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Journal articles on the topic 'Deletion 17p'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Zenz, Thorsten, Alexander Kröber, Katrin Scherer, et al. "Monoallelic TP53 inactivation is associated with poor prognosis in chronic lymphocytic leukemia: results from a detailed genetic characterization with long-term follow-up." Blood 112, no. 8 (2008): 3322–29. http://dx.doi.org/10.1182/blood-2008-04-154070.

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AbstractThe exact prognostic role of TP53 mutations (without 17p deletion) and any impact of the deletion without TP53 mutation in CLL are unclear. We studied 126 well-characterized CLL patients by direct sequencing and DHPLC to detect TP53 mutations (exons 2-11). Most patients with 17p deletions also had TP53 mutations (81%). Mutations in the absence of 17p deletions were found in 4.5%. We found a shorter survival for patients with TP53 mutation (n = 18; P = .002), which was more pronounced when analyzed from the time point of mutation detection (6.8 vs 69 months, P < .001). The survival w

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2

Zenz, Thorsten, Antonio Sarno, Sonja Häbe, et al. "17p Deletion in CLL: Detailed Analysis of TP53 Mutations, Alternative Mechanisms of p53 Inactivation, Clone Size and Clonal Evolution." Blood 112, no. 11 (2008): 782. http://dx.doi.org/10.1182/blood.v112.11.782.782.

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Abstract The prognosis of CLL with 17p deletion is very poor. While it is generally accepted that inactivation of p53 (by mutation) underlies refractoriness of CLL with 17p deletion, no study has analyzed a large cohort of CLL patients with 17p deletion with respect to TP53 mutations and investigated other mechanisms of p53 inactivation. In order to assess the incidence of TP53 mutations in CLL with 17p deletion we identified a large cohort of CLL cases with 17p deletion (n=217) and studied TP53 mutations in 124 of these patients. We used DHPLC to screen for TP53 mutations (Exons 2–11). Aberra

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3

Rudenko, Hannah C., Vasantha Brito-Babapulle, David Gonzalez, et al. "Combined aCGH and Mutational Analysis of CLL Patients with 17p Deletion." Blood 108, no. 11 (2006): 2091. http://dx.doi.org/10.1182/blood.v108.11.2091.2091.

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Abstract We have utilised aCGH (Breakthrough Breast Cancer Research Centre 5.8K array) and mutational analysis of the TP53 gene (exons 4–10) on 74 cases of CLL to define the extent of deletion at 17p, TP53 mutational status, additional genomic changes, and how this affects clinical outcome. 17p- cases were selected by FISH (n=37, Vysis LSI P53 probe) and 37 cases were selected as being representative of the survival curve of CLL patients without 17p-. FISH identified 22 cases with TP53- in ≥ 50% of cells, 4 cases with TP53- 20–50% and 11 cases with TP53- ≤ 20%. aCGH can detect abnormalities pr

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4

Stamatoullas, A., M. P. Callar, C. Bastard, et al. "121 Myelodysplastic syndrome and 17P deletion." Leukemia Research 21, no. 1 (1997): S31. http://dx.doi.org/10.1016/s0145-2126(97)81333-1.

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5

Schnaiter, Andrea, and Stephan Stilgenbauer. "17p Deletion in Chronic Lymphocytic Leukemia." Hematology/Oncology Clinics of North America 27, no. 2 (2013): 289–301. http://dx.doi.org/10.1016/j.hoc.2013.01.008.

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6

Ghia, Emanuela M., Laura Rassenti, and Thomas J. Kipps. "Early Events in the Clonal Evolution in Patients with Chronic Lymphocytic Leukemia Carrying TP53 Mutations and 17p Deletion." Blood 112, no. 11 (2008): 4165. http://dx.doi.org/10.1182/blood.v112.11.4165.4165.

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Abstract The leukemia cells of patients with chronic lymphocytic leukemia (CLL) may experience clonal evolution of TP53 mutations and/or deletions in the short arm of chromosome 17 (del(17p)). Such changes are associated with poor prognosis and resistance to standard chemotherapy. We evaluated for TP53 mutations and p53 protein expression before and after irradiation in leukemia cells with del(17p) of 14 patients at various times prior to therapy. The proportion of leukemia cells harboring del(17p) ranged from 3% to 99.5%, as assessed by fluorescence in situ hybridization (FISH). Four cases ha

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7

Zenz, Thorsten, Sonja Häbe, Tina Denzel, et al. "Detailed analysis of p53 pathway defects in fludarabine-refractory chronic lymphocytic leukemia (CLL): dissecting the contribution of 17p deletion, TP53 mutation, p53-p21 dysfunction, and miR34a in a prospective clinical trial." Blood 114, no. 13 (2009): 2589–97. http://dx.doi.org/10.1182/blood-2009-05-224071.

