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Leukemia

Relevant Articles About Research and Clinical Trials in Leukemia

RELATED :ALL (Acute Lymphoblastic Leukemia):AML (Acute Myeloid Leukemia):CLL (Chronic Lymphocytic Leukemia):CML (Chronic Myeloid Leukemia)

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ALL (Acute Lymphoblastic Leukemia)Other CancersBiological: BlinatumomabBiological: RituximabCyclophosphamideCytarabineDaunorubicinDaunorubicin HydrochlorideDexamethasoneEtoposideMercaptopurineMethotrexatePegaspargasePrednisoneProcedure: Allogeneic Hematopoietic Stem Cell TransplantationProcedure: Biospecimen CollectionProcedure: Bone Marrow AspirationProcedure: Bone Marrow BiopsyProcedure: Lumbar PunctureProcedure: X-Ray ImagingVincristineVincristine SulfateActiveNot RecruitingCanadaIsraelPuerto RicoUnited States 0NCT02003222Phase 3
Combination Chemotherapy With or Without Blinatumomab in Treating Patients With Newly Diagnosed BCR-ABL-Negative B Lineage Acute Lymphoblastic Leukemia

Combination Chemotherapy With or Without Blinatumomab in Treating Patients With Newly Diagnosed BCR-ABL-Negative B Lineage Acute Lymphoblastic Leukemia

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Effective T-ALL Treatment With Indisulam via RBM39 Mis-Splicing

KEY TAKEAWAYS

  • The study aimed to investigate the therapeutic efficacy of indisulam in T-ALL through RBM39 degradation and its impact on pre-mRNA splicing.
  • Researchers noted that indisulam treats T-ALL by inducing RBM39 degradation and pre-mRNA mis-splicing.

Despite the use of targeted therapeutic approaches, T-cell acute lymphoblastic leukemia (T-ALL) is still associated with a high incidence of complications and a poor prognosis. Indisulam (also known as E7070), a newly identified molecular glue compound, has demonstrated increased therapeutic efficacy in several types of cancer through the rapid degradation of RBM39.

Tongting Ji and the team aimed to evaluate the therapeutic potential of indisulam in T-ALL, elucidate its underlying mechanisms, and explore the role of the RBM39 gene.

They performed an inclusive analysis of the anticancer effects of indisulam using both in vivo and in vitro models. The construction of RBM39-knockdown cell lines with shRNA confirmed that the malignant phenotype of T-ALL cells relied on RBM39.

RNA sequencing revealed indisulam-induced splicing anomalies, while proteomic analysis identified protein changes induced by the drug. Comprehensive cross-analysis of these results, including patient samples, facilitated the identification and validation of downstream effectors and their functional roles.

About indisulam’s effects, significant antineoplastic activity was observed in T-ALL. It attenuates cell proliferation, promotes apoptosis, and interferes with cell cycle progression in vitro while facilitating tumor remission in T-ALL in vivo models.

This investigation provides evidence that the downregulation of RBM39 results in restricted proliferation of T-ALL cells both in vitro and in vivo, suggesting that RBM39 is a potential target for T-ALL treatment.

Indisulam’s efficacy is attributed to its ability to induce RBM39 degradation, causing widespread aberrant splicing and abnormal translation of the critical downstream effector protein, THOC1, ultimately leading to protein depletion. Moreover, the presence of DCAF15 is regarded as critical for the effectiveness of indisulam, and its absence negates the ability of indisulam to induce the desired functional alterations.

The study concluded that indisulam, by targeting RBM39 to induce tumor cell apoptosis, is an effective drug for treating T-ALL. Targeting RBM39 through indisulam leads to the mis-splicing of pre-mRNAs, resulting in the loss of key effectors such as THOC1.

