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Journal articles on the topic 'Ph+ Acute Lymphoblastic Leukemia'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Maslak, P. "Ph+ Acute Lymphoblastic Leukemia." ASH Image Bank 2003, no. 1105 (2003): 100869. http://dx.doi.org/10.1182/ashimagebank-2003-100869.

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2

AKAY, Olga Meltem, and Betül Zeynep ERSOY. "Ph-like Acute Lymphoblastic Leukemia." LLM Dergi 2, no. 3 (2018): 53–59. http://dx.doi.org/10.5578/llm.67277.

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3

Tran, Thai Hoa, and Mignon L. Loh. "Ph-like acute lymphoblastic leukemia." Hematology 2016, no. 1 (2016): 561–66. http://dx.doi.org/10.1182/asheducation-2016.1.561.

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Abstract Philadelphia chromosome–like acute lymphoblastic leukemia (Ph-like ALL) is a newly identified high-risk (HR) B-lineage ALL subtype, accounting for ∼15% of children with National Cancer Institute–defined HR B-ALL. It occurs more frequently in adolescents and adults, having been reported in as much as 27% of young adults with ALL between 21 and 39 years of age. It exhibits adverse clinical features, confers a poor prognosis, and harbors a diverse range of genetic alterations that activate cytokine receptor genes and kinase signaling pathways, making it amenable to treatment with tyrosin

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4

Conserva, Maria Rosa, Immacolata Redavid, Luisa Anelli, et al. "IKAROS in Acute Leukemia: A Positive Influencer or a Mean Hater?" International Journal of Molecular Sciences 24, no. 4 (2023): 3282. http://dx.doi.org/10.3390/ijms24043282.

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One key process that controls leukemogenesis is the regulation of oncogenic gene expression by transcription factors acting as tumor suppressors. Understanding this intricate mechanism is crucial to elucidating leukemia pathophysiology and discovering new targeted treatments. In this review, we make a brief overview of the physiological role of IKAROS and the molecular pathway that contributes to acute leukemia pathogenesis through IKZF1 gene lesions. IKAROS is a zinc finger transcription factor of the Krüppel family that acts as the main character during hematopoiesis and leukemogenesis. It c

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5

Tasian, Sarah K., Mignon L. Loh, and Stephen P. Hunger. "Philadelphia chromosome–like acute lymphoblastic leukemia." Blood 130, no. 19 (2017): 2064–72. http://dx.doi.org/10.1182/blood-2017-06-743252.

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AbstractPhiladelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL), also referred to as BCR-ABL1–like ALL, is a high-risk subset with a gene expression profile that shares significant overlap with that of Ph-positive (Ph+) ALL and is suggestive of activated kinase signaling. Although Ph+ ALL is defined by BCR-ABL1 fusion, Ph-like ALL cases contain a variety of genomic alterations that activate kinase and cytokine receptor signaling. These alterations can be grouped into major subclasses that include ABL-class fusions involving ABL1, ABL2, CSF1R, and PDGFRB that phenocopy BCR-ABL1 and

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6

Kohla, Samah, Sarah EL Kourashy, Zafar Nawaz, Reda Youssef, Ahmad Al-Sabbagh, and Feryal A. Ibrahim. "P190^BCR-ABL1 in a Patient with Philadelphia Chromosome Positive T-Cell Acute Lymphoblastic Leukemia: A Rare Case Report and Review of Literature." Case Reports in Oncology 14, no. 2 (2021): 1040–50. http://dx.doi.org/10.1159/000516270.

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T-acute lymphoblastic leukemia/lymphoblastic lymphoma (T-ALL/LBL) is rare and aggressive leukemia. Philadelphia chromosome positive (Ph+) is the most common cytogenetic abnormality in chronic myeloid leukemia (CML) and B-acute lymphoblastic leukemia (B-ALL). Ph+ T-ALL is exceeding rare and has a therapeutic and prognostic significance. The incidence and outcome of Ph+ T-ALL are unknown. Differentiation between Ph+ T-ALL/LBL and T-cell lymphoblastic crises of CML may be difficult. We report a rare case of adult de novo T-ALL with significant monocytosis, having Ph+ with (P190 <i>BCR-ABL1&

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7

Tran, Thai Hoa, and Sarah K. Tasian. "Clinical screening for Ph-like ALL and the developing role of TKIs." Hematology 2022, no. 1 (2022): 594–602. http://dx.doi.org/10.1182/hematology.2022000357.