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Abstract The prognosis of fludarabine (F)–refractory chronic lymphocytic leukemia (CLL) is very poor, and underlying mechanisms are only partly understood. To assess the contribution of p53 abnormalities to F-refractory CLL, we studied TP53 mutations in the CLL2H trial (subcutaneous alemtuzumab; n = 99). We found TP53 mutations in 37% of patients. Twelve of 67 (18%) patients without the 17p deletion showed a TP53 mutation and 50% showed evidence of uniparental disomy. A total of 75% of cases with TP53 mutation (without 17p−) showed clonal evolution/expansion. TP53 mutations had no impact on ov

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8

Soenen, Valérie, Claude Preudhomme, Christophe Roumier, Agnès Daudignon, Jean Luc Laı̈, and Pierre Fenaux. "17p Deletion in Acute Myeloid Leukemia and Myelodysplastic Syndrome. Analysis of Breakpoints and Deleted Segments by Fluorescence In Situ." Blood 91, no. 3 (1998): 1008–15. http://dx.doi.org/10.1182/blood.v91.3.1008.

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Abstract Recently, we and other groups reported in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) a strong correlation between cytogenetic rearrangements leading to 17p deletion, a typical form of dysgranulopoiesis combining pseudo-Pelger-Huët hypolobulation and small vacuoles in neutrophils, and p53 mutation. To gain further insight into this “17p-syndrome,” we studied 17 cases of AML and MDS with 17p deletion by whole chromosome painting (WCP) and fluorescence in situ hybridization (FISH) with probes spanning the 17p arm, including a p53 gene probe. Cytogenetically, 15 pati

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9

Soenen, Valérie, Claude Preudhomme, Christophe Roumier, Agnès Daudignon, Jean Luc Laı̈, and Pierre Fenaux. "17p Deletion in Acute Myeloid Leukemia and Myelodysplastic Syndrome. Analysis of Breakpoints and Deleted Segments by Fluorescence In Situ." Blood 91, no. 3 (1998): 1008–15. http://dx.doi.org/10.1182/blood.v91.3.1008.1008_1008_1015.

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Recently, we and other groups reported in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) a strong correlation between cytogenetic rearrangements leading to 17p deletion, a typical form of dysgranulopoiesis combining pseudo-Pelger-Huët hypolobulation and small vacuoles in neutrophils, and p53 mutation. To gain further insight into this “17p-syndrome,” we studied 17 cases of AML and MDS with 17p deletion by whole chromosome painting (WCP) and fluorescence in situ hybridization (FISH) with probes spanning the 17p arm, including a p53 gene probe. Cytogenetically, 15 patients had

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10

Chaudhury, Ateefa, Julio C. Chavez, and Javier Pinilla-Ibarz. "Utilization of Targeted Exome Sequencing to Determine Implications of TP53 Mutation Status in Relation to 17p Deletion in Chronic Lymphocytic Leukemia (CLL)." Blood 124, no. 21 (2014): 3287. http://dx.doi.org/10.1182/blood.v124.21.3287.3287.

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Abstract Background: Advances in molecular genetics have changed the risk stratification and treatment of patients with Chronic Lymphocytic Leukemia (CLL). Previous studies have shown the worst patient outcomes associated with 17p deletion from diminished overall and progression free survival, in addition to lack of response to conventional Fludarabine based chemotherapy regimens. More recently, analyses of the role of TP53 mutation utilizing next generation sequencing (NGS) in CLL patients has shown that it may also be associated with poor prognosis and similar outcomes to those patients with

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11

Forconi, Francesco, Andrea Rinaldi, Ivo Kwee, et al. "Identification of New Recurrent Lesions and Clinical Subsets by Genome-Wide DNA Profiling in Chronic Lymphocytic Leukemia with 17p Deletion." Blood 110, no. 11 (2007): 4696. http://dx.doi.org/10.1182/blood.v110.11.4696.4696.

