A N Mohamed

Children's Hospital of Michigan, Detroit, Michigan, United States

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Publications (61)249.86 Total impact

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    ABSTRACT: Secondary malignancies (SMs) in Hodgkin lymphoma (HL) are thought to be related to exposure to alkalating agents, topoisomerase II inhibitors and ionizing radiation, and tend to occur a decade after initial therapy. We report a 14 year old autistic male, who developed malignant fibrous histiocytoma (MFH) two years after autologous stem cell transplantation for advanced stage HL. The MFH and post-surgical reactive tissues exhibited multiple clonal abnormalities. In addition, PHA-stimulated peripheral blood lymphocytes showed increased frequency of non-clonal chromosomal aberrations. The potential role of genomic instability in early onset of SM in our patient is discussed.
    Pediatric Blood & Cancer 07/2011; 56(7):1143-5. · 2.35 Impact Factor
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    ABSTRACT: IKK-2 is an important regulator of the nuclear factor-κB (NF-κB) which has been implicated in survival, proliferation and apoptosis resistance of lymphoma cells. In this study, we investigated whether inhibition of IKK-2 impacts cell growth or cytotoxicity of selected conventional chemotherapeutic agents in non-Hodgkin's lymphoma.Two established model systems were used; Follicular (WSU-FSCCL) and Diffuse Large Cell (WSU-DLCL2) Lymphoma, both of which constitutively express p-IκB. A novel, selective small molecule inhibitor of IKK-2, ML120B (N-[6-chloro-7-methoxy-9H-β-carbolin-8-yl]-2-methylnicotinamide) was used to perturb NF-κB in lymphoma cells. The growth inhibitory effect of ML120B (M) alone and in combination with cyclophosphamide monohydrate (C), doxorubicin (H) or vincristine (V) was evaluated in vitro using short-term culture assay. We also determined efficacy of the combination in vivo using the SCID mouse xenografts. ML120B down-regulated p-IκBα protein expression in a concentration dependent manner, caused growth inhibition, increased G0/G1 cells, but did not induce apoptosis. There was no significant enhancement of cell kill in the M/C or M/H combination. However, there was strong synergy in the M/V combination where the vincristine concentration can be lowered by a hundred fold in the combination for comparable G2/M arrest and apoptosis. ML120B prevented vincristine-induced nuclear translocation of p65 subunit of NF-κB. In vivo, ML120B was effective by itself and enhanced CHOP anti-tumor activity significantly (P = 0.001) in the WSU-DLCL2-SCID model but did not prevent CNS lymphoma in the WSU-FSCCL-SCID model. For the first time, this study demonstrates that perturbation of IKK-2 by ML120B leads to synergistic enhancement of vincristine cytotoxicity in lymphoma. These results suggest that disruption of the NF-κB pathway is a useful adjunct to cytotoxic chemotherapy in lymphoma.
    Molecular Cancer 01/2010; 9:228. · 5.13 Impact Factor
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    ABSTRACT: t(8;21)(q22;q22) results in the AML1-ETO (A1E) fusion gene and is a common cytogenetic abnormality in acute myeloid leukemia (AML). Although insertions at the breakpoint region of the A1E fusion transcripts have been reported, additional structural alterations are largely uncharacterized. By RT-PCR amplifications and DNA sequencing, numerous in-frame and out-of-frame AML1b-ETO and AML1c-ETO transcripts were identified in 13 pediatric t(8;21) AMLs, likely resulting from alternate splicing, internal deletions and/or breakpoint region insertions involving both the AML1 (RUNX1) and ETO regions. The in-frame A1E fusion transcript forms represented minor forms. These structure alterations were found in AML1c-ETO but not AML1b-ETO transcripts in two adult t(8;21) AMLs. Although no analogous alterations were detected in native AML1b transcripts, identical alterations in native ETO transcripts were identified. When transfected into HeLa cells, only AML1b, and not the in-frame A1E forms, transactivated the GM-CSF promoter. In co-transfection experiments, the effects of A1E proteins on GM-CSF transactivation by AML1b ranged from repressive to activating. Our results demonstrate a remarkable and unprecedented heterogeneity in A1E fusion transcripts in t(8;21) myeloblasts and suggest that synthesis of alternate A1E transcript and protein forms can significantly impact the regulation of AML1 responsive genes.
