Clinical prognosis analysis of 54 pediatric patients with T-cell acute lymphoblastic leukemia

doi:10.21203/rs.3.rs-4779900/v1

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Clinical prognosis analysis of 54 pediatric patients with T-cell acute lymphoblastic leukemia

https://doi.org/10.21203/rs.3.rs-4779900/v1

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Background: T-cell acute lymphoblastic leukemia (T-ALL) is a rare and highly malignant neoplastic disease in children. Studying of its prognostic factors and clinical characteristics will bring certain reference value to clinical practice.

Procedure: The clinical data of 54 children with T-ALL admitted to our hospital were retrospectively analyzed, and the Kaplan-Meier method was used for analysis.

Results: The median survival time of the 54 children was 43.5 months. The complete remission rate after two courses was 90.74%, and the 3-year overall survival and disease-free survival rates were 81.48% and 77.78%, respectively. Ten(18.51%) of the 54 cases died, with six (11.11%) of them succumbing to recurrence. Univariate analysis revealed that age, gender, the initial count of white blood cells, remission status of day 19(D19) and day 35(D35), newly diagnosed lactate dehydrogenase levels, presence of a mediastinal mass, spleen infiltration, and adequacy of asparaginase treatment were statistically significant factors affecting the 3-year overall survival(OS) rate (P<0.05). Multivariate analysis revealed that age (P=0.004), D35 bone marrow remission (P<0.001), D35 MRD (P<0.001), and LDH (P=0.019) were independent risk factors influencing the 3-year os.

Conclusion: The overall efficacy of SCMC-ALL-2015(Shanghai Children's Medical Center-Acute Lymphoblastic Leukemia-2015) on pediatric T-ALL is good, and the death of a small number of children is mainly due to disease recurrence. Lactate dehydrogenase levels at the initial diagnosis, age, and remission status of D35 are independent risk factors.

T-cell acute lymphoid leukemia

childhood

efficacy

disease characteristics

prognostic analysis

T-cell acute lymphoblastic leukemia (T-ALL) is a highly proliferative malignancy derived from early T-cell progenitor cells[1–3]. Its etiology is still unclear and may be related to heredity, gene mutations, environmental pollution, physical radiation, and viral infection[4–7]. T-ALL accounts for only 10%~15% of acute lymphoblastic leukemia cases[8]. Patients with this type of leukemia are at risk of T-cell infiltration of organs, where invasive metastasis is the primary consequence of disease recurrence. This is closely associated with a poor prognosis. Chemokines, integrins, and Notch signaling pathways are all involved in the T-cell infiltration process [9–12]. Due to the low incidence of T-ALL in children, there are few reports in China. The Department of Pediatrics at Peking University People's Hospital has analyzed the clinical outcomes of 136 children with T-cell acute leukemia and discovered that the minimal residual disease on day 33 was a significant prognostic indicator[13]. This study retrospectively analyzed the clinical records and prognostic information of 54 cases of T-ALL in our hospital, collected over a period of more than 6 years. It summarized the clinical characteristics and identified adverse prognostic factors of T-ALL, providing valuable guidance for clinical practice.

Research Participants

A total of 54 children with T-ALL were admitted to our hospital from May 2015 to November 2020 selected. This study has been approved by the Ethics Committee of our hospital (approval number KY-2022-096-01), and all patients have signed the informed consent form in accordance with the Declaration of Helsinki. Enrollment criteria: (1) 0 ~ 14 years old; (2) All patients were diagnosed with T-ALL through morphological, immunological, genetic, and molecular biology examinations (MICM), meeting the diagnostic criteria outlined in the 2016 edition of the World Health Organization Classification of Tumors for Hematopoietic and Lymphoid Tissues. (3) The children have not received any leukemia-related treatment before coming to the department.

The enrolled patients were grouped according to gender, age, number of white blood cells at the first diagnosis, lactate dehydrogenase at the first diagnosis, mediastinal mass, spleen infiltration, liver infiltration, renal infiltration, D19 remission, D35 remission, and other factors.

Clinical Data Collection

Through the hospital's electronic medical record query system, hematology-oncology patient data registration specialist record book, regular telephone follow-up, and other methods, the medical history, laboratory examination reports, imaging data, prognosis, and other relevant data of the research subjects were collected and sorted.

