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Journal articles on the topic 'Inv 16'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

Lazarchick, J. "AML with inv(16)." ASH Image Bank 2004, no. 0214 (2004): 101005. http://dx.doi.org/10.1182/ashimagebank-2004-101005.

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2

Eskelin, Sebastian, and Tero Kivel?? "INV 16 Metastatic uveal melanoma." Melanoma Research 17, no. 1 (2007): A7—A8. http://dx.doi.org/10.1097/00008390-200702000-00026.

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3

Bennett, John M. "Inv(16) and eosinophilia in CMMoL." Cancer Genetics and Cytogenetics 101, no. 1 (1998): 81. http://dx.doi.org/10.1016/s0165-4608(97)00252-5.

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4

Maslak, P. "Acute Myeloid Leukemia with inv 16." ASH Image Bank 2002, no. 1029 (2002): 100528. http://dx.doi.org/10.1182/ashimagebank-2002-100528.

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5

Surapally, Sridevi, Daniel G. Tenen, and John A. Pulikkan. "Emerging therapies for inv(16) AML." Blood 137, no. 19 (2021): 2579–84. http://dx.doi.org/10.1182/blood.2020009933.

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Abstract The core binding factor composed of CBFβ and RUNX subunits plays a critical role in most hematopoietic lineages and is deregulated in acute myeloid leukemia (AML). The fusion oncogene CBFβ-SMMHC expressed in AML with the chromosome inversion inv(16)(p13q22) acts as a driver oncogene in hematopoietic stem cells and induces AML. This review focuses on novel insights regarding the molecular mechanisms involved in CBFβ-SMMHC–driven leukemogenesis and recent advances in therapeutic approaches to target CBFβ-SMMHC in inv(16) AML.

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6

Helbling, Daniel, Beatrice U. Mueller, Nikolai A. Timchenko, et al. "Inv (16) Suppresses CEBPA in Acute Myeloid Leukemia by Activation of Calreticulin." Blood 104, no. 11 (2004): 3388. http://dx.doi.org/10.1182/blood.v104.11.3388.3388.

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Abstract Inversion of chromosome 16 (inv(16)) results in the reciprocal chromosomal rearrangement of the CBFB and MYH11 genes and it is the hallmark of malignant cells observed in patients with acute myeloid leukemia (AML) subtype M4Eo. Alterations of structure or expression of CEBPA - a key myeloid transcription factor - have been implicated in particular subtypes of AML. To investigate the effects of inv(16) on CEBPA we conditionally expressed inv(16) in U937 cells and found that CEBPA mRNA levels remained unchanged. However, CEBPA protein and binding activity were suppressed by 100% and 71%

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7

Pelzer, Benedikt W., Anita Hollenbeck, Stefanie Weber та ін. "HIF-1α Promotes Cbfbeta-SMMHC-Induced Acute Myeloid Leukemia Development". Blood 128, № 22 (2016): 1559. http://dx.doi.org/10.1182/blood.v128.22.1559.1559.

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Abstract Acute myeloid leukemia (AML) develops by the acquisition of genomic alterations which initiate different pathways leading to full-blown malignancy. The type of genomic driver alteration governs AML biology and clinical disease course. Translocations involving the core-binding factor (CBF) complex such as t(8:21) and inv(16) represent distinct subgroups of AML genomic drivers. However, additional factors promoting CBF AML leukemogenesis remain largely unknown. Due to the hypoxic nature of the bone marrow the activation of the ubiquitous hypoxia-sensing pathway via HIF-1a might promote

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8

Li, Jianyong, Huifen Zhou, Lijuan Chen, et al. "Trisomy 22 as the Sole Abnormality Is an Important Marker for Inversion 16 in Acute Myeloid Leukemia." Blood 108, no. 11 (2006): 4445. http://dx.doi.org/10.1182/blood.v108.11.4445.4445.

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Abstract Inv(16) has been reported in 10%~12% of acute myeloid leukemia (AML), mostly being associated with the M4Eo subtype, and is associated with a relatively favorable outcome. However, it is a cryptic rearrangement and often difficult to recognize in conventional cytogenetics (CC). Trisomy 22 is an uncommon karyotypic aberration in AML and is often associated with inv(16)(p13q22). In order to explore the value of trisomy 22 in the diagnosis of AML with inv(16), dual-color interphase fluorescence in situ hybridization (FISH) was performed in 19 AML cases with trisomy 22 abnormality. The pr

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9

Bank, Ingrid E. M., Válerie de Haas, H. Berna Beverloo, Christian M. Zwaan, and Gertjan J. Kaspers. "Clinical and Prognostic Significance of Eosinophilia and Inv(16)/t(16;16) In Pediatric Acute Myelomonocytic Leukemia (AML-M4)." Blood 116, no. 21 (2010): 1664. http://dx.doi.org/10.1182/blood.v116.21.1664.1664.