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Abstract Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) is a common subtype of B-lineage acute lymphoblastic leukemia (B-ALL) with increasing frequency across the age spectrum. Characterized by a kinase-activated gene expression profile and driven by a variety of genetic alterations involving cytokine receptors and kinases, Ph-like ALL is associated with high rates of residual disease and relapse in patients treated with conventional chemotherapy. In this case-based review, we describe the biology of the 2 major ABL-class and JAK pathway genetic subtypes of Ph-like ALL

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8

De Vita, Serena, Silvia De Matteis, Luca Laurenti, et al. "Secondary Ph+ acute lymphoblastic leukemia after temozolomide." Annals of Hematology 84, no. 11 (2005): 760–62. http://dx.doi.org/10.1007/s00277-005-1093-6.

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9

Foà, Robin. "HOW I TREAT PH+ ACUTE LYMPHOBLASTIC LEUKEMIA." Hematology, Transfusion and Cell Therapy 47 (July 2025): 103869. https://doi.org/10.1016/j.htct.2025.103869.

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10

Vakana, Eliza, Jessica K. Altman, Heather Glaser, Nicholas J. Donato, and Leonidas C. Platanias. "Antileukemic effects of AMPK activators on BCR-ABL–expressing cells." Blood 118, no. 24 (2011): 6399–402. http://dx.doi.org/10.1182/blood-2011-01-332783.

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Abstract The mammalian target of rapamycin (mTOR) signaling pathway plays a critical role in growth and survival of BCR-ABL transformed cells. AMPK kinase is a metabolic sensor that exhibits suppressive effects on the mTOR pathway and negatively regulates mTOR activity. We report that AMPK activators, such as metformin and 5-aminoimidazole-4-carboxamide ribonucleotide, suppress activation of the mTOR pathway in BCR-ABL–expressing cells. Treatment with these inhibitors results in potent suppression of chronic myeloid leukemia leukemic precursors and Ph+ acute lymphoblastic leukemia cells, inclu

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11

Inaba, Hiroto, and Charles G. Mullighan. "Pediatric acute lymphoblastic leukemia." Haematologica 105, no. 11 (2020): 2524–39. http://dx.doi.org/10.3324/haematol.2020.247031.

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The last decade has witnessed great advances in our understanding of the genetic and biological basis of childhood acute lymphoblastic leukemia (ALL), the development of experimental models to probe mechanisms and evaluate new therapies, and the development of more efficacious treatment stratification. Genomic analyses have revolutionized our understanding of the molecular taxonomy of ALL, and these advances have led the push to implement genome and transcriptome characterization in the clinical management of ALL to facilitate more accurate risk-stratification and, in some cases, targeted ther

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12

Pui, Ching-Hon. "Precision medicine in acute lymphoblastic leukemia." Frontiers of Medicine 14, no. 6 (2020): 689–700. http://dx.doi.org/10.1007/s11684-020-0759-8.

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AbstractThe cure rate of childhood acute lymphoblastic leukemia (ALL) has exceeded 90% in some contemporary clinical trials. However, the dose intensity of conventional chemotherapy has been pushed to its limit. Further improvement in outcome will need to rely more heavily on molecular therapeutic as well as immuno-and cellular-therapy approaches together with precise risk stratification. Children with ETV6-RUNX1 or hyperdiploid > 50 ALL who achieve negative minimal residual disease during early remission induction are suitable candidates for reduction in treatment. Patients with Philadelph

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13

Nishida, Hiroko, Natsuko Yoshimizu, Hironori Ueno, et al. "Ph-positive acute lymphoblastic leukemia after long-term remission of Ph-positive acute myeloid leukemia." Leukemia Research 31, no. 3 (2007): 417–18. http://dx.doi.org/10.1016/j.leukres.2006.03.025.

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14

Heisterkamp, N., R. Jenkins, S. Thibodeau, JR Testa, K. Weinberg, and J. Groffen. "The bcr gene in Philadelphia chromosome positive acute lymphoblastic leukemia." Blood 73, no. 5 (1989): 1307–11. http://dx.doi.org/10.1182/blood.v73.5.1307.1307.

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Abstract In chronic myelogenous leukemia (CML) and in a percentage of childhood and adult acute lymphoblastic leukemia (ALL) the Philadelphia (Ph′) chromosome is present in the leukemic cells of patients. This chromosome is the result of a reciprocal translocation between chromosomes 9 and 22. In CML the break on chromosome 22 occurs within the major breakpoint cluster region (Mbcr) of the bcr gene. In this study, we report on the examination of DNAs from nine Ph′-chromosome positive ALL patients for rearrangements within the bcr gene using Southern blot analysis. Of nine patients having a kar

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15

Heisterkamp, N., R. Jenkins, S. Thibodeau, JR Testa, K. Weinberg, and J. Groffen. "The bcr gene in Philadelphia chromosome positive acute lymphoblastic leukemia." Blood 73, no. 5 (1989): 1307–11. http://dx.doi.org/10.1182/blood.v73.5.1307.bloodjournal7351307.