Treatment Options

All children were treated with the SCMC⁃ALL⁃2015 chemotherapy regimen, and specific chemotherapy regimens were described in the references[14]. Total chemotherapy regimen: ① Inducing remission treatment: VDLP regimen: Vincristine (VCR) 1.5mg/(m². d), d8, 15, 22, 29; Daunorubicin (DNR) 25mg/(m². d), d8, 15, 22; PEG-asparaginase (PEG-ASP) 2000U/(m². d), d6, 26; Prednisone (Pred) 40mg/(m². d), po tid d1-7; Intrathecal injection (I/T): d3, 10, 17, 24. ② Consolidation therapy: CAT regimen: Cyclophosphamide (CTX) 1000mg/(m². d), d1; Ara-C 100mg/(m². d), q12h d1-7; Mercaptopurine (6-mp): 75mg/(m². d), po d1-7; I/T: d1. ③ Central Prevention I: HD-MTX regimen: Methotrexate (MTX) 5g/(m².24h), q2w × 3 (d1, 15, 29); I/T: d1, 15, 29; Calcium folinate (CF): at 42h, 15mg/m2, q6h × 4; Mercaptopurine (6-mp): 25mg/m², d1-42, qn, po. ④ Re induction I: 1) VDLD regimen: VCR 1.5mg/(m². d), d1, 8, 15; DNR 25mg/(m². d), d1, 8; PEG-ASP 2000U/(m². d), d3; Dexamethasone (Dex): 8mg/(m². d), d1-7, d15-21 po tid; I/T: d1; 2) CAT scheme: CTX 1000mg/(m². d), d1; Ara-C 2g/m², q12h d1-2; 6-mp: 75mg/(m². d), po d1-7; I/T: d1. ⑤ Central Prevention II: MTX 5g/(m².24h), q2w × 2 (d1,15); I/T: d1, 15; CF: at 42h, 15mg/m², q6h × 4; 6-mp: 25mg/m², d1-28, qn, po. ⑥ Intermittent treatment I: MTX 20mg/m², qw x 8W; 6-mp 50mg/(m². d), po qn × 8W. ⑦ Re induction II: VDLD regimen (as above). ⑧ Maintenance therapy I: 1) MTX 20mg/m², qw x 8W; 6-mp: 50mg/(m². d), po qn x 8W; 2) CAT scheme (as above); 3) Dex 8mg/(m2. d), po d1-4; VCR 1.5mg/(m2. d), d1; Ara-C 2g/m2, q12h × 4; I/T d1. ⑨ Maintenance therapy II: MTX 20mg/m2, qw; 6-mp: 50mg/m2, qn; VCR 1.5mg/(m2. d), every d49; Dex 8mg/(m2. d), every d49-56. The total treatment period of the above plan was 24 months to 30 months. The total number of intrathecal injections was 20 times, and if there was central invasion, it is 24 times. All 54 children with T-ALL were classified into high-risk groups for treatment.

Efficacy Evaluation And Follow-up

Bone marrow aspiration examinations were performed at intervals of day19, day 35, and every six months during the maintenance therapy period, to assess the proportion of naive cells and measurable residual disease (MRD). The proportion of naive cells is less than 5% belongs to the M1 bone marrow image, 5%~25% belongs to the M2 bone marrow image, and more than 25% belongs to the M3 bone marrow image. MRD monitoring was marked by monoclonal antibody combinations to screen for the immunophenotypes co-expressed on tumor cells but not on normal cells, with a sensitivity of 10^− 4. MRD < 0.01% is considered negative, while MRD > 0.01% is considered positive. Complete remission (CR) is defined as M1 bone marrow image. Recurrence is defined as M2 or M3 bone marrow images or extramedullary recurrence. Overall survival (OS) refers to the time from the date of the first diagnosis to death or the end of follow-up. Event-free survival (EFS) refers to the time from the first diagnosis to the occurrence of the first event (such as relapse, death, or the follow-up cut-off). The follow-up deadline is June 30, 2023.

Statistical Methods

SPSS 22.0 was used to analyze the data, and the median and interquartile ranges were used to statistically describe the continuous variables, such as age. The Kaplan-Meier method was used to calculate the survival function, and the chi-square test was employed for univariate analysis, with p < 0.05 considered statistically significant.