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Abstract Abstract 1664 The prognosis of pediatric AML has improved considerably in the past decades, with overall long-term survival rates around 60%. This has been achieved by the more effective use of anti-leukemic drugs, improved supportive care and the use of risk-group stratification. A well-known prognostic factor is cytogenetics, and inv(16)(p13.1q22) or t(16;16)(p13.1q22) leading to the CBFβ-MYHII fusion gene and usually detected in AML FAB type M4, is associated with excellent outcome. However, information on cytogenetics is not always available due to lack of material, assay failures

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10

Pulsoni, Alessandro, Simona Iacobelli, Paola Fazi, et al. "AML-M4: Role of Eosinophilia and Cytogenetics on Treatment Response and Survival. The GIMEMA Experience." Blood 106, no. 11 (2005): 4501. http://dx.doi.org/10.1182/blood.v106.11.4501.4501.

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Abstract Background: The acute myeloid leukemia (AML)-M4 subtype is frequently associated to eosinophilia and/or to the cytogenetic alteration inv(16)/t(16;16). The presence of these features is generally associated with good prognosis, but the studies concerning their exact role are hampered by the low number of cases. We retrospectively analyzed patients with AML-M4 enrolled in two consecutive GIMEMA studies to assess the influence of eosinophilia and of the inv(16) cytogenetic abnormality on the prognosis of acute myelomonocytic leukemia (M4) and acute myelomonocytic leukemia with abnormal

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11

Kuwatsuka, Yachiyo, Koichi Miyamura, Ritsuro Suzuki, et al. "Hematopoietic stem cell transplantation for core binding factor acute myeloid leukemia: t(8;21) and inv(16) represent different clinical outcomes." Blood 113, no. 9 (2009): 2096–103. http://dx.doi.org/10.1182/blood-2008-03-145862.

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We analyzed 338 adult patients with acute myeloid leukemia (AML) with t(8;21) and inv(16) undergoing stem cell transplantation (SCT) who were registered in the Japan Society for Hematopoietic Cell Transplantation database. At 3 years, overall survival (OS) of patients with t(8;21) and inv(16) was 50% and 72%, respectively (P = .002). Although no difference was observed when restricted to allogeneic SCT in first complete remission (CR; 84% and 74%), OS of patients with t(8;21) and inv(16) undergoing allogeneic SCT in second or third CR (45% and 86% at 3 years; P = .008) was different. OS was no

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12

Marcucci, Guido, K. Mrózek, A. S. Ruppert, et al. "t(8;21) Acute Myeloid Leukemia (AML) Differs from inv(16) AML in Pretreatment Characteristics, Outcome and Prognostic Factors Predicting Outcome: A Cancer and Leukemia Group B (CALGB) Study." Blood 104, no. 11 (2004): 2017. http://dx.doi.org/10.1182/blood.v104.11.2017.2017.

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Abstract Since t(8;21) and inv(16) disrupt core binding factor in AML and confer a favorable prognosis, these cytogenetic groups are often treated similarly, but hitherto have not been compared in a large study. We compared 144 adult AML patients (pts) with t(8;21) with 168 with inv(16) enrolled on the cytogenetic study CALGB 8461. t(8;21) pts were less frequently white (P=.01), had lower hemoglobin levels (P=.03), WBC (P<.001) and % blood (P<.001) and BM blasts (P=.005), and had more frequently secondary chromosome aberrations (P<.001) than inv(16) pts, who more often had extramedull

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13

Simonis, Alexander, Norman F. Russkamp, Jan Mueller, et al. "Disruption of CSF-1R signaling inhibits growth of AML with inv(16)." Blood Advances 5, no. 5 (2021): 1273–77. http://dx.doi.org/10.1182/bloodadvances.2020003125.

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Key Points Human inv(16) AML cells express CSF-1R and are exposed to CSF-1 in vivo. Inhibition of CSF-1R signaling reduces viability of inv(16) AML cells in vitro and in therapeutic settings in humanized mice in vivo.

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14

Paschka, P., G. Marcucci, A. S. Ruppert, et al. "Mutations of KIT tyrosine kinase (TK) gene predict relapse in adult patients (pts) with core binding factor acute myeloid leukemia (CBF AML): A Cancer and Leukemia Group B (CALGB) study." Journal of Clinical Oncology 24, no. 18_suppl (2006): 2. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.2.

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2 Background: Multi-course high-dose cytarabine (HDAC) has largely improved the outcome of CBF AML pts with t(8;21)(q22;q22) and inv(16)(p13q22). Yet, ∼50% of pts relapse within 5 years (yrs), indicating the need for markers identifying high-risk pts who require more aggressive and/or novel therapies. KIT mutations (mKIT) of exons 17 (mKIT17) and 8 (mKIT8) are good candidates to be such markers. Previous studies showed that mKIT17 impacted adversely on outcome of t(8;21), but not inv(16), pts. Methods: Sixty-one pts with inv(16) and 49 with t(8;21), assigned to HDAC consolidation on CALGB prot

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15

Viswanatha, David S., I. Ming Chen, Pu Paul Liu та ін. "Characterization and Use of an Antibody Detecting the CBFβ-SMMHC Fusion Protein in inv(16)/t(16;16)-Associated Acute Myeloid Leukemias". Blood 91, № 6 (1998): 1882–90. http://dx.doi.org/10.1182/blood.v91.6.1882.

