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What Is a Blood Disorder?

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Blood disorders are physical conditions that prevent the normal function of blood in the body. A disorder may involve factors that interfere with the production of the individual components found in the blood, such as hemoglobin or blood proteins. The nature of a blood disorder may also include situations where the blood does not coagulate properly, or the blood cells themselves are malformed or infected.
There is a wide range of blood diseases known today. Anemia is one of the more common examples of a blood disorder. Sometimes referred to as tired blood, a person who is anemic is likely to have a lack of proteins and other elements in the blood. As a result, the blood cannot carry the needed nutrients to various parts of the body and the individual is likely to feel fatigued more often. Over time, anemia can also have a negative impact on the emotions, as the blood is unable to supply proper nutrition to the brain for the production of chemicals that help to maintain an even mood.
Sickle cell anemia is one of the more serious types of anemic blood disorder. In addition to fatigue, a person suffering with this disorder is also likely to experience a great deal of pain. The pain may be localized in one part of the body or migrate to different areas throughout the course of the day.
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Hemophilia is another relatively common blood disorder. Hemophiliacs suffer with a condition in which the blood lacks the normal ability to coagulate. This means that a minor cut or scratch that would be of little consequence to most people can be a serious issue for a hemophiliac or free bleeder. Special precautions must be taken to avoid cuts, since the blood loss can be quick and significant.
A blood disorder can also mean the presence of some sort of disease in the bloodstream. The presence of the disease in the blood means that it is possible to infect a number of vital organs if the condition is not caught and corrected in time. Bloodborne cancer, especially in the form of lymphoma or leukemia, are two prime examples.
Fortunately, many blood disorder problems can be treated successfully, if caught in the early stages. Some conditions, however, cannot be reversed. When that is the case, medical professionals may choose to administer medication on an ongoing basis to contain the blood disorder, or make use of transfusions as a means of weakening the disease to the point it can be contain. WWW.Wisegreek.com
Blood disorders
Introduction
Blood is a specialized body fluid that delivers necessary substances to the body's cells such as nutrients and oxygen and transports waste products away from those same cells. Blood accounts for 8% of the human body weight, with an average density of approximately 1060 kg/m3, very close to pure water's density of 1000 kg/m3.The average adult has a blood volume of roughly 5 litres (1.3 gal), composed of plasma and several kinds of cells (occasionally called corpuscles); these formed elements of the blood are erythrocytes (red blood cells), leukocytes (white blood cells), and thrombocytes (platelets). By volume, the red blood cells constitute about 45% of whole blood, the plasma about 54.3%, and white cells about 0.7%. Those disorders marked by aberrations in structure or function of the blood cells or the blood-clotting mechanism. Although many other diseases may be reflected by the blood and its constituents, the abnormalities of red cells, white cells, platelets, and clotting factors are considered to be primary hematologic disorders. Questgarden.com Blood www.nhlbi.nih.gov/health/health-topics/topics/anemia Overview
Blood is made up of many parts, including red blood cells, white blood cells, platelets (PLATE-lets), and plasma (the fluid portion of blood).
Red blood cells are disc-shaped and look like doughnuts without holes in the center. They carry oxygen and remove carbon dioxide (a waste product) from your body. These cells are made in the bone marrow—a sponge-like tissue inside the bones.
White blood cells and platelets (PLATE-lets) also are made in the bone marrow. White blood cells help fight infection. Platelets stick together to seal small cuts or breaks on the blood vessel walls and stop bleeding. With some types of anemia, you may have low numbers of all three types of blood cells. RBC Disorders http://en.wikipedia.org/wiki/Red_blood_cell Red blood cell
From Wikipedia, the free encyclopedia

Scanning electron micrograph of human red blood cells (ca. 6–8 μm in diameter; artificial colors)