General Information

Among the 54 children, 43 were boys and 11 were girls, resulting in a male-to-female ratio of 3.9:1. Out of these children, 32 were younger than 10 years old, while 22 were older than 10 years old. There were 28 cases (51.85%) with a white blood cell (WBC) count≤0×10⁹/L and 26 cases (48.15%) with a WBC count > 50×10⁹/L. 25 cases (46.30%) were diagnosed with lactate dehydrogenase (LDH)≤2000U/L, while 29 cases (53.70%) had LDH > 2000U/L. Among them, 24 cases (44.44%) were accompanied by mediastinal infiltration, 19 cases (35.19%) were accompanied by hepatic infiltration, and only 5 cases (9.26%) were accompanied by renal infiltration. There were 3 cases (5.56%) of tumor lysis that occurred at the initial stage, with all three children having an initial WBC≥180×10⁹/L and lactate dehydrogenase (LDH) levels > 3300. Among them, 2 cases were transferred to the pediatric intensive care unit due to tumor lysis syndrome and were transferred out after stabilization to continue chemotherapy. We used pegylated asparaginase(PEG-ASP) at a dose of 2000IU/m2 each time. The total course of treatment consisted of eight doses of PEG-ASP, with a total dose of 16000IU/m2. A total dose of less than 16000IU/m2 is considered insufficient. The summary data of all children is shown in Table 1.

Bone Marrow Examination

All children were tested for leukemia immunophenotyping at the initial diagnosis. T-lineage markers included CD7, cCD3, TCRαβ, TCRγδ, CD3, CD4, CD8, CD1a, CD2, CD5, and TDT. MRD was monitored by flow cytometry, using fluorescence in situ hybridization (FISH) to screen for mutant genes, including BCR-ABL1, MLL, TEL-AML1, PDGFRb, and C-myc. Among the 54 children, 2 were positive for the MLL gene and 1 case was positive for C-myc.

Efficacy Assessment And Prognostic Follow-up

After the diagnosis was confirmed, all 54 children received sequential chemotherapy. Forty-nine children (90.74%) achieved CR after two courses of treatment. Unfortunately, six children died due to recurrence during the follow-up period, resulting in a recurrence rate of 11.11%. Two cases of recurrence occurred in the central nervous system, two cases in the bone marrow, one case in the testes and bone marrow, and the last case in the central nervous system and bone marrow. Allogeneic hematopoietic stem cell transplantation was performed in two cases. In one case, the D35MRD was greater than 1%, while in the other case, MRD levels increased during maintenance therapy. Both children were still alive and free of disease at the time of follow-up.

The median survival time of the 54 children was 43.5 (1.27 ~ 86.60) months. The OS and 3-year disease-free survival (DFS) rates were 81.48% and 77.78%, respectively. Among them, 4 cases were lost to follow-up. Out of 54 cases, 44 (81.48%) were alive, while10 (18.52%) died. Among the deceased, 6 died due to relapse, and the remaining 4 cases passed away after not responding to initial treatment. The survival curve is depicted in Fig. 1.

Prognostic Factor Analysis

Univariate analysis revealed that splenic infiltration and renal infiltration were not statistically significant for 3-year OS (P > 0.05). While age (> 10 years), gender, number of leukocytes at first diagnosis (WBC > 50×10⁹/L), whether D19 bone marrow was in remission, D19MRD (≥0.01%), whether D35 bone marrow was in remission, D35MRD (≥0.01%), lactate dehydrogenase (LDH > 2000U/L), mediastinal mass, spleen infiltrate, and the total amount of asparaginase were statistically significant for 3-year OS (P < 0.05). The statistical results are shown in Table 2.

The factors with P < 0.05 in Table 2 were included in the Cox regression analysis. The results indicated that age, D35 bone marrow remission, D35 MRD, and LDH were independent risk factors influencing the 3-year overall survival rate of patients. The statistical results are shown in Table 3.

