A N Mohamed

Karmanos Cancer Institute, Detroit, MI, United States

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Publications (30)130.59 Total impact

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    ABSTRACT: Two elderly men with stage IV mantle cell lymphoma (MCL) rapidly developed a leukaemic phase with unusually high blast counts that proved fatal. One lymph node biopsy showed diffuse MCL, the other blastic morphology. In addition to t(11;14), there were t(8;14) and t(1;19) in case 1 and dup(8)(q24q13) in case 2. Fluorescence in situ hybridization revealed genomic fusion of IgH/MYC genes in case 1 and an extra copy of C-MYC gene in case 2. The genomic alteration of C-MYC oncogene is probably implicated in the blastic transformation and aggressive behaviour of the disease.
    British Journal of Haematology 11/2001; 115(1):66-8. · 4.94 Impact Factor
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    ABSTRACT: CD56, a neural adhesion molecule, is a marker of natural killer (NK) lymphocytes as well as a subgroup of CD8+ T cells. Normal lymphocytes with a CD56/CD4 phenotype are scarce. Physiologic increases may occur in patients with immunosuppression, chronic inflammation, and autoimmune disorders. We report 4 cases of lymphomas/leukemias with the unusual CD56/CD4 phenotype. Two were of T-cell and 2 of true NK-cell origin. The T-cell lymphomas had large granular lymphocyte morphologic features and splenomegaly. One patients had a benign course; the other died within months of the leukemia diagnosis. The 2 NK cell lymphomas had blastic morphologic features, initially involved skin, and had a very aggressive clinical course; 1 patient died of acute leukemia, and 1 had recurrence after bone marrow transplantation. Cytogenetic analyses did not show a consistent pattern of abnormalities. The NK lymphoma with acute leukemia had a t(2;5) but was CD30- and anaplastic lymphoma kinase negative. Although CD56+/CD4+ lymphomas/leukemias are a heterogeneous group, there may be a distinct subgroup of NK lymphoblastoid lymphomas of the skin, judging from our cases, as well as those previously reported.
    American Journal of Clinical Pathology 09/2001; 116(2):168-76. · 2.88 Impact Factor
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    ABSTRACT: We have identified 52 patients of follicular lymphoma (FL) with t(14;18)(q32;q21). Histologically, the lymphomas were placed into six groups according to their cellular composition and growth pattern. Chromosome analysis revealed that all cases but one had additional secondary chromosomal abnormalities. The most frequent numerical aberrations were gains of chromosomes 7 (38%), X (36%), 5 (15%), 12 (15%), 18/der(18)t(14;18) (25%), and 21 (15%). Structural abnormalities of chromosome 1 were seen in 19 tumors (36%) affecting both arms with breakpoints clustered at 1p36. Other structural abnormalities included partial deletions of 6q, 10q, and 13q. Breakpoint at 8q24 was seen in four cases. The chromosome aberrations were correlated with the morphological subtypes of follicular lymphoma. Gain of chromosome 7 appeared to be associated with follicular large cell lymphoma. The incidence of trisomy 5 and 12, and 13q- was higher in follicular lymphoma with aggressive histological features than in low-grade lymphoma. In addition, complexity of the karyotype and high degree of polyploidy increased with the grade. The most valuable cytogenetic markers in the t(14;18) lymphomas are those involving 8q24 which was found exclusively in the blastic/blastoid variant FL. Therefore, chromosome analysis in relation to histologic pattern of follicular lymphoma can provide additional information in predicting tumor evolution and transformation to a higher-grade malignancy.