3D rendering of red blood cells
Red blood cells, or erythrocytes, are the most common type of blood cell and the vertebrate organism's principal means of delivering oxygen (O2) to the body tissues via the blood flow through the circulatory system.[1] They take up oxygen in the lungs or gills and release it into tissues while squeezing through the body's capillaries.
The cytoplasm of erythrocytes is rich in hemoglobin, an iron-containing biomolecule that can bind oxygen and is responsible for the red color of the cells. The cell membrane is composed of proteins and lipids, and this structure provides properties essential for physiological cell function such as deformability and stability while traversing the circulatory system and specifically the capillary network.
In humans, mature red blood cells are flexible and oval biconcave disks. They lack a cell nucleus and most organelles, in order to accommodate maximum space for haemoglobin. Approximately 2.4 million new erythrocytes are produced per second.[2] The cells develop in the bone marrow and circulate for about 100–120 days in the body before their components are recycled by macrophages. Each circulation takes about 20 seconds. Approximately a quarter of the cells in the human body are red blood cells.[3][4]
Red blood cells are also known as RBCs, red cells,[5] red blood corpuscles (an archaic term), haematids, erythroid cells or erythrocytes (from Greek erythros for "red" and kytos for "hollow vessel", with -cyte translated as "cell" in modern usage). Packed red blood cells (pRBC) are red blood cells that have been donated, processed, and stored in a blood bank for blood transfusion.
History of RBC
The first person to describe red blood cells was the young Dutch biologist Jan Swammerdam, who had used an early microscope in 1658 to study the blood of a frog.[6] Unaware of this work, Anton van Leeuwenhoek provided another microscopic description in 1674, this time providing a more precise description of red blood cells, even approximating their size, "25,000 times smaller than a fine grain of sand".
In 1901, Karl Landsteiner published his discovery of the three main blood groups—A, B, and C (which he later renamed to O). Landsteiner described the regular patterns in which reactions occurred when serum was mixed with red blood cells, thus identifying compatible and conflicting combinations between these blood groups. A year later Alfred von Decastello and Adriano Sturli, two colleagues of Landsteiner, identified a fourth blood group—AB.
In 1959, by use of X-ray crystallography, Dr. Max Perutz was able to unravel the structure of hemoglobin, the red blood cell protein that carries oxygen.[7]

