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Journal articles on the topic 'Bande q13'

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Published: 4 June 2021

Last updated: 12 February 2022

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1

Taniwaki, M., K. Nishida, T. Takashima, et al. "Nonrandom chromosomal rearrangements of 14q32.3 and 19p13.3 and preferential deletion of 1p in 21 patients with multiple myeloma and plasma cell leukemia." Blood 84, no. 7 (1994): 2283–90. http://dx.doi.org/10.1182/blood.v84.7.2283.2283.

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Abstract Structural chromosomal abnormalities and their break-points were characterized in 17 patients with multiple myeloma (MM) and 4 with plasma cell leukemia by banding. Chromosome 14q32 translocations with a variety of partners were detected in 13 patients, and a variant translocation t(8;22)(q24.1;q11) was detected in 1. Three recurrent 14q32 translocations have been identified: t(6;14)(p21.1;q32.3) occurring in 3 cases, and t(11;14)(q13;q32.3) and t(14;18) (q32.3;q21.3) each occurring in 2 cases. Translocations t(1;14)(q21;q32.3), t(3;14)(p11;q32),t(7;14)(q11.2;q32.3), and t(11;14)(q23;

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2

Taniwaki, M., K. Nishida, T. Takashima, et al. "Nonrandom chromosomal rearrangements of 14q32.3 and 19p13.3 and preferential deletion of 1p in 21 patients with multiple myeloma and plasma cell leukemia." Blood 84, no. 7 (1994): 2283–90. http://dx.doi.org/10.1182/blood.v84.7.2283.bloodjournal8472283.

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Structural chromosomal abnormalities and their break-points were characterized in 17 patients with multiple myeloma (MM) and 4 with plasma cell leukemia by banding. Chromosome 14q32 translocations with a variety of partners were detected in 13 patients, and a variant translocation t(8;22)(q24.1;q11) was detected in 1. Three recurrent 14q32 translocations have been identified: t(6;14)(p21.1;q32.3) occurring in 3 cases, and t(11;14)(q13;q32.3) and t(14;18) (q32.3;q21.3) each occurring in 2 cases. Translocations t(1;14)(q21;q32.3), t(3;14)(p11;q32),t(7;14)(q11.2;q32.3), and t(11;14)(q23;q32.3) we

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3

Bernasconi, Paolo, Irene Dambruoso, Marina Boni, et al. "Fluorescence In Situ Hybridization (FISH) Reveals Unexpected Cryptic Chromosome 11 Defects in MDS/AML Patients." Blood 108, no. 11 (2006): 4413. http://dx.doi.org/10.1182/blood.v108.11.4413.4413.

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Abstract Conventional cytogenetics (CC) discovers clonal chromosomal defects in about 40–80% of de novo MDS/AML. However, due to the poor quality of metaphases, CC is often unable to reveal cryptic defects, precisely define chromosomal breakpoints and establish the nature of marker chromosomes. All these drawbacks may be overcome by FISH, a powerful technique with high sensitivity and specificity. Abnormalities of chromosome 11 long arm and of band 11p15 are seen in 5–7% and in 0.5% of de novo MDS/AML. Herein we report two patients diagnosed as AML evolved from MDS. On CC the karyotype of the

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4

Lemons, Richard S., Rafael Espinosa, Matt Rebentisch, Frank McCormick, Martha Ladner, and Michelle M. Le Beau. "Chromosomal localization of the gene encoding GTPase-activating protein (RASA) to human chromosome 5, bands q13–q15." Genomics 6, no. 2 (1990): 383–85. http://dx.doi.org/10.1016/0888-7543(90)90581-e.

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5

Cuneo, A., C. Mecucci, S. Kerim, et al. "Multipotent stem cell involvement in megakaryoblastic leukemia: cytologic and cytogenetic evidence in 15 patients." Blood 74, no. 5 (1989): 1781–90. http://dx.doi.org/10.1182/blood.v74.5.1781.1781.

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Abstract Cytologic and cytogenetic results obtained from patients fulfilling the FAB criteria for the diagnosis of acute nonlymphocytic leukemia (ANLL) of megakaryocytic lineage (ANLL-M7) are reported. Eleven cases were de novo ANLL-M7, of whom three presented with acute myelofibrosis. Four cases were megakaryoblastic transformations of chronic myelogenous leukemia (two cases), refractory anemia with excess of blasts (one case), and polycythemia vera (one case). Four patients showed a minority of granular blasts, with occasional Auer rods in one. Positive myeloperoxidase and/or sudan black-B s

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6

Cuneo, A., C. Mecucci, S. Kerim, et al. "Multipotent stem cell involvement in megakaryoblastic leukemia: cytologic and cytogenetic evidence in 15 patients." Blood 74, no. 5 (1989): 1781–90. http://dx.doi.org/10.1182/blood.v74.5.1781.bloodjournal7451781.

