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Understanding leukemia

Acute lymphoblastic leukemia (ALL)

ALL is the most common cancer in children, but it also occurs in adults. It develops quickly, yet thanks to modern treatment the great majority of children reach long-lasting remission, and for adults immunotherapy and targeted drugs have opened new options. This topic explains the types of ALL, how it is diagnosed and the stages of treatment.

Last updated: ~6 min read
Bone marrow smear in acute lymphoblastic leukemia: densely packed purple lymphoblasts with large nuclei and scant cytoplasm
Figure 1.Bone marrow smear in ALL: immature lymphoblasts fill the marrow.

01Short answer

Acute lymphoblastic leukemia (ALL) is the rapid growth of immature cells of the lymphoid line (lymphoblasts) in the bone marrow. The blasts suppress normal blood formation and can spread to the brain and spinal cord, lymph nodes, spleen, liver and testicles. There are two main types: B-cell (more common) and T-cell. In the US the median age at diagnosis is 18: more than half of cases occur in people under 20, but ALL can occur at any age. Genetic findings — such as the Philadelphia chromosome — shape treatment. Treatment usually has induction, consolidation and long maintenance phases and takes about 2–3 years in total; protecting the central nervous system is part of every phase. In children, 5-year survival is about 90%.

02Simple explanation

In ALL, the problem starts in the lymphoid family — the family that makes B and T lymphocytes. Genetic changes build up in a precursor cell, which stops maturing and multiplies quickly. These immature cells are called lymphoblasts.

The lymphoblasts pile up in the marrow and leave no room for healthy cells, causing tiredness, paleness, infections, fever, bruising and bleeding. ALL also often causes bone and joint pain (children may limp), swollen lymph nodes and an enlarged spleen and liver. Symptoms usually develop over a few weeks.

Lymphoblasts can pass from the blood into the fluid around the brain and spinal cord. Ordinary chemotherapy does not reach this area well, so treatment includes special “protection” — drugs are injected directly into the spinal fluid. This is called central nervous system (CNS) prophylaxis.

ALL treatment is long but comes in stages: first intensive induction (to reach remission), then consolidation (to destroy hidden cells) and finally about 2 years of maintenance, often as tablets at home. The long maintenance phase helps prevent relapse.

Childhood ALL is one of the great success stories of modern medicine: about 90% of children live at least 5 years, and most stay in long-lasting remission. Results in adults are more challenging, but targeted drugs, immunotherapy and CAR-T cell therapy have improved the picture considerably in recent years.

03Scientific explanation

Diagnosis relies on finding lymphoblasts in the marrow or blood and on immunophenotyping (flow cytometry). According to the NCI, precursor B-cell ALL cells typically express CD10, CD19, CD34 and nuclear TdT, while precursor T-cell ALL cells commonly express CD2, CD3, CD7, CD34 and TdT. WHO 2022 divides B-lymphoblastic leukemia/lymphoma into genetic subtypes (e.g. BCR::ABL1, KMT2A rearrangements, ETV6::RUNX1, hyperdiploidy, hypodiploidy, BCR::ABL1-like); T-ALL is a separate group. Mature B-cell Burkitt leukemia is treated not as ALL but as Burkitt lymphoma.

The Philadelphia chromosome — t(9;22), BCR::ABL1 — is found in about 20–30% of adults with ALL and becomes more common with age; it is rare in children. In Ph-positive ALL, tyrosine kinase inhibitors (e.g. imatinib, dasatinib, nilotinib) are added to chemotherapy or immunotherapy. BCR::ABL1-like (Ph-like) ALL has a gene-expression profile similar to Ph-positive ALL but lacks BCR::ABL1; it is often linked to other kinase changes and is considered unfavourable. In children, high hyperdiploidy (51–65 chromosomes) and ETV6::RUNX1 are favourable findings, while KMT2A rearrangements and hypodiploidy are unfavourable.

The treatment phases are induction (usually a corticosteroid, vincristine, asparaginase and/or an anthracycline), consolidation/intensification and maintenance (usually daily mercaptopurine and weekly methotrexate, with periodic vincristine/steroid pulses). CNS prophylaxis uses intrathecal chemotherapy (e.g. methotrexate), high-dose systemic chemotherapy and, rarely, radiation. In children, the risk group is based on age, white count, B or T lineage, genetics, CNS involvement and early treatment response (MRD). In adolescents and young adults, “pediatric-inspired” protocols have shown better results.