Effect of osmotic pressure on blood cells

Micrographs of the effects of osmotic pressure * Hemolysis is the general term for excessive breakdown of red blood cells. It can have several causes and can result in hemolytic anemia. * The malaria parasite spends part of its life-cycle in red blood cells, feeds on their hemoglobin and then breaks them apart, causing fever. Both sickle-cell disease and thalassemia are more common in malaria areas, because these mutations convey some protection against the parasite. * Polycythemias (or erythrocytoses) are diseases characterized by a surplus of red blood cells. The increased viscosity of the blood can cause a number of symptoms. * In polycythemia vera the increased number of red blood cells results from an abnormality in the bone marrow. * Several microangiopathic diseases, including disseminated intravascular coagulation and thrombotic microangiopathies, present with pathognomonic (diagnostic) red blood cell fragments called schistocytes. These pathologies generate fibrin strands that sever red blood cells as they try to move past a thrombus. * Hemolytic transfusion reaction is the destruction of donated red blood cells after a transfusion, mediated by host antibodies, often as a result of a blood type mismatch.
Several blood tests involve red blood cells, including the RBC count (the number of red blood cells per volume of blood), the hematocrit (percentage of blood volume occupied by red blood cells), and the erythrocyte sedimentation rate. Many diseases involving red blood cells are diagnosed with a blood film (or peripheral blood smear), where a thin layer of blood is smeared on a microscope slide. The blood type needs to be determined to prepare for a blood transfusion or an organ transplantation.
References
1. Jump up ^ "Blood Cells". 2. Jump up ^ Erich Sackmann, Biological Membranes Architecture and Function., Handbook of Biological Physics, (ed. R.Lipowsky and E.Sackmann, vol.1, Elsevier, 1995 3. ^ Jump up to: a b Laura Dean. Blood Groups and Red Cell Antigens 4. ^ Jump up to: a b Pierigè F, Serafini S, Rossi L, Magnani M (January 2008). "Cell-based drug delivery". Advanced Drug Delivery Reviews 60 (2): 286–95. doi:10.1016/j.addr.2007.08.029. PMID 17997501. 5. Jump up ^ Vinay Kumar, Abul K. Abbas, Nelson Fausto, Richard N. Mitchell (2007). Robbins Basic Pathology (8th ed.). Saunders. 6. Jump up ^ "Swammerdam, Jan (1637–1680)", McGraw Hill AccessScience, 2007. Accessed 27 December 2007. 7. Jump up ^ "Red Gold – Blood History Timeline". PBS. 2002. Retrieved 27 December 2007. 8. Jump up ^ Stephanie Pappas (May 2, 2012). "'Iceman' mummy holds world's oldest blood cells". Fox News. Retrieved May 2, 2012. 9. ^ Jump up to: a b Gulliver, G. (1875). "On the size and shape of red corpuscles of the blood of vertebrates, with drawings of them to a uniform scale, and extended and revised tables of measurements". Proceedings of the Zoological Society of London 1875: 474–495. 10. Jump up ^ Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN 0-13-981176-1. 11. Jump up ^ Snyder, Gregory K.; Sheafor, Brandon A. (1999). "Red Blood Cells: Centerpiece in the Evolution of the Vertebrate Circulatory System". Integrative and Comparative Biology 39 (2): 189. doi:10.1093/icb/39.2.189. 12. Jump up ^ Ruud JT (May 1954). "Vertebrates without erythrocytes and blood pigment". Nature 173 (4410): 848–50. Bibcode:1954Natur.173..848R. doi:10.1038/173848a0. PMID 13165664. 13. Jump up ^ Carroll, Sean (2006). The Making of the Fittest. W.W. Norton. ISBN 0-393-06163-9. 14. Jump up ^ Cohen, W. D. (1982). "The cytomorphic system of anucleate non-mammalian erythrocytes". Protoplasma 113: 23. doi:10.1007/BF01283036. 15. Jump up ^ Wingstrand KG (1956). "Non-nucleated erythrocytes in a teleostean fish Maurolicus mülleri (Gmelin)". Zeitschrift Für Zellforschung Und Mikroskopische Anatomie 45 (2): 195–200. doi:10.1007/BF00338830 (inactive 2009-12-02). PMID 13402080. 16. Jump up ^ Gregory, T. R. (2001). "The Bigger the C-Value, the Larger the Cell: Genome Size and Red Blood Cell Size in Vertebrates". Blood Cells, Molecules, and Diseases 27 (5): 830–843. doi:10.1006/bcmd.2001.0457. PMID 11783946. edit 17. Jump up ^ Wan J, Ristenpart WD, Stone HA (October 2008). "Dynamics of shear-induced ATP release from red blood cells". Proceedings of the National Academy of Sciences of the United States of America 105 (43): 16432–7. Bibcode:2008PNAS..10516432W. doi:10.1073/pnas.0805779105. PMC 2575437. PMID 18922780. 18. Jump up ^ Diesen DL, Hess DT, Stamler JS (August 2008). "Hypoxic vasodilation by red blood cells: evidence for an s-nitrosothiol-based signal". Circulation Research 103 (5): 545–53. doi:10.1161/CIRCRESAHA.108.176867. PMC 2763414. PMID 18658051. 19. Jump up ^ Kleinbongard P, Schutz R, Rassaf T et al. (2006). "Red blood cells express a functional endothelial nitric oxide synthase". Blood 107 (7): 2943–51. doi:10.1182/blood-2005-10-3992. PMID 16368881. 20. Jump up ^ Ulker P, Sati L, Celik-Ozenci C, Meiselman HJ, Baskurt OK (2009). "Mechanical stimulation of nitric oxide synthesizing mechanisms in erythrocytes". Biorheology 46 (2): 121–32. doi:10.3233/BIR-2009-0532. PMID 19458415. 21. Jump up ^ Benavides, Gloria A; Giuseppe L Squadrito, Robert W Mills, Hetal D Patel, T Scott Isbell, Rakesh P Patel, Victor M Darley-Usmar, Jeannette E Doeller, David W Kraus (2007-11-13). "Hydrogen sulfide mediates the vasoactivity of garlic". Proceedings of the National Academy of Sciences of the United States of America 104 (46): 17977–17982. Bibcode:2007PNAS..10417977B. doi:10.1073/pnas.0705710104. PMC 2084282. PMID 17951430. Retrieved 2010-03-03. 