Acute Lymphoblastic Leukemia (ALL): Understanding Your Pathology Report

Section Editor: David Li MD
June 22, 2026

Acute lymphoblastic leukemia (ALL) is a type of blood cancer that starts in the bone marrow, the soft, spongy tissue inside bones where blood cells are made. In ALL, the bone marrow makes large numbers of immature white blood cells called lymphoblasts, also called leukemic blasts. These abnormal cells grow quickly and crowd out the normal cells, so the bone marrow can no longer make enough healthy red blood cells, white blood cells, and platelets. ALL is most often diagnosed in children, but it also occurs in adults. When the same cancer forms a mass outside the bone marrow and blood rather than filling the marrow, it is called lymphoblastic lymphoma.

This article will help you understand the findings in your pathology report for acute lymphoblastic leukemia, what each term means, and why it matters for your care or the care of your child.

What are the types of acute lymphoblastic leukemia?

Acute lymphoblastic leukemia (ALL) is divided into types based on which kind of lymphocyte, a type of white blood cell, the leukemia comes from. There are two main types:

B-cell acute lymphoblastic leukemia (B-ALL) — The most common type, especially in children. It begins in immature B lymphocytes (B cells), white blood cells that normally make antibodies to help fight infection.
T-cell acute lymphoblastic leukemia (T-ALL) — Less common, and seen more often in older children, teenagers, and young adults. It begins in immature T lymphocytes (T cells), white blood cells that normally help control the immune response and fight viruses.

The type of ALL is one of the first things the care team determines, because B-cell and T-cell disease are treated somewhat differently. The articles linked above explain each type in more detail.

Who gets acute lymphoblastic leukemia?

Acute lymphoblastic leukemia (ALL) can occur at any age, but it is most commonly diagnosed in children between 2 and 5 years old. There is a second, smaller peak in adults over the age of 50. Overall, ALL is slightly more common in males than in females, and somewhat more common in people of Hispanic and white backgrounds. ALL is not contagious, and in almost all cases it is not caused by anything a person did or was exposed to.

What causes acute lymphoblastic leukemia?

The exact cause of acute lymphoblastic leukemia (ALL) is usually not known. ALL develops when the DNA inside a developing blood cell in the bone marrow is damaged, which causes the cell to grow out of control as a leukemic blast. A few factors are known to increase the risk:

Inherited genetic conditions — Some conditions present from birth, such as Down syndrome, are linked with a higher risk of ALL. Most people with these conditions never develop leukemia.
Previous cancer treatment — Earlier treatment with chemotherapy or radiation therapy can increase the risk.
Random DNA changes — In most cases, ALL happens because of mutations (changes in the DNA) that occur by chance in a single bone marrow cell. These changes are not inherited and cannot be passed to children.

What are the symptoms of acute lymphoblastic leukemia?

Most symptoms of acute lymphoblastic leukemia (ALL) happen because the leukemic blasts fill the bone marrow and prevent it from making enough normal blood cells. Common symptoms include:

Fatigue and weakness — caused by a shortage of red blood cells (anemia).
Frequent fevers and infections — caused by a shortage of normal infection-fighting white blood cells (neutropenia).
Easy bruising or bleeding — caused by low platelet counts (thrombocytopenia).
Bone or joint pain — caused by the buildup of leukemic blasts inside the bones.
Swollen lymph nodes, liver, or spleen — caused by leukemia cells collecting in these organs.
Unexplained weight loss or loss of appetite.

Because these symptoms can also be caused by many other, far more common conditions, blood tests and an examination of the bone marrow are needed to confirm the diagnosis.

How is the diagnosis made?

The diagnosis of acute lymphoblastic leukemia (ALL) is made by examining the blood and bone marrow. A complete blood count (CBC) is usually the first test. In ALL, the white blood cell count may be very high or very low, the red blood cell and platelet counts are often low, and immature lymphoblasts may be seen circulating in the blood.

Because blasts in the blood can resemble other immature cells, a bone marrow sample is needed to confirm the diagnosis. This is done with a bone marrow aspiration and biopsy, usually taken from the back of the hip bone after the area is numbed. A pathologist examines the sample under the microscope and counts the proportion of blasts. In ALL, the bone marrow is largely replaced by lymphoblasts that crowd out the normal blood-forming cells. The same disease is called lymphoblastic lymphoma instead of leukemia when it forms a mass (for example, in a lymph node) with little or no involvement of the blood and marrow.

Additional laboratory tests are used to classify the leukemia. Flow cytometry, a test that measures cell-surface proteins as cells pass through a laser beam, determines whether the blasts are of B-cell or T-cell origin and is the primary test for this purpose. Immunohistochemistry, which uses antibodies to detect specific proteins, may also be used. Chromosome studies and molecular tests look for the genetic changes described in the next section, which help guide treatment and predict outcome. Finally, a sample of the fluid around the brain and spinal cord (cerebrospinal fluid) is often collected via lumbar puncture to assess whether leukemia cells have spread to the central nervous system.

