Table of Contents
1. Introduction: What is B-cell ALL?
2. Epidemiology & Risk Factors
3. Pathophysiology & Genetic Basis
4. Symptoms & Red Flags
5. Diagnosis & Risk Stratification
6. Treatment Approach: Multiphase Strategy
• Induction
• Consolidation
• Maintenance
• Central Nervous System (CNS) Prophylaxis
7. Modern Therapies & Personalized Medicine
• Targeted therapy & TKIs (Ph+ B-ALL)
• Immunotherapies (Blinatumomab, Inotuzumab, CAR T-cell)
• Stem Cell Transplantation (Allogeneic HCT)
• Emerging treatments & clinical trials
8. Prognosis & Follow-up Care
9. How RecMed Supports Patients with B-cell ALL
10. FAQs
11. References
B-cell acute lymphoblastic leukemia (B-ALL) is a malignancy of immature B-cell progenitors (lymphoblasts) in the bone marrow, blood and sometimes extramedullary sites. It is the most common subtype of acute lymphoblastic leukemia (ALL).
In both children and adults, a multidisciplinary, risk-adapted, personalized treatment strategy is paramount for optimal outcomes.
B-ALL accounts for approximately 75–80% of ALL cases in children and ~75% of adult ALL.
Risk factors include: prior radiation exposure, inherited syndromes (e.g., Down syndrome), certain genetic predispositions, and exposures that may affect bone marrow function.
Emerging genome-wide studies are identifying ancestral susceptibility loci (e.g., in children of African ancestry) which may inform future prevention and risk stratification.
B-ALL arises when a B-cell precursor acquires genetic and epigenetic abnormalities that block differentiation and promote proliferation. Key features:
• Chromosomal translocations (e.g., t(12;21) ETV6-RUNX1, t(9;22) BCR-ABL1)
• Gene amplifications or deletions (e.g., iAMP21)
• High hyperdiploidy is a favorable prognostic factor in childhood B-ALL.
• Molecular profiling is increasingly important for treatment decisions.
Children or adults with B-ALL may present with:
• Fatigue, pallor, bleeding or bruising (thrombocytopenia)
• Fever, recurrent infections (neutropenia)
• Bone or joint pain (marrow expansion)
• Lymphadenopathy, splenomegaly
• CNS involvement: headache, vomiting, visual changes
Prompt recognition and referral to a hematology/oncology centre is critical.
Diagnosis includes:
• Peripheral blood counts & film, bone-marrow aspirate/biopsy with immunophenotyping
• Cytogenetic/molecular testing (e.g., BCR-ABL1, iAMP21, Ph-like ALL)
• Assessment of minimal residual disease (MRD) — major prognostic marker.
• While there is no traditional “stage” system for ALL, treatment is stratified by risk (age, white-cell count, genetic features, MRD)
The treatment of B-ALL involves several phases:
Induction
Aim: achieve complete remission (CR) by reducing blasts. Usually multi-agent chemotherapy over several weeks.
Consolidation
Purpose: eradicate residual disease, deepen remission, and prepare for further therapy.
Maintenance
Lower-intensity therapy given for many months (often 2-3 years) to sustain remission. For Ph-negative B-ALL in children, maintenance may include methotrexate and 6-mercaptopurine, sometimes alternating with immunotherapy (e.g., blinatumomab).
CNS Prophylaxis
Since leukemia cells may hide in the sanctuary of the CNS, prophylactic therapy (intrathecal chemotherapy, sometimes cranial irradiation) is standard.
Targeted therapy & TKIs (Ph+ B-ALL)
In Philadelphia-chromosome positive B-ALL, the addition of tyrosine kinase inhibitors (TKIs) alongside chemotherapy has dramatically improved outcomes.
Immunotherapies
• Blinatumomab (CD19 bispecific)
• Inotuzumab ozogamicin (CD22 antibody-drug conjugate)
• CAR T-cell therapy (e.g., tisagenlecleucel) for relapsed/refractory cases.
Stem-Cell Transplantation
Allogeneic hematopoietic stem-cell transplantation (allo-HSCT) remains a key option for high-risk or relapsed B-ALL. Personalized decisions based on risk, remission status and donor availability.
Emerging Treatments & Trials
Novel therapies (e.g., osteoclast-targeting, novel biomarkers) are under investigation in high-risk B-ALL.
Prognosis is highly variable depending on age, risk features, and response to therapy. In pediatric B-ALL, long-term survival can reach ~80-90%.
Follow-up includes: monitoring for relapse, late effects of therapy (cardiac, endocrine, fertility), and psychosocial support.
At RecMed Medical Travel (Istanbul, Türkiye), we offer:
• Advanced diagnostics: molecular profiling, MRD assessment
• Access to specialized treatment modalities: immunotherapy, CAR T-cell therapy, stem-cell transplant
• Multidisciplinary team approach: hematologists, oncologists, transplant specialists, genetic counselling
• International patient coordination: visas, accommodation, translation services, after-care planning
Our goal is to deliver personalized world-class care for B-cell ALL patients in an international setting.
Can B-cell ALL be cured?
Yes — many children and some adults achieve long-term remission or cure, especially with early diagnosis and risk-adapted therapy.
What is minimal residual disease (MRD) and why does it matter?
MRD refers to the small number of leukemic cells remaining after treatment; it’s one of the strongest prognostic factors and guides therapy escalation.
When is CAR T-cell therapy used in B-ALL?
Typically when B-ALL is relapsed or refractory to conventional therapy and the patient is eligible for advanced immunotherapy.
Does B-cell ALL affect adults and children differently?
Yes — children generally have better outcomes; adults tend to have more complex disease, different risk features and may require more intensive or novel therapies.
1. National Cancer Institute (NCI). Acute Lymphoblastic Leukemia Treatment (PDQ®).
2. Prognostic and Predictive Biomarkers in Precursor B-cell Acute Lymphoblastic Leukemia.
3. Management of B-cell lineage acute lymphoblastic leukemia.
4. Acute Lymphoblastic Leukemia, Version 2.2024, NCCN Clinical Practice Guidelines in Oncology (ALL).
5. Genome-wide association study of childhood B-cell ALL.
6. Nature article: Targeting osteoclasts in high-risk B-ALL.