22. Jump up ^ Kesava, Shobana (2007-09-01). "Red blood cells do more than just carry oxygen; New findings by NUS team show they aggressively attack bacteria too". The Straits Times. Retrieved 2013-03-26. 23. Jump up ^ Jiang N, Tan NS, Ho B, Ding JL (October 2007). "Respiratory protein-generated reactive oxygen species as an antimicrobial strategy". Nature Immunology 8 (10): 1114–22. doi:10.1038/ni1501. PMID 17721536. 24. ^ Jump up to: a b Kabanova S, Kleinbongard P, Volkmer J, Andrée B, Kelm M, Jax TW (2009). "Gene expression analysis of human red blood cells". International Journal of Medical Sciences 6 (4): 156–9. doi:10.7150/ijms.6.156. PMC 2677714. PMID 19421340. 25. Jump up ^ Zimmer, Carl (2007-03-27). "Scientists Explore Ways to Lure Viruses to Their Death". The New York Times. Retrieved 2013-03-26. 26. Jump up ^ Uzoigwe C (2006). "The human erythrocyte has developed the biconcave disc shape to optimise the flow properties of the blood in the large vessels". Medical Hypotheses 67 (5): 1159–63. doi:10.1016/j.mehy.2004.11.047. PMID 16797867. 27. Jump up ^ Gregory TR (2001). "The bigger the C-value, the larger the cell: genome size and red blood cell size in vertebrates". Blood Cells, Molecules & Diseases 27 (5): 830–43. doi:10.1006/bcmd.2001.0457. PMID 11783946. 28. Jump up ^ Goodman SR, Kurdia A, Ammann L, Kakhniashvili D, Daescu O (December 2007). "The human red blood cell proteome and interactome". Experimental Biology and Medicine 232 (11): 1391–408. doi:10.3181/0706-MR-156. PMID 18040063. 29. Jump up ^ Mary Louise Turgeon (2004). Clinical Hematology: Theory and Procedures. Lippincott Williams & Wilkins. p. 100. ISBN 9780781750073.[dead link] 30. Jump up ^ McLaren CE, Brittenham GM, Hasselblad V (April 1987). "Statistical and graphical evaluation of erythrocyte volume distributions". Am. J. Physiol. 252 (4 Pt 2): H857–66. PMID 3565597. 31. Jump up ^ Hillman, Robert S.; Ault, Kenneth A.; Rinder, Henry M. (2005). Hematology in Clinical Practice: A Guide to Diagnosis and Management (4 ed.). McGraw-Hill Professional. p. 1. ISBN 0-07-144035-6. 32. Jump up ^ Iron Metabolism, University of Virginia Pathology. Accessed 22 September 2007. 33. Jump up ^ Iron Transport and Cellular Uptake by Kenneth R. Bridges, Information Center for Sickle Cell and Thalassemic Disorders. Accessed 22 September 2007. 34. Jump up ^ Harrison, K. L. (1979). "Fetal Erythrocyte Lifespan". Journal of Paediatrics and Child Health 15 (2): 96–97. doi:10.1111/j.1440-1754.1979.tb01197.x. edit 35. Jump up ^ Lang F, Lang E, Föller M (2012). "Physiology and pathophysiology of eryptosis". Transfusion Medicine and Hemotherapy 39 (5): 308–314. doi:10.1159/000342534. PMC 3678267. PMID 23801921. 36. Jump up ^ Föller M, Huber SM, Lang F (October 2008). "Erythrocyte programmed cell death". IUBMB Life 60 (10): 661–8. doi:10.1002/iub.106. PMID 18720418. 37. ^ Jump up to: a b c Yazdanbakhsh K, Lomas-Francis C, Reid ME (October 2000). "Blood groups and diseases associated with inherited abnormalities of the red blood cell membrane". Transfusion Medicine Reviews 14 (4): 364–74. doi:10.1053/tmrv.2000.16232. PMID 11055079. 38. ^ Jump up to: a b c Mohandas N, Gallagher PG (November 2008). "Red cell membrane: past, present, and future". Blood 112 (10): 3939–48. doi:10.1182/blood-2008-07-161166. PMC 2582001. PMID 18988878. 39. Jump up ^ Rodi PM, Trucco VM, Gennaro AM (June 2008). "Factors determining detergent resistance of erythrocyte membranes". Biophysical Chemistry 135 (1–3): 14–8. doi:10.1016/j.bpc.2008.02.015. PMID 18394774. 40. Jump up ^ Hempelmann E, Götze O (1984). "Characterization of membrane proteins by polychromatic silver staining". Hoppe Seyler's Z Physiol Chem 365: 241–242. 41. Jump up ^ Iolascon A, Perrotta S, Stewart GW (March 2003). "Red blood cell membrane defects". Reviews in Clinical and Experimental Hematology 7 (1): 22–56. PMID 14692233. 42. Jump up ^ Denomme GA (July 2004). "The structure and function of the molecules that carry human red blood cell and platelet antigens". Transfusion Medicine Reviews 18 (3): 203–31. doi:10.1016/j.tmrv.2004.03.006. PMID 15248170. 43. Jump up ^ Tokumasu F, Ostera GR, Amaratunga C, Fairhurst RM (2012) Modifications in erythrocyte membrane zeta potential by Plasmodium falciparum infection. Exp Parasitol 44. Jump up ^ "Circular of Information for Blood and Blood Products" (pdf). American Association of Blood Banks, American Red Cross, America's Blood Centers. Retrieved 2010-11-01. 45. Jump up ^ First red blood cells grown in the lab, New Scientist News, 19 August 2008 46. Jump up ^ An X, Mohandas N (May 2008). "Disorders of red cell membrane". British Journal of Haematology 141 (3): 367–75 47. . doi:10.1111/j.1365-2141.2008.07091.x. PMID 18341630. * * * http://www.healthline.com/health/bleeding-disorders#Overview
Bleeding Disorders
A bleeding disorder is a condition that affects the way your blood normally clots. When you get injured, your blood normally begins to clot to prevent a massive loss of blood. Sometimes the mechanism that causes the blood to clot fails, resulting in rapid or prolonged bleeding.
Bleeding disorders don’t always affect blood leaving the body. There are many conditions that cause bleeding to occur under the skin or in the brain. * http://www.healthline.com/health/bleeding-disorders#Causes