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In chronic myelogenous leukemia (CML) and in a percentage of childhood and adult acute lymphoblastic leukemia (ALL) the Philadelphia (Ph′) chromosome is present in the leukemic cells of patients. This chromosome is the result of a reciprocal translocation between chromosomes 9 and 22. In CML the break on chromosome 22 occurs within the major breakpoint cluster region (Mbcr) of the bcr gene. In this study, we report on the examination of DNAs from nine Ph′-chromosome positive ALL patients for rearrangements within the bcr gene using Southern blot analysis. Of nine patients having a karyotypical

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16

Robinson, Adam C., Bernard L. Marini, Kristen M. Pettit, and Anthony J. Perissinotti. "Successful use of blinatumomab in a patient with acute lymphoblastic leukemia and severe hepatic dysfunction." Journal of Oncology Pharmacy Practice 26, no. 1 (2019): 200–205. http://dx.doi.org/10.1177/1078155219829534.

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Relapsed/refractory acute lymphoblastic leukemia poses a significant clinical challenge due to its poor prognosis, with survival rates of less than a year, even with novel therapies. Patients frequently experience toxicities from induction chemotherapy such as hepatotoxicity, which can limit therapeutic options upon relapse. Blinatumomab, a novel immunotherapy, has demonstrated excellent efficacy in relapsed/refractory acute lymphoblastic leukemia; however, there are limited data on use of this agent in patients with significant organ dysfunction. In this report, we describe the safe and effec

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17

Yalçın, Cumali, Fahir Özkalemkaş, Vildan Özkocaman, et al. "Philadelphia chromosome-positive acute lymphoblastic leukemia presenting with bilateral serous retinal detachment: A case report and review of the literature." Indian Journal of Ophthalmology - Case Reports 4, no. 1 (2024): 150–54. http://dx.doi.org/10.4103/ijo.ijo_645_23.

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We report a case who presented with bilateral serous retinal detachment (SRD) as the initial sign of Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL). A 49-year-old female presented with blurred vision. A colored fundus image of the patient revealed SRD around the posterior pole’s optic disc. Bone marrow aspiration showed infiltration with lymphoblasts. The patient was diagnosed with Ph+ ALL. SRD regressed in the color fundus image of the patient after induction chemotherapy and intrathecal methotrexate. The patient’s visual symptoms completely regressed. In conclusion,

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18

Herold, Tobias, Claudia D. Baldus, and Nicola Gökbuget. "Ph-like Acute Lymphoblastic Leukemia in Older Adults." New England Journal of Medicine 371, no. 23 (2014): 2235. http://dx.doi.org/10.1056/nejmc1412123.

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19

Chiaretti, Sabina, and Robin Foà. "Management of adult Ph-positive acute lymphoblastic leukemia." Hematology 2015, no. 1 (2015): 406–13. http://dx.doi.org/10.1182/asheducation-2015.1.406.

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Abstract Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL) has been regarded for decades as the ALL subgroup with the worse outcome. It represents the most frequent genetic subtype of adult ALL, and increases progressively with age. The introduction of tyrosine kinase inhibitors (TKIs) has enabled to obtain complete hematologic remissions (CHRs) in virtually all patients, including the elderly, to improve disease-free survival and overall survival, as well as to increase the percentage of patients who can undergo an allogeneic stem cell transplant (allo-SCT). The current management

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20

Wadhawan, Pallavi, Dhwanee Thakkar, D. S. Udayakumar, et al. "Fish-ing for PH-like acute lymphoblastic leukemia." Pediatric Hematology Oncology Journal 8, no. 4 (2023): S34. http://dx.doi.org/10.1016/j.phoj.2023.10.087.

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21

Govedarovic, Nenad. "Treatment of patients with acute lymphoblastic leukemia who are not suitable for high-dose chemotherapy and hematopoietic stem cell transplantation." Medical review 75, Suppl. 1 (2022): 19–23. http://dx.doi.org/10.2298/mpns22s1019g.

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Introduction. Acute lymphoblastic leukemia is a malignant disease characterized by the proliferation of precursor B-cells, Tcells or less often, precursors of NK-cells. B-cell acute lymphoblastic leukemia is more common in patients >60 years of age compared to patients <60 years of age (89% vs. 66%), and cytogenetic abnormalities such as t(9;22) (Ph+) are more common in older than younger patients (36% against 19%). Elderly patients often have a poor status and comorbidities, so poor disease outcome is more common. Clinical and biological features. B cell acute lymphoblastic leukemia is

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22

Zhao, Yanhong, Weihua Zhai, Aiming Pang, et al. "Efficacy and Safety of Olverembatinib-Based Therapies in Patients with Ph/BCR-ABL1-Positive Acute Lymphoblastic Leukemia." Blood 142, Supplement 1 (2023): 5893. http://dx.doi.org/10.1182/blood-2023-184565.