T-cell acute lymphoblastic leukemia is an aggressive hematologic malignancy characterized by the transformation and expansion of T-cell progenitor cells[15, 16]. Current treatments for T-ALL include high-intensity combination chemotherapy to achieve high overall survival rates, with promising efficacy observed in pediatric patients [17, 18]. Despite the high response rate after front-line treatment, a small number of pediatric patients still experience relapse[19], with a 10-year OS of 21% ± 8% for relapsed T-ALL[20], indicating a poor prognosis. Pei Zhengkang, a foreign scholar, believes that the prognosis of pediatric T-ALL is generally worse than that of B-ALL [21]. The reasons for this are as follows: (1) patients with T-ALL are usually older than patients with B-ALL, have poor tolerance to chemotherapy, especially dexamethasone and asparaginase, and have an increased risk of extramedullary recurrence; (2) the majority of patients with B-ALL have favorable genetic subtypes (such as ETV6-RUNX1 and hyperdiploid), which result in a better outcome compared to the T-ALL subtype; (3) patients with B-ALL are more likely to receive available targeted therapies, such as ABL tyrosine kinase inhibitors for Philadelphia chromosome-positive and some Philadelphia chromosome-like ALL, and multiple immunotherapies such as CAR-T for CD19-positive and CD22-positive B-ALL cases. However, new treatment options for T-ALL are limited [22–24]. Among the 54 children with T-ALL in this study, 22 (40.74%) were older than 10 years old, which is a relatively high proportion. The sensitivity of the chemotherapy drugs dexamethasone and asparaginase was lower in older children, consequently impacting the prognosis. Our univariate prognostic analysis also confirmed that age was one of the significant influencing factors for the 3-year OS. We conducted routine fusion gene testing on all children and identified 2 cases of MLL gene positivity and 1 case of C-myc positivity. Unfortunately, there were no specific targeted drug treatments available for these cases. One of the major barriers to targeting T-cell tumors is that the activation or clearance of normal or tumor T-cells can cause significant toxicity. Therefore, there is a need for the development of novel immunotherapies that are both safe and effective [25–27].

ALL often shows a very active proliferative rate and high tumor burden, characterized by elevated white blood cell counts and frequent thoracic masses and pleural effusions [28]. In this study, 26 (48.15%) of the 54 patients had a high WBC count (> 50×10⁹/L), including 24 cases (44.44%) with thoracic invasion, and 29 cases (53.70%) with lactate dehydrogenase levels > 2000 U/L at the initial stage, which was consistent with the literature report[29]. At present, measurable residual disease remains the best predictor of prognosis and clinical decision-making[30]. Our study demonstrates that MRD outcomes on D19 and D35 are closely linked to prognosis. Consequently, children with high MRD levels are more likely to experience recurrence and have a relatively poor prognosis. Large-scale studies have shown that the use of asparaginase is closely associated with improved survival rates. Patients who use asparaginase for more than 26 weeks have shown nearly a 20% increase in survival rates compared to those who use it for less than 26 weeks[31, 32]. Moreover, increasing the dosage of asparaginase may have a positive impact on controlling the recurrence of extramedullary leukemia[33]. Our study also suggests that the total amount of asparaginase has an impact on prognosis. Multivariate survival analysis revealed that LDH, D35 bone marrow remission, and D35 MRD were independent risk factors influencing the 3-year overall survival rate. This suggests that the tumor burden of children at the time of initial diagnosis and achieving remission on D35 (after 2 courses of induction therapy) had a significant impact on the prognosis.

In COG trials AALL0434, the 4-year event-free survival (EFS) and overall survival (OS) were 84.7% ± 2.3% and 89.0% ± 2.0%[34]. The patient's prognosis is better than ours. The reason may be that the chemotherapy regimen is different, and their HR patients were randomly assigned to receive or not receive courses of nelarabine[34]. A literature review summarizes all instances of T-ALL induction failure in two consecutive cross-border randomized trials (UKALL2003 and UKALL2011)[35]. The study found that the incidence of induction failure was 10.3%, which was significantly correlated with age.In the UKALL2011 study, chemotherapy incorporating nalabine was introduced, and the outcomes were reinforced with hematopoietic stem cell transplantation. However, the results did not show improvement[35]. Combining TAL1 lesions with mutations in the MYC and RAS pathways creates a genetic stratifier that can identify patients who are highly likely to not respond to conventional therapy[35]. Our study did not conduct thorough genomic profiling and did not identify potential subtypes of genetic diseases.