    Cancer Genetics and Cytogenetics 05/2001; 126(1):45-51. · 1.93 Impact Factor
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    ABSTRACT: Adenocarcinoma of the pancreas generally remains an incurable disease by available treatment modalities, demanding the development of a suitable cell-culture/animal model and the discovery and evaluation of novel therapeutic agents. We report the clonal preservation of a human pancreatic cell line (KCI-MOH1) established from a 74-year-old African-American man diagnosed with pancreatic cancer. Initially the human primary tumor was grown as a xenograft in SCID mice and, subsequently, a cell line was established from tumors grown as a xenograft as reported in our earlier publication. The molecular characterization of the primary tumor, the tumors grown as xenograft, and the cell line all revealed similar genotypic properties. By using an automated DNA sequencer, a K-ras mutation (codon 12, GGT to CGT, Gly to Arg) was detected in the pancreatic tumor tissue taken from the patient, whereas no p53 mutation was detected. The same K-ras mutation and unaltered p53 was also found in the xenograft tumor and in the KCI-MOH1 cell line. Chromosome analysis of the cultured cells revealed: 42,XY,add(3)(p11.2),der(7)t(7;12) (p22;q12),-10,-12,add (14)(p11),-18,add (20)(q13),-22/84, idemx2, which is the same chromosome complement found in xenograft tumors. The KCI-MOH1 cell line grows well in tissue culture and forms tumors in the SCID mice when implanted subcutaneously, as well as in orthotopic sites. The KCI-MOH1 cell line-derived SCID mouse xenograft model was used for efficacy evaluation of bryostatin 1, auristatin-PE, spongistatin 1, and gemcitabine alone and in combination. Tumor growth inhibition (T/C expressed as percentage), tumor growth delay (T - C), and log 10 kill for these agents were 38%, 22 days, and 0.53; 15%, 30 days, and 0.80; 24%, 25 days, and 0.66; and 10%, 33 days, and 0.90, respectively. When given in combination, two of seven gemcitabine + auristatin-PE-treated animals were free of tumors for 150 days and were considered cured. Animals treated with a combination of bryostatin 1 and gemcitabine and a combination of spongistatin and gemcitabine produced remissions in only one of seven mice. From these results, we conclude that (a) this is the first study illustrating that clonal characteristics of primary pancreatic tumors remained unchanged when implanted in mice and as a permanent cell line grown in vitro; and (b) there is a synergistic effect between gemcitabine and selected marine products tested in this study, which is more apparent in the gemcitabine and auristatin-PE combination. The results of this preliminary study suggest that these agents should be explored clinically in the treatment of pancreatic cancer.
    Pancreas 12/1999; 19(4):353-61. · 2.95 Impact Factor
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    ABSTRACT: Often the diagnosis of pancreas cancer needs to be established from limited cytology specimens or small biopsies. Most ductal adenocarcinomas are histologically well to moderately differentiated and mimicked closely by pancreatitis, and therefore the microscopic diagnosis can be difficult. In addition, there appears to be significant heterogeneity in the outcome of the patients with pancreatic cancer, which cannot be predicted accurately by current prognosticators such as the grade and stage of the tumor. Therefore, there is need for methods that can be used as adjuncts to routine diagnostic and prognostic parameters. This study was designed to test the utility of the fluorescent in situ hybridization (FISH) method in identifying the molecular alterations, particularly the ones that have been detected with relatively high frequency in pancreas cancer. Formalin-fixed and paraffin-embedded tissues of 10 cases were enumerated for chromosome 7, 8, 17, 18, and 20 copy numbers by using alpha-satellite probes, and for c-myc by using a gene-specific probe. The number of signals per nucleus (reflecting chromosomal copy number and status of c-myc amplification) were counted in more than two areas containing 50-500 cells. Because of tumor heterogeneity, monosomy (loss of one chromosome copy) was defined arbitrarily as one signal in >25% of nuclei. C-myc amplification was defined as more than two gene copies in >20% of the cells. The most frequent signal losses were found in chromosomes 8 (four of 10 cases) and chromosome 17 (four of 10), followed by 20 (three of 10) and 18 (two of 10). No loss of chromosome 7 was detected. In contrast, gains in chromosome copy number were identified in only one of 10 tumors, which showed gain of both chromosome 7 and 18. Amplification of c-myc gene was detected in two of 10 cases, but neither of the two had aneuploidy for chromosome 8, where the c-myc gene is located. In addition, loss in c-myc signal was observed in one case that also showed loss of chromosome 8 copy number. FISH can be used to detect chromosomal changes in pancreatic cancer; abundance of lytic enzymes in this organ is not an impediment for the applicability of this technique. Therefore it can potentially be used in the future as an adjunct to the conventional diagnostic and prognostic markers. This study confirms that loss of chromosomes, particularly chromosomes 17 and 18, which carry the p53 and DCC genes, are common in pancreas cancer. Chromosome 20 is also frequently lost. In addition, in this study, alterations of chromosome 8, which is seen commonly in prostatic adenocarcinoma but has not been previously documented in pancreatic cancer, also was detected in five of 10 tumors. Furthermore, amplification of the c-myc gene, which is located in chromosome 8, was found in the two of the remaining five cases. Further studies are needed to confirm this high incidence of chromosome 8 and c-myc alterations and their possible role in the pathogenesis of pancreatic adenocarcinoma.