    Oncogene 06/2008; 27(36):4933-42. · 8.56 Impact Factor
  • Christie L Boils, Anwar N Mohamed
    Acta Haematologica 02/2008; 119(2):65-8. · 0.89 Impact Factor
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    ABSTRACT: To evaluate the outcome of children with high hyperdiploid acute lymphoblastic leukemia (hHDALL) treated at the author's institution. One hundred thirty-five consecutive children with B-precursor ALL were diagnosed between 1991 and 2002: 38 (28.1%) hHDALL and 97 (71.9%) non-hHDALL. In the hHDALL group, 11/38 (28.9%) relapsed at a median interval of 2.8 years (range: 0.8-5.0 years) with 9/11 relapses occurring at the end or after the completion of therapy. Three (27.3%) relapses were isolated hematopoietic (BM), while eight (72.7%) were either isolated extramedullary (EM) relapses (n=6; Testis: 4; CNS: 2) or combined hematopoietic and extramedullary relapses (n=2; BM + CNS: 1; BM + Testis: 1). For the non-hHDALL group, 29/97 (29.9%) relapsed. Unlike the hHDALL group, the non-hHDALL group experienced hematopoietic relapses (62%; n=18) more frequently than isolated extramedullary (27.5%; n=8: Testis: 1; CNS: 7) or combined hematopoietic and extramedullary relapses (10.3%; CNS + BM: 3), with 24/29 (82.8%) of the relapses occurring on therapy. Relapses in hHDALL frequently involved EM sites (P=0.053). Presence of triple trisomy of +4,+10,+17 at diagnosis had a protective effect against relapse (P<0.05). Five-year EFS for the hHDALL and non-hHDALL patients was similar, 70.5+/-7.5% and 66.4+/-4.9%, respectively. Five-year OS for the hHDALL patients was significantly higher than for the non-hHDALL patients, 92+/-4.5% vs. 74.1+/-4.5%, P=0.038. Biologically significant differences exist between relapse patterns of hHDALL and non-hHDALL cases related to relapse sites and time periods when relapses occur. hHDALL relapses continue to be chemo-sensitive.
    American Journal of Hematology 01/2008; 83(1):34-40. · 4.00 Impact Factor
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    ABSTRACT: We identified 120 multiple myeloma (MM) cases with satisfactory cytogenetic evaluation and abnormal karyotypes. Hyperdiploid karyotype was found in 77 cases (64%), hypodiploid in 30 cases (25%), and the remaining 13 cases (11%) had a pseudodiploid karyotype. The most common numerical abnormalities were gains of chromosomes 15, 9, 3 followed by chromosomes 19, 11, 7, 21, and 5. Whole chromosome losses were also frequent involving primarily chromosomes X/Y, 8, 13, 14, and 22. Most cases showed also structural rearrangements leading to del(1p), dup(1q), del(5q), del(6q), del(8p), del(9p), del(13q), and del(17p). Chromosome 13/13q deletion was found in 52% of cases; complete loss of 13 was observed in 73% of cases, whereas 27% had interstitial deletions. In addition, 13/13q deletions occurred in 75% of nonhyperdiploid myeloma but only 39% of the hyperdiploid had 13/13q deletions. Translocations affecting 14q32/IGH region was seen 40 cases; t(11;14)(q13;q32) in 17 cases, t(14;16)(q32;q23) and t(8;14)(q24;q32) in three cases each, and t(6;14)(p21;q32) and t(1;14)(q21;q32) in two cases each. The remaining 14q32 translocations had various t(V;14) partners or of an undetermined origin. Remarkably, the 14q32/IGH translocations were less frequent in the hyperdiploid karyotypes than the nonhyperdiploid karyotypes (17 vs. 63%). Fourteen cases showed break at 8q24/CMYC site; seven of those had Burkitt's-type translocations. Our results revealed that conventional cytogenetics remains an important tool in elucidating the complex and divers genetic anomalies of MM. Cytogenetics identifies two distinct groups of MM, hyperdiploid and nonhyperdiploid, and establishes the presence of prognostic chromosomal markers such as 13/13q, 17p, 8q24, and 16q aberrations.