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Background Olverembatinib is an oral, third-generation BCR-ABL1 tyrosine kinase inhibitor (TKI) developed in China that could effectively target wild-type and mutant BCR-ABL1 kinase. It is effective and well-tolerated for patients with chronic myeloid leukemia. However, its efficacy and safety in patients with Ph/BCR-ABL1-Positive acute lymphoblastic leukemia are not entirely clear. This study aims to analyze the efficacy and safety of Olverembatinib-based therapies in patients with Ph/BCR-ABL1-Positive acute lymphoblastic leukemia. Methods Patients with Ph/BCR-ABL1-positive acute lymphoblasti

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23

Pushel, Irina, Byunggil Yoo, Daniel Louiselle, et al. "Single-Cell RNA Sequencing Facilitates Study of Cancer Mechanisms across Pediatric Leukemias." Blood 142, Supplement 1 (2023): 1614. http://dx.doi.org/10.1182/blood-2023-187340.

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Leukemia is the most common pediatric cancer, diagnosed in over 3,000 children annually in the US. While the prognosis for many pediatric leukemias has significantly improved with the addition of DNA sequencing to the diagnosis and treatment selection process, the molecular mechanisms driving some cases remain inscrutable. In this study, we performed single-cell RNA sequencing on a cohort of pediatric leukemia samples (n = 72) to explore intra- and inter-patient heterogeneity across multiple types of malignancies: acute megakaryoblastic leukemia (AMKL, n = 1), acute myeloid leukemia (AML, n =

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24

Chang, Bill H., Abdusebur Jemal, Jeffrey Tyner, Mathew Thayer, Markus Muschen, and Brian J. Druker. "YM155 sensitivity in pediatric acute lymphoblastic leukemia." Journal of Clinical Oncology 30, no. 15_suppl (2012): 9555. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.9555.

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9555 Background: Despite advances in treatment and outcomes in pediatric acute lymphoblastic leukemia, there continue to be subsets of patients that are refractory to standard intensive chemotherapy. Therefore, novel agents are needed to further advance treatment for this disease. YM155 (Astellas) is a selective suppressant of survivin expression. Survivin has been shown to be over-expressed in malignant cells and in relapsed ALL. Early adult phase I/II studies show promise in both tolerability and possible efficacy in B-cell malignancies. Methods: Fresh diagnostic leukemic patient samples, AL

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25

Demirkan, Fatih, Rafiye Ciftciler, Omur Gokmen Sevindik, et al. "Turkish Acute Lymphoblastic Leukemia Registry, Retrospective Phase Data." Blood 134, Supplement_1 (2019): 5073. http://dx.doi.org/10.1182/blood-2019-126006.

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Background and Aim: Significant developments have occurred in clinical management of acute lymphoblastic leukemia (ALL) in adults over recent decades. However, treatment results are still not satisfactory especially in routine practice. The aim of the study was to evaluate the general clinical features, treatment details and outcomes of a large group of patients followed up in multiple centers in Turkey with a diagnosis of ALL. Materials and Methods: A retrospective analysis of the data of patients with ALL was made, which are diagnosed and treated between January 2003 and June 2017 by differe

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26

Porazzi, Patrizia, Marco De Dominici, Joseph Salvino, and Bruno Calabretta. "Targeting the CDK6 Dependence of Ph+ Acute Lymphoblastic Leukemia." Genes 12, no. 9 (2021): 1355. http://dx.doi.org/10.3390/genes12091355.

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Ph+ ALL is a poor-prognosis leukemia subtype driven by the BCR-ABL1 oncogene, either the p190- or the p210-BCR/ABL isoform in a 70:30 ratio. Tyrosine Kinase inhibitors (TKIs) are the drugs of choice in the therapy of Ph+ ALL. In combination with standard chemotherapy, TKIs have markedly improved the outcome of Ph+ ALL, in particular if this treatment is followed by bone marrow transplantation. However, resistance to TKIs develops with high frequency, causing leukemia relapse that results in <5-year overall survival. Thus, new therapies are needed to address relapsed/TKI-resistant Ph+ ALL. W

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27

Harb, Jason G., Brenda I. Chyla, and Claudia S. Huettner. "Loss of Bcl-x in Ph+ B-ALL increases cellular proliferation and does not inhibit leukemogenesis." Blood 111, no. 7 (2008): 3760–69. http://dx.doi.org/10.1182/blood-2007-08-108803.

