1 and 2 of p16 gene deletion was detected in 8 of 21 patients(38.1%), and exon 1 and 2 of p15 gene deletion in 11 of 21 patients(52.3%). Aberrant p15 gene transcription was observed in two cases. CONCLUSION: High frequency of p16 and p15 gene deletions and aberrant transcription may be involved in the pathogenesis of childhood ALL.
UI - 12116073
AU - Liang DC; Shih LY; Yang CP; Hung IJ; Chen SH; Jaing TH; Liu HC; Chang WH
TI - Multiplex RT-PCR assay for the detection of major fusion transcripts in Taiwanese children with B-lineage acute lymphoblastic leukemia.
SO - Med Pediatr Oncol 2002 Jul;39(1):12-7
AD - Division of Pediatric Hematology-Oncology, Mackay Memorial Hospital, Taipei, Taiwan.
BACKGROUND: The classification of B-lineage acute lymphoblastic leukemia (ALL) by specific chromosomal translocations may have prognostic implications. Reverse transcriptase-polymerase chain reaction (RT-PCR) assay is a useful tool for the detection of fusion transcript resulting from specific chromosomal translocation of the leukemic cells. In general, fusion transcripts are determined individually, a process which is labor intensive in order to detect all major fusion transcripts. PROCEDURE: We use a multiplex RT-PCR assay to detect both the CML- and ALL-type BCR-ABL transcripts of the t(9;22), all described variants of the E2A-PBX1 transcripts of t(1;19), the MLL-AF4 transcripts of t(4;11), and all described variants of TEL-AML1 (also termed ETV6-CBFA2) of the cryptic t(12;21) in 165 leukemic samples at diagnosis. RESULTS: The study yielded a completely concordant result with those obtained by the individual RT-PCR assay. In this cohort of Taiwan children, the relative frequencies of the four translocations of B-lineage ALL were as following: 6% with ALL-type t(9;22)/BCR-ABL, 7% t(1;19)/E2A-PBX1, 3% t(4;11)/MLL-AF4, and 18% t(12;21)/TEL-AML1, comparable to those in the Western countries. CONCLUSION: Multiplex RT-PCR assay is an efficient, sensitive, accurate, and cost-effective diagnostic tool, which will likely improve our ability in accurately and rapidly risk-stratifying children with ALL. Copyright 2002 Wiley-Liss, Inc.
UI - 12116079
AU - Barr RD; Guo CY; Wiernikowski J; Webber C; Wright M; Atkinson S
TI - Osteopenia in children with acute lymphoblastic leukemia: a pilot study of amelioration with Pamidronate.
SO - Med Pediatr Oncol 2002 Jul;39(1):44-6
AD - Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada.
UI - 12008081
AU - Ravandi F; Cortes J; Estrov Z; Thomas D; Giles FJ; Huh YO; Pierce S;
TI - O'Brien S; Faderl S; Kantarjian HM CD56 expression predicts occurrence of CNS disease in acute lymphoblastic leukemia.
SO - Leuk Res 2002 Jul;26(7):643-9
AD - Department of Hematology/Oncology, University of Illinois, Chicago, IL, USA.
We examined the pre-treatment bone marrow samples from 200 consecutive adult patients with acute lymphoblastic leukemia (ALL) treated on various protocols at the University of Texas, M.D. Anderson Cancer Center between 1986 and 1998. Standard MFC techniques were used to determine CD56 expression on the leukemia blasts cells. The expression of CD56 was correlated with clinical characteristics at diagnosis, response to therapy, survival and disease-free survival.Blast expression of CD56 (> or = 20% of leukemic blasts) was seen in 16 (8%) of patients, with a median expression of 67% (range 20-99%). CD56 expression was associated with a higher incidence of central nervous system (CNS) disease at diagnosis (19% versus 4%; P=0.016). Incidence of CNS disease at any time was higher in patients with CD56+ disease (31% versus 14%; P=0.057). Among the 109 patients uniformly treated with the hyperCVAD regimen, CD56 expression was associated with a statistically significant higher incidence of CNS disease (33% versus 9%; P=0.026). CD56 expression in ALL is uncommon but may predict a higher risk for CNS disease. If these results are confirmed, CD56 expression could be used in combination with other high-risk features (e.g. lactate dehydrogenase (LDH), S-phase fraction, mature B-cell phenotype) to design a risk-oriented approach to CNS prophylaxis.
