Clinical features and initial treatment outcomes of pediatric B-cell acute lymphoblastic leukemia with P2RY8::CRLF2 fusion positivity: a case series

Introduction

Acute lymphoblastic leukemia (ALL) is the most common malignancy in children, and improvements in outcomes have largely resulted from risk-adapted, stratified therapy. In recent years, Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) has attracted increasing attention as a high-risk subtype. This entity is characterized by aberrant activation of kinase signaling pathways and, despite lacking the BCR::ABL1 fusion, carries a similarly unfavorable prognostic profile (1,2).

Among the various genetic alterations in Ph-like ALL, rearrangements of CRLF2 (cytokine receptor-like factor 2) represent the most common molecular event, accounting for approximately half of cases, and promote leukemogenesis mainly through activation of the JAK-STAT signaling pathway (3). The P2RY8::CRLF2 fusion is one of the major forms of CRLF2 rearrangement in children (4). Previous studies have suggested that patients harboring this fusion often present with high white blood cell (WBC) counts and older age at diagnosis features associated with clinical high-risk disease—and that early international studies reported poor responses to chemotherapy and higher relapse rates (3-5).

However, with the widespread use of contemporary intensified chemotherapy protocols, its prognostic significance remains controversial. Some studies indicate that intensive treatment may mitigate the adverse prognostic impact of this alteration. At present, systematic clinical data on P2RY8::CRLF2 fusion-positive ALL in Chinese pediatric populations remain limited.

Therefore, we retrospectively analyzed the clinical data of seven children with P2RY8::CRLF2 fusion-positive B-ALL to preliminarily characterize their clinical and biological features and early treatment responses, with the aim of providing evidence to support precise risk identification and individualized therapeutic strategies. We present this article in accordance with the AME Case Series reporting checklist (available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0320/rc).

Case presentation

Study population

This was a retrospective case series. Seven children with newly diagnosed P2RY8::CRLF2 fusion-positive B-cell acute lymphoblastic leukemia (B-ALL) who were diagnosed and treated in the Department of Hematology at the Children’s Hospital of Nanjing Medical University between September 2017 and July 2024 were consecutively included. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was conducted with approval from the Ethics Committee of Children’s Hospital of Nanjing Medical University (No. 202509031-1). Due to the retrospective nature of this analysis, the requirement for written informed consent from the patients’ parents or guardians was waived by the ethics committee.

Inclusion criteria were as follows: (I) age 0–18 years; (II) newly diagnosed B-ALL confirmed by MICM classification (morphology, immunology, cytogenetics, and molecular biology); (III) presence of the P2RY8::CRLF2 fusion confirmed by transcriptome sequencing or reverse transcription polymerase chain reaction (RT-PCR); and (IV) complete clinical and follow-up data. Exclusion criteria included: (I) secondary acute lymphoblastic leukemia; and (II) prior chemotherapy or radiotherapy before enrollment.

Diagnostic procedures and molecular testing

All patients were diagnosed by bone marrow morphology, with ≥20% lymphoblasts required for diagnosis. Immunophenotyping was performed by multiparameter flow cytometry. Leukemia cells expressing B-lineage markers such as CD19, CD10, and CD22, together with cytoplasmic CD79a positivity, were considered diagnostic. Cytogenetic analysis was performed using G-banding karyotyping. Fusion genes and gene mutations were screened using RNA-based transcriptome sequencing, and key mutations were confirmed by Sanger sequencing. Overexpression of CRLF2 was further evaluated using fluorescence in situ hybridization as supportive evidence.

Treatment protocols

All patients received risk-adapted chemotherapy according to the CCCG-ALL-2015 or CCCG-ALL-2020 protocols developed by the Chinese Children’s Cancer Group. The backbone chemotherapy of the CCCG-ALL protocols consisted of risk-adapted multi-agent therapy including glucocorticoids, vincristine, daunorubicin or other anthracycline exposure according to risk group, pegylated asparaginase, cyclophosphamide, cytarabine, 6-mercaptopurine, high-dose or escalating-dose methotrexate, and triple intrathecal therapy for central nervous system prophylaxis. Maintenance therapy mainly consisted of daily 6-mercaptopurine and weekly methotrexate, with protocol-defined vincristine/dexamethasone pulses. Treatment intensity and post-induction adjustments were guided by age, initial WBC count, sentinel cytogenetic/molecular lesions, and MRD response on day 19 and day 46. Initial risk stratification was based on age at diagnosis, WBC count, and immunophenotype. Risk group and treatment intensity were subsequently adjusted according to molecular and cytogenetic findings, as well as minimal residual disease (MRD) levels on day 19 and day 46 of induction therapy. One patient (Case 2) received the JAK inhibitor ruxolitinib early during induction therapy. Another patient (Case 7), whose MRD remained positive on day 19, underwent treatment intensification with the addition of ruxolitinib and the bispecific CD3/CD19 antibody blinatumomab.