    American Journal of Hematology 01/2008; 82(12):1080-7. · 4.00 Impact Factor
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    Sarah Dean, Anwar N Mohamed
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    ABSTRACT: We present a 30-year-old male patient diagnosed with myelodysplastic syndrome (MDS). Chromosome analysis of the bone marrow aspirate revealed a derivative chromosome resulting from an unbalanced 1;16 translocation causing the gain of 1q and loss of 16q. Dual color fluorescence in situ hybridization demonstrated that the 1q;16p derivative chromosome contained centromeric material derived from chromosome 1, and accordingly the translocation was designated as a der (1)t(1;16)(p11;p11.1). Review of literature revealed that 1;16 translocation in MDS is nonrandom and is always described as unbalanced, resulting in trisomy 1q and monosomy 16q.
    American Journal of Hematology 06/2007; 82(5):396-9. · 4.00 Impact Factor
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    ABSTRACT: We describe two patients with CML blast crisis with clonal evolution affecting 16q22 (t(16;16)(p13;q22) and inv(16)(p13;q22), abnormalities of core binding factor, usually found in de novo acute myeloid leukemia (AML)). The bone marrow of both cases showed myelomonocytic (M4) differentiation and eosinophilia. Both patients had prominent extramedullary disease and had poor response to treatment. A literature search focused on patients with CML and additional chromosome changes more typical of AML, revealed that the morphology of the blasts correlated with the finding typical of the underlying "AML" cytogenetic abnormality and an overall very poor clinical outcome, even in the groups with "favorable" AML type translocations.
    Leukemia Research 03/2006; 30(2):225-32. · 2.76 Impact Factor
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    ABSTRACT: We report on a 17-year-old boy with a unique lymphocyte mitomycin-C (MMC)-sensitive chromosomal breakage syndrome. He had failure to thrive, and has microcephaly, slight facial dysmorphism, and constitutional short stature but no other phenotypic or hematological manifestations of Fanconi anemia (FA). He developed B-cell lymphoma of the neck, which was treated with standard doses of alkylating agents. Major side effects related to chemotherapy did not occur. Normal erythrocyte corpuscular volume, MMC-insensitive fibroblasts, and the occurrence of lymphoma rather than AML sets this patient apart from typical FA. The combination of constitutional dwarfism, microcephaly, MMC-sensitive lymphocytes, and susceptibility to lymphoma represents an unusual constellation of symptoms among genetic disorders.
    Cancer Genetics and Cytogenetics 02/2006; 164(2):168-71. · 1.93 Impact Factor
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    ABSTRACT: T-cell/histiocyte-rich large B-cell lymphoma (TCHRLBCL) is a variant of large B-cell lymphoma only rarely encountered in children. Here we report the case of an 8-year-old African American boy with Epstein-Barr virus (EBV)-positive TCHRLBCL who initially presented with right submandibular, anterior cervical and supraclavicular lymphadenopathy. Cytogenetic analysis of the lymph node revealed a near-triploid karyotype with complex chromosomal aberrations. Although morphologically the bone marrow was normal, the same cytogenetically abnormal clone was detected. The patient responded to chemotherapy with CHOP (doxorubicin, cyclophosphamide, vincristine and prednisone) therapy, with disappearance of the abnormal clone from the bone marrow. The patient remains in remission 26 months after the initial diagnosis.
    Leukemia and Lymphoma 04/2005; 46(3):465-9. · 2.61 Impact Factor
  • Gail Bentley, Margarita Palutke, Anwar N Mohamed
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    ABSTRACT: The BCL2 gene was identified through molecular analysis of the breakpoints involved in the t(14;18)(q32;q21) found in the majority of follicular lymphomas (FL). Variant translocations leading to juxtaposing of the BCL2 with either the IGK or IGL gene have been recognized in B-cell malignant lymphoma, although they are rare. We identified seven lymphoma cases that had variant translocations. Three cases had simple translocations involving two chromosomal regions: t(18;22)(q21;q11.2) in two cases and t(2;18)(p11.2;q21) in the third case. Complex translocations affecting more than two chromosomes were seen in the remaining four cases. Fluorescence in situ hybridization using the LSI IGH/BCL2 DNA probes revealed rearrangements of the BCL2 gene locus in all cases. In addition, expression of BCL2 protein was seen in all cases; only five of the seven cases expressed BCL6 protein. Morphologically, the lymphomas were categorized as B-cell follicular lymphoma in six cases and in the seventh case as diffuse large cell lymphoma (Richter syndrome) transformed from preexisting chronic lymphocytic leukemia (CLL). In case 2, the variant t(18;22) was seen as a secondary aberration evolving from a trisomy 12 clone. The findings revealed that BCL2 rearrangements in some malignant lymphomas occur through variant simple or complex chromosomal translocations, but always involving the IGH, IGK, or IGL chromosomal site. In addition, fluorescence in situ hybridization proved to be an important tool in evaluating these cases by showing IGH/BCL2 gene fusion or repositioning of the BCL2 gene.