UI - 12008082
AU - Dorak MT; Oguz FS; Yalman N; Diler AS; Kalayoglu S; Anak S; Sargin D;
TI - Carin M A male-specific increase in the HLA-DRB4 (DR53) frequency in high-risk and relapsed childhood ALL.
SO - Leuk Res 2002 Jul;26(7):651-6
AD - Department of Epidemiology and International Health, School of Public Health, University of Alabama at Birmingham, AL 35294-0022, USA. email@example.com
Previous studies reported significant HLA-DR associations with various leukemias one of which is with HLA-DRB4 (DR53) family in male patients with childhood ALL. We have HLA-DR-typed 212 high-risk or relapsed patients with childhood (n=114) and adult (n=98) ALL and a total of 250 healthy controls (118 children, 132 adult) by PCR-SSP analysis. The members of the HLA-DRB3 (DR52) family were underrepresented in patients most significantly for HLA-DRB1*12 (P=0.0007) and HLA-DRB1*13 (P=0.0001). In childhood ALL, the protective effect of DRB3 was evident in homozygous form (P=0.001). The DRB4 marker frequency was increased in males with childhood ALL (67.4%) compared to age- and sex-matched controls (42.1%, P=0.003) and female patients (35.7%, P=0.004). Besides being a general marker for increased susceptibility to childhood ALL in males, HLA-DRB4 is over-represented in high-risk patients. These results further suggest that the HLA system is one of the components of genetic susceptibility to leukemia but mainly in childhood and in boys only.
UI - 11872238
AU - Brouwer RE; van der Heiden P; Schreuder GM; Mulder A; Datema G; Anholts
TI - JD; Willemze R; Claas FH; Falkenburg JH Loss or downregulation of HLA class I expression at the allelic level in acute leukemia is infrequent but functionally relevant, and can be restored by interferon.
SO - Hum Immunol 2002 Mar;63(3):200-10
AD - Laboratory of Experimental Hematology, Department of Hematology, Leiden, The Netherlands.
Human leukocyte antigen (HLA) class I expression at the allelic level was analyzed in 397 acute myeloid leukemia (AML) and 186 acute lymphoid leukemia (ALL) using a complement-dependent cytotoxicity assay. Impaired recognition possibly due to HLA downregulation was observed in 2% of the patients with AML and ALL in complete remission, and in 8%-15% in the groups with blasts. In 15 instances of diminished cytotoxicity, leukemic cells and control PHA blasts from the same patients were further analyzed using flow cytometry. In 4/6 ALL and 4/9 AML patients HLA downregulation or complete loss (2 patients) of cell surface expression could be confirmed. No genomic abnormalities were observed. In addition, 12 AML and 13 ALL patients were tested during relapse using flow cytometry. In 1/12 AML patients and 1/13 ALL patients allelic downregulation of cell surface expression was found. In two patients tested, downregulation or loss of cell surface expression of HLA class I antigens corresponded with impaired T cell mediated lysis by HLA restricted cytotoxic T lymphocyte.Treatment of the cells with alpha- or gamma-interferon could restore HLA class I expression and T-cell recognition. In conclusion, downregulation of cell surface expression of HLA class I expression at the allelic level in AML and ALL is infrequent but functionally relevant. HLA downregulation was reversible and T-cell recognition could be restored by alpha- or gamma-interferon.
UI - 12070010
AU - Davies SM; Bhatia S; Ross JA; Kiffmeyer WR; Gaynon PS; Radloff GA;
TI - Robison LL; Perentesis JP Glutathione S-transferase genotypes, genetic susceptibility, and outcome of therapy in childhood acute lymphoblastic leukemia.