Genetic changes and molecular testing in acute lymphoblastic leukemia

Acute lymphoblastic leukemia (ALL) is classified into subtypes based on the genetic changes found in leukemic blasts. These changes do not cause symptoms on their own, but they are among the most important findings on the report because they guide treatment and help predict how the leukemia will behave. The most relevant changes include:

Philadelphia chromosome (BCR::ABL1 fusion) — This change joins two genes, BCR and ABL1, to form a new gene that drives leukemia growth. B-ALL with this change is called Philadelphia chromosome-positive (Ph-positive) B-ALL. Its presence is used to decide whether to add a drug class called tyrosine kinase inhibitors, which block the abnormal protein produced by the fusion gene, to chemotherapy.
KMT2A rearrangement — A change involving the KMT2A gene. It is more common in infants and is generally linked with a higher risk of relapse, which may lead the team to consider more intensive treatment.
Chromosome number — Leukemic blasts with extra chromosomes (high hyperdiploidy) tend to have a more favorable outcome, while blasts with too few chromosomes (hypodiploidy) tend to have a higher risk.
Other defining changes — Many additional genetic patterns are recognized, including ETV6::RUNX1 (favorable) and a group called Philadelphia chromosome-like (Ph-like) B-ALL, which behaves like Ph-positive disease and may respond to targeted drugs even though the BCR::ABL1 fusion is absent.

After treatment begins, very sensitive tests, including flow cytometry, PCR, and next-generation sequencing, are used to detect small numbers of leukemia cells that may remain. This is called measurable (or minimal) residual disease, often abbreviated as MRD. The MRD result is one of the strongest predictors of whether the leukemia will return, and it is used to decide whether treatment should be intensified. The specific genetic subtypes are described in more detail in the articles on B-ALL and T-ALL linked above.

What is the prognosis for acute lymphoblastic leukemia?

Prognosis means the expected outcome of a disease. Unlike most solid tumors, acute lymphoblastic leukemia (ALL) is not given a stage based on size or spread, because it begins throughout the bone marrow and blood rather than as a single mass. Instead, the likely outcome is estimated from a combination of factors:

Age — Children, particularly those between 1 and 10 years old, generally do better than infants under 1 year and adults.
White blood cell count at diagnosis — A very high count is associated with a higher risk.
Genetic subtype — Changes such as high hyperdiploidy and ETV6::RUNX1 are favorable, while KMT2A rearrangement and hypodiploidy carry a higher risk.
Spread to the central nervous system — Leukemia cells found in the cerebrospinal fluid require additional treatment directed at the brain and spinal cord.
Response to treatment (MRD) — Reaching an MRD-negative result, meaning no leukemia can be detected by sensitive testing, is one of the most favorable signs.

Outcomes have improved substantially. Most children with ALL are now cured, with five-year survival above 90% for childhood B-ALL. Outcomes in adults have historically been lower, but they have improved with modern chemotherapy combined with immunotherapy, reaching four-year survival of roughly 80 to 85% in younger adults who can receive these treatments. Philadelphia chromosome-positive B-ALL, once considered high risk, now reaches five-year survival above 80% when tyrosine kinase inhibitors are combined with chemotherapy or immunotherapy. Your prognosis depends on your own combination of these factors, which your care team can explain in the context of your specific report.

What happens after a diagnosis of acute lymphoblastic leukemia?

Once acute lymphoblastic leukemia (ALL) is confirmed, the care team plans treatment based on the type (B-cell or T-cell), the genetic changes found, the patient’s age, and the overall risk. Treatment for ALL is typically delivered over about two to three years in phases. The findings on the pathology report shape several decisions:

Combination chemotherapy — The backbone of treatment, given in phases (often called induction, consolidation, and maintenance) to bring the leukemia into remission and keep it there.
Treatment aimed at the brain and spinal cord — Because ALL can spread to the central nervous system, chemotherapy is given into the cerebrospinal fluid through a lumbar puncture, and radiation is sometimes used.
Tyrosine kinase inhibitors — For Philadelphia chromosome-positive B-ALL, drugs such as imatinib, dasatinib, or ponatinib are added to target the BCR::ABL1 protein.
Immunotherapy — Drugs such as blinatumomab (which directs the patient’s own T cells against the leukemia) and inotuzumab ozogamicin are increasingly used in B-ALL, including to clear measurable residual disease.
CAR T-cell therapy — For B-ALL that has come back or not responded, a patient’s own T cells can be re-engineered to attack the leukemia. Approved options exist for children and young adults as well as for older adults.
Stem cell (bone marrow) transplant — An allogeneic transplant, using blood-forming cells from a donor, may be considered for higher-risk or relapsed disease.

T-cell ALL is treated with similar chemotherapy backbones, often including a drug called nelarabine. Throughout treatment, the MRD result is used to decide whether to intensify therapy or move toward a transplant. Care is provided by a team that usually includes a hematologist or oncologist, specialized nurses, and other supportive care specialists, and clinical trials are often available. Decisions about which of these approaches apply are made by the treatment team together with the patient or family, based on the specific findings in the report.

Questions to ask your doctor

What type of acute lymphoblastic leukemia do I have, B-cell or T-cell?
What did the flow cytometry and other tests show about the leukemia cells?
Were any genetic changes found, such as the Philadelphia chromosome (BCR::ABL1), a KMT2A rearrangement, or a change in chromosome number?
Am I (or is my child) considered standard risk or high risk, and what does that mean?
Has the leukemia spread to the cerebrospinal fluid or central nervous system?
Will I need treatment directed at the brain and spinal cord?
What treatment phases should I expect, and how long will treatment last?
Could a tyrosine kinase inhibitor, immunotherapy, or CAR T-cell therapy be part of my treatment?
How will measurable residual disease (MRD) be tested, and how will the results affect my treatment?
Might I need a stem cell (bone marrow) transplant?
What is my prognosis based on my specific test results?
Are there clinical trials that I should consider?