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Abstract The inv(16)(p13q22) and t(16;16)(p13;q22) cytogenetic abnormalities occur commonly in acute myeloid leukemia (AML), typically associated with French-American-British (FAB) AML-M4Eo subtype. Reverse transcriptase-polymerase chain reaction (RT-PCR) techniques have been recently developed to detect the presence of several variants of the resultant CBFB-MYH11 fusion gene that encodes a CBFβ-smooth muscle myosin heavy chain (SMMHC) fusion protein. We have now determined the clinical use of a polyclonal antibody [anti-inv(16) Ab] directed against a junctional epitope of the most common type

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16

Viswanatha, David S., I. Ming Chen, Pu Paul Liu та ін. "Characterization and Use of an Antibody Detecting the CBFβ-SMMHC Fusion Protein in inv(16)/t(16;16)-Associated Acute Myeloid Leukemias". Blood 91, № 6 (1998): 1882–90. http://dx.doi.org/10.1182/blood.v91.6.1882.1882_1882_1890.

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The inv(16)(p13q22) and t(16;16)(p13;q22) cytogenetic abnormalities occur commonly in acute myeloid leukemia (AML), typically associated with French-American-British (FAB) AML-M4Eo subtype. Reverse transcriptase-polymerase chain reaction (RT-PCR) techniques have been recently developed to detect the presence of several variants of the resultant CBFB-MYH11 fusion gene that encodes a CBFβ-smooth muscle myosin heavy chain (SMMHC) fusion protein. We have now determined the clinical use of a polyclonal antibody [anti-inv(16) Ab] directed against a junctional epitope of the most common type of CBFβ-

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17

Zhang, Lianjun, Le Xuan Truong Nguyen, Dijiong Wu, et al. "Anti-MiR-126 Therapy for Inv(16) Acute Myeloid Leukemia." Blood 134, Supplement_1 (2019): 3914. http://dx.doi.org/10.1182/blood-2019-123468.

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Inv(16)(p13q22) or t(16;16)(p13.1;q22) [hereafter inv(16)], a chromosomal rearrangement occurred in 5-12% acute myeloid leukemia (AML) patients, disrupts the core-binding factor (CBF) transcription complex and creates a leukemogenic fusion gene CBFb-MYH11 (CM). Only about 50% inv(16) patients achieve long-term survival with standard chemotherapy. Therefore, more effective therapies are necessary to improve outcomes. MicroRNAs (miRNAs) are small non-coding RNA molecules that inhibit multiple target gene expression. High miR-126 expression is a miRNA hallmark of inv(16) AML. However, the functio

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18

Paschka, P., M. D. Radmacher, G. Marcucci, et al. "Outcome prediction in adult core binding factor (CBF) acute myeloid leukemia (AML) with gene expression profiling: A Cancer and Leukemia Group B (CALGB) study." Journal of Clinical Oncology 25, no. 18_suppl (2007): 7011. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.7011.

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7011 Background: In CBF AML with t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22) [abbreviated inv(16)], KIT mutations (mutKIT) and, in inv(16), trisomy 22 predict outcome and may guide the development of novel risk-adapted therapies. However, prognosis of patients (pts) lacking the aforementioned markers is less clear. Therefore, we profiled gene expression in t(8;21) (n=22) or sole inv(16) (n=25) pts who lacked mutKIT to identify signatures predictive of outcome. All pts were treated on CALGB trials incorporating consolidation therapy with multiple courses of higher dose cytarabine. Met

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19

Quesnel, B., H. Kantarjian, J. P. Bjergaard, et al. "Therapy-related acute myeloid leukemia with t(8;21), inv(16), and t(8;16): a report on 25 cases and review of the literature." Journal of Clinical Oncology 11, no. 12 (1993): 2370–79. http://dx.doi.org/10.1200/jco.1993.11.12.2370.

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PURPOSE To analyze therapy-related acute myeloid leukemias (tAMLs) with t(8;21), inv(16), or t(8;16). PATIENTS AND METHODS Twenty-five patients with tAML and t(8;21)(q22;q22), inv(16)(p13;q22), or t(8;16)(p11;p13) from seven centers, along with 23 previously published cases, were studied. RESULTS Twenty-six, 16, and six patients, respectively, had t(8;21), inv(16), and t(8;16). Prior cancer was a solid tumor in 27 cases, and a hematologic malignancy in all other patients. Five patients had received prior radiotherapy (RT) alone, and 43 had received prior chemotherapy with or without RT. Prior

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20

Rao, Sridhar. "RUNX1 and inv(16) are frenemies in AML." Blood 136, no. 21 (2020): 2361–62. http://dx.doi.org/10.1182/blood.2020008802.