    Cancer Genetics and Cytogenetics 03/2005; 157(1):12-7. · 1.93 Impact Factor
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    ABSTRACT: We retrospectively analyzed the prognostic significance of mixed chimerism and associated clinical parameters in 80 patients following unmanipulated allogenic stem cell transplantation. Chimerism studies were performed on marrow aspirates using fluorescent in situ hybridization and variable number tandem repeats techniques at day +30, day +90 and +12 months. The median overall survival (OS) was 24 months (range, 1-56 months). Mixed chimerism was found in 23, 28 and 14% of patients at day +30 (1 month), +90 (3 months), and +12 months, respectively. Day +30 chimerism studies failed to provide any prognostic information. Day +90 mixed chimeras (MC) had significantly higher relapse rates compared to day +90 complete chimeras (CC) at 6 months (P=0.03) and 18 months when compared to MC (P=0.03) following transplant. The median OS in day +90 MC and day+90 CC were, respectively (95% CI, 2-35 months), compared to 47 months (95% CI, 20-74 months) (P=0.02). In conclusion, chimerism studies on day +30 could be reserved for patients who fail to demonstrate engraftment. Day +90 MC had higher relapse rates and lower OS, and therefore may be considered for novel therapies and future studies.
    Leukemia 11/2004; 18(10):1681-6. · 10.16 Impact Factor
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    ABSTRACT: The t(1;22)(p13;q13) is associated with acute megakaryoblastic leukemia (AMKL) seen mostly in young infants and known to have a poor prognosis. A 5-year-old child had prolonged prothrombin and partial thromboplastin times, low albumin, and decreased vitamin K-dependent coagulation factors and factor V activities at the time of AMKL diagnosis. All of these factors normalized following chemotherapy when remission was achieved. Cytogenetic analysis revealed a female karyotype with a balanced t(17;22)(q21;q13). Here, we present an AMKL pediatric case with a novel translocation and significant hepatocellular dysfunction that resolved with chemotherapy. The t(17;22) (q21;q13) may represent a variant of t(1;22)(p13;q13).
    Cancer Genetics and Cytogenetics 11/2004; 154(2):167-8. · 1.93 Impact Factor
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    ABSTRACT: Cytogenetic analyses of 16 cases of Wilms tumor with abnormal karyotypes were reviewed, 15 cases of unilateral tumor and 1 bilateral. Three tumors exhibited an unfavorable histology (i.e., anaplastic changes); the rest fell into the favorable histology group. Of the 17 tumors with abnormal clonal aberrations, 9 tumors were hyperdiploid (53%), 7 had pseudodiploid karyotypes (41%), and 1 was hypodiploid (6%). The most common numerical aberrations in descending order of frequency were gain of chromosomes 12, 8, and 6 and loss of chromosome 16. Structural rearrangements mostly involved chromosome 1, followed by chromosomes 7, 14, and 17. Clustering of breaks around 1p22 approximately p31-->pter resulting in partial loss of 1p was the most frequent structural aberration. Additionally, i(7q) was observed as a sole abnormality in two tumors and a 7p translocation in two other tumors. Two other recurrent abnormalities were a partial deletion of 14q, seen in three tumors, and complete loss of chromosome 14 in one tumor. All three Wilms tumors with unfavorable histology had abnormalities of 17p, resulting in TP53 gene deletion. These findings provide further support for the importance of gains of chromosomes 12, 8, and 6 and loss of 1p in the development of Wilms tumor. The results also support the association of unfavorable-histology Wilms tumors with TP53 deletion. The nonrandom losses of 16/16q, 7p, and 14q may point to the importance of genomic imbalance in the pathogenetic consequences and progression of Wilms tumor.