SO - Blood 2002 Jul 1;100(1):67-71
AD - Children's Oncology Group, Arcadia, CA 91066-6012, USA. firstname.lastname@example.org
The glutathione S-transferase (GST) genes are involved in the metabolism of environmental carcinogens and of some classes of chemotherapy drugs. GSTM1 and GSTT1 genotypes are polymorphic in humans, and the phenotypic absence of enzyme activity is caused by a homozygous inherited deletion of the gene. Previous, smaller studies of childhood acute lymphoblastic leukemia (ALL) provided contrasting data on the role of the GST genotype in susceptibility and treatment outcomes. We analyzed GST genotypes in 710 children with ALL treated by the Children's Cancer Group. Frequencies were compared with those of normal controls, and outcomes were analyzed according to genotype. Comparisons of gene frequencies in ALL case and control patients showed similar frequencies (54% vs 53% GSTM1 null in whites, P =.9; 40% versus 32% in blacks, P =.45; 16% versus 15% GSTT1 null in whites, P =.8; 17% versus 28% in blacks, P =.3). ALL was not associated with the GSTM1-null genotype or the double-null genotype in blacks or whites, in contrast to previous reports. Stratification of cases by age at diagnosis, sex, white blood cell count at diagnosis, B or T lineage, or cytogenetics revealed no differences in genotype frequencies. Analysis of treatment outcomes showed no differences in outcome according to GST genotype; in particular, there were no differences in frequencies of relapse at any site. These data, representing a larger series than any reported previously, suggest that GST genotype does not affect etiology or outcome of childhood ALL.
UI - 12086890
AU - Ferrando AA; Neuberg DS; Staunton J; Loh ML; Huard C; Raimondi SC; Behm
TI - FG; Pui CH; Downing JR; Gilliland DG; Lander ES; Golub TR; Look AT Gene expression signatures define novel oncogenic pathways in T cell acute lymphoblastic leukemia.
SO - Cancer Cell 2002 Feb;1(1):75-87
AD - Department of Pediatric Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02142, USA.
Human T cell leukemias can arise from oncogenes activated by specific chromosomal translocations involving the T cell receptor genes. Here we show that five different T cell oncogenes (HOX11, TAL1, LYL1, LMO1, and LMO2) are often aberrantly expressed in the absence of chromosomal abnormalities. Using oligonucleotide microarrays, we identified several gene expression signatures that were indicative of leukemic arrest at specific stages of normal thymocyte development: LYL1+ signature (pro-T), HOX11+ (early cortical thymocyte), and TAL1+ (late cortical thymocyte). Hierarchical clustering analysis of gene expression signatures grouped samples according to their shared oncogenic pathways and identified HOX11L2 activation as a novel event in T cell leukemogenesis. These findings have clinical importance, since HOX11 activation is significantly associated with a favorable prognosis, while expression of TAL1, LYL1, or, surprisingly, HOX11L2 confers a much worse response to treatment. Our results illustrate the power of gene expression profiles to elucidate transformation pathways relevant to human leukemia.
UI - 12086866
AU - Staudt LM
TI - It's ALL in the diagnosis.
SO - Cancer Cell 2002 Mar;1(2):109-10
AD - Metabolism Branch, Center for Cancer Research, National Cancer Institute, 9000 Rockville Pike, Bethesda, MD 20892, USA. Istaudt@mail.nih.gov
The molecular diagnosis of human cancer will hasten the development of treatments tailored to the abnormalities present in each patient's tumor cells. Recent gene expression profiling studies of pediatric acute lymphoblastic leukemia (ALL) suggest that the molecular diagnosis of these diseases is right around the corner.
UI - 12086872
AU - Yeoh EJ; Ross ME; Shurtleff SA; Williams WK; Patel D; Mahfouz R; Behm
TI - FG; Raimondi SC; Relling MV; Patel A; Cheng C; Campana D; Wilkins D; Zhou X; Li J; Liu H; Pui CH; Evans WE; Naeve C; Wong L; Downing JR Classification, subtype discovery, and prediction of outcome in pediatric acute lymphoblastic leukemia by gene expression profiling.