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21

Nakamura, Hideo, Takahiro Maeda, Tomoko Kohno, Naoki Sadamori, and Michito Ichimaru. "Hypoplastic acute leukemia associated with inv(16)(p13q22)." Cancer Genetics and Cytogenetics 51, no. 1 (1991): 63–66. http://dx.doi.org/10.1016/0165-4608(91)90009-j.

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22

Rauch, Philipp J., Jana M. Ellegast, Larisa V. Kovtonyuk, et al. "Inv(16) AML Engrafts Human Cytokine Knock-in Mice." Blood 128, no. 22 (2016): 1078. http://dx.doi.org/10.1182/blood.v128.22.1078.1078.

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Abstract Favorable-risk acute myeloid leukemia (AML) constitutes up to 40% of newly diagnosed AML cases. However, only 66% of younger and 33% of older patients are alive 3 years post diagnosis. Studying the biology of these entities in vivo has been inherently difficult: in fact, faithful xeno-engraftment of human AML in immunodeficient mice has been limited to higher-risk AML. To address this limitation we hypothesized that a human myelopoiesis-supportive environment may permit xeno-engraftment of favorable-risk AML: we transplanted primary human AML with isolated NPM1 mutation and AML with i

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23

Larmonie, Nicole S. D., Marry M. van den Heuvel-Eibrink, Askar Obulkasim, et al. "DNA Methylation Profiling of Pediatric AML Reveals That Hypomethylation of MN1 Is Characteristic of Inv(16) AML and a Driver of MN1 Overexpression." Blood 124, no. 21 (2014): 867. http://dx.doi.org/10.1182/blood.v124.21.867.867.

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Abstract Primary refractory and relapsed pediatric acute myeloid leukemia (AML) still lead to a significant number of childhood cancer deaths, despite the current chemotherapeutic regimens. AML leukemogenesis is driven by collaborative genetic abnormalities that induce hematopoietic maturation arrest and cell proliferation. Particular AML-associated maturation inhibiting aberrations are known to target chromatin regulators, thus directly influencing the transcriptional program of leukemic cells. Therapies targeting epigenetic processes, e.g. with hypomethylation-inducing agents, are therefore

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24

Bullinger, Lars, Claudia Scholl, Eric Bair, et al. "Identification of Distinct inv(16) Subclasses in Adult Acute Myeloid Leukemia Based on Gene Expression Profiling." Blood 104, no. 11 (2004): 2037. http://dx.doi.org/10.1182/blood.v104.11.2037.2037.

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Abstract Recurrent cytogenetic aberrations have been shown to constitute markers of diagnostic and prognostic value in acute myeloid leukemia (AML). However, even within the well-defined cytogenetic AML subgroup with an inv(16) we see substantial biological and clinical heterogeneity which is not fully reflected by the current classification system. To better characterize this cytogenetic group on the molecular level we profiled gene expression in a series of adult AML patients (n=26) with inv(16) using 42k cDNA microarrays. By unsupervised hierarchical clustering we observed that samples with

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25

Durst, Kristie L., Bart Lutterbach, Tanawan Kummalue, Alan D. Friedman, and Scott W. Hiebert. "The inv(16) Fusion Protein Associates with Corepressors via a Smooth Muscle Myosin Heavy-Chain Domain." Molecular and Cellular Biology 23, no. 2 (2003): 607–19. http://dx.doi.org/10.1128/mcb.23.2.607-619.2003.

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ABSTRACT Inversion(16) is one of the most frequent chromosomal translocations found in acute myeloid leukemia (AML), occurring in over 8% of AML cases. This translocation results in a protein product that fuses the first 165 amino acids of core binding factor β to the coiled-coil region of a smooth muscle myosin heavy chain (CBFβ/SMMHC). CBFβ interacts with AML1 to form a heterodimer that binds DNA; this interaction increases the affinity of AML1 for DNA. The CBFβ/SMMHC fusion protein cooperates with AML1 to repress the transcription of AML1-regulated genes. We show that CBFβ/SMMHC contains a

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26

Qi, Jing, Sandeep Singh, Qi Cai, et al. "Selective Targeting Of Inv(16)+ AML Stem Progenitor Cells By Inhibiting HDAC8." Blood 122, no. 21 (2013): 224. http://dx.doi.org/10.1182/blood.v122.21.224.224.

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Abstract Chromosomal inversion inv(16)(p13.1q22) which leads to the fusion of the transcription factor gene CBFb and the MYH11 gene, occurs in over 8% of acute myeloid leukemia (AML) cases. The fusion product CBFβ-SMMHC (CM) inhibits differentiation of hematopoietic stem and progenitor cells (HSPCs) and creates pre-leukemic populations predisposed to acute myeloid leukemia (AML) transformation. The mutations of tumor suppressor p53 occur in approximately half of all cases of human cancer, but TP53 mutations are relatively rare in inv(16) AML. We have previously shown that CM expression leads t

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27

Fasan, Annette, Claudia Haferlach, Karolína Perglerová, et al. "Landscape of Secondary Genetic Lesions in Acute Myeloid Leukemia with Inv(16)/CBFB-MYH11." Blood 126, no. 23 (2015): 801. http://dx.doi.org/10.1182/blood.v126.23.801.801.