In summary, T-cell acute lymphoblastic leukemia is a rare and highly malignant neoplastic disease in children. Chemotherapy is the primary treatment currently available. The SCMC-ALL-2015 regimen has shown good efficacy in achieving early response and improving long-term prognosis. Our study also found that lactate dehydrogenase levels (at the time of initial diagnosis), age, and D35 remission were independent risk factors affecting the prognosis. Due to the low incidence of the disease and the limited clinical sample size, some conclusions may be biased. Multi-center large-sample clinical studies are needed to further deepen the understanding of pediatric T-ALL.

Ethics approval and consent to participate
Ethical clearance was obtained from the Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University. Written informed consent was obtained from all parents

Consent for publication

Not applicable.

Competing interests
The authors declare no competing interests.

Author details

Department of Pediatrics, the Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University, 1 Huanghe West Road, Huaian 223000, China.

Funding

This study supported by Nanjing Medical University Science and Technology Development Fund Project (NMUB2018153).

Author Contribution

All authors contributed to the conception and design of the study. H.Q. independently performed the literature search, data collection, statistical analysis, and wrote the first draft of the manuscript. W.K. critically reviewed and revised the manuscript. All authors contributed to the article and read and approved the final manuscript as submitted.

Acknowledgements

The authors thank the support staff for their cooperation during this study.

Data Availability

The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.