* What Causes Bleeding Disorders to Occur?
Bleeding disorders are often caused by a failure of the blood to clot. Several conditions can affect the way the blood clots. Many causes are related to protein defects in the plasma (the liquid component of blood). These proteins are directly responsible for how the blood coagulates (clots). In some diseases, these proteins might be missing completely or they may be low in count. The majority of these defects are hereditary (passed from parent to child through genes). However, some may develop due to other medical conditions.
Other conditions that can cause bleeding disorders are: * liver disease * low red blood cell count * vitamin K deficiency * medication side-effects
Medications that inhibit the clotting of the blood are called anticoagulants.

http://www.healthline.com/health/bleeding-disorders#Types

* Types of Bleeding Disorders
There are several bleeding disorders that can be inherited (passed down through genetics) or acquired. Some cause bleeding spontaneously, whereas others cause bleeding following an accident.
The most common inherited bleeding disorders are: * hemophilia A and B: caused by a deficiency or lack of certain blood clotting proteins, called factors. This disorder causes heavy or unusual bleeding * factor II, V, VII, X, XII deficiency: relate to blood clotting problems or abnormal bleeding problems * von Willebrand’s disease: the most common inherited bleeding disorder; caused by a deficiency of von Willebrand factor, which helps blood platelets clump together and stick to a blood vessel wall
Certain diseases or medical conditions can also cause a deficiency of one or more blood clotting factors. The most common causes of acquired bleeding disorders are end-stage liver disease or vitamin K deficiency. According to the American Association of Clinical Chemistry (AACC), this is because most blood clotting factors are produced in the liver, and certain clotting factors are vitamin k dependent (AACC, 2011).