Response evaluation and follow-up

(I) Complete remission (CR): defined as <5% lymphoblasts in bone marrow with no clinical evidence of extramedullary leukemia. (II) MRD: bone marrow samples were evaluated on day 19 and day 46 of induction therapy. MRD was assessed by multiparameter flow cytometry using leukemia-associated immunophenotype detection. MRD <0.01% (<10⁻⁴) was considered negative. (III) Molecular response: the P2RY8::CRLF2 fusion transcript level was monitored by real-time quantitative PCR. Values below the detection limit were defined as molecular negativity. (IV) Adverse events: toxicities were graded and recorded according to the Common Terminology Criteria for Adverse Events of the U.S. National Institutes of Health.

Follow-up was conducted through outpatient visits and telephone contact. The last follow-up date was July 31, 2025. Endpoints were defined as relapse, death, or last follow-up. Event-free survival (EFS) was defined as the time from diagnosis to the first event (including relapse, treatment failure, or death) or last follow-up. Overall survival (OS) was defined as the time from diagnosis to death from any cause or last follow-up.

Statistical analysis

Statistical analyses were performed using SPSS version 26.0. Continuous variables with a normal distribution are presented as mean ± standard deviation, whereas non-normally distributed variables are described as median (range). Categorical variables are expressed as number of cases (percentage). As this study was a small-sample case series, no hypothesis testing for group comparisons was performed. Descriptive statistical methods were primarily used to summarize the clinical characteristics, treatment responses, and survival outcomes of the patients.

Clinical characteristics, treatment response, and outcomes

Baseline clinical characteristics

Baseline clinical features are summarized in Table 1. A total of seven children with P2RY8::CRLF2 fusion-positive B-ALL were included, comprising three males and four females (male-to-female ratio 0.75:1). The detection rate accounted for 0.86% of leukemia cases tested at our center during the same period. The median age at diagnosis was 3 years and 11 months (range, 9 months to 12 years 11 months).

The median WBC count at diagnosis was 25.65×10⁹/L [range, (4.34–131.12)×10⁹/L]. Five patients (71.4%) had WBC counts >10×10⁹/L, and three (42.8%) had WBC counts >50×10⁹/L. All patients (7/7, 100%) had a precursor B-cell immunophenotype. According to the CCCG-ALL risk stratification criteria, one patient was classified as low risk and six as intermediate risk. At diagnosis, 5 patients (71.4%) presented with extramedullary involvement such as hepatomegaly, splenomegaly, or lymphadenopathy. One patient (14.3%) had skeletal involvement manifested as ankle joint swelling and pain.

Cytogenetic and molecular findings are summarized in in Table 2. Concomitant genetic abnormalities included RAS pathway mutations in three patients, PAX5 fusions in two patients, IGH fusion in one patient, and JAK mutation in one patient. All fluorescence in situ hybridization (FISH) tests were negative. Cerebrospinal fluid examinations were also negative in all patients, with no evidence of central nervous system leukemia (CNSL).

Treatment response and early outcomes

Table 3 summarizes the treatment regimens, treatment responses, and follow-up outcomes of the patients. All patients completed induction chemotherapy. Two patients received treatment according to the CCCG-ALL-2015 protocol; among them, Case 2 had persistent MRD positivity on day 19 of induction and, after multidisciplinary discussion, ruxolitinib was added to the induction regimen. Five patients were treated according to the CCCG-ALL-2020 protocol. One patient (Case 7) showed a poor early treatment response, with persistent MRD positivity on both day 19 and day 46, and subsequently received combined therapy with ruxolitinib and blinatumomab.

On day 19 of induction therapy, 5 patients (71.4%) had bone marrow MRD levels <0.01%. One patient (Case 2) had an MRD level of 0.05%, and another patient (Case 7) had an MRD level of 1.88%. By day 46 of induction therapy, six patients achieved MRD <0.01%, with concurrent disappearance of the P2RY8::CRLF2 fusion transcript. In Case 7, MRD decreased to 0.04% after salvage immunotherapy (and subsequently became undetectable on follow-up testing), achieving molecular remission. All seven patients achieved CR, resulting in a 100% CR rate at the end of induction therapy.

Adverse events

All treatment-related adverse events were reversible. The main toxicities included infections in 5 patients (71.4%), such as pneumonia, sepsis, and enteritis; hepatic dysfunction in 3 patients (42.9%); and mucositis in 2 patients (28.6%). Most events were grade 2–3. All adverse events improved with appropriate supportive care, and no treatment-related deaths occurred.

Follow-up and survival outcomes

As of the last follow-up (July 31, 2025), Cases 1–4 had completed protocol therapy and discontinued treatment, all maintaining CR. Cases 5–7 remained in the maintenance phase of therapy. The EFS and OS rates were both 100%. The median follow-up duration was 32 months (range, 13–96 months). No hematologic or extramedullary relapse was observed during follow-up.