This study was funded by the National Key R&D Program of China (2022YFC2502700); National Natural Science Foundation (82072767, 82141110, 82203442, 82373414, 82172840, 82300182); Natural Science Foundation of Jiangsu Province (BK20220047); Jiangsu province’s science and technology support program (Social Development) project (BE2021657, BE2021654, BE2022732); Medical Research Project of Jiangsu Provincial Health and Family Planning Commission (Key Project ZD2021006); Suzhou Health Talent Training Project (GSWS2020047, GSWS2021028, GSWS2022062, GSWS2023048); the Science and Technology Development Project of Suzhou City (SKJY2021109, SKJY2021111, SKJY2021112, SKY2022170, SKY2022175, SKY2023192) and Jiangsu Provincial Health Commission Scientific Research Project (Z2022031, ZD2022056, M2022102, H2023106) and National Outstanding Youth Cultivation Program Project (YYJQ004).

Source: https://pubmed.ncbi.nlm.nih.gov/39044280/

Ji T, Yang Y, Yu J, et al. (2024). “Targeting RBM39 through indisulam induced mis-splicing of mRNA to exert anti-cancer effects in T-cell acute lymphoblastic leukemia.” J Exp Clin Cancer Res. 2024 Jul 24;43(1):205. doi: 10.1186/s13046-024-03130-8. PMID: 39044280; PMCID: PMC11267830.

Pharmacodynamic Parameters and Ibrutinib Response in CLL

KEY TAKEAWAYS

  • The PK-E3I observational study aimed to investigate how transient vs pHL affects outcomes in patients with CLL treated with ibrutinib.
  • Researchers noted that tHL is linked to reduced response duration, indicating the need for therapy adjustment after 3 months.

One of the 1 clinical observations of ibrutinib activity in the treatment of chronic lymphocytic leukemia (CLL) is a rapid decline in lymph node size. This phenomenon is accompanied by hyperlymphocytosis, either transient or prolonged, which is associated with distinct clinical responses and thus impacts long-term outcomes. Understanding the factors that determine different disease courses upon ibrutinib treatment remains a scientific challenge.

Sarah Cadot and the team aimed to assess the effects of transient versus prolonged hyperlymphocytosis (pHL) on clinical outcomes and pharmacodynamic parameters in patients with CLL undergoing ibrutinib treatment.

They performed an inclusive analysis from 2016 to 2021 with 2 cohorts of patients with CLL (cohort 1, n = 41; cohort 2, n = 81), reflecting the typical clinical characteristics of CLL. Such as a Male/Female sex ratio of 2/1, a median age of 70 years at diagnosis, and patients in first-line (1L) therapy (27%) or relapsed/refractory (R/R) patients (73%).

The study tracked blood cell counts over 2 years of ibrutinib treatment and included immunophenotyping and whole-body magnetic resonance imaging (MRI) in cohort 1. Data were integrated into a newly developed mathematical model, combining dynamical and statistical approaches, to identify biological mechanisms associated with different clinical responses.

The analysis revealed that ibrutinib-induced lymphocytosis delineates 2 patients with CLL subgroups: transient hyperlymphocytosis (tHL) and pHL.

Differences between the two groups were determined by baseline parameters such as absolute counts of CD4+ T lymphocytes (P = 0.026), regulatory CD4 T cells (P = 0.007), programmed cell death protein 1 (PD1), and CD69 expression on B leukemic cells, CD19/CD5high/CXCR4low levels (P = 0.04), and lymph node cellularity.

The study found that patients with tHL had a lower duration of response and poorer clinical outcomes. The mathematical modeling reproduced patient-specific dynamics and highlighted that differences between the 2 groups were largely due to the production of leukemic B cells in lymph node compartments and, to a lesser extent, T lymphocytes and leukemic B cell egress into the bloodstream.

Access to additional longitudinal MRI data could further elucidate leukemic B cell dynamics in lymph nodes and validate the relevance of the 2 distinct patient groups.

The study concluded that the multidisciplinary approach improved the understanding of ibrutinib response by identifying new pharmacodynamic parameters before and during treatment. It highlighted that tHL is associated with reduced duration of response and poorer clinical outcomes. Consequently, the findings support the need for adjusted management of ibrutinib therapy after 3 months.