    Cancer Genetics and Cytogenetics 01/2004; 148(1):66-70. · 1.93 Impact Factor
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    ABSTRACT: Acute myelogenous leukemia (AML) is a heterogeneous disease consisting of a variety of different leukemic subtypes. While acute promyelocytic leukemia displays marked sensitivity to the differentiating effects of trans-retinoic acid (tRA), other subtypes of AML display resistance. We now describe a novel compound (E)-4-[3-(1-adamantyl)-4-hydroxyphenyl]-3-chlorocinnamic acid (3-Cl-AHPC/MM002) that induces apoptosis in the tRA-resistant leukemia cell lines M07e, KG-1, and HL-60R, and in tRA-resistant patient leukemic blasts. The 3-Cl-AHPC totally inhibits leukemia colony formation at concentrations that inhibit committed human bone marrow stem cell proliferation, that is, granulocyte/macrophage colony-forming units (CFU-GMs) by only 30%. Exposure to 3-Cl-AHPC results in caspase activation and the cleavage of poly(adenosine diphosphate) (poly(ADP)) ribose polymerase. While activation of the extracellular signal-regulated kinase (ERK) and p38 pathways is not necessary for 3-Cl-AHPC-mediated apoptosis, maximal apoptosis requires c-Jun N-terminal kinase (JNK) activation. The 3-Cl-AHPC-mediated cleavage of the antiapoptotic B-cell leukemia XL (Bcl-XL) protein to a proapoptotic 18-kDa product is found in both the M07e cell line and patient leukemic blasts. The 3-Cl-AHPC treatment of mice bearing the AML 1498 cell line results in a 3.3-log kill in the leukemic blasts. While 3-Cl-AHPC does not activate retinoic nuclear receptors, it is a potent inducer of apoptosis in AML cells and may represent a novel therapy in the treatment of this disease.
    Blood 12/2003; 102(10):3743-52. · 9.78 Impact Factor
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    ABSTRACT: Imatinib mesylate is a tyrosine kinase inhibitor with high affinity for the BCR-ABL fusion protein expressed by the hematopoietic cells in chronic myelogenous leukemia (CML). Some patients with chronic-phase or accelerated-phase CML either relapse after an initial response or are refractory to imatinib, prompting us to evaluate the efficacy of dose increase in such patients. Twelve chronic-phase patients initially receiving 400 mg/day and 4 patients with accelerated phase initially receiving either 400 mg/day (two patients) or 600 mg/day (two patients) had their dose increased (14 to 800 mg/day and 2 to 600 mg/day) because of progressive disease (usually clonal evolution) or inadequate cytogenetic response after at least 1 year of therapy. Six patients had major cytogenetic responses after dose increase (3 complete and 3 partial). Two others had minor cytogenetic responses. Two patients with clonal evolution transiently lost the additional clonal aberrations. Almost all of the responses occurred within 6 months, and were typically 3-6 months in duration. However, 3 patients have continuing major cytogenetic responses of >18 months duration. Dose increase was well tolerated, with thrombocytopenia, mild leukopenia, and exacerbation of prior edema being the most common adverse events. Although increasing the dose of imatinib can benefit a subgroup of patients with CML with either an inadequate cytogenetic response or disease progression, our results suggest the majority will not have a sustained meaningful response, and that other options, such as allogeneic stem cell transplant or investigational therapies, also need to be considered at the time of dose increase.
    Clinical Cancer Research 06/2003; 9(6):2092-7. · 7.84 Impact Factor
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    ABSTRACT: The acquisition of secondary chromosomal aberrations in chronic myeloid leukemia (CML) patients with Philadelphia chromosome-positive (Ph+) karyotype signifies clonal evolution associated with disease progression to accelerated/blastic phase. Therefore, these aberrations are of clinical and biological importance. We identified 58 cases with secondary abnormalities in addition to t(9;22)(q34;q11.2) or its variants in a review of 137 CML patients treated with imatinib mesylate (STI571). Clinically 13 patients were in chronic phase, 24 in accelerated phase, and 21 in blastic phase. More than 50% of cases showed the major routes of CML clonal evolution [+8, i(17q), +Ph, and/or +19]. The remainder exhibited minor routes of secondary abnormalities with -17/17p-, 11p-/rearr(11p), and -7/rearr(7) as the most frequent abnormalities. Of particular interest, one case developed an inv(16)(p13q22) as a secondary anomaly during blastic transformation. The bone marrow was consistent with myelomonocytic morphology with eosinophilia. Cytogenetic responses to imatinib mesylate occurred in 15 of 58 (26%) patients; 12 achieved complete cytogenetic remission, 2 had a major response, and 1 had a minor response, with most responses noted within 3-6 months. Seven patients remain in remission >17-30 months, 2 patients relapsed between 12 and 19 months on therapy, and 1 patient was treated by bone marrow transplantation. Although some Ph+ CML patients with clonal evolution can have a complete cytogenetic response to imatinib mesylate, responses tend to be brief, and such patients may benefit from subsequent stem cell transplantation. Therefore, CML patients with clonal evolution may require therapy additional to imatinib mesylate for maximal eradication of the Ph+ leukemic cells.