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Abstract Introduction: Acute myeloid leukemia (AML) with inv(16)(p13q22) or t(16;16)(p13;q22) accounts for 5-7% of adult AML and overall is associated with a favorable outcome. However, secondary genetic lesions have been shown to negatively impact on outcome. Aims: To assess the frequency and clinical impact of additional mutations and chromosomal aberrations in AML with inv(16)/CBFB-MYH11. Patients: We analyzed 138 patients (pts) who were referred to our laboratory for diagnosis of de novo AML between 2005 and 2014 (54 females; 84 males; median age 54 years, range: 20-88 years). All patients

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28

Hajkova, Hana, Markus H. Y. Fritz, Jiri Schwarz та ін. "CBFβ/MYH11 Hypomethylation Signature In Patients With Acute Myeloid Leukaemia". Blood 122, № 21 (2013): 3774. http://dx.doi.org/10.1182/blood.v122.21.3774.3774.

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Abstract It has been shown that changes in DNA methylation pattern in patients with acute myeloid leukaemia (AML) may both reflect specific molecular abnormalities or characterize a group of patients without a known molecular aberration. Studying genes that are epigenetically deregulated in different groups of patients may contribute to a more detailed understanding of pathways involved in leukemic transformation. For 15 samples (14 AMLs of diverse clinical and genetic background and pool of CD34+ control samples) SureSelectXT Human Methyl-Seq system (Agilent) was used to interrogate DNA methy

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29

Schlenk, R. F., A. Benner, J. Krauter, et al. "Individual Patient Data–Based Meta-Analysis of Patients Aged 16 to 60 Years With Core Binding Factor Acute Myeloid Leukemia: A Survey of the German Acute Myeloid Leukemia Intergroup." Journal of Clinical Oncology 22, no. 18 (2004): 3741–50. http://dx.doi.org/10.1200/jco.2004.03.012.

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PurposeTo evaluate prognostic factors for relapse-free survival (RFS) and overall survival (OS) and to assess the impact of different postremission therapies in adult patients with core binding factor (CBF) acute myeloid leukemias (AML).Patients and MethodsIndividual patient data–based meta-analysis was performed on 392 adults (median age, 42 years; range, 16 to 60 years) with CBF AML (t(8;21), n = 191; inv(16), n = 201) treated between 1993 and 2002 in prospective German AML treatment trials.ResultsRFS was 60% and 58% and OS was 65% and 74% in the t(8;21) and inv(16) groups after 3 years, res

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30

Dissing, M., M. M. Le Beau, and J. Pedersen-Bjergaard. "Inversion of chromosome 16 and uncommon rearrangements of the CBFB and MYH11 genes in therapy-related acute myeloid leukemia: rare events related to DNA-topoisomerase II inhibitors?" Journal of Clinical Oncology 16, no. 5 (1998): 1890–96. http://dx.doi.org/10.1200/jco.1998.16.5.1890.

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PURPOSE To evaluate the frequency of inversion of chromosome 16 (inv[16]) and the type of rearrangement of the CBFB and MYH11 genes in therapy-related acute myeloid leukemia (t-AML) and to evaluate a possible relationship to specific types of previous chemotherapy. PATIENTS AND METHODS Cytogenetic studies were performed in 180 consecutive patients with therapy-related myelodysplasia (t-MDS) or t-AML in Copenhagen and in 270 consecutive patients in Chicago. Leukemic cells were available for studies of the molecular biology in 72 patients, including four with inv(16). RESULTS An inv(16)(p13q22)

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31

Haferlach, T., M. Winkemann, H. Loffler, et al. "The abnormal eosinophils are part of the leukemic cell population in acute myelomonocytic leukemia with abnormal eosinophils (AML M4Eo) and carry the pericentric inversion 16: a combination of May-Grunwald- Giemsa staining and fluorescence in situ hybridization." Blood 87, no. 6 (1996): 2459–63. http://dx.doi.org/10.1182/blood.v87.6.2459.bloodjournal8762459.

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The French-American-British subtype acute myelomonocytic leukemia with abnormal eosinophils (FAB AML M4Eo) with pericentric inversion of chromosome 16 is cytomorphologically defined by a myelomonoblastic blast population and abnormal eosinophils. Until now, it remained an open question whether these abnormal eosinophils are part of the malignant clone or an epiphenomenon. We analyzed five cases of AML M4Eo with inv(16) and combined May-Grunwald-Giemsa staining with fluorescence in situ hybridization using yeast artificial chromosome clone 854E2, which spans the inv(16) breakpoint on 16p. In th

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32

Han, Se young, Krzysztof Mrózek, Jenna Voutsinas, et al. "Secondary cytogenetic abnormalities in core-binding factor AML harboring inv(16) vs t(8;21)." Blood Advances 5, no. 10 (2021): 2481–89. http://dx.doi.org/10.1182/bloodadvances.2020003605.