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Abstract The kinase inhibitors imatinib mesylate and dasatinib are the preferred treatment for Philadelphia chromosome–positive (Ph+) leukemias, and they are highly successful in the chronic phase of chronic myeloid leukemia (CML). However, they are not efficient in Ph+ B-cell acute lymphoblastic leukemia (B-ALL). Ph+ leukemia cells are highly resistant to apoptosis, and evidence from cell lines and primary cells suggest Bcl-xL as a critical mediator of resistance to apoptosis: however, this concept has never been rigorously tested in an animal model. To clarify the role of Bcl-xL in Ph+ B-ALL

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28

Austin, Publishing Group. "Isolated Unilateral Optic Nerve Involvement as the Presenting Feature of Early Relapse in Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia." Annals of Hematology & Oncology 11, no. 4 (2024): 1463. https://doi.org/10.26420/annhematoloncol.2024.1463.

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Central Mervous System involvement (CNS) in Acute Lymphoblastic Leukemia (ALL) can be present at initial diagnosis or at disease relapse and early detection is crucial for prompt intervention. Optic nerve infiltration by leukemic cells is an oncologic emergency that requires urgent therapy to spare vision along with systemic therapy, with limited data about the optimal therapeutic strategy. Isolated optic nerve Involvement at relapse is rare; described in Philadelphia chromosome negative (Ph-) ALL in 2.2% of relapses in children and exceeding rare in Philadelphia chromosome positive (Ph+) case

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29

Shiraz, Parveen, Kimberly J. Payne, and Lori Muffly. "The Current Genomic and Molecular Landscape of Philadelphia-like Acute Lymphoblastic Leukemia." International Journal of Molecular Sciences 21, no. 6 (2020): 2193. http://dx.doi.org/10.3390/ijms21062193.

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Philadelphia (Ph)-like acute lymphoblastic leukemia (ALL) is a high-risk B-cell Acute Lymphoblastic Leukemia (B-ALL) characterized by a gene expression profile similar to Ph-positive B-ALL but lacking the BCR-ABL1 translocation. The molecular pathogenesis of Ph-like B-ALL is heterogenous and involves aberrant genomics, receptor overexpression, kinase fusions, and mutations leading to kinase signaling activation, leukemogenic cellular proliferation, and differentiation blockade. Testing for the Ph-like signature, once only a research technique, is now available to the clinical oncologist. The p

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30

Yoon, Jae-Ho, Hanwool Cho, Seug Yun Yoon, et al. "Genetic Characteristics and Long-Term Outcomes of Korean Adult Patients with Ph-like Acute Lymphoblastic Leukemia Versus Non-Ph-like Acute Lymphoblastic Leukemia." Blood 132, Supplement 1 (2018): 4087. http://dx.doi.org/10.1182/blood-2018-99-118067.

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Abstract Background: Recently, a high-risk subgroup of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) called Philadelphia chromosome (Ph)-like ALL was identified in adolescents and young adults. However, there are conflicting data regarding the incidence and prognosis of Ph-like ALL in adult patients, and no data have yet been introduced in Asian countries. Aim: We tried to identify the prevalence and genetic characteristics of Ph-like ALL in adult patients with newly diagnosed BCP-ALL. Furthermore, we analyzed the clinical characteristics, long-term outcomes, and prognostic impact of

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31

Cho, Young Jin, Bin Zhang, Vesa Kaartinen, et al. "Generation of rac3 Null Mutant Mice: Role of Rac3 in Bcr/Abl-Caused Lymphoblastic Leukemia." Molecular and Cellular Biology 25, no. 13 (2005): 5777–85. http://dx.doi.org/10.1128/mcb.25.13.5777-5785.2005.

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ABSTRACT Numerous studies indirectly implicate Rac GTPases in cancer. To investigate if Rac3 contributes to normal or malignant cell function, we generated rac3 null mutants through gene targeting. These mice were viable, fertile, and lacked an obvious external phenotype. This shows Rac3 function is dispensable for embryonic development. Bcr/Abl is a deregulated tyrosine kinase that causes chronic myelogenous leukemia and Ph-positive acute lymphoblastic leukemia in humans. Vav1, a hematopoiesis-specific exchange factor for Rac, was constitutively tyrosine phosphorylated in primary lymphomas fr

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32

Kurzrock, R., M. Shtalrid, M. Talpaz, WS Kloetzer, and JU Gutterman. "Expression of c-abl in Philadelphia-positive acute myelogenous leukemia." Blood 70, no. 5 (1987): 1584–88. http://dx.doi.org/10.1182/blood.v70.5.1584.1584.