    Pancreas 04/1999; 18(2):111-6. · 2.95 Impact Factor
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    ABSTRACT: A patient with Turner's syndrome was found to have generalized infantile myofibromatosis with visceral involvement at birth. The infant was treated with interferon-alpha because of the size of the lesions. Two months after treatment, the lesions appeared to have decreased in size and showed evidence of maturation with decreased apoptosis on histologic examination. Interferon-alpha treatment might induce regression of myofibromatosis.
    Journal of Pediatrics 12/1998; 133(5):694-6. · 4.04 Impact Factor
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    ABSTRACT: The down-regulation of multidrug resistance (mdr1) gene expression as detected by competitive reverse transcription-PCR and the antitumor activity of bryostatin 1 (Bryo1) are investigated in a newly established cell line from a patient with relapsed diffuse large cell lymphoma (DLCL). The cell line (WSU-DLCL2) grows in liquid culture and forms s.c. tumors in mice with severe combined immune deficiency. WSU-DLCL2 is a mature B-cell line (IgG lambda) that is negative for EBV nuclear antigen, expresses the multidrug resistance phenotype, and has t(14;18)(q32;q21) plus other chromosomal aberrations. Exposure of the WSU-DLCL2 cells to Bryo1 in culture reversed the multidrug resistance phenotype within 24 h. A functional assay revealed a 4-fold increase in [3H]vincristine accumulation in Bryo1-treated cells compared with control. Vincristine (VCR), doxorubicin, Bryo1, and 1-beta-D-arabinofuranosylcytosine showed no clinically significant activity when given alone to WSU-DLCL2-bearing severe combined immune deficiency mice. However, when given 24 h before each cytotoxic agent, Bryo1 substantially increased the antitumor activity of VCR but not 1-beta-D-arabinofuranosylcytosine. There was a statistically significant (P < 0.001) decrease in the expression of P-glycoprotein in WSU-DLCL2 tumors taken from Bryo1-treated animals compared with untreated controls. In vivo, a competitive reverse transcription-PCR assay revealed decreased mdr1 RNA expression 24 h after Bryo1 treatment. These findings taken together indicate that Bryo1-induced down-regulation of mdr1 might be one mechanism by which Bryo1 potentiates VCR activity. The sequential use of both agents resulted in clinically significant antitumor activity in this lymphoma model.
    Clinical Cancer Research 06/1998; 4(5):1305-14. · 7.84 Impact Factor
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    ABSTRACT: Adenocarcinoma of the pancreas is currently the fifth leading cause of death in the United States. It remains generally incurable by available treatment modalities. We report here on the characterization of a permanent pancreatic cell line (KCI-MOH1), established as a xenograft in severe combined immune deficient (SCID) mice, from a 74 year-old African American male patient diagnosed with pancreatic cancer. Sections from paraffin-embedded tumors excised from SCID mice revealed typical adenocarcinoma of the pancreas. Karyotypic analysis of cultured cells derived from tumors grown in SCID mice revealed a male karyotype with multiple clonal aberrations: 42, XY, add (3)(p11.2), der(7) t(7;12) (p22;q12), -10, -12, add (14)(p11), -18, add (20)(q13)-22/84, idemx2. Immunostaining of KCI-MOH1 tissues shows strong expression of p53 and p21 proteins. The xenograft model was established by transplanting the KCI-MOH1 cells subcutaneously (s.c.) in SCID mice. When the s.c. tumor was transplanted in vivo to other SCID mice, the success rate was 100%, with a doubling time of 8.5 days. The SCID mouse xenograft model was used to test the efficacy of selected standard chemotherapeutic drugs (taxol, gemcitabine, 5-fluorouracil, and Ara-C) and novel biological agents (Bryostatin 1 and Auristatin-PE). Results show that gemcitabine, Ara-C, and Bryostatin 1 were active against KCI-MOH1. The xenograft described herein can be used as an animal model to facilitate the development of novel therapeutic agents against human pancreatic cancers.
