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Results for “Precursor Cell Lymphoblastic Leukemia-Lymphoma”

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PubMedDate not supplied

The detection of oral Candida in pediatric leukemia patients.

Among leukemia patients, a significant number of deaths are due to Candida septicemia, many of which are associated with previous oral infections. Oral candidiasis detection methods vary, and the relationship between oral candidiasis and Candida colonization (CC) is not well defined. The main objectives of this study were to compare the incidence of CC in a healthy and leukemic population, and also to evaluate the efficacy of three simple and inexpensive methods of detecting oral CC in predicting the occurrence of oral candidiasis. A secondary objective was to portray speciation in the examined populations. Forty-two pediatric leukemia patients and 42 healthy, age-, race-, and gender-matched control patients participated in this study. The three methods of detection were cytological examination of the oral mucosa, and direct culture methods from mucosal smears using Sabouraud's dextrose agar (Becton Dickinson Microbiology Systems, Cockeysville, MD) and Oricult-N (Orion Diagnostica, Espoo, Finland). This study demonstrated an increased prevalence of CC in pediatric leukemia patients with the direct culture method detecting CC in a significantly greater proportion of the population (Oricult-N,P = 0.034; Sabouraud's dextrose agar, P = 0.0036). Candida albicans was the predominant species. Further study is needed to determine the clinical significance of oral CC and its relationship to oral candidiasis and systemic infection in pediatric leukemia patients.

Adolescent↗

PubMed1992

[CD10(CALLA)-negative acute lymphoblastic leukemia. A group with a bad prognosis].

The results of 188 patients with acute lymphoblastic leukemia, studied between 1985 and 1990, showed that 8 cases were CD10 negative, Dr, and CD19 positive. These findings indicate cell dedifferentiation and poor prognosis. The patients age ranged from 2 to 30 years, with a mean of 11 years. The male/female ratio was 5/3. Lymph node enlargement and splenomegaly were found in the 8 patients. With the exception of one patient in whom leucopenia was present, the white cell counts were always higher than 30,000/dl. The karyotype was studied in four cases, and all of them were hyperdiploid. This is the first report in Venezuela of cases with acute lymphoblastic leukemia - CD 10 negative.

Adolescent↗

PubMed1992

[A case of acute lymphocytic leukemia transformed from malignant lymphoma].

We report a case of malignant lymphoma in a 15-year-old male. He had erythema and nodular lesions, hepatomegaly, and splenomegaly with high fever for one month. Laboratory examination revealed a normal blood routine test, a few lymphomatic cells in the bone marrow, and histopathologic changes characteristic of malignant lymphoma in a skin biopsy. Two months later, a second bone marrow examination showed 90% prolymphoblasts. The peripheral blood count revealed WBC 108 x 10(9)/L; among these, prolymphoblasts accounted for 92%. The patient was diagnosed as acute lymphocytic leukemia, and died 2 days later. The diagnosis and transformation from malignant lymphoma to acute lymphocytic leukemia are discussed.

Adolescent↗

PubMed1992

[Leopard spot chorioretinopathy. Initial manifestation of recurrent acute lymphocytic leukemia].

An 11-year-old girl with a history of acute lymphocytic leukemia of the central nervous system had attained complete remission for almost 3 1/2 years after combination chemotherapy and radiotherapy when she developed iritis and chorioretinopathy of the right eye. Neither an anterior chamber tap nor a diagnostic vitrectomy revealed leukemic cells. Both nonspecific anti-inflammatory therapy and antiviral treatment were unsuccessful. Finally, lymphoblasts were detected in the cerebrospinal fluid and in the bone marrow after repeated lumbar puncture and bone marrow aspiration. Combination chemotherapy alone was resumed, resulting in the resolution of all acute ocular symptoms and bone marrow involvement. Only the leopard-spot-like pigmentary fundus changes persisted. The child has now remained in continuous complete remission for 1 1/2 years.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1992

Long term endocrine complications of acute leukemia therapy--a case report.

We report a patient with acute lymphoblastic leukemia who underwent treatment comprising chemotherapy, radiotherapy (cranial and testicular) and then a bone marrow transplant from an identical twin. He was cured of his leukemia and has been disease-free for nine years. With long term survival, there were problems, notably those of growth and endocrine insufficiency, which needed special considerations in management.