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Abstract The identical cytogenetic marker, t(9;22)(q34;q11) (Philadelphia [Ph] translocation), is found in approximately 90%, 20%, and 2% of adult patients with chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), and acute myelogenous leukemia (AML), respectively. In CML, the molecular events resulting from the Ph translocation include a break within the bcr locus on chromosome 22, transfer of the c-abl protooncogene from chromosome 9 to 22, and formation of an aberrant 210- kD bcr-abl fusion protein (p210bcr-abl). Recently, the absence of bcr rearrangement and expression o

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33

Kurzrock, R., M. Shtalrid, M. Talpaz, WS Kloetzer, and JU Gutterman. "Expression of c-abl in Philadelphia-positive acute myelogenous leukemia." Blood 70, no. 5 (1987): 1584–88. http://dx.doi.org/10.1182/blood.v70.5.1584.bloodjournal7051584.

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The identical cytogenetic marker, t(9;22)(q34;q11) (Philadelphia [Ph] translocation), is found in approximately 90%, 20%, and 2% of adult patients with chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), and acute myelogenous leukemia (AML), respectively. In CML, the molecular events resulting from the Ph translocation include a break within the bcr locus on chromosome 22, transfer of the c-abl protooncogene from chromosome 9 to 22, and formation of an aberrant 210- kD bcr-abl fusion protein (p210bcr-abl). Recently, the absence of bcr rearrangement and expression of a disti

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34

Sandberg, Avery A., Rodman Morgan, Thomas J. Kipps, Barbara K. Hecht, and Frederick Hecht. "The Philadelphia (Ph) chromosome in leukemia. II. Variant Ph translocations in acute lymphoblastic leukemia." Cancer Genetics and Cytogenetics 14, no. 1-2 (1985): 11–21. http://dx.doi.org/10.1016/0165-4608(85)90210-9.

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35

Gökbuget, Nicola, and Dieter Hoelzer. "Treatment of Adult Acute Lymphoblastic Leukemia." Hematology 2006, no. 1 (2006): 133–41. http://dx.doi.org/10.1182/asheducation-2006.1.133.

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Abstract In the early 1980s, adult acute lymphoblastic leukemia (ALL) was a rarely curable disease with overall survival < 10%. After adapting combinations employed by pediatric groups, the outcome improved to 30–40%. A period of stagnation followed with improvement only in distinct subgroups. In the past 5 years, however, striking new developments have been noticeable. Progress has been made in molecular diagnostics of ALL. Improvements to standard therapy including stem cell transplantation (SCT) have occurred and a variety of new drugs for ALL are under evaluation. Rapid diagnosis and cl

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36

Voncken, JW, C. Morris, P. Pattengale, et al. "Clonal development and karyotype evolution during leukemogenesis of BCR/ABL transgenic mice." Blood 79, no. 4 (1992): 1029–36. http://dx.doi.org/10.1182/blood.v79.4.1029.1029.

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Abstract The Philadelphia (Ph) translocation is responsible for the generation of the chimeric BCR/ABL oncogene. The Ph chromosome constitutes the earliest detectable chromosome abnormality in chronic myelogenous leukemia and is also found in acute lymphoblastic leukemia. Mice transgenic for a P190 BCR/ABL-producing DNA construct develop lymphoblastic leukemia/lymphoma and provide an opportunity to study early stages of the disease as well as progression. In this study, we have karyotyped the bone marrow of 10 19-day-old BCR/ABL P190 transgenic mice from a line that reproducibly develops leuke

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Voncken, JW, C. Morris, P. Pattengale, et al. "Clonal development and karyotype evolution during leukemogenesis of BCR/ABL transgenic mice." Blood 79, no. 4 (1992): 1029–36. http://dx.doi.org/10.1182/blood.v79.4.1029.bloodjournal7941029.

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The Philadelphia (Ph) translocation is responsible for the generation of the chimeric BCR/ABL oncogene. The Ph chromosome constitutes the earliest detectable chromosome abnormality in chronic myelogenous leukemia and is also found in acute lymphoblastic leukemia. Mice transgenic for a P190 BCR/ABL-producing DNA construct develop lymphoblastic leukemia/lymphoma and provide an opportunity to study early stages of the disease as well as progression. In this study, we have karyotyped the bone marrow of 10 19-day-old BCR/ABL P190 transgenic mice from a line that reproducibly develops leukemia/lymph

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38

Minieri, Valentina, Marco De Dominici, Marja T. Nevalainen, and Bruno Calabretta. "Targeting the STAT5 pathway in Ph+ acute lymphoblastic leukemia." Oncotarget 9, no. 95 (2018): 36726–27. http://dx.doi.org/10.18632/oncotarget.26412.