Discussion

This study retrospectively analyzed the clinical characteristics and early treatment outcomes of seven children with P2RY8::CRLF2 fusion-positive B-ALL. The results showed that the median age at onset was less than 4 years, with a nearly equal sex distribution. Common clinical manifestations included skin bleeding, ecchymosis, and lymphadenopathy, while a minority of patients presented with bone pain as the initial symptom. These findings are consistent with previous reports and suggest that the clinical presentation of P2RY8::CRLF2 fusion-positive B-ALL lacks specific features, and the diagnosis still relies on molecular testing (3). Under the CCCG-ALL-2015 and CCCG-ALL-2020 protocols, most patients achieved favorable early MRD responses, and one patient with persistent MRD positivity converted to MRD negativity after salvage immunotherapy. During the current follow-up period, all patients remained in CR; however, these observations should be interpreted cautiously because of the small sample size, heterogeneous treatment exposure, and relatively short follow-up in some patients.

Interestingly, the median age in our cohort was younger than that reported in several earlier studies of CRLF2-rearranged or Ph-like ALL, whereas a substantial proportion of patients still showed elevated WBC counts and extramedullary involvement. This discrepancy may reflect differences in patient selection, ethnic background, molecular screening strategies, and treatment era. Given the descriptive nature of the present case series, our cohort should not be considered representative of all pediatric patients with P2RY8::CRLF2 fusion-positive B-ALL. Rather, these cases provide real-world clinical observations from a Chinese pediatric center and highlight the need for broader multicenter validation.

Previous studies have shown that the P2RY8::CRLF2 fusion represents an important molecular event in high-risk pediatric B-ALL. It can lead to aberrant activation of the JAK–STAT signaling pathway and is often accompanied by IKZF1 deletions, providing a molecular basis for poor prognosis (3,4,6,7). In addition, mutations in RAS-related genes (such as KRAS and NRAS) are frequently observed in CRLF2-rearranged ALL (8). In a previous Chinese pediatric cohort, Dou et al. analyzed CRLF2 gene expression in 271 children with non-Down syndrome ALL and did not identify a significant association with JAK mutations (9). Another retrospective study by Xu et al. in adult patients with P2RY8::CRLF2 fusion-positive B-ALL found that, in addition to JAK mutations, alterations in RAS pathway genes (such as NRAS and PTPN11) and the transcriptional corepressor gene BCORL1 were relatively common (10). In the present cohort, three of seven patients harbored RAS pathway mutations, whereas only one patient had a JAK mutation. Although the small sample size precludes estimation of mutation prevalence, this finding is biologically plausible and should be interpreted in the context of previous genomic studies. Large-scale genomic analyses of pediatric B-ALL and B-other/Ph-like ALL have shown that kinase-activating lesions may involve not only the JAK-STAT pathway but also the RAS/RAF/MAPK pathway. Therefore, the RAS pathway alterations observed in our cohort support the molecular heterogeneity of P2RY8::CRLF2 fusion-positive B-ALL rather than defining a distinct mutation pattern in Chinese children. To place our findings into the context of published evidence and to partly compensate for the absence of an internal comparison group, we summarized selected representative studies of P2RY8::CRLF2-positive, CRLF2-rearranged, B-other, and Ph-like B-ALL in Table 4.

In addition to kinase pathway alterations, two patients in our cohort harbored PAX5 fusions. PAX5 is a key transcription factor required for B-cell lineage commitment, and PAX5 rearrangements may disrupt normal B-cell differentiation and contribute to leukemogenesis (16). Although no clear difference in early treatment response was observed in the two patients with PAX5 fusions, the coexistence of PAX5-related lesions with P2RY8::CRLF2 fusion further supports the molecular heterogeneity of this subgroup. Larger cohorts with integrated genomic and transcriptomic profiling are required to clarify whether these concurrent lesions influence MRD response or relapse risk.

The absence of a contemporaneous internal comparison group is an important limitation of this study. Because P2RY8::CRLF2 fusion-positive B-ALL is rare and because molecular diagnostic approaches evolved during the study period, retrospectively selecting CRLF2-high-expression cases or other high-risk B-ALL subgroups as controls may introduce substantial selection bias. Therefore, we did not perform formal comparative analyses. Instead, we contextualized our observations with published cohorts of P2RY8::CRLF2-positive, CRLF2-rearranged, B-other, and Ph-like B-ALL. The purpose of the present study is not to redefine risk stratification or establish a treatment recommendation, but to provide detailed real-world clinical and molecular observations of this rare subgroup.