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Abstract Chronic lymphocytic leukemia (CLL) with deletion of 17p(p53) locus (17p- CLL) identifies the most aggressive CLL subset, due to active disease course and resistance to current treatments. Intrinsic mechanisms of the poor prognosis of 17p- CLL are scarcely known. In order to identify additional lesions occurring in 17p- CLL which contribute to prognosis, we performed genome-wide DNA profiling in 18 cases of 17p- CLL (median follow-up 25 months, range 4–107), using high-resolution single-nucleotide polymorphism (SNP) arrays (Affymetrix Human Mapping Nsp 250 k arrays). Chromosomal 11q, 1

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12

Zenz, Thorsten, Barbara Eichhorst, Raymonde Busch, et al. "TP53 Mutation and Survival in Chronic Lymphocytic Leukemia." Journal of Clinical Oncology 28, no. 29 (2010): 4473–79. http://dx.doi.org/10.1200/jco.2009.27.8762.

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Purpose The precise prognostic impact of TP53 mutation and its incorporation into treatment algorithms in chronic lymphocytic leukemia (CLL) is unclear. We set out to define the impact of TP53 mutations in CLL. Patients and Methods We assessed TP53 mutations by denaturing high-performance liquid chromatography (exons 2 to 11) in a randomized prospective trial (n = 375) with a follow-up of 52.8 months (German CLL Study Group CLL4 trial; fludarabine [F] v F + cyclophosphamide [FC]). Results We found TP53 mutations in 8.5% of patients (28 of 328 patients). None of the patients with TP53 mutation

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13

Zenz, Thorsten, and Stephan Stilgenbauer. "CLL 17p deletion: more than ‘miR’ly p53?" Blood 116, no. 6 (2010): 859–60. http://dx.doi.org/10.1182/blood-2010-04-281253.

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14

Steichen-Gersdorf, E., M. Baumgartner, A. Kreczy, H. Maier, and F.-M. Fink. "Deletion mapping on chromosome 17p in medulloblastoma." British Journal of Cancer 76, no. 10 (1997): 1284–87. http://dx.doi.org/10.1038/bjc.1997.549.

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15

Teleanu, Veronica, Jennifer Edelmann, Claudia Haferlach, et al. "Genomic Mechanisms of 17p / TP53 Loss in Primary “ultra High-risk” and Refractory Chronic Lymphocytic Leukemia: Results from the CLL2O Trial." Blood 124, no. 21 (2014): 2184. http://dx.doi.org/10.1182/blood.v124.21.2184.2184.

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Abstract Background: Unraveling the cytogenetic background helped to decipher the molecular basis of many hematologic cancers and to develop specific therapies. Recently, using chromosome banding analysis (CBA), jumping translocations were identified as a cause of 17p loss in multiple myeloma, providing new insights into the origin of clonal evolution and copy number alterations (CNA) (Sawyer et al, Blood 2014). In chronic lymphocytic leukemia (CLL) the genomic mechanisms leading to 17p loss are not fully understood. Aims: Characterization of underlying mechanisms of 17p loss using CBA and cor

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16

Drach, Johannes, Jutta Ackermann, Elke Fritz, et al. "Presence of a p53 Gene Deletion in Patients With Multiple Myeloma Predicts for Short Survival After Conventional-Dose Chemotherapy." Blood 92, no. 3 (1998): 802–9. http://dx.doi.org/10.1182/blood.v92.3.802.415a17_802_809.

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In multiple myeloma (MM), previous studies showed that mutations of the p53 gene are rare events in patients with newly diagnosed disease, but it is not known whether deletions of p53 are of any significance in MM. To address this question, we used interphase fluorescence in situ hybridization (FISH) with a DNA probe specific for the p53 locus at 17p13 and investigated bone marrow plasma cells from 72 patients with MM (59 patients = 81.9% before therapy). By FISH, deletions of p53, which were found to be predominantly monoallelic, were detected in 32.8% and 54.5% of patients with newly diagnos

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17

Brito-Babapulle, Vasantha, Hannah Rudenko, Claire Dearden, et al. "Bacterial Artificial Chromosome (BAC) Array CGH Study of B-CLL Patients with 17p13 Deletion." Blood 106, no. 11 (2005): 2110. http://dx.doi.org/10.1182/blood.v106.11.2110.2110.

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Abstract B-cell chronic lymphocytic leukaemia is characterised by a highly variable clinical course. Clone specific chromosomal imbalances have a significant prognostic ability with deletion of 17p13 being associated with advanced disease and resistance to therapy, deletion of 11q with progressive disease and extensive lymphadenopathy, deletion of 13q14 on its own with good prognosis and trisomy 12 with atypical morphology and an intermediate prognosis. In the MRC CLL 4 trial, a randomised study of conventional therapy with chlorambucil vs fludarabine either on its own or in combination with c

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18

Bellucco, Fernanda T., Natália Nunes, Mileny E. S. Colovati, et al. "Miller-Dieker Syndrome due to a 5.5-Mb 17p Deletion in a 17;Y Pseudodicentric Chromosome." Cytogenetic and Genome Research 152, no. 1 (2017): 29–32. http://dx.doi.org/10.1159/000477920.