Immunotherapy has a special place in B-ALL: blinatumomab (a bispecific antibody that “links” T cells to CD19-bearing leukemia cells), inotuzumab ozogamicin (an antibody-drug conjugate aimed at CD22) and CD19-directed CAR-T cell therapy (tisagenlecleucel, brexucabtagene autoleucel). The NCI also lists the menin inhibitor revumenib among targeted treatments for acute leukemia with a KMT2A rearrangement. MRD is one of the strongest prognostic markers in ALL and influences decisions about intensifying treatment or transplant. In the US, overall 5-year relative survival for ALL is 73.2% (SEER, 2016–2022) — considerably higher in children and lower in older adults.

04What happens in the body?

B-cell and T-cell ALL

By looking at markers on the surface of the blasts, flow cytometry shows whether they belong to the B or T line. B-ALL is more common. T-ALL is relatively more common in teenage and young adult males and can cause a thymus mass in the chest — if it presses on the airway, that is an emergency.

Two groups of round cells on a dark background: small teal points of light glow on the surface of one group and amber points on the other, with a thin line of light between them.
Figure 2.Flow cytometry identifies the B or T line from markers on the surface of the blasts.

Genetics shapes treatment

Cytogenetics, FISH and molecular tests look for the Philadelphia chromosome, KMT2A rearrangements, hyperdiploidy and other changes. For example, in Ph-positive ALL targeted tablets are added to treatment. These results define the risk group and how intensive treatment needs to be.

A long but staged journey

Induction usually lasts several weeks and consolidation several months, while maintenance continues for about 2 years, mostly at home with regular check-ups. In every phase, a drug is injected into the spinal fluid to protect the brain and spinal cord.

A side view of a translucent human head and spine; a soft teal protective light flows along the brain and spinal canal, dark navy background, calm atmosphere.
Figure 3.CNS prophylaxis: medicine is delivered into the fluid around the brain and spinal cord.

Immunotherapy and MRD

Blinatumomab, inotuzumab and CAR-T cell therapy are a major advance, especially in relapsed or treatment-resistant B-ALL, and some protocols now use them earlier. MRD tests measure invisible residual disease and help fine-tune the treatment plan.

05ALL: from cell to treatment plan

How ALL develops and is treated, in four steps.

Genetic change — Mutations build up in a lymphoid precursor cell.1Genetic changeMutations build up in a lymphoid precursor cell.
Lymphoblasts multiply — The marrow fills with immature cells.2Lymphoblasts multiplyThe marrow fills with immature cells.
Spread is possible — Lymph nodes, spleen, CNS, thymus.3Spread is possibleLymph nodes, spleen, CNS, thymus.
Diagnosis and risk — Flow cytometry, genetics, MRD.4Diagnosis and riskFlow cytometry, genetics, MRD.
Induction → remissionAbout 98% of children reach remission.
CNS protectionDrugs are given into the spinal fluid.
Long maintenanceAbout 2 years, to prevent relapse.

06Main groups of ALL

GroupWhat does it mean?Treatment feature
B-ALL (Ph-negative)The most common form; blasts carry CD19, CD10 and othersStandard chemotherapy protocols; CD19/CD22-directed immunotherapy is possible
Ph-positive B-ALLBCR::ABL1 (t(9;22)); about 20–30% of adultsTyrosine kinase inhibitors are added to treatment
BCR::ABL1-like (Ph-like) B-ALLA profile similar to Ph-positive, but without BCR::ABL1Usually more intensive treatment; targeted drugs are being studied in some cases
KMT2A-rearranged ALLEspecially common in infants; considered unfavourableIntensive treatment; menin inhibitors may be an option at relapse
T-ALLBlasts carry CD3, CD7 and others; a thymus mass may be presentSpecific protocols; CNS prophylaxis is especially important
Burkitt leukemia (mature B)MYC rearrangement; grows very fastTreated as Burkitt lymphoma rather than as ALL

* This table is a simplified overview; protocols for children and adults differ. Your hematologist will explain your subtype and what it means.