SO - Cancer Cell 2002 Mar;1(2):133-43
AD - Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Treatment of pediatric acute lymphoblastic leukemia (ALL) is based on the concept of tailoring the intensity of therapy to a patient's risk of relapse. To determine whether gene expression profiling could enhance risk assignment, we used oligonucleotide microarrays to analyze the pattern of genes expressed in leukemic blasts from 360 pediatric ALL patients. Distinct expression profiles identified each of the prognostically important leukemia subtypes, including T-ALL, E2A-PBX1, BCR-ABL, TEL-AML1, MLL rearrangement, and hyperdiploid >50 chromosomes. In addition, another ALL subgroup was identified based on its unique expression profile. Examination of the genes comprising the expression signatures provided important insights into the biology of these leukemia subgroups. Further, within some genetic subgroups, expression profiles identified those patients that would eventually fail therapy. Thus, the single platform of expression profiling should enhance the accurate risk stratification of pediatric ALL patients.
UI - 11866371
AU - Levien MG
TI - Osteonecrosis as a complication of treating acute lymphoblastic leukemia in children: a report from the Children's Cancer Group.
SO - Clin Pediatr (Phila) 2002 Jan-Feb;41(1):63-4
AD - Cleveland Clinic Foundation, USA.
UI - 12146036
AU - Kashima K; Nagahama J; Sato K; Tanamachi H; Gamachi A; Daa T; Nakayama
TI - I; Yokoyama S Detection of the HTLV-I gene on cytologic smear slides.
SO - Acta Cytol 2002 Jul-Aug;46(4):709-12
AD - Department of Pathology, Oita Medical University Hospital, First Department of Pathology, Oita Medical University, Oita, Japan. email@example.com
OBJECTIVE: To apply the polymerase chain reaction (PCR) for detection of the HTLV-I gene from cytologic smear slides. STUDY DESIGN: Samples were from seven cases of serum anti-ATL antibody (ATLA)-positive T-cell lymphoma and three from ATLA-negative T-cell lymphoma. Six of the seven ATLA-positive cases were confirmed to be ATLL by Southern blotting. From the seventh case a fresh sample for blotting could not obtained. DNA was extracted from the cytologic smear slides of all 10 cases; they had been stained with Papanicolaou or May-Giemsa stain, digested with proteinase K and precipitated with phenol and ethanol. The target sequence in the pX region of the HTLV-I gene was amplified by PCR. RESULTS: All seven ATLA-positive cases, including one that had not yet been confirmed by Southern blotting, showed a single band, as predicted, while the three ATLA-negative cases showed no band. CONCLUSION: If cytologic smear slides are available but a fresh sample is not, the PCR method should provide evidence that the virus is present since in our study sufficient DNA templates were successfully extracted from the stained cytologic smear slides for detection of the virus.
UI - 12142782
AU - Kham SK; Tan PL; Tay AH; Heng CK; Yeoh AE; Quah TC
TI - Thiopurine methyltransferase polymorphisms in a multiracial asian population and children with acute lymphoblastic leukemia.
SO - J Pediatr Hematol Oncol 2002 Jun-Jul;24(5):353-9
AD - Department of Pediatrics, National University of Singapore, Singapore.
The purpose of this study was to determine the frequency of thiopurine methyltransferase (TPMT) polymorphisms in a multiracial Asian population and to assess its relevance in the management of childhood acute lymphoblastic leukemia (ALL). Six hundred unrelated cord blood samples from 200 Chinese, Malay, and Indian healthy newborns were collected at the National University Hospital, Singapore; an additional 100 children with ALL were analyzed for five of the commonly reported TPMT variant alleles using polymerase chain reaction/restriction fragment length polymorphism and allele-specific polymerase chain reaction-based assays. In the cord blood study, the TPMT*3C variant was detected in all three ethnic groups; Chinese, Malays, and Indians had allele frequencies of 3%, 2.3%, and 0.8%, respectively. The TPMT*3A variant was found only among the Indians at a low allele frequency of 0.5%. The TPMT*6 variant was found in one Malay sample. Among the children with ALL, two white and one Chinese were heterozygous for the TPMT*3A variant and showed intermediate sensitivity to 6-mercaptopurine during maintenance therapy. Three Chinese patients and one Malay patient were heterozygous for the TPMT*3C variant. Mercaptopurine sensitivity could be validated in only one out of four TPMT*3C heterozygous patients. The overall allele frequency of the TPMT variants in this multiracial population was 2.5%. The TPMT*3C was the most common variant allele; TPMT*3A and TPMT*6 were rare. These results support the feasibility of performing TPMT genotyping in all children diagnosed with acute leukemia to minimize toxicity from thiopurine chemotherapy.