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Miller-Dieker syndrome (MDS) is a contiguous gene deletion syndrome in which almost all patients present de novo 17p13.3 deletions. We report on a male infant with MDS and an unusual unbalanced translocation involving chromosomes Y and 17 that resulted in a large 5.5-Mb 17pterp13.2 deletion and a karyotype with 45 chromosomes. Apart from the deletion of the MDS critical region, the deletion of additional distal genes seemed to have no major influence on the patient's phenotype, since he did not show any unusual clinical findings that are not commonly described in MDS patients.

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19

Fiegl, Michael, Martin Erdel, Inge Tinhofer, et al. "Clinical Outcome of B-Cell Chronic Lymphocytic Leukemia Following Alemtuzumab Therapy: Retrospective Study within Various Cytogenetic Risk Categories." Blood 112, no. 11 (2008): 3164. http://dx.doi.org/10.1182/blood.v112.11.3164.3164.

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Abstract B-cell chronic lymphocytic leukemia (CLL) with 17p deletion responds poorly to chemotherapeutic agents. This retrospective study evaluated the benefit of alemtuzumab monotherapy in unselected patients with advanced CLL, categorized by cytogenetic profile. Methods: This is the largest data base with efficacy analysis of alemtuzumab in CLL stratified according to cytogenetics. Detailed data analysis was done in 138 CLL patients, in whom cytogenetic analysis was performed by FISH using the standard CLL analysis categorized according to Doehner et al. (N Engl J Med343, 1910; 2000). Respon

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20

Zenz, Thorsten, Julia Mohr, Eric Eldering, et al. "miR-34a as part of the resistance network in chronic lymphocytic leukemia." Blood 113, no. 16 (2009): 3801–8. http://dx.doi.org/10.1182/blood-2008-08-172254.

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Abstract 17p (TP53) deletion identifies patients with chronic lymphocytic leukemia (CLL) who are resistant to chemotherapy. The members of the miR-34 family have been discovered to be direct p53 targets and mediate some of the p53-dependent effects. We studied miR-34a and miR-34b/c expression in a large cohort to define their potential role in refractory CLL. While no expression of miR-34b/c could be detected, we found variable expression levels of miR-34a. miR-34a levels were up-regulated after DNA damage in the presence of functional p53, but not in cases with 17p deletion (P < .001). We

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21

Bastard, Christian, Christophe Fruchart, Gregory Raux, Francoise Parmentier, Dominique Vaur, and Herve Tilly. "Comparison of a Quantitative PCR Method with FISH for the Assessment of the Four Aneuploïdies Commonly Evaluated in CLL Patients." Blood 108, no. 11 (2006): 4950. http://dx.doi.org/10.1182/blood.v108.11.4950.4950.

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Abstract Four chromosomal defects associated with prognosis have been identified in CLL patients, namely deletions of the 13q13-q14, 11q22 and 17p13 regions and trisomy 12. Due to the low proliferation index of these tumors and to the fact that some defects can be cryptic, the detection of these abnormalities by conventional cytogenetics is difficult. Therefore, the resulting aneuploidies are usually evaluated by fluorescent in situ hybridisation (FISH). As probes are expensive and FISH time consuming, we aimed to compare a quantitative PCR method - quantitative PCR of short fluorescent fragme

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22

Zweegman, Sonja, and Niels W. C. J. van de Donk. "Deletion 17p: a matter of size and number?" Blood 137, no. 9 (2021): 1135–36. http://dx.doi.org/10.1182/blood.2020009102.

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23

Zenz, Thorsten, Peter Dreger, Sascha Dietrich, et al. "Allogeneic Stem Cell Transplantation Can Overcome the Adverse Prognostic Impact of TP53 Mutation In Chronic Lymphocytic Leukemia (CLL): Results From the GCLLSG CLL3x Trial." Blood 116, no. 21 (2010): 2357. http://dx.doi.org/10.1182/blood.v116.21.2357.2357.