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Cytologic and cytogenetic results obtained from patients fulfilling the FAB criteria for the diagnosis of acute nonlymphocytic leukemia (ANLL) of megakaryocytic lineage (ANLL-M7) are reported. Eleven cases were de novo ANLL-M7, of whom three presented with acute myelofibrosis. Four cases were megakaryoblastic transformations of chronic myelogenous leukemia (two cases), refractory anemia with excess of blasts (one case), and polycythemia vera (one case). Four patients showed a minority of granular blasts, with occasional Auer rods in one. Positive myeloperoxidase and/or sudan black-B stainings

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7

Redner, Robert L., Lydia C. Contis, Carol Evans, Maureen E. Sherer, and Sofia Shekhter-Levin. "A Novel t(3;17) Variant of Acute Promyelocytic Leukemia with Rearrangement of the RARA Locus." Blood 104, no. 11 (2004): 4428. http://dx.doi.org/10.1182/blood.v104.11.4428.4428.

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Abstract The vast majority of patients with Acute Promyelocytic Leukemia (APL, FAB M3) have the t(15;17)(q12;q21) chromosomal translocation. This introduces the gene for PML into the retinoic acid receptor alpha (RARA) locus, which leads to expression of a PML-RARA fusion. There is convincing evidence that expression of PML-RARA underlies the APL phenotype. Yet, there have been identified rare cases of APL that do not manifest t(15;17). Many of these cases exhibit cryptic rearrangements of PML and RARA. However, in a number of cases it has clearly been shown that a fusion protein different tha

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8

Luke, Sunny, Ram S. Verma, Rhandy Pebenito, and Michael J. Macera. "Inversion-duplication of bands q13→q21 of human chromosome 9." American Journal of Medical Genetics 40, no. 1 (1991): 57–60. http://dx.doi.org/10.1002/ajmg.1320400111.

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9

Shardy, Deborah L., Mohammed F. Azim, Rizwan C. Naeem, and Sharon E. Plon. "Identification of the Novel Chromosomal Translocation t(17;19)(q23;q13) in a Pediatric Patient with Acute Myeloid Leukemia." Blood 106, no. 11 (2005): 4344. http://dx.doi.org/10.1182/blood.v106.11.4344.4344.

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Abstract Chromosomal rearrangements have been associated with many hematologic malignancies. Identification of the genes involved in several of these rearrangements has provided information about the development of malignancy and has led to therapeutic interventions. Historically, a considerable number of pediatric acute myeloid leukemia (AML) cases have been reported as cytogenetically normal. However, with improved cytogenetic techniques and the use of fluorescent in situ hybridization (FISH), new translocations are now being identified. We present the case of a 10-year-old male with AML (FA

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10

Kottaridis, Panagiotis, Diana Brazma, Julie Howard-Reeves, Helen Mazzullo, and Elisabeth P. Nacheva. "A Cell Line SYRMO Derived From AML with EVI 1 Rearrangements Following Imatinib Mesylate Therapy for Chronic Myeloid Leukaemia." Blood 116, no. 21 (2010): 4470. http://dx.doi.org/10.1182/blood.v116.21.4470.4470.

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Abstract Abstract 4470 Chronic Myeloid Leukaemia (CML) is a malignant disorder of the haematopoeitic stem cell, usually characterised by the t(9;22) giving rise to the Philadelphia chromosome (Ph), and by the BCR-ABL gene rearrangement at the molecular level. Imatinib mesylate (IM), which targets the tyrosine kinase (TK) activity of BCR-ABL, has become the first line therapy for CML patients. Dasatinib or Nilotinib is now indicated as a second line therapy for patients who develop resistance or intolerance to IM. Here we report the case of a 51 year old woman who was diagnosed in Cyprus (2007)

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11

Li, Guang, Nan Hu, Alisa M. Goldstein, et al. "Allelic loss on chromosome bands 13q11-q13 in esophageal squamous cell carcinoma." Genes, Chromosomes and Cancer 31, no. 4 (2001): 390–97. http://dx.doi.org/10.1002/gcc.1158.