Adolescent↗

PubMed1992

Bone marrow transplantation in Ramathibodi Hospital: progress report.

Bone marrow transplantation has become the accepted treatment for several hematologic disorders. We have done 3 autologous and 6 allogeneic bone marrow transplantations at Ramathibodi Hospital since July 1989 in patients with acute lymphoblastic leukemia, acute non-lymphocytic leukemia, chronic myeloid leukemia, non-Hodgkin's lymphoma and severe aplastic anemia. Only one patient with aplastic anemia had late graft rejection, but the rest of them engrafted and did well during the median follow up period of 317 days (range: 39 to 962 days) post transplantation. None of the allogeneic BMT had graft-versus-host disease. We use cyclosporin and short course methotrexate for post transplantation immunosuppression.

Adolescent↗

PubMedDate not supplied

Treatment of testicular relapse in childhood acute lymphoblastic leukemia.

The experience of rescue therapy for 6 patients of childhood acute lymphoblastic leukemia (ALL) with testicular relapse is reported. In two patients, testicular relapse occurred 1 and 4 years off therapy, respectively. Two patients had testicular relapse on therapy. The remaining 2 patients had testicular relapse after premature discontinuation of therapy by the parents. Isolated testicular relapse was found in 2 patients. The rest of the testicular relapses were concurrent with either bone marrow (BM) or central nervous system (CNS) relapses. The rescue therapy included bilateral testicular irradiation 24 Gy, and systemic reinduction chemotherapy, followed by maintenance therapy as that of TCL 821 or TCL 842 protocol for high risk patients of ALL. CNS prophylaxis, which included intrathecal medication and/or cranial irradiation 18 Gy (if not given before), was also given. After testicular relapse, one had subsequent BM and CNS relapses and received more aggressive chemotherapy. Another one had subsequent CNS relapse 4 months after another premature withdrawal of treatment. One patient, who presented with CNS leukemia at diagnosis, had concurrent testicular and CNS relapses and died of CNS leukemia 3 months later. The remaining 5 patients remained in continuous complete remission for 26 to 95 months with a median duration of 54 months.

Child↗

PubMedDate not supplied

[Lymphoblastic lymphoma in the adult].

We report a series of 57 adults patients with lymphoblastic lymphoma treated at our Institution between 1975 and 1987. Mediastinal involvement was seen in 74% (42 cases); extranodal involvement (not including bone marrow) in 24% (14 cases); stage IV in 84% (48 patients) and leukemic phase in 19% (11 patients). In 15 cases immunologic studies were performed 14 proved to be of T type and the other one lack both T and B markers. Survival and duration of remission was better when the patients were treated with aggressive chemotherapy that included maintenance and central nervous system prophylaxis. In the multivariable analysis we observed that mediastinal mass, attainment of a complete remission and high levels of lactic dehidrogenase were associated with a worse prognosis. We believe that patients with lymphoblastic lymphoma have an aggressive disease and that the treatment should be more aggressive than in other non-Hodgkin's lymphomas, and include central nervous system prophylaxis.

Adolescent↗

PubMed1977

Enzyme markers in leukaemia.

Explore the source record for details and available documents.

Biomarkers, Tumor↗

PubMed1979

Complications of tumour overkill when associated with high dose methotrexate therapy.

Three patients, in whom tumour overkill by cytotoxic treatment, including high dose methotrexate with folinic acid rescue, resulted in the 'phosphate shower syndrome' (hyper-uricaemia, hyperkalaemia and hyperphosphataemia with hypocalcaemia and tetany, with metabolic acidosis and acute renal impairment) are described. Severe methotrexate toxicity occurred in two of these patients. High dose methotrexate would appear contra-indicated in situations where massive tumour lysis is possible.

Adolescent↗

PubMed2026

Case Report: Immune-driven clonal selection underlying lineage switch from B-Precursor acute lymphoblastic leukemia to acute myeloid leukemia following inotuzumab ozogamicin.

