It is the most common cancer in children, with: a peak incidence between ages 2 and 5 another peak after age 50. About 15 people per 1 million are affected by ALL.

Accueil Patient care Acute Lymphoblastic Leukemias

Acute Lymphoblastic Leukemias

Q: What are the causes?

Its origin is often unknown, and it is not contagious.The “blasts” accumulate in your bone marrow, which can no longer properly produce normal blood cells.

Q: Which tests are used to make the diagnosis?

The diagnosis of ALL is based on: A blood test (CBC) to measure the different blood cells and identify any abnormalities (such as low red blood cells, white blood cells, or platelets). A bone marrow examination (bone marrow aspirate/biopsy) to identify abnormal cells, their chromosomes, and genes. A cerebrospinal fluid (CSF) analysis to check for possible neurological involvement.

Q: What are the symptoms?

Fatigue, paleness, palpitations, and shortness of breath: signs of anemia (low red blood cells) Fever and infections (especially lung infections): signs of leukopenia or neutropenia (low white blood cells) Bleeding (especially from mucous membranes) and bruising: signs of thrombocytopenia (low platelets) These signs reflect bone marrow failure: the bone marrow is unable to produce enough red blood cells, white blood cells, and platelets. Tumor syndrome: certain organs may swell due to the accumulation of lymphoblasts (spleen, lymph nodes, testicles…). Sometimes: bone or joint pain and neurological symptoms may occur.

What is leukemia?

Definition

Your blood contains cancer cells. These are immature blood cells called “blasts.”

Leukemia

The disease develops rapidly, and treatment must begin within days of the diagnosis.

Acute

An abnormality occurs in the differentiation of lymphoid cells in the bone marrow.

Lymphoblastic

Your blood contains cancer cells. These are immature blood cells called “blasts.”

Leukemia

The disease develops rapidly, and treatment must begin within days of the diagnosis.

Acute

An abnormality occurs in the differentiation of lymphoid cells in the bone marrow.

Lymphoblastic

Types of Acute Lymphoblastic Leukemia

85%

B-cell phenotype

15%

T-cell phenotype

Understanding acute lymphoblastic leukemia

What are the causes?

Its origin is often unknown, and it is not contagious.
The “blasts” accumulate in your bone marrow, which can no longer properly produce normal blood cells.

What are the risk factors?

Exposure to ionizing radiation or certain chemicals (such as benzene), as well as chemotherapy and radiotherapy used to treat other cancers.

Certain genetic disorders (Trisomy 21, Fanconi anemia, Li-Fraumeni syndrome, etc.) and pre-existing blood disorders (myeloproliferative syndromes).

What are the symptoms?

Fatigue, paleness, palpitations, and shortness of breath: signs of anemia (low red blood cells)
Fever and infections (especially lung infections): signs of leukopenia or neutropenia (low white blood cells)
Bleeding (especially from mucous membranes) and bruising: signs of thrombocytopenia (low platelets)

These signs reflect bone marrow failure: the bone marrow is unable to produce enough red blood cells, white blood cells, and platelets.

Tumor syndrome: certain organs may swell due to the accumulation of lymphoblasts (spleen, lymph nodes, testicles…).

Sometimes: bone or joint pain and neurological symptoms may occur.

Who is affected?

It is the most common cancer in children, with:

a peak incidence between ages 2 and 5
another peak after age 50.

About 15 people per 1 million are affected by ALL.

Which tests are used to make the diagnosis?

The diagnosis of ALL is based on:

A blood test (CBC) to measure the different blood cells and identify any abnormalities (such as low red blood cells, white blood cells, or platelets).

A bone marrow examination (bone marrow aspirate/biopsy) to identify abnormal cells, their chromosomes, and genes.

A cerebrospinal fluid (CSF) analysis to check for possible neurological involvement.

Treatment of Acute Lymphoblastic Leukemia

Treatment Objectives

The treatment aims to eliminate the “blasts”, allowing the normal bone marrow to rebuild healthy blood cell populations (red blood cells, white blood cells, and platelets).