UI - 12145681
AU - van der Velden VH; Jacobs DC; Wijkhuijs AJ; Comans-Bitter WM; Willemse
TI - MJ; Hahlen K; Kamps WA; van Wering ER; van Dongen JJ Minimal residual disease levels in bone marrow and peripheral blood are comparable in children with T cell acute lymphoblastic leukemia (ALL), but not in precursor-B-ALL.
SO - Leukemia 2002 Aug;16(8):1432-6
AD - Department of Immunology, Erasmus MC, Erasmus University Medical Center, Rotterdam, The Netherlands.
Sensitive and quantitative detection of minimal residual disease (MRD) in bone marrow (BM) samples of children with acute lymphoblastic leukemia (ALL) is essential for evaluation of early treatment response. In this study, we evaluated whether the traumatic BM samplings can be replaced by peripheral blood (PB) samplings. MRD levels were analyzed in follow-up samples of 62 children with precursor-B-ALL (532 paired BM-PB samples) and 22 children with T-ALL (149 paired BM-PB samples) using real-time quantitative PCR (RQ-PCR) analysis of immunoglobulin and T cell receptor gene rearrangements with sensitivities of 10(-3) to 10(-5) (one ALL cell in 10(3) to 10(5) normal cells). In 14 of the 22 T-ALL patients, detectable MRD levels were found in 67 paired BM-PB samples: in 47 pairs MRD was detected both in BM and PB, whereas in the remaining pairs very low MRD levels were detected in BM (n = 11) or PB (n = 9) only. The MRD levels in the paired BM-PB samples were very comparable and strongly correlated (r(s) = 0.849). Comparable results were obtained earlier by immunophenotyping in 26 T-ALL patients (321 paired BM-PB samples), which also showed a strong correlation between MRD levels in paired BM and PB samples (r(s) = 0.822). In 39 of the 62 precursor-B-ALL patients, MRD was detected in 107 BM-PB pairs: in 48 pairs MRD was detected in both BM and PB, in 47 pairs MRD was solely detected in BM (at variable levels), and in 12 pairs only the PB sample was MRD-positive at very low levels (=10(-4)). Furthermore, in the 48 double-positive pairs, MRD levels in BM and PB varied enormously with MRD levels in BM being up to 1000 times higher than in the corresponding PB samples. Consequently, BM samples cannot easily be replaced by PB sampling for MRD analysis in childhood precursor-B-ALL, in line with their BM origin. In T-ALL, which are of thymic origin, BM sampling might be replaced by PB sampling, because the dissemination of T-ALL cells to BM and PB appears to be comparable.
UI - 12145701
AU - Alves S; Amorim A; Ferreira F; Norton L; Prata MJ
TI - The GSTM1 and GSTT1 genetic polymorphisms and susceptibility to acute lymphoblastic leukemia in children from north Portugal.
SO - Leukemia 2002 Aug;16(8):1565-7
UI - 11154239
AU - Carter TL; Watt PM; Kumar R; Burton PR; Reaman GH; Sather HN; Baker DL;
TI - Kees UR Hemizygous p16(INK4A) deletion in pediatric acute lymphoblastic leukemia predicts independent risk of relapse.
SO - Blood 2001 Jan 15;97(2):572-4
AD - Division of Children's Leukaemia and Cancer Research, TVWT Institute for Child Health Research, University of Western Australia, West Perth.
