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Acute lymphocytic leukemia

Acute lymphoblastic leukemia (ALL), also known as acute lymphocytic leukemia, is a cancer of the white blood cells, characterised by the overproduction and continuous multiplication of malignant and immature white blood cells (referred to as lymphoblasts) in the bone marrow. It is a hematological malignancy. It is fatal if left untreated as ALL spreads into the bloodstream and other vital organs quickly (hence "acute"). It mainly affects young children and adults over 50. more...

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Symptoms

Initial symptoms of ALL are quite aspecific, but worsen to the point that medical help is sought:

  • Generalised weakness and fatigue
  • Anemia
  • Frequent or unexplained fever and infections
  • Weight loss and/or loss of appetite
  • Excessive bruising or bleeding from wounds, nosebleeds, petechiae (red pinpoints on the skin)
  • Bone pain, joint pains (caused by the spread of "blast" cells to the surface of the bone or into the joint from the marrow cavity)
  • Breathlessness
  • Enlarged lymph nodes, liver and/or spleen

The signs and symptoms of ALL result from the lack of normal and healthy blood cells because they are crowded out by malignant and immature white blood cells. Therefore, people with ALL experience symptoms from their red blood cells, white blood cells, and platelets not functioning properly. Laboratory tests which might show abnormalities include blood counts, renal functions, electrolytes and liver enzymes.

Diagnosis

Diagnosing leukemia usually begins with a medical history and physical examination. If there is a suspicion of leukemia, the patient will then proceed to undergo a number of tests to establish the presence of leukemia and its type. Patients with this constellation of symptoms will generally have had blood tests, such as a full blood count.

These tests may include complete blood count (blasts on the blood film generally lead to the suspicion of ALL being raised). Nevertheless, 10% have a normal blood film, and clinical suspicion alone may be the only reason to perform a bone marrow biopsy, which is the next step in the diagnostic process.

Bone marrow is examined for blasts, cell counts and other signs of disease. Pathological examination, cytogenetics (e.g. presence of the Philadelphia chromosome) and immunophenotyping establish whether the "blast" cells began from the B lymphocytes or T lymphocytes.

If ALL has been established as a diagnosis, a lumbar puncture is generally required to determine whether the malignant cells have invaded the central nervous system (CNS).

Lab tests (mentioned above) and clinical information will also determined if any other medical imaging (such as ultrasound or CT scanning) may be required to find invasion of other organs such as the lungs or liver.

Pathophysiology

The etiology of ALL remains uncertain although some doctors believe that ALL develops from a combination of genetic and environmental factors. However, there is no definite way of determining the cause of leukemia.

Scientific research has shown that all malignancies are due to subtle or less subtle changes in DNA that lead to unimpaired cell division and breakdown of inhibitory processes. In leukemias, including ALL, chromosomal translocations occur regularly. It is thought that most translocations occur before birth during fetal development. These translocations may trigger oncogenes to "turn on", causing unregulated mitosis where cells divide too quickly and abnormally, resulting in leukemia. There is little indication that propensity for ALL is passed on from parents to children.

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Genetic variants may ease leukemia risk - acute lymphocytic leukemia - Brief Article
From Science News, 11/6/99 by N. Seppa

People with acute lymphocytic leukemia are more likely than healthy people to have the common version of a gene that plays a role in regulating folic acid metabolism in the body, a new study shows.

The gene encodes the enzyme methylene-tetrahydrofolate reductase (MTHFR), which acts on folic acid, a vitamin critical for DNA synthesis and repair. The common MTHFR gene produces a version of this enzyme that directs some of the folic acid toward other biological processes, reducing the amount available for proper DNA maintenance, the researchers find. Scientists have evidence that poor DNA repair triggers the growth of cancerous cells.

Folic acid deficiency may thus play a role in acute lymphocytic leukemia, a team of U.S. and British scientists report in the Oct. 26 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES (PNAS). As many as two-thirds of people have the common form of the MTHFR gene.

Using blood DNA, the researchers compared the genetic makeup of 308 patients in England that have various leukemias with that of 491 healthy adults matched for sex, age, lifestyle, and geographic location. Most of the patients had acute myeloid leukemia and were no more likely to have the gene variation than healthy volunteers were.

However, the 71 patients with acute lymphocytic leukemia were significantly more likely to carry the common gene version than were 114 matched healthy people, says study coauthor Christine F. Skibola, a toxicologist at the University of California, Berkeley School of Public Health.

The healthy people were four times as likely to have a variation at a site on the gene called MTHFR-677 than were patients with lymphocytic leukemia, also called acute lymphoblastic leukemia. The healthy participants were also three times as likely to have a change at another site, MTHFR-1298, as these leukemia patients, Skibola says.

The study "is very provocative and may provide some insight into the development of [acute lymphocytic leukemia]," says Joseph R. Bertino, a pharmacologist at Memorial Sloan-Kettering Cancer Center in New York.

Earlier work showed that folic acid deficiency causes breaks in chromosomes, which contain DNA, and that folic acid supplements can prevent such breaks. Also, two previous studies linked the less common MTHFR-677 form with a reduced risk of colon cancer.

The new study reinforces the value of dietary folic acid, says Bruce N. Ames of the Department of Cell and Molecular Biology at Berkeley in the same issue of PNAS. "Chromosome breaks could contribute to the increased risk of cancer associated with [folic-acid] deficiency in humans," he says.

Bertino cautions, however, that the same variants of MTHFR that may help protect people against lymphocytic leukemia also seem to hike blood concentrations of homocysteine, a chemical linked to cardiovascular problems.

COPYRIGHT 1999 Science Service, Inc.
COPYRIGHT 2000 Gale Group

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