Most studies have reported that high CRLF2 expression is associated with an unfavorable prognosis (3,4,17,18). However, some reports have suggested no clear association between CRLF2 overexpression and long-term relapse or survival outcomes (19-21). It should be noted that the P2RY8::CRLF2 fusion and CRLF2 overexpression are not completely equivalent. Overexpression of CRLF2 can arise through multiple mechanisms, including IGH::CRLF2 rearrangements, P2RY8::CRLF2 fusion, or other regulatory abnormalities, and several studies have linked it to adverse prognosis. Nevertheless, the favorable early responses observed in our cohort suggest that the prognostic impact of CRLF2-related abnormalities may be modified by MRD-guided risk adaptation, treatment intensity, coexisting genetic lesions, and the use of individualized targeted or immunotherapeutic interventions. Because several patients remain on therapy and the follow-up duration is limited, long-term prognostic conclusions cannot be drawn from the present series.

In terms of treatment strategies, targeted and immunotherapeutic approaches were used in selected patients as individualized interventions. Case 2 received the JAK inhibitor ruxolitinib in combination with risk-adapted multi-agent chemotherapy, while Case 7 received ruxolitinib and blinatumomab because of persistent MRD positivity after induction therapy; both patients ultimately achieved MRD negativity. However, because these patients received combination therapy and no control group was available, the contribution of ruxolitinib or blinatumomab to treatment response cannot be determined from this case series. Previous studies have suggested that in CRLF2-rearranged Ph-like ALL models, JAK inhibitors may act synergistically with standard induction agents such as vincristine, dexamethasone, and L-asparaginase (22). Meanwhile, ruxolitinib, a JAK1/2 inhibitor, is being explored in clinical trials in combination with chemotherapy (15). A study reported by Alghandour also indicated that patients with JAK2-mutated Ph-like ALL may benefit from ruxolitinib, although treatment responses appear to vary among individuals (23). Although exploratory studies have suggested potential benefit of ruxolitinib in CRLF2-rearranged B-ALL, robust clinical evidence from large cohorts is still lacking. Therefore, its use should currently be regarded as an individualized exploratory strategy rather than a standard recommendation. In the present study, ruxolitinib was not used according to a prospective protocol, and its use should therefore be interpreted as real-world individualized treatment rather than evidence supporting routine upfront application. In contrast, blinatumomab has demonstrated efficacy in achieving molecular remission in relapsed or refractory B-ALL, and its combination with frontline therapy in intermediate- and high-risk patients also warrants further investigation (24).

The present study has several limitations. First, this was a single-center retrospective case series with only seven patients, and the rarity of P2RY8::CRLF2 fusion-positive B-ALL limited the feasibility of expanding the cohort within the current study period. Second, no contemporaneous internal comparison group was included. Although comparison with CRLF2-high-expression cases or other high-risk B-ALL subgroups would be informative, such retrospective selection may be biased because molecular testing strategies, treatment protocols, and follow-up duration differed across patients and time periods. Third, treatment exposure was heterogeneous: two patients were treated according to the CCCG-ALL-2015 protocol, five according to the CCCG-ALL-2020 protocol, and two received additional targeted or immunotherapeutic agents. Therefore, treatment efficacy cannot be attributed to any single intervention. Fourth, the follow-up duration remains limited, and some patients are still receiving maintenance therapy, preventing reliable assessment of long-term EFS, OS, and relapse risk. Finally, the study did not include integrated multi-omics profiling or functional validation of the concurrent mutations. These limitations indicate that prospective multicenter studies with standardized molecular testing and longer follow-up are needed to define the biological and prognostic significance of P2RY8::CRLF2 fusion-positive pediatric B-ALL.

Conclusions

In conclusion, this single-center case series suggests that pediatric P2RY8::CRLF2 fusion-positive B-ALL is molecularly heterogeneous and may include RAS pathway co-lesions. Favorable early responses were observed in our patients under contemporary MRD-guided chemotherapy with individualized targeted or immunotherapeutic interventions. However, the small sample size, lack of a contemporaneous control group, heterogeneous treatment exposure, and limited follow-up preclude conclusions regarding long-term prognosis or treatment efficacy. Prospective multicenter studies are needed to define optimal risk stratification and precision therapy for this rare subgroup.

Acknowledgments

We gratefully acknowledge the pathologists in our hospital for their expertise and generous provision of data.

Footnote

Reporting Checklist: The authors have completed the AME Case Series reporting checklist. Available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0320/rc

Peer Review File: Available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0320/prf

Funding: This research was supported by Special Fund for Health Science and Technology Development in Nanjing (No. JQX19008) and Nanjing Medical Science and Technology Development Project (No. YKK21149).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-2026-0320/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was conducted with approval from the Ethics Committee of Children’s Hospital of Nanjing Medical University (No. 202509031-1). Due to the retrospective nature of this analysis, the requirement for written informed consent from the patients’ parents or guardians was waived by the ethics committee.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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