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12

Claeysen, S., P. Faye, M. Sebben, et al. "Assignment of 5-Hydroxytryptamine Receptor (HTR4) to human chromosome 5 bands q31→q33 by in situ hybridization." Cytogenetic and Genome Research 78, no. 2 (1997): 133–34. http://dx.doi.org/10.1159/000134646.

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13

Vernon, J. L., P. C. Burr, J. E. Wiley, and M. A. Farwell. "Assignment¹ of the mitochondrial translation elongation factor Ts gene (TSFM) to human chromosome 12 bands q13→q14 by in situ hybridization and with somatic cell hybrids." Cytogenetic and Genome Research 89, no. 3-4 (2000): 145–46. http://dx.doi.org/10.1159/000015596.

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14

Elwood, S. A., and J. B. Simeonsson. "Studies of the Spectral Dependence of Photoionization Spectrometry Measurements of NO in Air." Applied Spectroscopy 54, no. 2 (2000): 190–96. http://dx.doi.org/10.1366/0003702001949384.

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The relative merits of five laser excitation schemes have been evaluated for photoionization spectrometry (PIS) measurements of NO in air. All five schemes utilize wavelengths near 215 nm, which correspond to excitation of rovibronic transitions in the A 2Σ+–X 2πi (1,0) bands of NO. Photoionization of the excited NO molecules is accomplished by using wavelengths ranging from 215 to 1064 nm. Excitation spectra of the five PIS schemes reveal a significant enhancement when 355 nm radiation is used for photoionization. The enhancement is hypothesized to be related to a resonance or near-resonance

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15

Eme, John, and Wayne A. Bennett. "Acute temperature quotient responses of fishes reflect their divergent thermal habitats in the Banda Sea, Sulawesi, Indonesia." Australian Journal of Zoology 57, no. 5 (2009): 357. http://dx.doi.org/10.1071/zo09081.

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We measured metabolic rates of six Indo-Pacific fishes from different thermal habitats at 26°C and after acute transfer to 32°C. Temperature–metabolism relationships were expressed as temperature quotients (Q10) and ranged from ~1.0 in tidepool-dwelling common (Bathygobius fuscus) and sandflat (Bathygobius sp.) gobies to 2.65 and 2.29 in reef-associated white-tailed humbug (Dascyllus aruanus) and nine-banded cardinalfish (Apogon novemfasciatus), respectively. Squaretail mullet (Liza vaigiensis) and blackspot sergeant (Abudefduf sordidus) displayed Q10 responses of 2.03 and 1.26, respectively.

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16

van Woerden, Geeske M. "Measuring Electroencephalography: The Ups and Downs of Delta and Beta Bands as Biomarkers for 15q11-q13–Related Disorders." Biological Psychiatry 85, no. 9 (2019): e45-e46. http://dx.doi.org/10.1016/j.biopsych.2019.03.002.

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17

Raimondi, S. C., F. G. Behm, P. K. Roberson, et al. "Cytogenetics of pre-B-cell acute lymphoblastic leukemia with emphasis on prognostic implications of the t(1;19)." Journal of Clinical Oncology 8, no. 8 (1990): 1380–88. http://dx.doi.org/10.1200/jco.1990.8.8.1380.

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In earlier studies of the cytogenetic characteristics of leukemic lymphoblasts from children with pre-B-cell acute lymphoblastic leukemia (ALL), we concluded that certain chromosomal abnormalities explain, in part, the increased presence of high-risk features at diagnosis and the less favorable response to therapy among patients with this immunologic subclass of ALL. With extended follow-up and a larger patient population, we have further evaluated the biologic and clinical aspects of pre-B leukemia. Of 686 cases of ALL with adequate immunophenotyping, 150 were classified as pre-B cell. Sevent

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18

Starke, Heike, Jörg Seidel, Wolfram Henn, et al. "Homologous sequences at human chromosome 9 bands p12 and q13-21.1 are involved in different patterns of pericentric rearrangements." European Journal of Human Genetics 10, no. 12 (2002): 790–800. http://dx.doi.org/10.1038/sj.ejhg.5200889.

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19

Giagounidis, Aristoteles A. N., Sabine Haase, Ulrich Germing та ін. "Treatment of myelodysplastic syndrome with isolated del(5q) including bands q31–q33 with a combination of all-trans-retinoic acid and tocopherol-α: a phase II study". Annals of Hematology 84, № 6 (2005): 389–94. http://dx.doi.org/10.1007/s00277-005-1027-3.