    Pancreas 02/1998; 16(1):19-25. · 2.95 Impact Factor
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    ABSTRACT: We describe t(8;16)(p11;p13) acute myeloid leukaemia (AML-M4) in a 12-year-old white male with a history of prenatal X-ray exposure. He had skin and bone involvement and some of the leukaemic blasts showed haemophagocytosis, characteristic features seen in t(8;16) AML. 20% of the reported cases of t(8;16)(p11;p13) AML are therapy-related and this case further supports the possible role of the ionizing radiation in the development of this disorder.
    British Journal of Haematology 10/1996; 94(4):702-4. · 4.94 Impact Factor
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    ABSTRACT: A 38-year-old white man was diagnosed with B-cell chronic lymphocytic/prolymphocytic leukemia (CLL/PLL). The disease was unresponsive to a variety of chemotherapeutic regimes. One year after diagnosis, L3 blasts appeared in peripheral blood associated with more aggressive course. There was no change in the B-cell phenotype at that time, but cytogenetic analysis revealed the appearance of t(8;22)(q24;q11) and -21 superimposed on the original karyotype: 46,XY,+3,der(3)t(3;17)(p11;q12), t(11;14)(q13;q32),-17. These results indicate that the lymphoblastic transformation in our case emerged from the pre-existing B-lymphocytic clone.
    Cancer Genetics and Cytogenetics 03/1996; 86(2):143-6. · 1.93 Impact Factor
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    ABSTRACT: Chronic lymphocytic leukemia (CLL), a proliferative disease of mature looking B lymphocytes, is the commonest leukemia in western countries. It remains incurable by available treatment modalities. We report on the establishment of a permanent, EBV-negative, B-CLL line (WSU-CLL) from the peripheral blood of a patient with CLL. The cells grow as suspension in liquid culture, express IgG lambda and other B cell markers and show lg heavy and light gene rearrangements. Karyotypic analysis shows 45,X,del(3)(p14;p24),t(4;12;12) (q31;q22;p13), t(5;12) (q31;p13), add(16)(q24)X2, t(18;21) (q12;p12). WSU-CLL forms colonies when grown on soft agar. A xenograft model was established by injecting the WSU-CLL cells subcutaneously (s.c.) in severe combined immune deficient (SCID) mice. When the s.c. tumor was transplanted in vivo to other SCID mice, the success rate was 100% with a doubling time of 7.3 days. The CLL-SCID xenograft model was used to test the efficacy of selected standard chemotherapy drugs and new therapeutic agents against WSU-CLL. The cell line and the xenograft described can be used as a model to facilitate the development of new therapeutic agents against CLL in man.
    Leukemia 02/1996; 10(1):130-7. · 10.16 Impact Factor
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    ABSTRACT: A reciprocal translocation, t(10;22)(q22;q11), resulting in a masked Ph chromosome was identified in a patient diagnosed with chronic myeloid leukemia (CML). Both homologs of chromosome 9 were of the normal pattern. Two signals for the ABL probe, both of them hybridized to chromosome 9, were demonstrated via fluorescence in situ hybridization (FISH). Furthermore, cohybridization with two differently labeled BCR/ABL translocation DNA probes indicated a BCR/ABL fusion apparently located on 9q34. Molecular studies revealed a rearrangement of the BCR region and expression of a chimeric BCR/ABL mRNA of CML configuration. These findings indicate that the BCR/ABL fusion resulted from an unusual relocation of the BCR gene from its normal position on 22q11 to 9q34 adjacent to the ABL gene.
    Genes Chromosomes and Cancer 07/1995; 13(2):133-7. · 3.55 Impact Factor
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    ABSTRACT: A balanced reciprocal translocation, t(6;9)(p21;q34), was identified in a female patient diagnosed with chronic myeloid leukemia (CML). Both homologs of chromosome 22 were of normal length and morphology. Southern blotting revealed a bcr rearrangement with BglII and HindIII. Two signals for the abl probe were demonstrated by fluorescence in situ hybridization (FISH), one on the normal chromosome 9 and the second on a chromosome 22. Thus, molecular rearrangement of bcr resulted from insertion of an abl gene within the bcr region despite absence of a Ph chromosome.