The genes at the INK4A/ARF locus at 9p21 are frequently involved in human cancer. Virtually all p16(INK4A) exon 2 (henceforth called p16) inactivation in pediatric acute lymphoblastic leukemia (ALL) occurs by gene deletion. The results of this study illustrate that real-time quantitative polymerase chain reaction is capable of detecting gene deletion in primary patient specimens with a precision not previously achieved by conventional methods. Importantly, this assay includes the detection of hemizygous deletions. The study revealed, strikingly, that the risk ratio for relapse for hemizygous deletion compared with no deletion was 6.558 (P =.00687) and for homozygous deletion was 11.558 (P =.000539). These results confirm and extend the authors' previous findings that homozygous deletion of p16 in pediatric ALL patients is an independent prognostic indicator of outcome from therapy.
UI - 11405214
AU - Graf Einsiedel H; Taube T; Hartmann R; Eckert C; Seifert G; Wellmann S;
TI - Henze G; Seeger K Prognostic value of p16(INK4a) gene deletions in pediatric acute lymphoblastic leukemia.
SO - Blood 2001 Jun 15;97(12):4002-4
UI - 11778693
AU - Moynet D; Pouliquen JF; Londos-Gagliardi D; Buigues RP; Moreau JF;
TI - Bedjabaga I; Georges MC; Talarmin A; Joubert M; Fleury H; Vincendeau P; Guillemain B High variability of HTLV-I in a remote population of Gabon as compared to that of a similar population of French Guiana.
SO - Virus Genes 2001 Dec;23(3):257-61
AD - Immunologie Moleculaire et Parasitologie, Universite Bordeaux2, France. firstname.lastname@example.org
An anomalous high frequency of ATL was observed in a remote 'noir maroons' village of French Guiana. Since it is not clear if HTLV-I is responsible for different frequencies of disease in different geographical areas, we undertook a comparison of the population with a similar one located in Gabon. We found a much higher degree of gp46 surface envelope glycoprotein sequence conservation in the Guianese village than in the Gabonese one.
UI - 11899114
AU - Ou SX; Han D; Severson RK; Chen Z; Neglia JP; Reaman GH; Buckley JD;
TI - Robison LL Birth characteristics, maternal reproductive history, hormone use during pregnancy, and risk of childhood acute lymphocytic leukemia by immunophenotype (United States).
SO - Cancer Causes Control 2002 Feb;13(1):15-25
AD - Department of Pediatrics, University of Minnesota, Minneapolis, USA. Xiao-Ou.Shu@mcmail.vanderbilt.edu
OBJECTIVE: To investigate the associations of birth characteristics and maternal reproductive factors with risk of childhood acute lymphoblastic leukemia (ALL) by immunophenotypic subtypes. METHODS: Data collected from a case-control study including 1842 ALL cases (age < 15 years) and 1986 individually matched controls were analyzed. Exposure information was obtained through telephone interviews of parents. RESULTS: Factors associated with risk of ALL from all subgroups combined included high birth weight (OR = 1.4, 95% CI = 1.1-1.8), high birth order (OR = 2.0, 95% CI = 1.3-3.0 for fourth-born child compared to first-born child). young maternal age (<20 compared to 25-29, OR = 1.4, 95% CI = 1.1-1.9), advanced paternal age (>39 compared to 25-29, OR = 1.4, 95% CI = 1.0-1.9), induced abortion prior to the index pregnancy (OR = 1.2, 95% CI = 1.0-1.4), and oral contraceptive use during the index pregnancy (OR = 1.5, 95% CI = 1.0-2.2) with children under the age of 2 (OR = 5.1, 95% CI = 1.0-24.7) being the predominantly affected group. Risk of early pre-B-cell ALL increased with advanced paternal age (OR = 1.7, 95% CI = 1.1-2.7) and high birth order (OR = 2.0, 95% CI = 1.1-3.6), while risk of pre-B-cell ALL increased with both younger (OR = 3.4, 95% CI = 1.4-8.4) and advanced maternal age (OR = 2.6, 95% CI = 1.1-5.9). T-cell ALL was associated with high birth weight (OR = 2.4, 95% CI = 1.1-5.5) and history of induced abortion (OR = 2.4, 95% CI = 1.3-4.5). CONCLUSION: This study suggests that the association of ALL with birth characteristics and maternal reproductive factors varies with the immunophenotype of the ALL. Future studies are needed to better understand the effect of maternal hormone in the development of subtype of childhood ALL.