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20

Kurniali, Peter C., Anas Al-Janadi, Hongyan Chai, and Sainan Wei. "Cryptic Unbalanced Chromosomal Changes in a Case of Chronic Lymphocytic Leukemia / Small Lymphocytic Lymphoma (CLL/SLL) Identified By Single Nucleotide Polymorphism (SNP) Microarray, but Not By Conventional Karyotyping." Blood 124, no. 21 (2014): 5649. http://dx.doi.org/10.1182/blood.v124.21.5649.5649.

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Abstract Genomic abnormalities have been widely used to diagnose and provide prognostic significance in many hematologic malignancies (HM). The use of conventional G-banded chromosome and fluorescence in situ hybridization (FISH) analyses sometimes fail to detect genomic abnormalities due to the need for actively dividing cells and lower resolution of chromosome analysis (G-banded), as well as the inability to detect copy number of neutral loss of heterozygocity (G-banded and FISH). The addition of single nucleotide polymorphism (SNP) microarray has been shown to increase the detection rate of

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21

Raimondi, SC, FG Behm, PK Roberson, et al. "Cytogenetics of childhood T-cell leukemia." Blood 72, no. 5 (1988): 1560–66. http://dx.doi.org/10.1182/blood.v72.5.1560.1560.

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Abstract The karyotypes of 57 cases of childhood T-cell acute lymphoblastic leukemia (ALL) were analyzed to establish the cytogenetic profile in this disease. Three questions were of particular interest. Do the chromosomal changes in T-cell ALL preferentially affect bands where genes encoding the T-cell receptor for antigen (TCR) have been mapped? Do alterations involving the TCR gene regions appear with any notable frequency in B-progenitor ALL? Do chromosomal abnormalities in this disease relate to stage of T-cell ontogeny? A relatively high proportion of cases (65%) had a pseudodiploid kary

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22

Raimondi, SC, FG Behm, PK Roberson, et al. "Cytogenetics of childhood T-cell leukemia." Blood 72, no. 5 (1988): 1560–66. http://dx.doi.org/10.1182/blood.v72.5.1560.bloodjournal7251560.

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The karyotypes of 57 cases of childhood T-cell acute lymphoblastic leukemia (ALL) were analyzed to establish the cytogenetic profile in this disease. Three questions were of particular interest. Do the chromosomal changes in T-cell ALL preferentially affect bands where genes encoding the T-cell receptor for antigen (TCR) have been mapped? Do alterations involving the TCR gene regions appear with any notable frequency in B-progenitor ALL? Do chromosomal abnormalities in this disease relate to stage of T-cell ontogeny? A relatively high proportion of cases (65%) had a pseudodiploid karyotype at

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23

Xie, Y., and W. A. Muller. "Assignment of PECAM1 to human chromosome bands 17q22→q23 by in situ hybridization." Cytogenetic and Genome Research 74, no. 1-2 (1996): 156. http://dx.doi.org/10.1159/000134406.

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24

Bloomfield, CD, AI Goldman, G. Alimena, et al. "Chromosomal abnormalities identify high-risk and low-risk patients with acute lymphoblastic leukemia." Blood 67, no. 2 (1986): 415–20. http://dx.doi.org/10.1182/blood.v67.2.415.415.

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Abstract The importance of banded chromosome analyses in predicting long-term outcome in acute lymphoblastic leukemia (ALL) was evaluated in this follow-up study of 329 patients from the Third International Workshop on Chromosomes in Leukemia. Patients were divided into ten groups according to pretreatment karyotype: no abnormalities, one of the following structural abnormalities [the Philadelphia chromosome, translocations involving 8q24,t(4;11), 14q+, 6q-] or, in the remaining cases, modal number [less than 46, 46, 47 to 50, greater than 50]. Achievement and duration of complete remission (C

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25

Bloomfield, CD, AI Goldman, G. Alimena, et al. "Chromosomal abnormalities identify high-risk and low-risk patients with acute lymphoblastic leukemia." Blood 67, no. 2 (1986): 415–20. http://dx.doi.org/10.1182/blood.v67.2.415.bloodjournal672415.

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The importance of banded chromosome analyses in predicting long-term outcome in acute lymphoblastic leukemia (ALL) was evaluated in this follow-up study of 329 patients from the Third International Workshop on Chromosomes in Leukemia. Patients were divided into ten groups according to pretreatment karyotype: no abnormalities, one of the following structural abnormalities [the Philadelphia chromosome, translocations involving 8q24,t(4;11), 14q+, 6q-] or, in the remaining cases, modal number [less than 46, 46, 47 to 50, greater than 50]. Achievement and duration of complete remission (CR) and su

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26

Inazawa, J., K. Inoue, H. Nishigaki, et al. "Assignment of the human myeloperoxidase gene (MPO) to bands q21.3→q23 of chromosome 17." Cytogenetic and Genome Research 50, no. 2-3 (1989): 135–36. http://dx.doi.org/10.1159/000132742.