    Cancer Genetics and Cytogenetics 04/1995; 80(1):60-2. · 1.93 Impact Factor
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    ABSTRACT: Mammalian spermiogenesis is marked by the initial disruption of the nuclear-histone-DNA complex by the transition proteins for ultimate replacement with protamines. The genes for three of these low molecular weight basic nuclear proteins exist as a single linear array of PRM1, PRM2, and TNP2 on human chromosome 16p13.2. To begin to address the mechanism governing their transcriptional potentiation, a region of approximately 40 kilo-bases of the human genome encompassing these genes was introduced into the germ line of mice. Fluorescence in situ hybridization and Southern analysis showed that this segment of the human genome integrated into independent chromosomal sites while maintaining its fidelity. Transcript analysis demonstrated that the expression of the endogenous mouse protamine Prm1 and Prm2 genes as well as the mouse transition protein Tnp2 gene were expressed along with their human transgene counterparts. The pattern of expression of these transgenic human genes within this multigenic cluster faithfully represented that observed in vivo. In addition, all members of this transgenic gene cluster were expressed in proportions similar to those in human testis. Copy number-dependent and position-independent expression of the transgenic construct demonstrated that the corresponding biological locus was contained within this segment of the human genome. Furthermore, DNase I sensitivity established that in sperm the human PRM1-->PRM2-->TNP2 genic domain was contained as an approximately 28.5-kilobase contiguous segment bounded by an array of nuclear matrix associated topoisomerase II consensus sites. This is the first description of a multigenic male gamete-specific domain as a fundamental gene regulatory unit. A model of haploid-specific gene determination is presented.
    Journal of Biological Chemistry 04/1995; 270(15):8755-62. · 4.65 Impact Factor
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    ABSTRACT: A case of acute myeloid leukemia (M-3) with complex karyotypic aberrations and double minute (dmin) chromosomes is presented. The patient had no history of prior exposure to mutagenic or carcinogenic agents or of other malignancies. She died from CNS involvement six weeks after the initial diagnosis. We used comparative genomic hybridization to identify the amplified sequences presumed to represent the dmin of the leukemic cells; the tumor/normal ratios indicated increased signal intensity at 8q24. This localization prompted investigation by semi-quantitative PCR that revealed amplification of the MYC oncogene. The extent of chromosome aberrations and the oncogene amplification, both linked with poor prognosis, may relate to the rapid course of this patient's disease.
    Genes Chromosomes and Cancer 12/1993; 8(3):185-9. · 3.55 Impact Factor
  • American journal of diseases of children (1960) 12/1993; 147(11):1254-5.
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    ABSTRACT: A new human B-cell line, WSU-FSCCL, was established from the peripheral blood of a patient with low-grade follicular small cleaved cell lymphoma in leukemic phase. Both the fresh lymphoma cells and the established cell line exhibit t(14;18)(q32;q21) and t(8;11)(q24;q21) chromosomal translocations, 6q-, 1p+, and +i(1q). PCR analysis confirmed the juxtaposition of the major breakpoint-cluster region of bcl-2 with immunoglobulin heavy chain (JH) gene rearrangements. Southern analysis demonstrated that the 8q24 breakpoint was 5' of c-myc exon 1. The new line grows as a single-cell suspension with a doubling time of approximately 26 hours. It expresses cytoplasmic and cell surface IgM-kappa and reacts with monoclonal antibodies to B-cell antigens. Cells are negative for T-cell and myeloid/monocyte antigens as well as for Epstein-Barr virus nuclear antigen (EBNA). DNA histogram generated by flow cytometry indicated a near diploid stemline. While t(14;18) is common in follicular lymphomas, the t(8;11) is unusual in lymphomas, although it does involve a region frequently aberrant on chromosome 8. The rearrangement of c-myc may have conferred an aggressive clinical behavior seen in the terminal phase of the disease. The role of 11q21 remains undetermined.
    Cancer Genetics and Cytogenetics 11/1993; 70(1):62-7. · 1.93 Impact Factor
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    ABSTRACT: Waldenström's macroglobulinemia (WM) represents an indolent incurable human B-cell tumor. We have successfully established a permanent cell line, WSU-WM, without growth factors or viral transformation, from the pleural effusion of a 60-year-old man with IgM kappa WM. Phenotypic characterization of WSU-WM shows IgM lambda and expression of other B-cell markers. Karyotypic analysis shows a male chromosome complement with several clonal aberrations, including t(8;14)(q24;q32). Molecular characterization shows deletion of kappa and rearrangement of lambda light chain genes indicating a class switching. Both the secretory (s mu) and membrane (m mu) components of IgM are expressed. In addition, the breakpoint on 8q24 is downstream of exon 3 of the c-myc oncogene. WSU-WM grows in liquid culture and soft agar. When cells were injected subcutaneously in immune deficient mice, six of seven SCID mice developed subcutaneous tumors as opposed to three of seven in the athymic nude mice. When a WSU-WM SCID tumor was passaged in vivo in the SCID mice, the take rate was 100%. This xenograft model and a soft agar disk-diffusion assay were used to test the efficacy of standard chemotherapy agents against this tumor in vivo and in vitro, respectively. The cell line and the assays described herein can be used as a model to facilitate the discovery of new therapeutic agents or modalities for this disease.
