Leukemia

Practice Essentials

Leukemias are a group of diseases that result from the unregulated clonal proliferation of cells secondary to genetic abnormalities in a hematopoietic cell. Compared to normal cells, a high rate of proliferation and low rate of apoptosis offers leukemic cells a growth advantage. Leukemias eventually result in bone marrow failure.1

Depending on the percentage of blasts or leukemia cells in the blood or bone marrow, leukemias are classified as either chronic or acute. They are also classified as myeloid or lymphoid based on the predominant type of malignant cell.2

The four most common types of leukemia seen in the United States are acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), and chronic myeloid leukemia (CML). These constitute 10%, 33%, 35%, and 14% of nationwide leukemia cases, respectively. The other 8% of cases consist of other types of leukemia.2

ALL is the most common type of leukemia in children, accounting for 77% of cases of pediatric leukemia.1,3 AML is the most common type of acute leukemia in adults.3

In the United States, there are over 60,000 new cases of leukemia and over 20,000 deaths annually. Risk factors for leukemia include certain genetic and infectious diseases as well as exposure to ionizing radiation or certain medications.2

The presenting signs and symptoms of leukemia are usually related to the associated cytopenias or organ infiltration.3 These include fever, fatigue, headache, hepatomegaly, splenomegaly, bone pain, pallor, petechiae, bruising, and weight loss.4

Treatment for leukemia depends on the type of disease and age of the patient among other factors, but may consist of chemotherapy, immunotherapy, radiation therapy, targeted drug therapy, and/or hematopoietic stem cell transplantation.5

Pathophysiology

Acute Lymphoblastic Leukemia 

ALL develops when hematopoietic progenitor cells of the bone marrow or lymphatic system develop into malignant clones. These nonfunctional immature cells infiltrate the bone marrow, leading to anemia, neutropenia, and thrombocytopenia.6

While the resulting symptoms from bone marrow infiltration are often why patients present for diagnosis, lymphoblasts can also accumulate in extramedullary sites such as the meninges, gonads, thymus, liver, lymph nodes, and spleen, which can cause additional symptomatology.6,7

ALL is further divided into subtypes, which are determined by immunologic, cytogenetic, and molecular genetic properties.7

Acute Myeloid Leukemia

AML represents a spectrum of hematogenous malignancies resulting from genetic mutations in hematopoietic stem cells. Like ALL, malignant cells in AML have an increased ability to replicate and survive compared to normal cells, resulting in anemia, thrombocytopenia, and neutropenia.8,9

Because cloned stem cells have not yet differentiated in AML, the leukemic cells may have morphologic or immunophenotypic characteristics of erythroblasts, megakaryocytes, monocytes, eosinophils, basophils, mast cells, myelocytes, or promyelocytes. When one of these cell lines is dominant, it may be referred to in the name of the disease.8,9 

Chronic Lymphocytic Leukemia

CLL results from clonal B cell proliferation and is associated with lymphadenopathy, splenomegaly, and cytopenias. In order to be defined as CLL, 5 × 109/mL malignant cells must be present in the blood.10,11

The resulting lymphocytosis can lead to cytopenias and their associated symptoms. Patients may also have lymphadenopathy or splenomegaly. However, some patients are asymptomatic and may never need treatment.10,11

As the disease progresses, there is ongoing dysregulation of cellular and humoral immunity, leading to hypogammaglobulinemia and increased propensity for serious and life-threatening infections.10,11

Chronic Myeloid Leukemia

Most cases of CML result from a reciprocal balanced translocation between the long arms of chromosomes 9 and 22, which is known as the Philadelphia (Ph) chromosome. This cytogenetic abnormality leads to the BCR-ABL1 gene product, which codes for a tyrosine kinase.12,13

Other less common forms of CML include atypical CML, chronic myelomonocytic leukemia, juvenile myelomonocytic leukemia, chronic neutrophilic leukemia, chronic eosinophilic leukemia, and chronic basophilic leukemia.12,13 

Etiology

The etiology of nearly all cases of childhood ALL is unknown. However, some genetic and environmental factors are associated with a predisposition for the development of ALL. Conditions such as Down syndrome, ataxia-telangiectasia, and neurofibromatosis type 1 are known to be associated with ALL, as is exposure to diagnostic radiation.1

Aside from the association with certain genetic syndromes, there is also a genetic predisposition for ALL in family members of affected patients, as identical twins have a 5-fold increased risk of developing the disease.6