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Abstract Abstract 2357 There is ample evidence that poor-risk CLL, as defined by fludarabine refractoriness or the presence of deletion 17p-, can be successfully treated by allogeneic stem cell transplantation (alloSCT). It is unknown, however, whether alloSCT can also overcome the treatment resistance associated with TP53 mutations seen under conventional fludarabine combination therapy. Therefore we have assessed the impact of TP53 mutations on the outcome of alloSCT with the patient cohort enrolled on the CLL3X trial of the German CLL Study Group. Patients and Methods: The CLL3X trial inclu

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24

Greipp, Patricia T., Stephanie A. Smoley, David S. Viswanatha, et al. "Very High Risk CLL Characterized by a “Double Hit” Clone with Both 11q22 and 17p13 Deletion." Blood 120, no. 21 (2012): 2486. http://dx.doi.org/10.1182/blood.v120.21.2486.2486.

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Abstract Abstract 2486 In patients with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL), deletion of 17p13 (17p-) resulting in loss of one allele of TP53 and 11q22 (11q-) resulting in loss of one allele of ATM predicts a significantly poorer prognosis. These lesions are nearly always monoallelic in patients with CLL and their consequences are considerably influenced by the integrity of the remaining allele. A dysfunctional mutation in the remaining allele, resulting in more aggressive disease, ultimately occurs in most patients with 17p- (> 80%) but fewer patients with 11q- (3

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25

Drach, Johannes, Jutta Ackermann, Elke Fritz, et al. "Presence of a p53 Gene Deletion in Patients With Multiple Myeloma Predicts for Short Survival After Conventional-Dose Chemotherapy." Blood 92, no. 3 (1998): 802–9. http://dx.doi.org/10.1182/blood.v92.3.802.

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Abstract In multiple myeloma (MM), previous studies showed that mutations of the p53 gene are rare events in patients with newly diagnosed disease, but it is not known whether deletions of p53 are of any significance in MM. To address this question, we used interphase fluorescence in situ hybridization (FISH) with a DNA probe specific for the p53 locus at 17p13 and investigated bone marrow plasma cells from 72 patients with MM (59 patients = 81.9% before therapy). By FISH, deletions of p53, which were found to be predominantly monoallelic, were detected in 32.8% and 54.5% of patients with newl

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26

Ferrajoli, Alessandra, Michael J. Keating, William G. Wierda, et al. "Lenalidomide Is Active in Patients with Relapsed/Refractory Chronic Lymphocytic Leukemia (CLL) Carrying Unfavorable Chromosomal Abnormalities." Blood 110, no. 11 (2007): 754. http://dx.doi.org/10.1182/blood.v110.11.754.754.

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Genomic abnormalities, according to the Dohner hierarchical classification, are an important prognostic factor in chronic lymphocytic lymphoma (CLL). Specific chromosomal aberrations, such as a deletion 17p (P53 abnormalities) and deletion 11q (ATM defects), are associated with aggressive disease and inferior response to purine analogue-based chemotherapy. Lenalidomide is an immunomodulatory agent that has demonstrated clinical efficacy in patients with relapsed or refractory CLL in 2 separate phase II clinical trials (Chanan-Khan et al. JCO 2006; Ferrajoli et al. Blood 2006 abst). To investig

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27

Gonzalez, David, Pilar Martinez, Rachel Wade, et al. "Mutational Status of the TP53 Gene as a Predictor of Response and Survival in CLL Patients with and without 17p Deletion." Blood 112, no. 11 (2008): 784. http://dx.doi.org/10.1182/blood.v112.11.784.784.

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Abstract Background: Deletion of 17p in chronic lymphocytic leukaemia (CLL) is associated with resistance to conventional therapy and a poor clinical outcome. Though TP53 mutations have been described in some of these cases, the extent to which they occur in CLL patients and their clinical implications remain unclear. We investigated the prognostic value of TP53 mutations in the clinical course of CLL patients. Methods: We analysed 529 CLL samples from the UK LRF CLL4 clinical trial (Chlorambucil vs Fludarabine±Cyclophosphamide) for the presence of TP53 mutations and their association with res

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28

Zenz, Thorsten, Julia Mohr, Eric Eldering, et al. "Mir-34a as Part of the Chemotherapy Resistance Network in Chronic Lymphocytic Leukemia." Blood 112, no. 11 (2008): 1209. http://dx.doi.org/10.1182/blood.v112.11.1209.1209.