Lineage switch (LS), defined as a change in leukemic lineage during the disease course, is a rare but clinically significant event in acute leukemia and is typically associated with poor prognosis. Although LS has been increasingly reported following targeted immunotherapies, the clonal mechanisms underlying this phenomenon remain incompletely understood, particularly in cases without KMT2A rearrangement. We report a case of LS from B-precursor acute lymphoblastic leukemia (BCP-ALL) to acute myeloid leukemia (AML) following treatment with the CD22-targeted antibody-drug conjugate inotuzumab ozogamicin. To elucidate the clonal architecture underlying LS, targeted next-generation sequencing was performed on bone marrow samples obtained at multiple time points throughout the disease course. Genomic analysis demonstrated that the lymphoid and myeloid disease phases shared ancestral genetic alterations but displayed distinct mutational profiles. At the time of LS, TP53 and SMC1A mutations newly emerged, whereas only a subset of mutations detected at ALL relapse was retained. These findings suggest that the AML phase most likely resulted from the selective expansion of a genetically distinct subclone derived from a common progenitor, rather than the direct transdifferentiation of the dominant ALL clone, consistent with immunotherapy-driven clonal selection. Longitudinal genomic profiling revealed stepwise clonal evolution during disease progression, supporting a model of immunotherapy-driven clonal selection leading to LS. This case provides molecular evidence suggesting that immune-targeted therapy can promote expansion of minor pre-existing subclones with alternative lineage potential within a common progenitor even in non-KMT2A-rearranged leukemia. Our findings highlight the importance of comprehensive genomic monitoring during immunotherapy to identify therapy-resistant subclones and better understand mechanisms of lineage plasticity in acute leukemia.

Humans↗

PubMedDate not supplied

The expression of the ras p21 oncoprotein in the bone marrow smears of children with acute leukemia.

Point mutations of the ras genes have been detected in various hematologic malignancies. This genetic event may either occur in all malignant cells or be acquired by different subclones, which however, cannot be demonstrated adequately by analyzing only DNA derived from patient specimens. The availability of the ras p21 monoclonal antibody (MoAb) Y 13259 makes possible the direct study of the distribution of the ras gene product in human malignant cells. In this report the expression of the ras p21 oncoprotein in the bone marrow smears of 35 children with acute leukemia has been analyzed. The smears were treated with the MoAb Y 13259, biotinylated goat anti-rat IgG, streptavidin, peroxidase and stained with diaminobenzidine (DAB). The intensity of the staining was evaluated by two independent observers as negative or equivocal (-/+), moderate (+) or intense (++), by counting one thousand cells. Patients were also classified according to the percentage of the stained cells into four groups (0, I, II, III). It was found that 22/35 (63%) were (+) or (++) positive as follows: 11/21 (52%) with ALL CALLA (+), 2/2 ALL-B, 3/3 ALL-T and 6/9 AML. In Group 0 (none of the blasts was stained) were 13/35 (37%), as well as in Group I (1 to 25% of the blasts stained 1+ or 2+ positive), while in Group II (26 to 50% positive stained) 3/35 and in Group III (more than 51% stained) 6/35, all of which were AML (6/9). It is concluded that the immunohistochemical analysis of the ras p21 in blast cells of children with acute leukemia may demonstrate that ras gene expression in some subclones, the intensity and percentage of which may be of some clinical importance.

Acute Disease↗

PubMed2025

Cytogenetic and molecular characterization of an atypical ETP-ALL case with BCL2 dependency: therapeutic implications for Venetoclax use.

BACKGROUND: Early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) is a rare, high-risk subtype of T-ALL characterized by distinctive immunophenotypic and genomic features. It is often associated with induction failure and frequent relapses. Despite recent advances in its molecular characterization, the prognosis remains dismal, and effective targeted therapies are limited. METHODS AND RESULTS: We report a pediatric, multi-refractory ETP-ALL case with novel cytogenetic alterations, including a 4q deletion and a t(16;18)(q24;q21) translocation. Molecular profiling revealed progressive activation of the BCL2 pathway and disruption of Th17-related immune markers. Ex vivo sensitivity assays performed at different disease stages demonstrated increasing BCL2 dependency. Based on these findings, venetoclax was administered on a compassionate-use basis, resulting in rapid hematologic recovery and a marked reduction in blast percentage. CONCLUSIONS: This case highlights the role of clonal evolution and immune deregulation in accompanying BCL2 addiction in relapsed ETP-ALL. Altogether, our findings underscore the therapeutic potential of venetoclax in refractory pediatric ETP-ALL cases with progressive BCL2 dependency.