    Blood 07/1993; 81(11):3034-42. · 9.78 Impact Factor
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    ABSTRACT: Although some patients with malignant gliomas respond to treatment with chemotherapeutic agents like BCNU, tumor recurrence inevitably occurs, heralding the development of chemoresistance. Treating and/or preventing chemoresistance requires distinguishing newly developed resistance from the presence of intrinsically resistant cells in the primary tumor population. This study relates the chromosomal complements of freshly resected astrocytomas to the cells' chemosensitivity and ultimately to the patients' response to treatment. The authors dissociated 31 freshly resected human gliomas (5 astrocytomas, 10 anaplastic astrocytomas, 16 glioblastomas multiforme) into single cells, and performed cytogenetic analysis and BCNU sensitivity testing using the colony-forming assay (CFA) on first division cells from these tumors. The major cytogenetic abnormalities involved the loss of a sex chromosome in all three classes of gliomas and the gain of chromosome 7 in anaplastic astrocytoma and glioblastoma multiforme; clonal marker chromosomes were observed in only anaplastic astrocytoma and glioblastoma multiforme with no common rearrangement observed among the tumors. The five astrocytomas were near-diploid (2n+/-, 35-57 chromosomes/cell), and all were resistant to BCNU. Seven of ten anaplastic astrocytomas were composed primarily of 2n+/- cells and were BCNU resistant. Three other anaplastic astrocytomas had a 39% or greater representation of 4n+/- cells (88-101 chromosomes/cell), and these tumors were sensitive to BCNU. Ten of 16 glioblastomas multiforme were composed predominantly of 2n+/- cells and were resistant to carmustine. Six other glioblastomas multiforme had at least 41% 3n+/- (58-87 chromosomes/metaphase) and 4n+/- cell populations and were sensitive to carmustine. Thus, gliomas demonstrating BCNU sensitivity were more than 60% hyperdiploid (60 or more chromosomes/metaphase) with 1 to 8 clonal marker chromosomes and multiple clonal populations involving complex karyotypic deviations. In contrast, all 22 resistant tumors were composed primarily of near-diploid cells. Only 4 of 22 tumors had a clonal marker, and the chromosome ploidy changes were less extensive. In freshly resected untreated human gliomas, BCNU is most effective against hyperdiploid cells that have extensive ploidy changes and chromosome rearrangement, whereas resistance to carmustine is characteristic of near-diploid populations with few ploidy changes and rearranged chromosomes. This observation was consistent for all three classes of gliomas.
    Cancer 07/1993; 71(12):4007-21. · 5.20 Impact Factor
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    ABSTRACT: Results of cell culture and cytogenetic analysis (standard and fluorescent in situ hybridization, FISH) of two sporadic gastrinomas are reported. Maintenance of hormonal activity was assessed by detection of gastrin levels during the first 3 months in culture. Case 1 showed clonal aberrations consisting of two marker chromosomes: marker 1 is a large metacentric chromosome and marker 2 is a small acrocentric chromosome. Case 2 showed a constitutional polymorphism with chromosome 15p+ and a clone in the tumor cell culture with trisomy for chromosome 3. To our knowledge, this is the first cytogenetic report of sporadic gastrinomas (Zollinger-Ellison syndrome).
    Cancer Genetics and Cytogenetics 06/1993; 67(1):44-9. · 1.93 Impact Factor

Publication Stats

444 Citations
130.59 Total Impact Points

Institutions

  • 1999
    • Karmanos Cancer Institute
      • Division of Hematology and Oncology
      Detroit, MI, United States
  • 1993
    • Harper University Hospital
      Detroit, Michigan, United States
    • University of California, San Francisco
      • Department of Laboratory Medicine
      San Francisco, California, United States
  • 1988–1989
    • Wayne State University
      • Department of Internal Medicine
      Detroit, MI, United States