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39

Alam, Arif, Khaled al Qawasmeh, Jihad Kanbar, et al. "Philadelphia Positive Acute Lymphoblastic Leukemia (Ph+ ALL), Tawam Experience." Blood 126, no. 23 (2015): 4867. http://dx.doi.org/10.1182/blood.v126.23.4867.4867.

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Abstract Acute lymphoblastic leukemia (ALL) is a relatively rare lymphoid disorder with approximately 11 cases per million persons per year in United States. It is seen more commonly in children however adults are also affected with the median age approximately 39 years. The prognosis is influenced by the age of the patient and genetic findings. Abnormal cytogenetic is present in approximately 80 % of the patients. Philadelphia chromosome t (9;22) is seen in approximately 30 % of adult patients (Ph + ALL) and imparts a poor prognosis. Allogeneic stem cell transplant remains one of the corner s

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40

Foà, Robin. "Ph-Positive Acute Lymphoblastic Leukemia — 25 Years of Progress." New England Journal of Medicine 392, no. 19 (2025): 1941–52. https://doi.org/10.1056/nejmra2405573.

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Ottmann, Oliver G., and Barbara Wassmann. "Treatment of Philadelphia Chromosome–Positive Acute Lymphoblastic Leukemia." Hematology 2005, no. 1 (2005): 118–22. http://dx.doi.org/10.1182/asheducation-2005.1.118.

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Abstract Philadelphia chromosome positive (Ph+) acute lymphoblastic leukemia (ALL) includes at least one-quarter of all adults with ALL. Until recently, conventional chemotherapy programs that have been effective in other precursor B-cell ALL cases have been unable to cure patients with this diagnosis. Allogeneic stem cell transplantation early in first remission has been the recommended therapy. The availability of imatinib mesylate and other tyrosine kinase inhibitors and small molecules that affect the BCR/ABL signaling pathways may be changing the treatment paradigm and the prognosis for t

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Carthikeyan, Subramaniam Murali, and Perumal Kalaiyarasi Jayachandran. "Dasatinib—A Generation Ahead." Indian Journal of Medical and Paediatric Oncology 42, no. 02 (2021): 172–76. http://dx.doi.org/10.1055/s-0041-1732822.

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AbstractDasatinib is a highly potent second-generation (2G) tyrosine kinase inhibitor (TKI) used in the management of Philadelphia (Ph) chromosome-positive leukemias, chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL). In CML, dasatinib produces higher rates of early and deeper molecular responses compared with imatinib. The drug has its share of toxicities, namely, cytopenias, cardiovascular, and pleural effusion. This review describes the pharmacological aspects of dasatinib, clinically relevant toxicities, and their management.

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Gökbuget, Nicola. "Treatment of older patients with acute lymphoblastic leukemia." Hematology 2016, no. 1 (2016): 573–79. http://dx.doi.org/10.1182/asheducation-2016.1.573.

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AbstractThe treatment of older patients with acute lymphoblastic leukemia (ALL) is an unmet medical need. With increasing age, ALL patients have a significantly lower clinical remission rate, higher early mortality, higher relapse rate, and poorer survival compared with younger patients. This is only partly explained by a higher incidence of poor prognostic factors in the older age group. Most importantly, intensive chemotherapy with or without stem cell transplantation (SCT) is less well tolerated in older patients. Some progress has been made with delivering age-adapted, moderately intensive

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Jelinek, Jaroslav, Yasuhiro Oki, Vazganush Gharibyan, et al. "JAK2 mutation 1849G>T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome–negative CML, and megakaryocytic leukemia." Blood 106, no. 10 (2005): 3370–73. http://dx.doi.org/10.1182/blood-2005-05-1800.

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AbstractAn activating 1849G&gt;T mutation of JAK2 (Janus kinase 2) tyrosine kinase was recently described in chronic myeloproliferative disorders (MPDs). Its role in other hematologic neoplasms is unclear. We developed a quantitative pyrosequencing assay and analyzed 374 samples of hematologic neoplasms. The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but less prevalent in acute myeloid leukemia (AML) with an antecedent PV or myelofibrosis (5 [36%] of 14 patients). JAK2 mutation was also detected in 3 (19%) of 16 patients with Philadelphia-chromosome (Ph)–

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Park, Eugene, Enzi Jiang, Yao-Te Hsieh, et al. "Targeting Survivin In Recalcitrant Acute Lymphoblastic Leukemia." Blood 116, no. 21 (2010): 3263. http://dx.doi.org/10.1182/blood.v116.21.3263.3263.