The study was funded by Institut National du Cancer within the framework of C15093BS-Cancer Plan (SC, SK, LD, LY, AQM); Agence Nationale de la Recherche within the framework of LABEX-TOUCAN (SC, CL, LY, AQM); Centre National de la Recherche Scientifique within the framework of EDYLE (SC, CA, CD, LD, LY, FC, AQM); La Ligue contre le Cancer, within the framework of Comites 11,32,65 (LY, AQM).

Source: https://pubmed.ncbi.nlm.nih.gov/39037964/

Clinical Trial: https://clinicaltrials.gov/study/NCT02824159

Cadot S, Audebert C, Dion C, et al. (2024). “New pharmacodynamic parameters linked with ibrutinib responses in chronic lymphocytic leukemia: Prospective study in real-world patients and mathematical modeling.” PLoS Med. 2024 Jul 22;21(7):e1004430. doi: 10.1371/journal.pmed.1004430. PMID: 39037964.

Malnutrition Role in Car T-Cell Therapy Success and Survival

KEY TAKEAWAYS

  • The study aimed to investigate the impact of malnutrition and cachexia on the outcomes and survival of patients undergoing CAR T-cell therapy.
  • Researchers noticed that pre-treatment malnutrition and cachexia were significantly linked to poorer CAR T-cell therapy outcomes and reduced OS; further research is ongoing.

Chimeric Antigen Receptor (CAR) T-cell therapy has emerged as a revolutionary treatment for patients with refractory or relapsed B-cell malignancies specifically referred to as B-cell acute lymphoblastic leukemia (B-ALL). However, a significant proportion of patients experience negative outcomes, including severe inflammatory toxicities and relapse.

Cachexia and malnutrition are known secondary syndromes in many patients with cancer, attributed to the effects of active malignancy, systemic inflammation, and cumulative treatment burden; however, further research is required to accurately characterize these issues in patients with CAR T-cell.

B. Cucchiaro and the team aimed to explore the changes in nutritional status (malnutrition and cachexia) in CAR T-cell therapy patients and the potential impact on patient outcomes including survival. Additionally, they described the utilization of dietetic resources in this specific patient population in a London tertiary referral center.

They performed an inclusive analysis of adult hematology patients receiving licensed CD19-targeting CAR T-cell therapy. Data were collected from the time of treatment consent through to the day of discharge, including body weight, C-reactive protein, albumin, lactate dehydrogenase, nutrition-risk screening scores (hospital-specific), and dietetic input.

Clinical outcomes such as 12-month all-cause mortality, intensive care unit (ICU) admission, high-grade toxicities, and length of hospital stay (LoS) were also recorded. Cachexia and malnutrition were defined using the modified Glasgow Prognostic Score (mGPS) and Global Leadership Initiative on Malnutrition (GLIM) consensus, respectively.

About 114 patients (55.6 ± 15.1 years; 57% males) with B-cell non-Hodgkin’s lymphoma (n = 109) and B-ALL (n = 5), receiving axicabtagene ciloleucel (n = 89) and tisagenlecleucel (n = 25) were included. The median LoS for treatment was 34 (27-38) days. Prior to treatment, 31.5% of patients developed malnutrition, with pre-cachexia/refractory cachexia (mGPS) identified in 43.6% of patients.

This altered nutritional status pre-treatment was significantly associated with adverse patient outcomes post-infusion; mGPS was independently associated with inferior overall survival (OS) (HR = 3.158, CI = 1.36-7.323, P = 0.007), with malnutrition and mGPS associated with increased LoS (P = 0.037), sepsis (P = 0.022), and ICU admission (P = 0.039).

During admission, patients experienced significant body weight loss (-5.6% (-8.8 to -2.4); P < 0.001), with 68.4% developing malnutrition. Malnutrition screening during admission identified 57% of patients at risk, with 66.6% of patients referred to dietetics; however, there was a lack of malnutrition screening and dietetic referrals prior to treatment.

The study concluded that pre-treatment malnutrition and cachexia were significantly associated with adverse CAR T-cell therapy outcomes, with mGPS cachexia status independently linked to inferior OS. Further research in this novel area is essential to confirm the extent and impact of nutritional issues, assist with implementing dietetic pathways, and identify potential interventions to optimize outcomes.