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Abstract The central role of 17p (TP53) deletion and 11q (ATM) deletion in identifying patients with CLL who respond sub-optimally to chemotherapy suggests a prominent role of the DNA damage pathway in CLL. MiR34s have been shown to be direct p53 targets and mediate some of the p53 dependent effects. To assess the role of miR-34s in a large cohort of CLL patients (n=60), we studied miR34a and miR34b/c levels together with a detailed assessment of the DNA damage response. While no expression of miR-34b/c could be detected, we found diverse expression levels of miR34a. MiR34a levels in CLL are u

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29

Bomben, Riccardo, Maria Francesca Rossi, Tiziana D'Agaro, et al. "Clinical Impact of Clonal and Subclonal TP53 Mutations in Chronic Lymphocytic Leukemia." Blood 132, Supplement 1 (2018): 945. http://dx.doi.org/10.1182/blood-2018-99-111452.

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Abstract Introduction. The clinical course of patients with chronic lymphocytic leukemia (CLL) is highly heterogeneous. The deletions/mutations of 17p/TP53 are predictors of chemorefractoriness, and for this reason, in the management algorithm of CLL patients, when present, indicate treatment with with chemo-free regimens also in the context of first-line therapy. Recent studies based on ultra-deep-next generation sequencing (NGS) have shown that TP53 mutations can be present at very low clonal abundance in tumor cell populations, although whether these mutations may have a detrimental clinica

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30

Yuan, Ying‐Ying, Hua‐Yuan Zhu, Jia‐Zhu Wu, et al. "The percentage of cells with 17p deletion and the size of 17p deletion subclones show prognostic significance in chronic lymphocytic leukemia." Genes, Chromosomes and Cancer 58, no. 1 (2018): 43–51. http://dx.doi.org/10.1002/gcc.22692.

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31

Yu, Lijian, Haesook T. Kim, Siddha Kasar, et al. "Comprehensive Genetic Characterization of 17p Deleted CLL Identifies Predictors of Overall Survival." Blood 126, no. 23 (2015): 2907. http://dx.doi.org/10.1182/blood.v126.23.2907.2907.

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Abstract Many studies have shown that deletion at chromosome 17p targeting the TP53 gene, or del(17p), is associated with poor prognosis in chronic lymphocytic leukemia (CLL). Despite this, not all del(17p) CLL progresses rapidly to treatment and has short survival. We hypothesized that other coexisting genetic aberrations may contribute to the poor clinical outcome and heterogeneity of del(17p) cases. To assess this, we analyzed copy number alterations (CNAs) using Affymetrix SNP array data from 200 CLL patients (55 with del(17p)), and somatic mutation profile by whole exome sequencing (WES;

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32

Abbas, Naeem, Samra Waheed, Aisha Jamal, Ali Saleem, and Tahir Sultan Shamsi. "Acute Leukemia of Ambiguous Lineage with a Rare Abnormality Del17p by FISH Analysis." National Journal of Health Sciences 5, no. 2 (2020): 79–82. http://dx.doi.org/10.21089/njhs.52.0079.

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Abstract: The World Health Organization (WHO) has categorized acute undifferentiated leukemia (AUL) as a rare subtype of acute leukemia of ambiguous lineage (ALAL). The prognosis of AUL is considered poor and it expresses no known lineage-specific markers. In majority of the cases, AUL has been associated with karyotypic abnormalities, most commonly deletion 5q and complex karyotype. Deletion 17p correlation with acute myeloid leukemia and myelodysplastic syndome has been previously established and is associated with poorer outcomes. Herein we are reporting a case of forty years old male who w

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33

Gogia, Ajay, Ritu Gupta, Lalit Kumar, Atul Sharma, and Lata Soni. "Chronic lymphocytic leukemia with deletion 17p: An Indian scenario." South Asian Journal of Cancer 08, no. 01 (2019): 40–51. http://dx.doi.org/10.4103/sajc.sajc_287_18.

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34

Ferretti, Elisabetta, Enrico De Smaele, Lucia Di Marcotullio, Isabella Screpanti, and Alberto Gulino. "Hedgehog checkpoints in medulloblastoma: the chromosome 17p deletion paradigm." Trends in Molecular Medicine 11, no. 12 (2005): 537–45. http://dx.doi.org/10.1016/j.molmed.2005.10.005.

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35

Ghia, Paolo. "Ibrutinib holds promise for patients with 17p deletion CLL." Lancet Oncology 17, no. 10 (2016): 1342–43. http://dx.doi.org/10.1016/s1470-2045(16)30442-9.

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36

Anagnostopoulos, Athanasios K., Chrissa Papathanassiou, Kalliopi Karamolegou, et al. "Proteomic Studies of Pediatric Medulloblastoma Tumors with 17p Deletion." Journal of Proteome Research 14, no. 2 (2015): 1076–88. http://dx.doi.org/10.1021/pr501219f.