Humans↗

PubMed2026

Late acquisition of BCR::ABL1 during clonal evolution of SAMD9-associated MDS with phenotypic shift from AML to B-ALL.

We describe a unique case of SAMD9-associated myelodysplastic syndrome (MDS) with monosomy 7 that evolved over 16 years into BCR::ABL1-positive acute myeloid leukemia (AML) and subsequently manifested as B-cell acute lymphoblastic leukemia (B-ALL). Genomic analysis at AML diagnosis revealed a germline SAMD9 mutation together with somatic RUNX1 and PPM1D mutations, supporting stepwise clonal evolution, with BCR::ABL1 emerging as a late leukemogenic event. The dominant leukemic population at AML onset showed myeloid morphology and immunophenotype, whereas a minor CD19+CD10+ population was already detectable. Following venetoclax and azacitidine therapy, the dominant leukemic phenotype shifted to B-ALL while retaining BCR::ABL1 positivity. Detection of the Philadelphia chromosome in mature neutrophils at both AML onset and ALL relapse supported multilineage involvement of a multipotent BCR::ABL1-positive clone. Ponatinib achieved disease control. This case highlights late acquisition of BCR::ABL1 during SAMD9-associated clonal evolution and therapy-driven phenotypic shift within a shared Ph-positive leukemic stem-cell hierarchy.

Humans↗

PubMed2026

Clinical and molecular prognostic factors in newly diagnosed pediatric T-cell lymphoblastic lymphoma: a prospective, multicenter, single-arm phase 2 clinical trial.

BACKGROUND: Poor early treatment response in T-cell lymphoblastic lymphoma (T-LBL) is associated with an unfavorable prognosis. This multicenter prospective study evaluated the efficacy of the response-adjusted Chinese Children's Cancer Group (CCCG-LBL-2016) protocol for pediatric T-LBL and examined clinical and molecular prognostic factors. METHODS: Clinical and laboratory data from seven pediatric oncology centers were analyzed. A sub-cohort of 23 patients underwent exploratory integrated genomic analysis, including targeted next-generation sequencing, RNA sequencing, and copy-number array analysis. Survival was evaluated using the Kaplan-Meier method, and prognostic factors were analyzed using multivariable Cox proportional hazards regression. RESULTS: A total of 163 patients (median age: 108 months; 116 males, 47 females) were enrolled, most with advanced disease (stage III: 81.0%; stage IV: 17.8%). Patients were stratified into the low-risk (R1, n = 2) and intermediate-risk groups (R2, n = 161); thirty one patients in the R2 group were escalated to the high-risk intensified regimen (R3) due to poor early response. The 3-year overall survival (OS) was 78.6% ± 3.3% and event-free survival (EFS) was 73.9% ± 3.5%. Outcomes differed by risk group (P < 0.05), with 3-year OS and EFS of 100% and 100% in R1, 82.6% ± 3.4% and 79.5% ± 3.4% in R2, and 58.6% ± 9.1% and 48.3% ± 9.1% in R3. Progression or recurrence occurred in 42 patients (median: 7 months; 3-year OS: 17.1% ± 6.3%). Clinical risk factors included R3 assignment and elevated lactate dehydrogenase. In the exploratory molecular sub-cohort, recurrent alterations included CDKN2A (39.1%), NOTCH1 (26.1%), FBXW7 (21.7%), and MTAP/PIK3R1/NRAS (13.0%). Exploratory multivariable Cox regression analysis identified that CDKN2A alteration was associated with an increased risk of progression or recurrence (hazard ratio = 35.89, 95% confidence interval: 3.07-419, P = 0.004). CONCLUSIONS: Adjusting the risk stratification based on treatment response significantly improved the overall prognosis of T-LBL. However, survival rates remain very low among patients who experience disease progression or recurrence. The preliminarily explored molecular genetic risk factors might contribute to further risk stratification and provide potential therapeutic targets.

Humans↗

PubMed2025

The super-enhancer regulatory gene SH2D1A promotes the progression of T cell acute lymphoblastic leukemia by activating CHI3L2.