07Key terms

ALL
Acute lymphoblastic leukemia — a leukemia in which lymphoblasts multiply quickly.
Lymphoblast
An immature cell of the lymphoid line.
B-ALL / T-ALL
Types of ALL depending on whether the blasts come from the B or T line.
Philadelphia chromosome
A shortened chromosome 22 carrying BCR::ABL1, formed by t(9;22).
Intrathecal
Given into the fluid around the spinal cord.
CNS prophylaxis
Treatment that protects the brain and spinal cord from leukemia.
Maintenance
Long, gentler treatment to prevent relapse.
Blinatumomab
A bispecific antibody that directs T cells to CD19-bearing leukemia cells.
CAR-T
A patient’s own T cells, modified in the lab to attack leukemia.
MRD
Measurable residual disease — a very small number of leukemia cells left in remission.

08Key points

  • ALL is an acute leukemia in which lymphoid blasts multiply quickly in the marrow.
  • It is the most common cancer in children, but also occurs in adults.
  • There are two main types: B-ALL (more common) and T-ALL.
  • Genetic findings (e.g. the Philadelphia chromosome) shape treatment.
  • Treatment consists of induction, consolidation and about 2 years of maintenance.
  • Protecting the brain and spinal cord is an important part of treatment.
  • About 90% of children live at least 5 years; new immunotherapies are available for adults.
  • MRD is one of the most important measures of treatment response.

09Frequently asked questions

Why does ALL treatment take so long?

Because leukemia cells can hide even after remission. Research has shown that long, gentle maintenance treatment lowers the risk of relapse. During maintenance, most people live at home and can return to school or work.

Why are lumbar punctures done so often?

Both to check whether there are leukemia cells in the spinal fluid and to give drugs directly there to protect the CNS. Pain relief is used during the procedure, and children often have brief sedation.

Is Philadelphia-positive ALL worse?

In the past, Ph-positive ALL had a difficult outlook. Today, tyrosine kinase inhibitors and immunotherapy have improved results considerably. Your hematologist will explain what to expect in your situation.

Is ALL in adults different from ALL in children?

Yes, for several reasons: adults more often have unfavourable genetic changes (such as Ph), and they may tolerate treatment less well. So results in adults are not as good as in children, but new treatments are narrowing the gap.

Is CAR-T therapy suitable for everyone?

No. CAR-T is usually approved for relapsed or treatment-resistant B-ALL, with certain age and other conditions. It can cause serious side effects and is given in specialised centres. Your hematologist can assess whether it may suit you.

Will I need a transplant?

Not everyone does. A transplant is considered mainly for high-risk disease, MRD-positive status or after relapse. Most children reach long-lasting remission without a transplant.

10Questions for your doctor

Take these questions to your appointment. The ones you save are collected on the “My questions” page and stay on this device only.

  1. Is my ALL B-cell or T-cell?

  2. Has the Philadelphia chromosome been checked, and what is the result?

  3. What treatment is planned to protect the brain and spinal cord?

  4. How long will all the phases of treatment take?

My questions

12Sources

  1. National Cancer Institute (NCI). Adult Acute Lymphoblastic Leukemia Treatment (PDQ®) — Patient Version
  2. National Cancer Institute (NCI). Adult Acute Lymphoblastic Leukemia Treatment (PDQ®) — Health Professional Version
  3. National Cancer Institute (NCI). Childhood Acute Lymphoblastic Leukemia Treatment (PDQ®) — Patient Version
  4. National Cancer Institute (NCI), SEER. Cancer Stat Facts: Acute Lymphocytic Leukemia (ALL)
  5. American Cancer Society. Key Statistics for Acute Lymphocytic Leukemia (ALL)
  6. American Cancer Society. How Is Acute Lymphocytic Leukemia Classified?
  7. American Cancer Society. Signs and Symptoms of Acute Lymphocytic Leukemia (ALL)
  8. American Cancer Society. Typical Treatment of Acute Lymphocytic Leukemia
  9. NHS. Acute lymphoblastic leukaemia — Symptoms
  10. National Cancer Institute (NCI). NCI Dictionary of Cancer Terms: Philadelphia chromosome
  11. Leukemia (Nature) — WHO 5th edition. WHO Classification of Haematolymphoid Tumours: Lymphoid Neoplasms
  12. National Cancer Institute (NCI). CAR T Cells: Engineering Patients’ Immune Cells to Treat Their Cancers
Medical disclaimerThis information is for educational purposes only and does not replace medical advice.
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