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37

Ise, Mikiko, Hideki Tsujimura, Chikara Sakai, and Kyoya Kumagai. "Hepatic Extramedullary Disease in Multiple Myeloma With 17p Deletion." Clinical Lymphoma Myeloma and Leukemia 14, no. 5 (2014): e165-e168. http://dx.doi.org/10.1016/j.clml.2014.04.002.

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38

Cogen, Philip H., Laleh Daneshvar, Andrew K. Metzger, and Michael S. B. Edwards. "Deletion mapping of the medulloblastoma locus on chromosome 17p." Genomics 8, no. 2 (1990): 279–85. http://dx.doi.org/10.1016/0888-7543(90)90283-z.

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39

Fésüs, Viktória, Dóra Marosvári, Béla Kajtár, et al. "A TP53-mutáció-analízis jelentősége krónikus lymphocytás leukaemiában." Orvosi Hetilap 158, no. 6 (2017): 220–28. http://dx.doi.org/10.1556/650.2017.30656.

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Abstract: Introduction: In recent years much progress has been made in the therapy of chronic lymphocytic leukaemia, as the new innovative medicine proved to be effective in managing patients carrying TP53 abnormalities. To identify all these patients, it is essential to screen for both forms of TP53 defects, including both 17p deletions and TP53 mutations. Aim: The aim of this study was to determine the frequency of TP53 mutations and their association with 17p deletions in a large Hungarian cohort of 196 patients suffering from chronic lymphocytic leukaemia. Method: We performed mutation ana

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Brown, Jennifer R., Megan Hanna, Bethany Tesar, et al. "High Resolution Genomic Analysis In CLL Demonstrates Genomic Stability In Untreated Patients and Novel Markers of Progression In Treated Patients." Blood 116, no. 21 (2010): 2426. http://dx.doi.org/10.1182/blood.v116.21.2426.2426.

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Abstract Abstract 2426 Chronic lymphocytic leukemia is the most common leukemia of adults but still incurable. Prognosis at diagnosis is widely variable, and the key cytogenetic abnormalities determined by FISH remain one of the best predictors of prognosis and treatment response. We therefore undertook very high resolution genomic analysis of 161 CLLs with matched germline samples using Affymetrix 6.0 SNP arrays, in an effort to identify additional predictors of prognosis, and have also performed gene expression profiling on most of this patient cohort. The median age at diagnosis for the coh

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Ho, Park Jong, Baek Hee Jong, Zo Joe Ill, Lee Choon Tack, Kim Chang Min, and Shim Young Mog. "High Prevalence of p53 Gene Mutation in Esophageal Cancer." Asian Cardiovascular and Thoracic Annals 5, no. 4 (1997): 213–19. http://dx.doi.org/10.1177/021849239700500407.

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Tissue samples from 24 patients with esophageal cancer were studied to determine the incidence and clinical implications of alterations of the p53 gene. Allelic deletion of chromosome 17p and mutation of the p53 gene were determined by Southern blot analysis and polymerase chain reaction single-stranded conformation polymorphism. Nucleotide sequence analysis was performed using the direct sequencing method when abnormalities were detected. Eighteen of the 24 cases of esophageal cancer showed either gene deletions or mutations of the p53 gene. Among 15 tumors with p53 gene deletion or mutation,

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Schichman, Steven A., Annjanette Stone, Maria Winters, et al. "Whole Genome Copy Number Variation Analysis of Chronic Lymphocytic Leukemia (CLL) Cells From Early-Intermediate Stage, High Risk CLL Patients Prior to First Treatment Reveals New Loss of Heterozygosity and Duplication Events in the CLL Genome." Blood 114, no. 22 (2009): 1265. http://dx.doi.org/10.1182/blood.v114.22.1265.1265.

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Abstract Abstract 1265 Poster Board I-287 Introduction Fluorescence in situ hybridization (FISH), in combination with other markers, is used as a prognostic tool for CLL patients at diagnosis. The presence or absence of trisomy 12 and deletions at 13q, 11q, and 17p helps to predict disease progression and to stratify patients for therapeutic decisions. We hypothesized that whole genome single nucleotide polymorphism (SNP)-based copy number variation (CNV) analysis would capture all of the information in current CLL FISH panels and would reveal new CNV features in the CLL genome. Patients and M

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Mohr, Julia, Thorsten Zenz, Dirk Winkler, et al. "The Response to DNA Damage in CLL Cells Is Partly Determined by the Type of TP53 Mutation and Genomic Aberrations." Blood 112, no. 11 (2008): 3119. http://dx.doi.org/10.1182/blood.v112.11.3119.3119.