UI - 11899117
AU - Ekstrom K; Wuu J; Hsieh CC; Glimelius B; Lambe M
TI - Childbearing and the risk of leukemia in Sweden.
SO - Cancer Causes Control 2002 Feb;13(1):47-53
AD - Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden. email@example.com
OBJECTIVE: The possible influence of childbearing on the development of leukemias in females has received little attention, in spite of consistent findings of lower incidence rates in females than in males. A nested case-control study was undertaken to explore if parity and age at first birth affect the risk of developing these malignancies. METHODS: In a nationwide cohort defined by a population-based Fertility Register, we identified 356 women with chronic myeloid leukemia (CML), 819 with acute nonlymphocytic leukemia (ANLL), and 179 with acute lymphocytic leukemia (ALL). For each case, five age-matched controls were selected. Odds ratios were estimated by conditional logistic regression analyses. RESULTS: There was some evidence of weak negative associations between parity and age at first birth for CML. Compared to nulliparous women there was a tendency of a temporal risk reduction of CML for the first 10 years following a delivery. The risk of ANLL was slightly lower in parous compared to nulliparous women. Neither parity nor age at first birth was related to the risk of ALL. CONCLUSIONS: We conclude that if pregnancy-related hormonal or immunological factors have an effect on the development of leukemia, it is minor and confined to the myeloid types, chiefly CML. Our study gives some support for treating the leukemias as separate entities based on both cell lineage and form in future etiologic studies.
UI - 12091359
AU - Hotfilder M; Rottgers S; Rosemann A; Jurgens H; Harbott J; Vormoor J
TI - Immature CD34+CD19- progenitor/stem cells in TEL/AML1-positive acute lymphoblastic leukemia are genetically and functionally normal.
SO - Blood 2002 Jul 15;100(2):640-6
AD - Department of Pediatric Hematology and Oncology, University Children's Hospital Muenster, Germany.
One important question in stem cell biology of childhood acute lymphoblastic leukemia (ALL) is whether immature CD34+CD19- cells are part of the leukemic cell clone. CD34+CD19- cells from the bone marrow of 9 children with TEL/AML1-positive ALL were purified by flow sorting and subjected to reverse transcriptase-polymerase chain reaction (RT-PCR), fluorescence in situ hybridization, and methylcellulose cultures. In 3 of 8 patients analyzed by RT-PCR, no TEL/AML1-positive cells could be detected in the CD34+CD19- cell fraction. Altogether, the percentage of TEL/AML1-positive cells was low: 1.6% (n = 8; SD 2.2%) by nested real-time RT-PCR and 2.5% (n = 5; SD 2.6%) by fluorescence in situ hybridization. This correlated with the percentage of contaminating CD19+ leukemic cells in the CD34+CD19- cell fraction in 6 control sorts (mean 4.6%, SD 3.6%), indicating that the low levels of leukemic cells detected in the CD34+CD19- cell fraction could be attributed to sorter errors. Methylcellulose cultures in 3 patients provided further evidence that CD34+CD19- cells represent a candidate normal cell population. The clonogenicity of the CD34+CD19- cell fraction was similar to normal progenitors, including growth of primitive granulocyte, erythroid, macrophage, megakaryocyte colony-forming units. Each of 92 colonies from cultures with CD34+CD19- cells tested negative for TEL/AML1. In conclusion, our data support the hypothesis that the leukemia in TEL/AML1-positive childhood ALL originates in a CD19+ lymphoid progenitor. This has many therapeutic implications, eg, for purging of autologous stem cell products, flow cytometric monitoring of minimal residual disease, and targeting immunotherapy against the leukemic cell clone.
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