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27

Espinosa III, R. E., R. S. Lemons, R. K. Permian, W. L. Kuo, M. R. Rosner, and M. M. Le Beau. "Localization of the gene encoding insulin-degrading enzyme to human chromosome 10, bands q23→q25." Cytogenetic and Genome Research 57, no. 4 (1991): 184–86. http://dx.doi.org/10.1159/000133142.

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28

Popescu, Nicholas C., C. Richter King, and Matthias H. Kraus. "Localization of the human erbB-2 gene on normal and rearranged chromosomes 17 to bands q12–21.32." Genomics 4, no. 3 (1989): 362–66. http://dx.doi.org/10.1016/0888-7543(89)90343-1.

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29

Raghoebier, S., JH van Krieken, JC Kluin-Nelemans, et al. "Oncogene rearrangements in chronic B-cell leukemia." Blood 77, no. 7 (1991): 1560–64. http://dx.doi.org/10.1182/blood.v77.7.1560.1560.

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Abstract Forty-four B-chronic lymphocytic leukemias (CLL) were studied by Southern blot analysis using probes for the Ig genes and bcl-1, bcl-2 (major, minor and 5′ breakpoint region), bcl-3, c-myc, and retinoblastoma (Rb) loci. Eight cases had three or more rearranged JH bands, indicating oligoclonality, clonal evolution, or chromosomal translocation. One case had a rearrangement of the bcl-1 locus and three of the bcl-2 locus. In the first case, comigration of the rearranged bcl-1 and JH sequences indicated a t(11;14)(q13;q32) translocation, which, in contrast to previously described cases,

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30

Raghoebier, S., JH van Krieken, JC Kluin-Nelemans, et al. "Oncogene rearrangements in chronic B-cell leukemia." Blood 77, no. 7 (1991): 1560–64. http://dx.doi.org/10.1182/blood.v77.7.1560.bloodjournal7771560.

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Forty-four B-chronic lymphocytic leukemias (CLL) were studied by Southern blot analysis using probes for the Ig genes and bcl-1, bcl-2 (major, minor and 5′ breakpoint region), bcl-3, c-myc, and retinoblastoma (Rb) loci. Eight cases had three or more rearranged JH bands, indicating oligoclonality, clonal evolution, or chromosomal translocation. One case had a rearrangement of the bcl-1 locus and three of the bcl-2 locus. In the first case, comigration of the rearranged bcl-1 and JH sequences indicated a t(11;14)(q13;q32) translocation, which, in contrast to previously described cases, seems to

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31

Schaffner, Claudia, Stephan Stilgenbauer, Gudrun A. Rappold, Hartmut Döhner, and Peter Lichter. "Somatic ATM Mutations Indicate a Pathogenic Role of ATM in B-Cell Chronic Lymphocytic Leukemia." Blood 94, no. 2 (1999): 748–53. http://dx.doi.org/10.1182/blood.v94.2.748.

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Abstract Deletion in chromosome bands 11q22-q23 is one of the most common chromosome aberrations in B-cell chronic lymphocytic leukemia (B-CLL). It is associated with extensive lymph node involvement and poor survival. The minimal consensus deletion comprises a segment, which contains the ATM gene presenting an interesting candidate gene, as mutations in ATM predispose A-T patients to lymphoid malignancies. To investigate a potential pathogenic role of ATM in B-cell tumorigenesis, we performed mutation analysis of ATM in 29 malignant lymphomas of B-cell origin (B-CLL = 27; mantle cell lymphoma

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32

Schaffner, Claudia, Stephan Stilgenbauer, Gudrun A. Rappold, Hartmut Döhner, and Peter Lichter. "Somatic ATM Mutations Indicate a Pathogenic Role of ATM in B-Cell Chronic Lymphocytic Leukemia." Blood 94, no. 2 (1999): 748–53. http://dx.doi.org/10.1182/blood.v94.2.748.414k02_748_753.