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Abstract A central role of the DNA damage response pathway and particularly p53 has been suggested by the prognostic role of 17p and 11q deletions in CLL. In the critical regions, two prominent genes are located that are involved in the cells’ response to DNA damage. Functional assessment of p53 may be of help to more precisely define a subgroup of patients with defects in the DNA damage response pathway. The most commonly used assays include FACS measurement of induction of p53/p21 after DNA damage, induction of p53 by nutlins or the measurement of transcriptional targets of p53 by RT-PCR or

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Sebaa, Amel, Lionel Ades, Fanny Baran-Marzack, et al. "Incidence of 17p deletions andTP53mutation in myelodysplastic syndrome and acute myeloid leukemia with 5q deletion." Genes, Chromosomes and Cancer 51, no. 12 (2012): 1086–92. http://dx.doi.org/10.1002/gcc.21993.

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Dun, Karen. "Fish analysis of 17p deletion: Lessons learned from the EQA." Pathology 52 (February 2020): S28. http://dx.doi.org/10.1016/j.pathol.2020.01.117.

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Peacock, J., A. Bagchi, S. Egan, and M. Taylor. "PM-16 * AN ANIMAL MODEL OF 17p DELETION IN MEDULLOBLASTOMA." Neuro-Oncology 17, suppl 3 (2015): iii34. http://dx.doi.org/10.1093/neuonc/nov061.138.

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Badoux, Xavier C., Michael Keating, Susan O'Brien, et al. "Patients with Relapsed CLL and 17p Deletion by FISH Have Very Poor Survival Outcomes." Blood 114, no. 22 (2009): 1248. http://dx.doi.org/10.1182/blood.v114.22.1248.1248.

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Abstract Abstract 1248 Poster Board I-270 Background There has recently been substantial work to identify factors that correlate with clinical outcome for patients with CLL. Identifying and validating factors may give understanding and insight into the biology of the disease and may help guide management of patients. TP53 is a gene located on the short arm of chromosome 17 (17p). The protein product of TP53, p53, is a transcription factor that regulates cell cycle and functions as a tumor suppressor. Therefore, p53 is critically important for the survival of CLL cells. In addition, p53 is crit

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Thakurta, Anjan, Maria Ortiz, Pedro Blecua, et al. "High subclonal fraction of 17p deletion is associated with poor prognosis in multiple myeloma." Blood 133, no. 11 (2019): 1217–21. http://dx.doi.org/10.1182/blood-2018-10-880831.

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Abstract Deletions of chromosome 17p (del17p) that span the TP53 gene are associated with poor outcome in multiple myeloma (MM), but the prognostic value of del17p cancer clonal fraction (CCF) remains unclear. We applied uniform cytogenetic assessments in a large cohort of newly diagnosed MM (NDMM) patients carrying varying levels of del17p. Incremental CCF change was associated with shorter survival, and a robust CCF threshold of 0.55 was established in discovery and replication data sets. After stratification on the 0.55-CCF threshold, high-risk patients had statistically significantly poore

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Tam, Constantine S., Tait D. Shanafelt, William G. Wierda, et al. "De Novo Deletion 17p13.1 Chronic Lymphocytic Leukemia Shows Significant Clinical Heterogeneity: The MD Anderson/Mayo Clinic Experience." Blood 112, no. 11 (2008): 1056. http://dx.doi.org/10.1182/blood.v112.11.1056.1056.

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Abstract Figure Figure In order to characterize the clinical course of patients (pts) with deletion 17p13.1 (17p-) CLL, we identified 100 consecutive treatment-naïve pts with 17p- from the MD Anderson Cancer Center (MDACC, n=61) and Mayo Clinic (n=39) clinical databases. The diagnosis of 17p- was established by FISH with a median time from initial diagnosis to FISH documenting 17p- of 9 months. Median age was 64 yrs (60 for MDACC pts & 70 for Mayo pts) and Rai stage was 0, 1–2 and 3–4 in 34%, 49% and 17% pts respectively. 17p- was the sole FISH abnormality in 29%. Unmutated IgVH and ZAP-7

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Rossi, Davide, Lodovico Terzi-di-Bergamo, Lorenzo De Paoli, et al. "Molecular prediction of durable remission after first-line fludarabine-cyclophosphamide-rituximab in chronic lymphocytic leukemia." Blood 126, no. 16 (2015): 1921–24. http://dx.doi.org/10.1182/blood-2015-05-647925.

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