Certain types of ALL are associated with infectious agents. These include adult T-cell leukemia, which is associated with human T-cell leukemia virus I (HTLV-I). HTLV-I is endemic in Japan and the Caribbean.6

Although most patients with AML have not been exposed to a causative environmental factor, there are four established environmental factors associated with the development of AML. These are high-dose radiation, high-dose benzene, smoking, and chemotherapy. Obesity is an additional risk factor for AML.8

Among the chronic leukemias, CML is associated with exposure to high doses of ionizing radiation, but it is not associated with any chemical agents and is not typically identified as a secondary malignancy. By contrast, CLL is one of the only leukemias that is not associated with exposure to radiation. However, CLL is strongly associated with family history. Those with a first-degree relative with CLL have an 8.5-fold increased risk of developing the disease and 10% of patients with CLL have a first- or second-degree relative with the disease.10-13

Epidemiology

Acute Lymphoblastic Leukemia

Sixty percent of cases of ALL occur in children. There is a biphasic age distribution, with one peak at ages two to five years and a second peak after age 50 years. ALL is the most common cancer in children. It accounts for 75% of leukemias in patients less than age 15 years and is the second leading cause of death in this age group.6,7,15

In adults, ALL represents 20% of all acute leukemias and the lifetime risk is the same for men and women. Although the incidence of ALL is higher in children, more deaths occur in adults.6,7,15

Acute Myeloid Leukemia

Eighty percent of acute leukemias in adults are classified as AML. In pediatric patients, AML represents 15% to 20% of acute leukemias. AML is the most common form of leukemia in neonates, but its prevalence decreases in older children and adolescents. AML occurs somewhat more commonly in men than women and the median age of onset is 68 years.8,14

Chronic Lymphocytic Leukemia

Although the prevalence of CLL has increased in recent decades, this is thought to be secondary to improved therapies for the disease and decreased morbidity and mortality from other diseases.10

CLL occurs mostly in older adults, with a median age of onset of 71 years, and is very rare in children. It is the most common type of leukemia found in the United States overall and occurs equally in men and women.10,16

Chronic Myeloid Leukemia

CML represents about 15% of all leukemia cases in the United States. The incidence increases with age, with less than 10% of cases occurring in individuals under 20 years old.12,13

Over the past two decades, the development of successful treatments for CML has led to a decrease in annual mortality rate from 10%-20% to 2%. As a result, the prevalence of the disease has increased as patients live longer. Before 2000, the prevalence of CML in the United States was 25,000 to 30,000 cases. Today, it is 100,000 cases.12,13  

Prognosis

The prognosis for leukemia varies substantially by patient age and type of leukemia.

Survival rates for acute forms of childhood leukemia have improved dramatically in recent decades. The 5-year survival rate for ALL in children is 90%. However, it is important to note that chronic medical conditions are more common in children who have been treated for ALL, so comprehensive long-term follow-up is essential. Childhood AML has an 85% to 90% remission rate and a survival rate of 60% to 70%.1

For adults with AML, chromosomal findings at diagnosis are prognostic for survival. Patients are classified as having a favorable, intermediate, or adverse cytogenetic risk based on the presence or absence of certain chromosomal findings. In addition to gene mutations, deregulation or overexpression of certain genes also plays a role in determining disease prognosis. Other patient specific factors such as age and leukocyte count at presentation also influence prognosis.9

Age at diagnosis, white blood cell count, immunophenotype, and cytogenetic and genetic variations all contribute to risk stratification and prognostic determination for adults with ALL. Minimal residual disease (MRD) is also an important consideration for assessing ALL prognosis.6

The prognosis for CML was greatly improved with the development of tyrosine kinase inhibitors (TKIs). The life expectancy of those with chronic phase CML is close to that of the general population and the 5-year survival is now greater than 90%. Prior to the use of TKIs, the median survival was 4 to 7 years.12,17

CLL prognosis is highly variable. The median survival is 10 years, but can range from 2 to 20 or more years. Some patients with low stage disease at diagnosis can survive for 5 to 20 years without any treatment. Factors affecting prognosis of CLL include lymphocyte doubling time and specific genetic abnormalities.16 

Patient Education

American Cancer Society

https://www.cancer.org/cancer/leukemia.html

American Society of Hematology

https://www.hematology.org/education/patients/blood-cancers/leukemia

Leukemia & Lymphoma Society

https://www.lls.org/leukemia

National Cancer Institute

https://www.cancer.gov/types/leukemia

National Library of Medicine

https://medlineplus.gov/leukemia.html

 

References

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