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Deletion in chromosome bands 11q22-q23 is one of the most common chromosome aberrations in B-cell chronic lymphocytic leukemia (B-CLL). It is associated with extensive lymph node involvement and poor survival. The minimal consensus deletion comprises a segment, which contains the ATM gene presenting an interesting candidate gene, as mutations in ATM predispose A-T patients to lymphoid malignancies. To investigate a potential pathogenic role of ATM in B-cell tumorigenesis, we performed mutation analysis of ATM in 29 malignant lymphomas of B-cell origin (B-CLL = 27; mantle cell lymphoma, [MCL] =

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33

La Starza, R., I. Wlodarska, A. Aventin, et al. "Molecular Delineation of 13q Deletion Boundaries in 20 Patients With Myeloid Malignancies." Blood 91, no. 1 (1998): 231–37. http://dx.doi.org/10.1182/blood.v91.1.231.

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Abstract Fluorescent in situ hybridization (FISH) analysis with a panel of DNA probes for 13q13.1-q14.3 was performed on 20 cases of myeloid malignancies, of which 17 showed a del(13)(q) and three had translocations affecting 13q. By chromosome morphology, deletions consistently involved bands q14 and q21. In addition to confirming the chromosome data, FISH allowed us to delineate a commonly deleted region that was flanked by YAC 833A2 and YAC 854D4. Three cases with 13q translocations unexpectedly showed accompanying cryptic microdeletions of 13q, and in one case the commonly deleted region c

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34

La Starza, R., I. Wlodarska, A. Aventin, et al. "Molecular Delineation of 13q Deletion Boundaries in 20 Patients With Myeloid Malignancies." Blood 91, no. 1 (1998): 231–37. http://dx.doi.org/10.1182/blood.v91.1.231.231_231_237.

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Fluorescent in situ hybridization (FISH) analysis with a panel of DNA probes for 13q13.1-q14.3 was performed on 20 cases of myeloid malignancies, of which 17 showed a del(13)(q) and three had translocations affecting 13q. By chromosome morphology, deletions consistently involved bands q14 and q21. In addition to confirming the chromosome data, FISH allowed us to delineate a commonly deleted region that was flanked by YAC 833A2 and YAC 854D4. Three cases with 13q translocations unexpectedly showed accompanying cryptic microdeletions of 13q, and in one case the commonly deleted region could be n

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35

Oudat, Raida, Zebunnisa Khan, and Armand B. Glassman. "A Unique, Complex Variant Philadelphia Chromosome Translocation in a Patient With Typical Chronic Myelogenous Leukemia." Archives of Pathology & Laboratory Medicine 125, no. 3 (2001): 437–39. http://dx.doi.org/10.5858/2001-125-0437-aucvpc.

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Abstract The Philadelphia (Ph) chromosome [der(22) t(9;22)(q34;q11)] is the characteristic chromosomal abnormality found in chronic myelogenous leukemia (CML). This chromosome has been reported in patients with other chromosomal abnormalities. In this study, we describe a patient with hematologically typical chronic-phase CML with an unusual and complex translocation involving chromosomes 9, 11, and 22. These complex translocations were identified by G-banded conventional cytogenetics and confirmed by fluorescence in situ hybridization (FISH) using whole chromosome painting probes (wcp). To th

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36

Sembries, Sabine, Heike Pahl, Stephan Stilgenbauer, Hartmut Döhner, and Folke Schriever. "Reduced Expression of Adhesion Molecules and Cell Signaling Receptors by Chronic Lymphocytic Leukemia Cells With 11q Deletion." Blood 93, no. 2 (1999): 624–31. http://dx.doi.org/10.1182/blood.v93.2.624.

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Abstract Deletions in chromosome bands 11q22-q23 were recently shown to be one of the most frequent chromosome aberrations in B-cell chronic lymphocytic leukemia (B-CLL). Patients suffering from B-CLL with 11q deletion are characterized by extensive lymphadenopathy, rapid disease progression, and short survival times. Phenotypic and functional characteristics of B-CLL cells with 11q deletion that may help to explain the pathophysiology of this entity are yet unknown. In the present study, B-CLL cells with (n = 19) and without (n = 19) 11q deletion were analyzed for their expression of function

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Sembries, Sabine, Heike Pahl, Stephan Stilgenbauer, Hartmut Döhner, and Folke Schriever. "Reduced Expression of Adhesion Molecules and Cell Signaling Receptors by Chronic Lymphocytic Leukemia Cells With 11q Deletion." Blood 93, no. 2 (1999): 624–31. http://dx.doi.org/10.1182/blood.v93.2.624.402k10_624_631.