    Clinical Cancer Research 04/2003; 9(4):1333-7. · 7.84 Impact Factor
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    ABSTRACT: A 6-year-old girl with hypereosinophilia was found to have a familial constitutional translocation t(5;9)(q11;q34). Flow cytometry and gene rearrangement studies did not show any clonal T-helper cell proliferation. Presence of cryptic Philadelphia translocation was ruled out by reverse transcription polymerase chain reaction. Abelson oncogene translocation on chromosome 5 was confirmed by fluorescent in situ hybridization. This is the first example of a familial translocation involving the abelson oncogene and association with hypereosinophilia. The authors discuss a novel mechanism of hypereosinophilia involving the hybrid product of the abelson oncogene with an unknown partner gene on chromosome 5 (probably granzyme-A).
    Journal of Pediatric Hematology/Oncology 02/2003; 25(1):82-4. · 0.97 Impact Factor
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    ABSTRACT: We present three cases with presumptive evidence of mantle cell lymphoma (MCL) that were submitted for cytogenetic evaluation. Chromosome analysis showed a normal karyotype in two cases, while the third case showed the composite karyotype; 45,XY,t(1;22)(p13;q13),23,del(10)(q22),add(15)(q22),add(17)(p13). The characteristic t(11;14)(q13;q32) for MCL was not observed by conventional karyotyping in any of the cases. We furthermore evaluated the specimens by fluorescence in situ hybridization (FISH) using the dual-color LSI IgH/CCND1 DNA probe. Fusion signals, consistent with t(11;14)(q13;q32), were observed in 65% and 85% of interphase cells in cases 1 and 2, respectively, while the metaphases from both cases revealed a normal pattern. All abnormal metaphases as well as 57% of interphase cells from case 3 displayed a fusion signal. In the abnormal metaphase cells, the fused signal was located on the normally looking 14q32, suggesting that the IgH/CCND1 fusion resulted from the insertion of the CCND1 gene into 14q32 adjacent to the IgH gene. Thus, FISH confirmed the diagnosis of MCL by showing the IgH/CCND1 fusion. In addition, these findings indicate that the sensitivity of FISH is superior to that of conventional cytogenetics in detecting t(11;14)(q13;q32) associated with MCL.
    Cancer Genetics and Cytogenetics 08/2002; 136(2):108-12. · 1.93 Impact Factor
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    ABSTRACT: We describe two cases of hepatoblastoma occurring in an 18-month-old boy and a 3-month-old girl. Cytogenetic analysis of the primary tumors revealed gain of 2q and 20 in both cases. In case 1, t(7;8;11) was seen as a secondary abnormality. Other chromosomal aberrations seen in case 2 were unbalanced t(1;1) and t(2;11), resulting in partial gains of 1q and 2q. These results support previous reports that gains of 2q and 20 and rearrangement of chromosome 1 are strongly associated with hepatoblastoma and may be essential for establishing this neoplasm. The 11q and 7q abnormalities may represent a pathway of genetic evolution associated with hepatoblastoma progression.
    Cancer Genetics and Cytogenetics 04/2002; 133(2):179-82. · 1.93 Impact Factor

Publication Stats

802 Citations
249.86 Total Impact Points

Institutions

  • 2004–2011
    • Children's Hospital of Michigan
      Detroit, Michigan, United States
  • 2002–2008
    • Detroit Medical Center
      • Division of Pathology
      Detroit, Michigan, United States
  • 1988–2008
    • Wayne State University
      • • Department of Pathology
      • • School of Medicine
      • • Department of Internal Medicine
      Detroit, Michigan, United States
  • 1999–2006
    • Karmanos Cancer Institute
      • Division of Hematology and Oncology
      Detroit, MI, United States
  • 1993
    • University of California, San Francisco
      • Department of Laboratory Medicine
      San Francisco, California, United States
  • 1992
    • Harper University Hospital
      Detroit, Michigan, United States