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Abstract Patients with core-binding factor (CBF) acute myeloid leukemia (AML), caused by either t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), have higher complete remission rates and longer survival than patients with other subtypes of AML. However, ∼40% of patients relapse, and the literature suggests that patients with inv(16) fare differently from those with t(8;21). We retrospectively analyzed 537 patients with CBF-AML, focusing on additional cytogenetic aberrations to examine their impact on clinical outcomes. Trisomies of chromosomes 8, 21, or 22 were significantly more common i

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33

Marlton, P., DF Claxton, P. Liu, et al. "Molecular characterization of 16p deletions associated with inversion 16 defines the critical fusion for leukemogenesis." Blood 85, no. 3 (1995): 772–79. http://dx.doi.org/10.1182/blood.v85.3.772.bloodjournal853772.

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The inversion of chromosome 16 [inv(16)] in acute myeloid leukemia (AML) is associated with a p-arm deletion in a subset of patients. The inversion results in two fusion genes: 5′-CBFB/MYH11–3′ on 16p and 5′- MYH11/CBFB-3′ on 16q. We have studied cells from 42 patients with inv(16) (38 patients) or t(16;16) (four patients) to define the frequency and characteristics of the deletion further. Using fluorescence in situ hybridization (FISH) with probes from cosmids, cosmid contigs, and yeast artificial chromosomes (YACs), we found that six patients with inv(16) had a deletion of between 150 and 3

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34

Sangle, Nikhil A., and Sherrie L. Perkins. "Core-Binding Factor Acute Myeloid Leukemia." Archives of Pathology & Laboratory Medicine 135, no. 11 (2011): 1504–9. http://dx.doi.org/10.5858/arpa.2010-0482-rs.

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Core-binding factor acute myeloid leukemia (AML) is cytogenetically defined by the presence of t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), commonly abbreviated as t(8;21) and inv(16), respectively. In both subtypes, the cytogenetic rearrangements disrupt genes that encode subunits of core-binding factor, a transcription factor that functions as an essential regulator of normal hematopoiesis. The rearrangements t(8;21) and inv(16) involve the RUNX1/RUNX1T1 (AML1-ETO) and CBFB/MYH11 genes, respectively. These 2 subtypes are categorized as AML with recurrent genetic abnormalities, and

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35

Kundu, Mondira, and Pu Paul Liu. "Function of the inv(16) fusion gene CBFB-MYH11." Current Opinion in Hematology 8, no. 4 (2001): 201–5. http://dx.doi.org/10.1097/00062752-200107000-00004.

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36

Dwyre, Denis M., and Mohamed Osman. "AML with inv(16) with numerous Charcot-Leyden crystals." Blood 134, no. 21 (2019): 1876. http://dx.doi.org/10.1182/blood.2019002684.

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Adya, N., Y. Chen, E. Hilgenfeld, et al. "Characterizing gene expression profile of Inv(16)-associated leukemia." Nature Genetics 27, S4 (2001): 37. http://dx.doi.org/10.1038/86966.

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Pulikkan, John Anto, Mahesh Hegde, Houda Belaghzal та ін. "CBFβ-SMMHC Inhibition Disrupts Enhancer Chromatin Dynamics and Represses MYC Transcriptional Program in Inv(16) Leukemia". Blood 130, Suppl_1 (2017): 784. http://dx.doi.org/10.1182/blood.v130.suppl_1.784.784.

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Abstract Chromatin complexes regulate gene expression in normal and malignant hematopoiesis. The significance of transcription factor deregulation on the control of epigenetic dynamics in leukemia is poorly understood. The leukemia fusion CBFβ-SMMHC is expressed in inv(16) acute myeloid leukemia (AML), and deregulates the activity of the transcription factor RUNX1. This fusion protein blocks myeloid differentiation, expands pre-leukemic myeloid progenitor cells, and drives AML development. The CBFβ-SMMHC inhibitor, AI-10-49, specifically disrupts its binding to RUNX1 resulting in an acute RUNX

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Kim, Hyung-Gyoon, Kyoko Kojima, C. Scott Swindle, et al. "FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia." Blood 111, no. 3 (2008): 1567–74. http://dx.doi.org/10.1182/blood-2006-06-030312.

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Abstract The inversion of chromosome 16 in the inv(16)(p13q22) is one of the most frequent cytogenetic abnormalities observed in acute myeloid leukemia (AML). The inv(16) fuses the core binding factor (CBF) beta subunit with the coiled-coil rod domain of smooth muscle myosin heavy chain (SMMHC). Expression of CBFβ-SMMHC in mice does not promote AML in the absence of secondary mutations. Patient samples with the inv(16) also possess mutually exclusive activating mutations in either N-RAS, K-RAS, or the receptor tyrosine kinases, c-KIT and FLT3, in almost 70% of cases. To test whether an activat

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Bullinger, Lars, Stephan Kurz, Konstanze Dohner, et al. "Gene Expression Profiling Identifies Distinct Subclasses in Core Binding Factor Acute Myeloid Leukemia." Blood 106, no. 11 (2005): 673. http://dx.doi.org/10.1182/blood.v106.11.673.673.

