BCR-ABL1 fusion

WWOX2 serves as a tumor suppressor, whereas FUT1 functions as a promoter of malignancy. The interplay between tumor inducers and suppressors may serve as a survival mechanism for cancer cells, a subject that has received limited research attention.

Circulating miRNAs are valuable biomarkers for TKI resistance in CML. Targeting HMGB1-associated miRNAs, together with combined CBD and IM treatment, may help re-establish apoptotic regulation and overcome resistance mechanisms.

Consistent with prior preclinical studies, we demonstrate that dasatinib and ponatinib, unlike SRC sparing TKIs (imatinib, nilotinib), antagonize blinatumomab's T-cell engaging efficacy by potently inhibiting LCK Y394 phosphorylation, a critical step in proximal TCR signaling. We show that TKI-induced T-cell suppression and antagonism can be significantly improved by supplementing co-cultures with common gamma-chain cytokines, particularly IL-7. IL-7 robustly enhances human T-cell proliferation, reduces exhaustion, and significantly improves blinatumomab's cytotoxic efficacy in the presence of Src/BCRABL1 TKIs.

Finally, the duplex FA-eLCR successfully detected the BCR/ABL1p210 transcripts in patients with chronic myeloid leukemia (CML) and monitored the change of transcripts during treatment, with 100 % concordance to reverse transcription-quantitative polymerase chain reaction, highlighting its high potential in the early diagnosis and minimal residual disease (MRD) monitoring of CML. This work presents a novel strategy to address nonspecific amplification in LCR and introduces a cost-effective, highly sensitive platform for molecular diagnosis in clinical setting.

P3, N=150, Recruiting, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College.; Institute of Hematolog | Not yet recruiting --> Recruiting

PREPARE-ALL identifies twice as many relapses as clinicians and serves as a practical decision-support tool for early relapse triage and treatment planning, enabling timely therapeutic adjustments and improved outcomes in pediatric ALL.

Additionally, the development of new therapeutic approaches is examined as a forward-looking tactic to produce more profound and long-lasting molecular responses which include immune-based therapies, combinatorial approaches, and promising third-generation TKIs. This review aims to improve patient outcomes and identify future avenues in CML research by combining new information with existing knowledge.

BM fibrosis is a critical factor influencing the response to TKIs in CML patients. Lower grades of fibrosis correlate with higher response rates and better clinical outcomes, suggesting the importance of early intervention and tailored treatment approaches based on fibrosis grading.

Our findings indicate that CAPE could serve as an adjunctive therapy for CML against drug resistance caused by the T315I mutation through a mechanism that does not directly inhibit BCR-ABL1. This study underscores the promise of targeting mitochondrial metabolism as a novel approach for overcoming therapeutic resistance in CML.

Tyrosine kinase inhibitors restore the distribution of memory T cells in patients with chronic myeloid leukemia (CML), but T cell exhaustion remains an issue. This situation highlights the need for alternative activation strategies to enhance immunity.

Multidisciplinary methods are crucial for diagnosing CML blast crisis. Orelabatinib shows efficacy, and more research on personalized treatment is needed.

At the time of initial diagnosis, the patient presented with a primary tumor in the right thigh and extensive metastatic involvement affecting both lungs, pleura, mediastinum, pelvic cavity, and the right inguinal region, resulting in the classification of the case as high-risk. In addition to conventional multimodal therapy, early intervention using tyrosine kinase inhibitors was implemented, leading to the achievement of an early complete response.