The study received no funds and was in part supported by the Clinical Academic Pathway provided through the CNMAR.

Source: https://pubmed.ncbi.nlm.nih.gov/38901943/

Cucchiaro B, Davies NA, Weekes CE, et al. (2024). “Malnutrition and cachexia are associated with poor CAR T-cell therapy outcomes including survival.” Clin Nutr ESPEN. 2024 Aug;62:206-215. doi: 10.1016/j.clnesp.2024.05.020. Epub 2024 May 28. PMID: 38901943.

Ferroptosis and Its Impact on CML Diagnosis and Therapy

Ferroptosis and Its Impact on CML Diagnosis and Therapy

KEY TAKEAWAYS

  • The study aimed to investigate the role of ferroptosis in CML to uncover its impact on disease progression, treatment response, and potential therapeutic strategies.
  • Researchers noticed that ferroptosis signatures in CML offer key diagnostic and therapeutic insights.

The relationship between ferroptosis and the progression and treatment of hematological tumors has been extensively studied, although its precise association with chronic myeloid leukemia (CML) remains uncertain.

Fangmin Zhong and the team aimed to assess the potential of targeting ferroptosis as a novel therapeutic strategy for drug-resistant CML.

They performed an inclusive analysis using multi-transcriptome sequencing data to assess the ferroptosis levels in CML samples and their correlation with the tumor microenvironment, disease progression, and treatment response. Machine learning algorithms were employed to identify diagnostic ferroptosis-related genes (FRGs).

The consensus clustering algorithm was applied to determine ferroptosis-related molecular subtypes. Clinical samples from patients were collected and sequenced to validate bioinformatics findings. Additionally, cell experiments were conducted to evaluate the therapeutic efficacy of induced ferroptosis in drug-resistant CML.

The ferroptosis scores were significantly lower in samples from patients with CML compared to normal samples, and these scores further decreased with disease progression and non-response to treatment. Most FRGs were downregulated in CML samples. A high ferroptosis score was also associated with greater immunosuppression and increased activity of metabolic pathways.

Through support vector machine recursive feature elimination (SVM-RFE), least absolute shrinkage selection operator (LASSO), and random forest (RF) algorithms, 5 FRGs (ACSL6, SLC11A2, HMOX1, SLC38A1, AKR1C3) with high diagnostic value were identified.

The clinical diagnostic value of these five FRGs and their effectiveness in differentiating CML from other hematological malignancies were validated using additional validation cohorts and a real-world cohort.

Significant differences were found in immune landscape, chemosensitivity, and immunotherapy responsiveness between the 2 ferroptosis-related molecular subtypes. Cellular experiments confirmed that CML-resistant cells are more sensitive to the induction of ferroptosis and that this can enhance the sensitivity of imatinib treatment.

The study concluded that the molecular signature of ferroptosis in CML samples reveals significant diagnostic and therapeutic insights. The identified FRGs have reliable clinical diagnostic value, and the characterization of ferroptosis-related molecular subtypes provides valuable information for tailoring patient-specific treatment strategies.

Targeting and inducing ferroptosis shows considerable promise as an effective therapeutic approach for overcoming drug resistance in CML.

The study was funded by the National Natural Science Foundation of China (82160405, 82160038, 82301578, 82170140 and 82370146), the Natural Science Foundation of Jiangxi Province (20232BAB216037, 20232BAB216050), the Key Research and Development Program of Shaanxi Province (2024SF-YBXM-151), and the Shaanxi Fundamental Science Research Project for Chemistry and Biology (Grant No. 23JHZ007).

Source: https://pubmed.ncbi.nlm.nih.gov/39026664/

Zhong F, Zhang X, Wang Z, et al. (2024). “The therapeutic and biomarker significance of ferroptosis in chronic myeloid leukemia. Front Immunol.” 2024 Jul 4;15:1402669. doi: 10.3389/fimmu.2024.1402669. PMID: 39026664; PMCID: PMC11254662.