Huang YH, Wan CL, Dai HP, Xue SL: Targeted therapy and immunotherapy for T cell acute lymphoblastic leukemia/lymphoma. ANN HEMATOL 2023, 102(8):2001-2013.
Duffield AS, Mullighan CG, Borowitz MJ: International Consensus Classification of acute lymphoblastic leukemia/lymphoma. VIRCHOWS ARCH 2023, 482(1):11-26.
Shiraz P, Jehangir W, Agrawal V: T-Cell Acute Lymphoblastic Leukemia-Current Concepts in Molecular Biology and Management. BIOMEDICINES 2021, 9(11).
Gocho Y, Liu J, Hu J, Yang W, Dharia NV, Zhang J, Shi H, Du G, John A, Lin TN et al: Network-based systems pharmacology reveals heterogeneity in LCK and BCL2 signaling and therapeutic sensitivity of T-cell acute lymphoblastic leukemia. NAT CANCER 2021, 2(3):284-299.
Vadillo E, Dorantes-Acosta E, Pelayo R, Schnoor M: T cell acute lymphoblastic leukemia (T-ALL): New insights into the cellular origins and infiltration mechanisms common and unique among hematologic malignancies. BLOOD REV 2018, 32(1):36-51.
Dai YT, Zhang F, Fang H, Li JF, Lu G, Jiang L, Chen B, Mao DD, Liu YF, Wang J et al: Transcriptome-wide subtyping of pediatric and adult T cell acute lymphoblastic leukemia in an international study of 707 cases. P NATL ACAD SCI USA 2022, 119(15):e2120787119.
Baran N, Lodi A, Dhungana Y, Herbrich S, Collins M, Sweeney S, Pandey R, Skwarska A, Patel S, Tremblay M et al: Inhibition of mitochondrial complex I reverses NOTCH1-driven metabolic reprogramming in T-cell acute lymphoblastic leukemia. NAT COMMUN 2022, 13(1):2801.
Karrman K, Johansson B: Pediatric T-cell acute lymphoblastic leukemia. GENE CHROMOSOME CANC 2017, 56(2):89-116.
Gianni F, Belver L, Ferrando A: The Genetics and Mechanisms of T-Cell Acute Lymphoblastic Leukemia. CSH PERSPECT MED 2020, 10(3).
Steimle T, Dourthe ME, Alcantara M, Touzart A, Simonin M, Mondesir J, Lhermitte L, Bond J, Graux C, Grardel N et al: Clinico-biological features of T-cell acute lymphoblastic leukemia with fusion proteins. BLOOD CANCER J 2022, 12(1):14.
Salmeron-Villalobos J, Ramis-Zaldivar JE, Balague O, Verdu-Amoros J, Celis V, Sabado C, Garrido M, Mato S, Uriz J, Ortega MJ et al: Diverse mutations and structural variations contribute to Notch signaling deregulation in paediatric T-cell lymphoblastic lymphoma. PEDIATR BLOOD CANCER 2022, 69(11):e29926.
Grazioli P, Orlando A, Giordano N, Noce C, Peruzzi G, Scafetta G, Screpanti I, Campese AF: NF-kappaB1 Regulates Immune Environment and Outcome of Notch-Dependent T-Cell Acute Lymphoblastic Leukemia. FRONT IMMUNOL 2020, 11:541.
Xue YJ, Wang Y, Lu AD, Jia YP, Zuo YX, Ding MM, Zeng HM, Zhang LP: Clinical Analysis of Pediatric T-Cell Acute Lymphoblastic Leukemia Using the MRD-Oriented Strategy System. CL LYMPH MYELOM LEUK 2023, 23(7):477-483.
Chu J, Cai H, Cai J, Bian X, Cheng Y, Guan X, Chen X, Jiang H, Zhai X, Fang Y et al: Prognostic significance of steroid response in pediatric acute lymphoblastic leukemia: The CCCG-ALL-2015 study. FRONT ONCOL 2022, 12:1062065.
Drobna M, Szarzynska-Zawadzka B, Dawidowska M: T-cell acute lymphoblastic leukemia from miRNA perspective: Basic concepts, experimental approaches, and potential biomarkers. BLOOD REV 2018, 32(6):457-472.
Karrman K, Johansson B: Pediatric T-cell acute lymphoblastic leukemia. GENE CHROMOSOME CANC 2017, 56(2):89-116.
Raetz EA, Teachey DT: T-cell acute lymphoblastic leukemia. HEMATOL-AM SOC HEMAT 2016, 2016(1):580-588.
Lato MW, Przysucha A, Grosman S, Zawitkowska J, Lejman M: The New Therapeutic Strategies in Pediatric T-Cell Acute Lymphoblastic Leukemia. INT J MOL SCI 2021, 22(9).
Laukkanen S, Veloso A, Yan C, Oksa L, Alpert EJ, Do D, Hyvarinen N, McCarthy K, Adhikari A, Yang Q et al: Therapeutic targeting of LCK tyrosine kinase and mTOR signaling in T-cell acute lymphoblastic leukemia. BLOOD 2022, 140(17):1891-1906.
Reismuller B, Attarbaschi A, Peters C, Dworzak MN, Potschger U, Urban C, Fink FM, Meister B, Schmitt K, Dieckmann K et al: Long-term outcome of initially homogenously treated and relapsed childhood acute lymphoblastic leukaemia in Austria--a population-based report of the Austrian Berlin-Frankfurt-Munster (BFM) Study Group. BRIT J HAEMATOL 2009, 144(4):559-570.
Teachey DT, Pui CH: Comparative features and outcomes between paediatric T-cell and B-cell acute lymphoblastic leukaemia. LANCET ONCOL 2019, 20(3):e142-e154.
Pui CH, Evans WE: Treatment of acute lymphoblastic leukemia. NEW ENGL J MED 2006, 354(2):166-178.
Chohan KL, Siegler EL, Kenderian SS: CAR-T Cell Therapy: the Efficacy and Toxicity Balance. CURR HEMATOL MALIG R 2023, 18(2):9-18.
Zhang X, Zhu L, Zhang H, Chen S, Xiao Y: CAR-T Cell Therapy in Hematological Malignancies: Current Opportunities and Challenges. FRONT IMMUNOL 2022, 13:927153.
Ghione P, Moskowitz AJ, De Paola N, Horwitz SM, Ruella M: Novel Immunotherapies for T Cell Lymphoma and Leukemia. CURR HEMATOL MALIG R 2018, 13(6):494-506.
Inaba H, Pui CH: Immunotherapy in pediatric acute lymphoblastic leukemia. CANCER METAST REV 2019, 38(4):595-610.
Lu P, Liu Y, Yang J, Zhang X, Yang X, Wang H, Wang L, Wang Q, Jin D, Li J et al: Naturally selected CD7 CAR-T therapy without genetic manipulations for T-ALL/LBL: first-in-human phase 1 clinical trial. BLOOD 2022, 140(4):321-334.
Sanchez-Martin M, Ferrando A: The NOTCH1-MYC highway toward T-cell acute lymphoblastic leukemia. BLOOD 2017, 129(9):1124-1133.
Burns MA, Place AE, Stevenson KE, Gutierrez A, Forrest S, Pikman Y, Vrooman LM, Harris MH, Hunt SK, O'Brien JE et al: Identification of prognostic factors in childhood T-cell acute lymphoblastic leukemia: Results from DFCI ALL Consortium Protocols 05-001 and 11-001. PEDIATR BLOOD CANCER 2021, 68(1):e28719.
Petit A, Trinquand A, Chevret S, Ballerini P, Cayuela JM, Grardel N, Touzart A, Brethon B, Lapillonne H, Schmitt C et al: Oncogenetic mutations combined with MRD improve outcome prediction in pediatric T-cell acute lymphoblastic leukemia. BLOOD 2018, 131(3):289-300.
Gupta S, Wang C, Raetz EA, Schore R, Salzer WL, Larsen EC, Maloney KW, Mattano LJ, Carroll WL, Winick NJ et al: Impact of Asparaginase Discontinuation on Outcome in Childhood Acute Lymphoblastic Leukemia: A Report From the Children's Oncology Group. J CLIN ONCOL 2020, 38(17):1897-1905.
Schore RJ, Devidas M, Bleyer A, Reaman GH, Winick N, Loh ML, Raetz EA, Carroll WL, Hunger SP, Angiolillo AL: Plasma asparaginase activity and asparagine depletion in acute lymphoblastic leukemia patients treated with pegaspargase on Children's Oncology Group AALL07P4(.). LEUKEMIA LYMPHOMA 2019, 60(7):1740-1748.
Heo YA, Syed YY, Keam SJ: Pegaspargase: A Review in Acute Lymphoblastic Leukaemia. DRUGS 2019, 79(7):767-777.
Hayashi RJ, Winter SS, Dunsmore KP, Devidas M, Chen Z, Wood BL, Hermiston ML, Teachey DT, Perkins SL, Miles RR et al: Successful Outcomes of Newly Diagnosed T Lymphoblastic Lymphoma: Results From Children's Oncology Group AALL0434. J CLIN ONCOL 2020, 38(26):3062-3070.
O'Connor D, Demeulemeester J, Conde L, Kirkwood A, Fung K, Papaleonidopoulou F, Bloye G, Farah N, Rahman S, Hancock J et al: The Clinicogenomic Landscape of Induction Failure in Childhood and Young Adult T-Cell Acute Lymphoblastic Leukemia. J CLIN ONCOL 2023, 41(19):3545-3556.