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Deletions in chromosome bands 11q22-q23 were recently shown to be one of the most frequent chromosome aberrations in B-cell chronic lymphocytic leukemia (B-CLL). Patients suffering from B-CLL with 11q deletion are characterized by extensive lymphadenopathy, rapid disease progression, and short survival times. Phenotypic and functional characteristics of B-CLL cells with 11q deletion that may help to explain the pathophysiology of this entity are yet unknown. In the present study, B-CLL cells with (n = 19) and without (n = 19) 11q deletion were analyzed for their expression of functionally rele

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38

Testa, J. R., T. Taguchi, A. G. Knudson, and O. Hino. "Localization of the interferon-α gene cluster to rat chromosome bands 5q31→q33 by fluorescence in situ hybridization." Cytogenetic and Genome Research 60, no. 3-4 (1992): 247–49. http://dx.doi.org/10.1159/000133350.

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39

Verma, Ram S., Robert A. Conte, Sami L. Sayegh, and Debasis Kanjilal. "The interstitial deletion of bands q33-35 of long arm of chromosome 7: a review with a new case report." Clinical Genetics 41, no. 2 (2008): 82–86. http://dx.doi.org/10.1111/j.1399-0004.1992.tb03638.x.

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40

Chaudhary, Renuka, Bhanu P. Chowdhary, Ingrid Harbitz, and Ingemar Gustavsson. "Localization of the Ceruloplasmin (CP) Gene to the q32-q33 Bands of Chromosome 13 in Pigs by in Situ Hybridization." Hereditas 119, no. 1 (2004): 7–10. http://dx.doi.org/10.1111/j.1601-5223.1993.00007.x.

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41

Rubnitz, JE, FG Behm, AM Curcio-Brint, et al. "Molecular analysis of t(11;19) breakpoints in childhood acute leukemias." Blood 87, no. 11 (1996): 4804–8. http://dx.doi.org/10.1182/blood.v87.11.4804.bloodjournal87114804.

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MLL is fused to ENL or ELL in acute leukemias that contain t(ll;19)(q23;p13). Although ENL and ELL localize to chromosome 19, bands p13.3 and p13.1, respectively, these breakpoints are not always readily distinguished by standard cytogenetics. We therefore used reverse transcriptase-polymerase chain reaction (RT-PCR) assays to analyze 26 cases of childhood acute leukemia containing t(11;19) to determine the frequencies of ENL and ELL involvement. All 17 cases of acute lymphoblastic leukemia (ALL) had MLL/ENL fusion transcripts. By contrast, of the 9 cases of acute myeloid leukemia (AML) analyz

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42

Quintrell, N., R. Lebo, H. Varmus, et al. "Identification of a human gene (HCK) that encodes a protein-tyrosine kinase and is expressed in hemopoietic cells." Molecular and Cellular Biology 7, no. 6 (1987): 2267–75. http://dx.doi.org/10.1128/mcb.7.6.2267.

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We have isolated cDNAs representing a previously unrecognized human gene that apparently encodes a protein-tyrosine kinase. We have designated the gene as HCK (hemopoietic cell kinase) because its expression is prominent in the lymphoid and myeloid lineages of hemopoiesis. Expression in granulocytic and monocytic leukemia cells increases after the cells have been induced to differentiate. The 57-kilodalton protein encoded by HCK resembles the product of the proto-oncogene c-src and is therefore likely to be a peripheral membrane protein. HCK is located on human chromosome 20 at bands q11-12, a

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43

Quintrell, N., R. Lebo, H. Varmus, et al. "Identification of a human gene (HCK) that encodes a protein-tyrosine kinase and is expressed in hemopoietic cells." Molecular and Cellular Biology 7, no. 6 (1987): 2267–75. http://dx.doi.org/10.1128/mcb.7.6.2267-2275.1987.

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Abstract:

We have isolated cDNAs representing a previously unrecognized human gene that apparently encodes a protein-tyrosine kinase. We have designated the gene as HCK (hemopoietic cell kinase) because its expression is prominent in the lymphoid and myeloid lineages of hemopoiesis. Expression in granulocytic and monocytic leukemia cells increases after the cells have been induced to differentiate. The 57-kilodalton protein encoded by HCK resembles the product of the proto-oncogene c-src and is therefore likely to be a peripheral membrane protein. HCK is located on human chromosome 20 at bands q11-12, a

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44

Rimokh, R., F. Berger, G. Delsol, et al. "Detection of the chromosomal translocation t(11;14) by polymerase chain reaction in mantle cell lymphomas." Blood 83, no. 7 (1994): 1871–75. http://dx.doi.org/10.1182/blood.v83.7.1871.1871.