Your doctor may suggest participating in a clinical trial to gain access to an innovative drug and/or contribute to improving medical practices.

Treatment is carried out in several phases.

Prephase

1 week

Corticosteroid therapy: taking corticosteroids, which are anti-inflammatory medications

Lumbar puncture: to analyze cerebrospinal fluid (CSF) and administer chemotherapy

Pre-chemotherapy assessments: evaluation of various organs through blood tests, echocardiography, possible CT scan, fertility preservation, and placement of a central venous catheter

These steps help determine the characteristics of the disease necessary to start an appropriate treatment.

Induction phase

5–6 weeks of hospitalization (to minimize the risk of infection)

Corticosteroid therapy: taking corticosteroids, which are anti-inflammatory medications

Intravenous combination chemotherapy: several chemotherapy drugs given together (vincristine, anthracyclines, cyclophosphamide, asparaginase)

Lumbar puncture

To eliminate blasts present in the bone marrow and blood.

This phase causes aplasia (a drop in blood cell counts), temporarily lowering the immune defenses. Antibiotics or platelet and red blood cell transfusions may be required.

A bone marrow examination is performed at the end to check whether the blasts have been eliminated. If successful, this is called complete remission.

Treatment is adapted for patients over 65 years old (adjusted chemotherapy doses), B-cell ALL (addition of immunotherapy), patients with the Philadelphia chromosome (targeted therapy added in all phases).

Consolidation phase + delayed intensification

Several months, with hospital stays of 3–7 days interspersed with time at home.

High-dose consolidation chemotherapy given in cycles

Immunotherapy (Blinatumomab) to help the patient’s immune system destroy residual leukemia cells

Lumbar punctures

To eliminate residual disease and reduce the risk of relapse.

Between consolidation cycles, a delayed intensification phase is performed.

Corticosteroid therapy (anti-inflammatory medications) and intravenous combination chemotherapy (same as in the induction phase) are used.

Usually performed on an outpatient basis, but hospitalization is often required to monitor for infection risk in case of severe white blood cell reduction (aplasia).

Cranial radiotherapy (use of high-energy beams to destroy cancer cells) concludes the intensive treatment phase.

For patients at high risk of relapse, a stem cell transplant may be performed to replace diseased bone marrow with healthy marrow from a compatible donor (often a family member). For patients with the Philadelphia chromosome, consolidation consists of alternating high-dose chemotherapy and Blinatumomab combined with targeted therapy. The targeted therapy continues during the maintenance phase, which also includes re-induction cycles.

Maintenance phase

2 years, on an outpatient basis

Two oral chemotherapy treatments

Monthly intravenous chemotherapy and corticosteroids → only during the first year

In some cases, you may be invited to participate in a clinical research trial. You will be required to sign a written consent form and will have the right to withdraw from the trial at any time without providing a reason.

Research

The biology of T-cell ALL and B-cell ALL. Understanding the molecular mechanisms of tumor progression

For a subgroup of B-cell ALL patients with a gene rearrangement, monitoring the disease through this rearrangement is more reliable than traditional methods. This improves the assessment of patient outcomes.

Emmanuelle Clappier and her team

The fundamental mechanisms of T-cell ALL development: receptors, epigenetics, genomics, and more.

Some T-cell ALL (so-called PI3K pathway-altered) are highly dependent on glucose and, when glucose is scarce, use glutamine instead. Using inhibitors to block these pathways offers a promising and innovative therapeutic approach.

Vahid Asnafi and Elizabeth Macintyre and their team

The dynamic interactions between T-ALL leukemia cells and their microenvironment, particularly the vascular components.

A microfluidic “on-chip” vascular network and a bio-fabricated human bone marrow and brain system in a preclinical model to study the vascular system’s response to leukemia-induced specific stimuli.

Diana Passaro and her team

The interaction of T-ALL and B-ALL leukemia cells with the various components of the bone marrow.

Identification of a population of dormant leukemia cells that are resistant to chemotherapy, providing new prognostic and therapeutic insights. Development of a humanized bone model, which will allow the study of intercellular interactions that induce chemoresistance in leukemia cells.

Françoise Pflumio and her team