General classification[ edit ] Clinically and pathologically, leukemia is subdivided into a variety of large groups. The first division is between its acute and chronic forms:
Normal lymphoblasts develop into mature, infection-fighting B-cells or T-cells, also called lymphocytes. Signals in the body control the number of lymphocytes so neither too few nor too many are made. In ALL, both the normal development of some lymphocytes and the control over the number of lymphoid cells become defective.
In childhood ALL, this process begins at conception with the inheritance of some of these genes. These genes, in turn, increase the risk that more mutations will occur in developing lymphoid cells.
Certain genetic syndromes, like Down Syndromehave the same effect. Environmental risk factors are also needed to help create enough genetic mutations to cause disease.
Since they have the same genes, different environmental exposures explain why one twin gets ALL and the other does not. Aside from the KMT2A rearrangement, only one extra mutation is typically found.
These genes play important roles in cellular development, proliferation, and differentiation.
Significant risk of disease occurs when a person inherits several of these mutations together. Down syndromeFanconi anemiaBloom syndromeX-linked agammaglobulinemiasevere combined immunodeficiencyShwachman-Diamond syndromeKostmann syndromeneurofibromatosis type 1ataxia-telangiectasiaparoxysmal nocturnal hemoglobinuriaand Li-Fraumeni syndrome.
This result is questioned as no causal mechanism linking electromagnetic radiation with cancer is known. The mechanism connecting high birth weight to ALL is also not known. Delayed development of the immune system due to limited disease exposure may result in excessive production of lymphocytes and increased mutation rate during an illness.
Several studies have identified lower rates of ALL among children with greater exposure to illness early in life. Very young children who attend daycare have lower rates of ALL. Evidence from many other studies looking at disease exposure and ALL is inconclusive.
These changes include chromosomal translocationsintrachromosomal rearrangementschanges in the number of chromosomes in leukemic cells, and additional mutations in individual genes. This move can result in placing a gene from one chromosome that promotes cell division to a more actively transcribed area on another chromosome.
The result is a cell that divides more often. An example of this includes the translocation of C-MYCa gene that encodes a transcription factor that leads to increased cell division, next to the immunoglobulin heavy - or light-chain gene enhancersleading to increased C-MYC expression and increased cell division.
The result is the combination of two usually separate proteins into a new fusion protein. This protein can have a new function that promotes the development of cancer. These mutations produce a cell that divides more often, even in the absence of growth factors. Gaining at least five additional chromosomes, called high hyperdiploidy, occurs more commonly.
Less often, chromosomes are lost, called hypodiploidywhich is associated with a poorer prognosis. In childhood ALL, for example, one fusion gene translocation is often found along with six to eight other ALL-related genetic changes. These lymphoblasts build up in the bone marrow and may spread to other sites in the body, such as lymph nodesthe mediastinumthe spleenthe testiclesand the brainleading to the common symptoms of disease.
While many symptoms of ALL can be found in common illnesses, persistent or unexplained symptoms raise suspicion of cancer.
Because many features on the medical history and exam are not specific to ALL, further testing is often needed. A large number of white blood cells and lymphoblasts in the circulating blood can be suspicious for ALL because they indicate a rapid production of lymphoid cells in the marrow.
The higher these numbers typically points to a worse prognosis. Brain and spinal column involvement can be diagnosed either through confirmation of leukemic cells in the lumbar puncture or through clinical signs of CNS leukemia as described above.
Laboratory tests that might show abnormalities include blood count, kidney function, electrolyte, and liver enzyme tests. Cytogenetic testing on the marrow samples can help classify disease and predict how aggressive the disease course will be.Facts & Figures about Leukemia Although leukemia often is thought to be a childhood disease, in fact, the disease strikes 10 times as many adults as children.
According to the National Cancer Institute (NCI), about 52, new leukemia cases were diagnosed in the United States in Leukemia occurs most often in adults older than 55, but it is also the most common cancer in children younger than Explore the links on this page to learn more about the types of leukemia plus treatment, statistics, research, and clinical trials.
Symptoms of Acute Lymphoblastic Leukemia. ALL can cause a variety of symptoms. Some of these can be vague and not specific just to leukemia. They include: Fatigue; Fever; Loss of appetite or weight; Night sweats; Many symptoms of acute lymphoblastic leukemia are the result of a shortage of normal blood cells.
Leukemia is a cancer of the early blood-forming cells. Most often, leukemia is a cancer of the white blood cells, but some leukemias start in other blood cell types. There are several types of leukemia, which are divided based mainly on whether the leukemia is acute (fast growing) or chronic (slower growing), and whether it starts in myeloid.
Pancreatic cancer is the fourth leading cause of cancer death in this country. Get more facts about pancreatic cancer from MD Anderson, one of the nation’s top-ranked cancer centers. What is acute lymphoblastic leukemia?
Acute lymphoblastic leukemia (ALL) is a cancer of the white blood cells that normally fight infection. Its signs and symptoms resemble other common illnesses, which often leads to other treatments before the leukemia diagnosis is made.
What are the signs and symptoms of ALL?