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive leukemia subtype and a prevalent malignancy in children, with poor prognosis, high relapse rates, and drug resistance. Recent research has shown that super-enhancer-regulated genes play crucial roles in T-ALL progression. In this study, we identified SH2 domain containing 1 A (SH2D1A) as a gene regulated by super-enhancers, and is overexpressed, which correlates with unfavorable clinical outcomes in T-ALL. To investigate its role, we silenced SH2D1A expression in T-ALL cell models using RNA interference. This led to a significant reduction in cell proliferation, colony formation, and promoted apoptosis, as demonstrated by CCK-8 assays, soft agar colony formation, and flow cytometry analysis. In vivo, knockdown of SH2D1A significantly inhibited tumor growth and prolonged survival in mice bearing T-ALL. Mechanistically, we found that SH2D1A contributes to T-ALL progression by upregulating CHI3L2, a downstream effector that promotes cell proliferation and inhibits apoptosis. Using ChIP-Seq and RNA-seq technologies, we confirmed that SH2D1A regulates CHI3L2 expression through super-enhancer-mediated regulation in T-ALL cells. Our findings suggest that SH2D1A and CHI3L2 act as oncogenes in T-ALL, and may represent novel therapeutic targets. This research offers new insights into the molecular mechanisms of T-ALL and highlights potential avenues for therapeutic intervention.

Precursor T-Cell Lymphoblastic Leukemia-Lymphoma↗

PubMed2026

Deletion of 9p drives B-ALL through heterozygous inactivation of Pax5 and Cd72 in preleukemic cells.

The contribution of 9p deletion to B cell acute lymphoblastic leukemia (B-ALL) has remained elusive since its discovery more than 40 years ago. Here we show that loss of CD72 is recurrent in B-ALL cases containing PAX5 deletions, and that Cd72 haploinsufficiency drives B-ALL development in Pax5+/- mice. Mechanistically, Cd72+/-;Pax5+/- precursor B cells exhibited an inflammatory transcriptional profile characterized by a decrease in Myd88 expression, a finding that aligns with our previous studies of B-ALL development in Pax5+/- mice following exposure to immune stressors. These combined genomic analyses and functional models provide compelling evidence that co-deletion of 2 contiguous genes, Pax5 and Cd72, drives B cell leukemogenesis.

Animals↗

PubMed2026

Inhibition of the atypical kinase WNK1 as a therapeutic strategy in TAL-related T-cell acute lymphoblastic leukemia.

Driver mutations in T-cell acute lymphoblastic leukemia (T-ALL) rarely affect druggable kinases. However, these kinases can be aberrantly activated or repressed as secondary oncogenic events. Thus, integrating unbiased phosphoproteomics with genomic approaches may offer novel opportunities for target discovery and therapeutic interventions. In our study, we identified WNK1 (with no lysine [K]) as a potential target in T-ALL by pairing a list of vulnerable kinases with data from a phosphoproteomic screen of T-ALL cell lines. We subsequently validated WNK1 by loss-of-function-based studies and tested WNK inhibitors in several in vitro and in vivo T-ALL models and clinical T-ALL samples. We showed that therapeutic WNK1 repression promotes polyploidy, resulting in cell proliferation arrest, and morphometric changes, such as incomplete cell division or chromosome segregation through altered mitotic spindle assembly and abscission defects. Furthermore, we found that WNK1 is overexpressed in the TAL1/2-related subgroup, but not in normal thymus or lymph nodes, suggesting a potential translational area for clinical exploitation in poor-prognosis T-ALL carrying PTEN mutations and del(6q). Our work also reports a functional contribution of WNK1 in the leukemia establishment and progression. Structurally WNK1 is an atypical serine/threonine kinase that diverges from canonical kinases by lacking the conserved lysine in subdomain II, instead featuring a cysteine in subdomain I, which is critical for adenosine triphosphate (ATP) binding. This unusual structural configuration creates a distinct ATP-binding pocket with limited sequence similarity to conventional kinases, offering a unique opportunity to develop highly selective small molecules. Targeting this atypical ATP domain could thus provide a therapeutic advantage and broaden the treatment landscape for T-ALL.

WNK Lysine-Deficient Protein Kinase 1↗