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Abstract Recurrent cytogenetic aberrations have been shown to constitute markers of diagnostic and prognostic value in acute myeloid leukemia (AML). However, even within well-defined cytogenetic AML subgroups with an inv(16) or a t(8;21) we see substantial biological and clinical heterogeneity which is not fully reflected by the current classification system. Therefore, we profiled gene expression in a large series of adult AML patients with core binding factor (CBF) leukemia [inv(16) n=55, t(8;21) n=38] using a whole genome DNA microarray platform in order to better characterize this disease

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41

Mrózek, Krzysztof, Thomas W. Prior, Colin Edwards, et al. "Comparison of Cytogenetic and Molecular Genetic Detection of t(8;21) and inv(16) in a Prospective Series of Adults With De Novo Acute Myeloid Leukemia: A Cancer and Leukemia Group B Study." Journal of Clinical Oncology 19, no. 9 (2001): 2482–92. http://dx.doi.org/10.1200/jco.2001.19.9.2482.

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PURPOSE: To prospectively compare cytogenetics and reverse transcriptase–polymerase chain reaction (RT-PCR) for detection of t(8;21)(q22;q22) and inv(16)(p13q22)/t(16;16)(p13;q22), aberrations characteristic of core-binding factor (CBF) acute myeloid leukemia (AML), in 284 adults newly diagnosed with primary AML. PATIENTS AND METHODS: Cytogenetic analyses were performed at local laboratories, with results reviewed centrally. RT-PCR for AML1/ETO and CBFβ/MYH11 was performed centrally. RESULTS: CBF AML was ultimately identified in 48 patients: 21 had t(8;21) or its variant and AML1/ETO, and 27 h

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Claxton, DF, P. Liu, HB Hsu, et al. "Detection of fusion transcripts generated by the inversion 16 chromosome in acute myelogenous leukemia." Blood 83, no. 7 (1994): 1750–56. http://dx.doi.org/10.1182/blood.v83.7.1750.1750.

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Abstract Pericentric inversion of chromosome 16 [inv(16)(p13q22)] and the related t(16;16)(p13;q22) are seen in a subset of acute myelogenous leukemia (AML) phenotypically and prognostically differing from other cases. We have recently shown that inv(16) results in fusion of CBFB/PEBP2B, a gene encoded at 16q22 to MYH11, a smooth muscle myosin heavy chain gene encoded at 16p13. Chimeric transcripts consisting of upstream CBFB fused to downstream MYH11 coding sequences result from this fusion. In this study we have examined a series of 37 of these cases using reverse transcriptase-polymerase ch

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Claxton, DF, P. Liu, HB Hsu, et al. "Detection of fusion transcripts generated by the inversion 16 chromosome in acute myelogenous leukemia." Blood 83, no. 7 (1994): 1750–56. http://dx.doi.org/10.1182/blood.v83.7.1750.bloodjournal8371750.

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Pericentric inversion of chromosome 16 [inv(16)(p13q22)] and the related t(16;16)(p13;q22) are seen in a subset of acute myelogenous leukemia (AML) phenotypically and prognostically differing from other cases. We have recently shown that inv(16) results in fusion of CBFB/PEBP2B, a gene encoded at 16q22 to MYH11, a smooth muscle myosin heavy chain gene encoded at 16p13. Chimeric transcripts consisting of upstream CBFB fused to downstream MYH11 coding sequences result from this fusion. In this study we have examined a series of 37 of these cases using reverse transcriptase-polymerase chain react

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van der Reijden, BA, JG Dauwerse, JW Wessels, et al. "A gene for a myosin peptide is disrupted by the inv(16)(p13q22) in acute nonlymphocytic leukemia M4Eo." Blood 82, no. 10 (1993): 2948–52. http://dx.doi.org/10.1182/blood.v82.10.2948.bloodjournal82102948.

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Chromosome 16 aberrations are well known in acute nonlymphocytic leukemia (ANLL). The most frequent chromosome 16 aberration in ANLL subtype M4Eo is the inv(16)(p13q22). Recently, we showed that in 5 inv(16) patients with ANLL M4Eo the short arm breakpoints are clustered within a 14-kb genomic EcoRI fragment. We report here the identification of a gene situated in the 14-kb fragment. The gene, which codes for a myosin peptide, is disrupted by the inversion of chromosome 16 in the 5 patients. To the best of our knowledge, this is the first report of a myosin gene disrupted in leukemia.

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Ellegast, Jana M., Philipp J. Rauch, Larisa V. Kovtonyuk, et al. "inv(16) and NPM1mut AMLs engraft human cytokine knock-in mice." Blood 128, no. 17 (2016): 2130–34. http://dx.doi.org/10.1182/blood-2015-12-689356.