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Abstract Abstract 3263 Background: Despite the recent advances in chemotherapy for acute lymphoblastic leukemia (ALL), the development of drug resistance and long-term side effects of current treatments warrant new treatment modalities. Survivin/BIRC5, an inhibitor of apoptosis protein, is critical for the survival and proliferation of cancerous cells, is expressed in AML and ALL cells, and has been implicated in leukemia relapse. In the present study, we test the hypothesis that survivin is critical to the pathway of self-renewal of drug-resistant ALL cells. Methods: For gain of function stud

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Marini, Bernard L., Yihan Sun, Patrick W. Burke, and Anthony J. Perissinotti. "Successful reintroduction of blinatumomab in a patient with relapsed/refractory acute lymphoblastic leukemia following grade 4 cytokine release syndrome." Journal of Oncology Pharmacy Practice 24, no. 1 (2016): 67–73. http://dx.doi.org/10.1177/1078155216676633.

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Relapsed/refractory acute lymphoblastic leukemia poses a clinical challenge due to its poor prognosis and lack of effective treatment. Blinatumomab, a novel immunotherapy, has demonstrated excellent efficacy in relapsed/refractory acute lymphoblastic leukemia; however, life-threatening toxicities such as cytokine release syndrome have been reported in pivotal clinical trials. In this report, we describe the safe reintroduction of blinatumomab in an adult patient with relapsed Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia after experiencing grade 4 blinatumomab-induced cyt

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Meyer, Renata A., Harald Herrmann, Karoline V. Gleixner, et al. "Identification of Heat Shock Protein 32 (Hsp32) as a Novel Target in Acute Lymphoblastic Leukemia (ALL)." Blood 112, no. 11 (2008): 1616. http://dx.doi.org/10.1182/blood.v112.11.1616.1616.

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Abstract Heat shock proteins (Hsp) are increasingly employed as therapeutic targets in various solid tumors and leukemias. We have recently shown that Hsp32 is expressed in leukemic cells and serves as a survival-factor and molecular target in Ph+ chronic myeloid leukemia. In the present study, we examined the expression and functional role of Hsp32 in acute lymphoblastic leukemia (ALL). Leukemic cells were obtained from patients with Ph+ ALL (n=5) and Ph− ALL (n=5). In addition, Ph+ ALL cell lines (Z-119, BV-173, TOM-1, NALM-1) and Ph− ALL cell lines (RAJI, RAMOS, REH, BL-41) were used. As as

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Saleh, Khalil, Alexis Fernandez, and Florence Pasquier. "Treatment of Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia in Adults." Cancers 14, no. 7 (2022): 1805. http://dx.doi.org/10.3390/cancers14071805.

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Philadelphia-chromosome positive acute lymphoblastic leukemia (Ph+ ALL) is the most common subtype of B-ALL in adults and its incidence increases with age. It is characterized by the presence of BCR-ABL oncoprotein that plays a central role in the leukemogenesis of Ph+ ALL. Ph+ ALL patients traditionally had dismal prognosis and long-term survivors were only observed among patients who underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT) in first complete remission (CR1). However, feasibility of allo-HSCT is limited in this elderly population. Fortunately, development of in

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Nardi, Valentina, Nora Ku, Matthew J. Frigault, et al. "Clinical response to larotrectinib in adult Philadelphia chromosome–like ALL with cryptic ETV6-NTRK3 rearrangement." Blood Advances 4, no. 1 (2020): 106–11. http://dx.doi.org/10.1182/bloodadvances.2019000769.

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Key Points Larotrectinib has clinical activity in adult Ph-like acute lymphoblastic leukemia with ETV6-NTRK3 rearrangements. ETV6-NTRK3 rearrangements can be cryptic and subclonal in Ph-like ALL at diagnosis and selected for with aggressive therapy.

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Hunger, Stephen P. "Tyrosine Kinase Inhibitor Use in Pediatric Philadelphia Chromosome–Positive Acute Lymphoblastic Anemia." Hematology 2011, no. 1 (2011): 361–65. http://dx.doi.org/10.1182/asheducation-2011.1.361.

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Abstract Until recently, pediatric Philadelphia chromosome–positive (Ph+) acute lymphoblastic leukemia (ALL) was associated with an extremely poor outcome when treated with chemotherapy alone, and only modest survival benefits were obtained with the widespread use of hematopoietic stem cell transplantation (HSCT). The development of first-generation (imatinib) and second-generation (dasatinib and nilotinib) tyrosine kinase inhibitors (TKIs) that target the BCR-ABL1 fusion protein produced by the Ph chromosome revolutionized the treatment of chronic myelogenous leukemia (CML). The Children's On

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