Analysis of Genomic Breaks in CML and BCR::ABL1 ALL

KEY TAKEAWAYS

  • The study aimed to investigate the genomic breakpoints on the BCR side leading to p210 and p190 fusion proteins in both CML and ALL.
  • Breakpoint localization in ALL and CML is primarily influenced by chromatin accessibility and developmental stage, rather than specific DNA motifs.

The BCR::ABL1 is a hallmark of chronic myeloid leukemia (CML) and is also found in acute lymphoblastic leukemia (ALL). Most genomic breaks on the BCR side occur in 2 regions – Major and minor – leading to p210 and p190 fusion proteins, respectively.

Lenka Hovorkova and the team aimed to assess the genomic breakpoint patterns associated with BCR::ABL1 in 971 patients, highlighting differences between CML and BCR::ABL1-positive ALL.

They performed an inclusive analysis of 971 patients, including adults and children with CML and ALL: pediatric ALL (n = 353), pediatric CML (n = 197), adult ALL (n = 166), and adult CML (n = 255 patients). Using multiplex long-distance PCR or next-generation sequencing, they characterized the BCR::ABL1 genomic fusion and developed the “Break-App” web tool for breakpoint visualization and analysis. Statistical analyses employed Pearson’s Chi-Squared test, Kolmogorov-Smirnov test, and logistic regression.

Detailed analysis showed a non-random distribution of breaks in both BCR regions, whereas ABL1 breaks were distributed more evenly. However, a significant difference in the distribution of breaks between CML and ALL was found. No association of breakpoints with any type of interspersed repeats or DNA motifs was observed.

With a few exceptions, the primary structure of the fusions suggests that non-homologous end joining is responsible for the BCR and ABL1 gene fusions. Analysis of reciprocal ABL1::BCR fusions in 453 patients showed mostly balanced translocations without major deletions or duplications.

The study concluded that physical colocalization and chromatin accessibility, varying with the developmental stage of the cell, significantly influence breakpoint localization in BCR::ABL1-positive ALL and CML genomes, overriding the influence of specific DNA motifs.

The study was supported by the Czech Health Research Council (NU21-03-00128), Charles University (GAUK 327322), by the project from Ministry of Health, Czech Republic 00064203 (University Hospital Motol, Prague, Czech Republic), MH CZ – DRO (IHBT, 00023736), by the project National Institute for Cancer Research (Program EXCELES, ID Project No. LX22NPO5102), and Cancer Australia PdCCRS1128727 (RS).

Source: https://pubmed.ncbi.nlm.nih.gov/38970095/

Hovorkova L, Winkowska L, Skorepova J, et al. (2024). “Distinct pattern of genomic breakpoints in CML and BCR::ABL1-positive ALL: analysis of 971 patients.” Mol Cancer. 2024 Jul 5;23(1):138. doi: 10.1186/s12943-024-02053-4. PMID: 38970095; PMCID: PMC11229488.

GJA9-MYCBP and PVT1 as Diagnostic Biomarkers for ALL

KEY TAKEAWAYS

  • The study aimed to investigate the expression levels of lncRNA GJA9-MYCBP and PVT1 in blood samples from patients with ALL.
  • Researchers noticed that the upregulation of lncRNA GJA9-MYCBP and PVT1 may serve as a potential diagnostic biomarker for ALL.

Acute lymphoblastic leukemia (ALL) is the most prevalent childhood blood cancer, with long noncoding RNAs (lncRNAs) implicated in its pathogenesis. LncRNAs are increasingly recognized as vital for diagnosing and prognosticating ALL.

Kamal Shahamiri and the team aimed to evaluate GJA9-MYCBP and PVT1 expression in ALL and healthy blood samples.

They performed an inclusive analysis using 40 pairs of ALL and healthy individual samples. Patients’ clinicopathological characteristics were evaluated alongside the expression of MYC and each candidate lncRNA using quantitative real-time PCR.

The results showed that lncRNA GJA9-MYCBP and PVT1 were significantly upregulated in ALL samples compared with healthy ones. Similarly, mRNA levels of MYC were increased in ALL samples than in control ones.