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van der Reijden, BA, JG Dauwerse, JW Wessels, et al. "A gene for a myosin peptide is disrupted by the inv(16)(p13q22) in acute nonlymphocytic leukemia M4Eo." Blood 82, no. 10 (1993): 2948–52. http://dx.doi.org/10.1182/blood.v82.10.2948.2948.

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Abstract Chromosome 16 aberrations are well known in acute nonlymphocytic leukemia (ANLL). The most frequent chromosome 16 aberration in ANLL subtype M4Eo is the inv(16)(p13q22). Recently, we showed that in 5 inv(16) patients with ANLL M4Eo the short arm breakpoints are clustered within a 14-kb genomic EcoRI fragment. We report here the identification of a gene situated in the 14-kb fragment. The gene, which codes for a myosin peptide, is disrupted by the inversion of chromosome 16 in the 5 patients. To the best of our knowledge, this is the first report of a myosin gene disrupted in leukemia.

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Markus, Jan, Matthew T. Garin, Naomi Galili, et al. "Methylation-Independent Silencing of the Tumor Suppressor p15INK4B by CBFb-SMMHC in Acute Myeloid Leukemias with inv(16)." Blood 106, no. 11 (2005): 1615. http://dx.doi.org/10.1182/blood.v106.11.1615.1615.

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Abstract The tumor suppressor INK4B(p15) gene is silenced by CpG island hypermethylation in a majority of acute myeloid leukemias (AML). This silencing can be reversed by the treatment with hypomethylating agents, and these agents are currently being tested for therapeutic intervention. So far, it was not investigated whether or not the INK4B is hypermethylated in all cytogenetic subtypes of AML. Our experiments, which compare levels of INK4B methylation in AML with inv(16), t(8:21) and t(15;17) reveal a strikingly low level of methylation in all leukemias with inv(16). This contrasts with sig

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Paschka, Peter, Guido Marcucci, Amy S. Ruppert, et al. "Adverse Prognostic Significance of KIT Mutations in Adult Acute Myeloid Leukemia With inv(16) and t(8;21): A Cancer and Leukemia Group B Study." Journal of Clinical Oncology 24, no. 24 (2006): 3904–11. http://dx.doi.org/10.1200/jco.2006.06.9500.

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Purpose To analyze the prognostic impact of mutated KIT (mutKIT) in core-binding factor acute myeloid leukemia (AML) with inv(16)(p13q22) and t(8;21)(q22;q22). Patients and Methods Sixty-one adults with inv(16) and 49 adults with t(8;21), assigned to postremission therapy with repetitive cycles of higher dose cytarabine were analyzed for mutKIT in exon 17 (mutKIT17) and 8 (mutKIT8) by denaturing high-performance liquid chromatography and direct sequencing at diagnosis. The median follow-up was 5.3 years. Results Among patients with inv(16), 29.5% had mutKIT (16% with mutKIT17 and 13% with sole

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Marcucci, Guido, Krzysztof Mrózek, Amy S. Ruppert, et al. "Prognostic Factors and Outcome of Core Binding Factor Acute Myeloid Leukemia Patients With t(8;21) Differ From Those of Patients With inv(16): A Cancer and Leukemia Group B Study." Journal of Clinical Oncology 23, no. 24 (2005): 5705–17. http://dx.doi.org/10.1200/jco.2005.15.610.

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Purpose Because both t(8;21) and inv(16) disrupt core binding factor (CBF) in acute myeloid leukemia (AML) and confer relatively favorable prognoses, these cytogenetic groups are often treated similarly. Recent studies, however, have shown different gene profiling for the two groups, underscoring potential biologic differences. Therefore, we sought to determine whether these two cytogenetic groups should also be considered separate entities from a clinical standpoint. Patients and Methods We analyzed 144 consecutive adults with t(8;21) and 168 with inv(16) treated on Cancer and Leukemia Group

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Prébet, Thomas, Nicolas Boissel, Sarah Reutenauer, et al. "Acute Myeloid Leukemia With Translocation (8;21) or Inversion (16) in Elderly Patients Treated With Conventional Chemotherapy: A Collaborative Study of the French CBF-AML Intergroup." Journal of Clinical Oncology 27, no. 28 (2009): 4747–53. http://dx.doi.org/10.1200/jco.2008.21.0674.

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Purpose Acute myeloid leukemia (AML) with translocation (t) (8;21) or inversion (inv) (16) is associated with a favorable prognosis when treated with intensive chemotherapy. In elderly patients, these AML types are rare, and intensive treatments are much less tolerated. We conducted a retrospective study to evaluate the characteristics and outcome of AML with t(8;21) or inv(16) in the elderly. Patients and Methods Patients with t(8;21) or inv(16) AML who were age 60 years or older and who received at least one course of induction chemotherapy were included. Postremission therapy consisted of l

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