Table 1 to 3 are available in the Supplementary Files section.

No competing interests reported.

Download PDF

Version 1

posted

You are reading this latest preprint version

Clinical prognosis analysis of 54 pediatric patients with T-cell acute lymphoblastic leukemia

Status:

Version 1

Abstract

Figures

Background

Materials and Methods

Research Participants

Clinical Data Collection

Treatment Options

Efficacy Evaluation And Follow-up

Statistical Methods

Results

General Information

Bone Marrow Examination

Efficacy Assessment And Prognostic Follow-up

Prognostic Factor Analysis

Discussion

Conclusion

Declarations

Ethics approval and consent to participate
Ethical clearance was obtained from the Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University. Written informed consent was obtained from all parents

Consent for publication

Competing interests
The authors declare no competing interests.

Author details

Funding

Author Contribution

Acknowledgements

Data Availability

References

Tables

Additional Declarations

Supplementary Files

Status:

Version 1

Clinical prognosis analysis of 54 pediatric patients with T-cell acute lymphoblastic leukemia

Status:

Version 1

Abstract

Figures

Background

Materials and Methods

Research Participants

Clinical Data Collection

Treatment Options

Efficacy Evaluation And Follow-up

Statistical Methods

Results

General Information

Bone Marrow Examination

Efficacy Assessment And Prognostic Follow-up

Prognostic Factor Analysis

Discussion

Conclusion

Declarations

Ethics approval and consent to participate Ethical clearance was obtained from the Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University. Written informed consent was obtained from all parents

Consent for publication

Competing interests The authors declare no competing interests.

Author details

Funding

Author Contribution

Acknowledgements

Data Availability

References

Tables

Additional Declarations

Supplementary Files

Status:

Version 1

Ethics approval and consent to participate
Ethical clearance was obtained from the Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University. Written informed consent was obtained from all parents

Competing interests
The authors declare no competing interests.