Receiver operating characteristic curve analysis indicated a satisfactory diagnostic efficacy (P-value <.0001), suggesting that lncRNA GJA9-MYCBP and PVT1 may serve as a diagnostic biomarker for ALL. Linear regression analysis unveiled positive correlations between the expression level of MYC and lncRNA GJA9-MYCBP and PVT1 in patients with ALL (P-values <.01).

The study concluded that the upregulation of lncRNA GJA9-MYCBP and PVT1 may signify a diagnostic biomarker for ALL, affirming their clinical diagnostic significance.

This study was funded by the Research Fund of Shahrekord University of Medical Science (5677).

Source: https://pubmed.ncbi.nlm.nih.gov/38994720/

Shahamiri K, Alghasi A, Saki N, et al. (2024). “Upregulation of the long noncoding RNA GJA9-MYCBP and PVT1 is a potential diagnostic biomarker for acute lymphoblastic leukemia.” Cancer Rep (Hoboken). 2024 Jul;7(7):e2115. doi: 10.1002/cnr2.2115. PMID: 38994720; PMCID: PMC11240143.

Comparative BCR-ABL1 Prevalence in CML & General Populations

KEY TAKEAWAYS

  • The study aimed to compare BCR-ABL1 prevalence in CML pts’ relatives vs. the general population for familial CML insights.
  • Researchers found a higher BCR-ABL1 prevalence in CML relatives, suggesting familial influence in CML occurrence, tempered by other factors; further studies warranted.

The role of familial influence in chronic myeloid leukaemia (CML) occurrence is sparsely explored. A previous study was conducted to determine the prevalence of harboring BCR::ABL1 in the adult normal population (StudyN).

Jew Win Kuan and the team aimed to explore how often BCR-ABL1 is found in first-degree relatives of patients (pts) with CML (StudyR) vs. the StudyN, aiming to understand familial factors in CML occurrence.

Researchers designed a cross-sectional study StudyR using convenience sampling, recruiting first-degree relatives of pts with CML aged ≥ 18 years old without a history of hematological tumors. Real-time quantitative polymerase chain reaction standardized at the International Scale (BCR::ABL1-qPCRIS) was performed according to standard laboratory practice and the manufacturer’s protocol.

About 96 first-degree relatives from 41 families participated in the study, with an average age of 39 and a male-to-female ratio of 0.88. Each family had a median of 2 relatives (ranging from 1 to 5). Of these, 18 (19%) were parents, 39 (41%) were siblings, and 39 (41%) were offspring of the pts with CML.

StudyR found that 4% (4 out of 96) of first-degree relatives harbored BCR-ABL1, a higher prevalence compared to the 0.5% (1 out of 190) found in the normal population in StudyN. All 4 positive relatives were female, and among them, 3 were also found to be positive in StudyN.

The mean age was 39, younger than the average age of 45 in StudyN. BCR-ABL1-qPCRIS levels ranged from 0.0017%IS to 0.0071%IS, similar to levels observed in StudyN (0.0023%IS to 0.0032%IS) and in another referenced study (0.006%IS to 0.016%IS).

The study concluded that the prevalence of harboring BCR-ABL1 in the first-degree relatives of known pts with CML was higher than that observed in the normal population. This finding suggests the potential existence of familial influence in pts with CML occurrence.

However, it also indicated that this influence might be tempered by other dominant factors, such as genetic dilutional effects and protective genetic factors. The gender and ethnic associations observed were inconsistent with typical CML epidemiology, hinting at a potentially higher familial influence among females.

Further investigation into this topic is warranted, ideally through larger studies with longer follow-up periods, to better understand these complexities.

This study was funded by UNIMAS under Research ID: F05/IMPACT/2114/2021 and the open access funding was provided by Universiti Malaysia Sarawak.

Source: https://pubmed.ncbi.nlm.nih.gov/38877512/

Kuan JW, Su AT, Sim SP, et al. (2024). “Higher prevalence of harbouring BCR::ABL1 in first-degree relatives of chronic myeloid leukaemia (CML) patients compared to normal population.” BMC Cancer. 2024 Jun 14;24(1):734. doi: 10.1186/s12885-024-12102-2. PMID: 38877512; PMCID: PMC11179337.

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