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Abstract The t(11;14)(q13;q32) and its molecular counterpart, BCL1 rearrangement, are consistent features of mantle cell lymphoma (MCL). Rearrangement is thought to deregulate the nearby CCND1 (BCL1/PRAD1) proto-oncogene, a member of the cyclin G1 gene family, and thereby to contribute to tumorigenesis. We and others have previously shown that the BCL1 locus is rearranged in 55% to 60% of MCL patients and that, on chromosome 11, more than 80% of the breakpoints are localized within a 1-kbp DNA segment known as the major translocation cluster (MTC). We have determined the nucleotide sequence fo

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45

Rimokh, R., F. Berger, G. Delsol, et al. "Detection of the chromosomal translocation t(11;14) by polymerase chain reaction in mantle cell lymphomas." Blood 83, no. 7 (1994): 1871–75. http://dx.doi.org/10.1182/blood.v83.7.1871.bloodjournal8371871.

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Abstract:

The t(11;14)(q13;q32) and its molecular counterpart, BCL1 rearrangement, are consistent features of mantle cell lymphoma (MCL). Rearrangement is thought to deregulate the nearby CCND1 (BCL1/PRAD1) proto-oncogene, a member of the cyclin G1 gene family, and thereby to contribute to tumorigenesis. We and others have previously shown that the BCL1 locus is rearranged in 55% to 60% of MCL patients and that, on chromosome 11, more than 80% of the breakpoints are localized within a 1-kbp DNA segment known as the major translocation cluster (MTC). We have determined the nucleotide sequence for a porti

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46

Garcia, Emilio, Jeffrey Elliott, Ann Gorvad, et al. "A Continuous High-Resolution Physical Map Spanning 17 Megabases of the q12, q13.1, and q13.2 Cytogenetic Bands of Human Chromosome 19." Genomics 27, no. 1 (1995): 52–66. http://dx.doi.org/10.1006/geno.1995.1007.

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47

Lafage, Marina, Isabelle Clauss, Dominique Couez, Jacqueline Simonetti, Marc G. Wathelet, and Georges Huez. "The interferon- and virus-inducible IFI-56K and IFI-54K genes are located on human chromosome 10 at bands q23–q24." Genomics 13, no. 2 (1992): 458–60. http://dx.doi.org/10.1016/0888-7543(92)90272-t.

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48

Zhang, J., P. Meltzer, R. Jenkins, XY Guan, and J. Trent. "Application of chromosome microdissection probes for elucidation of BCR- ABL fusion and variant Philadelphia chromosome translocations in chronic myelogenous leukemia." Blood 81, no. 12 (1993): 3365–71. http://dx.doi.org/10.1182/blood.v81.12.3365.3365.

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Abstract Fluorescence in situ hybridization (FISH) has become an increasingly important method for assessing chromosome rearrangement. The reciprocal translocation constituting the Philadelphia (Ph) chromosome [t(9;22)(q34;q11)] characterizes more than 90% of patients with chronic myelogenous leukemia (CML). However, in the remaining cases the Ph chromosome (genetically characterized by the fusion of the BCR-ABL genes) is thought to arise through complex translocations that are often not readily apparent using routine chromosome-banding analysis. For this reason we have developed unique band-s

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49

Zhang, J., P. Meltzer, R. Jenkins, XY Guan, and J. Trent. "Application of chromosome microdissection probes for elucidation of BCR- ABL fusion and variant Philadelphia chromosome translocations in chronic myelogenous leukemia." Blood 81, no. 12 (1993): 3365–71. http://dx.doi.org/10.1182/blood.v81.12.3365.bloodjournal81123365.

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Abstract:

Fluorescence in situ hybridization (FISH) has become an increasingly important method for assessing chromosome rearrangement. The reciprocal translocation constituting the Philadelphia (Ph) chromosome [t(9;22)(q34;q11)] characterizes more than 90% of patients with chronic myelogenous leukemia (CML). However, in the remaining cases the Ph chromosome (genetically characterized by the fusion of the BCR-ABL genes) is thought to arise through complex translocations that are often not readily apparent using routine chromosome-banding analysis. For this reason we have developed unique band-specific p

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50

Phillips, J. C. "Assignment¹ of LHX1 to human chromosome bands 17q11.2→q12 by use of radiation hybrid mapping and somatic cell hybridization." Cytogenetic and Genome Research 97, no. 1-2 (2002): 140D. http://dx.doi.org/10.1159/000064048.

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