Identification of Bleeding Disorders| Symptoms
The main sign of a bleeding disorder is prolonged or excessive bleeding. The bleeding is normally heavier than normal and unprovoked.
Other signs of a bleeding disorder include: * unexplained bruising * heavy menstrual bleeding * frequent nosebleeds

http://www.healthline.com/health/bleeding-disorders#Diagnosis

* Diagnosing a Bleeding Disorder
To diagnose a bleeding disorder, your doctor will go over your medical history. During this part of the exam, the doctor will ask questions about any medical conditions you may have and any medications you may be taking.
Make sure to mention: * additional symptoms * how often you experience the bleeding * how long the bleeding episode lasts * what you were doing before the bleeding began
After gathering this information, your doctor will administer tests that include: * complete blood count (CBC): to check the amount of blood loss as well as the amount of red and white blood cells you have) * platelet aggregation test * bleeding time: to see how fast your blood vessels close to prevent bleeding

Identification of Bleeding Disorders| Symptoms
The main sign of a bleeding disorder is prolonged or excessive bleeding. The bleeding is normally heavier than normal and unprovoked.
Other signs of a bleeding disorder include: * unexplained bruising * heavy menstrual bleeding * frequent nosebleeds
Read more

* http://www.healthline.com/health/bleeding-disorders#Treatments * * Treatments Options for Bleeding Disorders
Treatment options vary depending on the cause for the bleeding.
Iron Supplementation
If you have significant blood loss, your doctor may prescribe iron supplements to replenish the amount of iron in your body. A low iron level can result in iron deficiency anemia. This condition can make you feel weak, short of breath, and light-headed. In addition to treatment with iron, you may need a blood transfusion.
Blood Tranfusion
A blood transfusion replaces the lost blood with blood taken from a donor. The donor blood has to match your blood type to prevent complications. This procedure is only offered in the hospital.
Additional treatments include: * factor replacement * fresh frozen plasma transfusion * * Complications of Bleeding Disorders
The best outcome results from seeking early treatment. Complications can arise if treatment is sought too late. Complications can also arise if the disorder is severe or causes excessive blood loss.
Common complications of bleeding disorders include: * bleeding into the brain * bleeding within the intestines * bleeding into the joints * joint pain

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leukemia
From Wikipedia, the free encyclopedia
For the journal, see Leukemia (journal). For animal diseases, see Leucosis. Leukemia | Classification and external resources | A Wright's stained bone marrow aspirate smearfrom a patient with precursor B-cell acute lymphoblastic leukemia. | ICD-10 | C91-C95 | ICD-9 | 208.9 | ICD-O: | 9800-9940 | DiseasesDB | 7431 | MedlinePlus | 001299 | MeSH | D007938 |
Leukemia (American English) or leukaemia (British English) is a type of cancer of the blood or bone marrow characterized by an abnormal increase of immature white blood cells called "blasts". Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader group of diseases affecting the blood, bone marrow, and lymphoid system, which are all known as hematological neoplasms.
Leukemia is a treatable disease. Most treatments involve chemotherapy, medical radiation therapy, hormone treatments, or bone marrow transplant. The rate of cure depends on the type of leukemia as well as the age of the patient. Children are more likely to be permanently cured than adults. Even when a complete cure is unlikely, most people with a chronic leukemia and many people with an acute leukemia can be successfully treated for years. Sometimes, leukemia is the effect of another cancer, known as blastic leukemia, which usually involves the same treatment, although it is usually unsuccessful.
Leukemia can affect people at any age. In 2000 approximately 256,000 children and adults around the world had developed some form of leukemia, and 209,000 have died from it.[1] About 90% of all leukemias are diagnosed in adults.[2]
The name comes from Ancient Greek λευκός leukos "white", and αἷμα haima "blood"[3]
Contents
[hide] * 1 Classification * 2 Signs and symptoms * 3 Causes * 4 Diagnosis * 5 Treatment * 5.1 Acute lymphoblastic * 5.2 Chronic lymphocytic * 5.3 Acute myelogenous * 5.4 Chronic myelogenous * 5.5 Hairy cell * 5.6 T-cell prolymphocytic * 5.7 Juvenile myelomonocytic * 6 Epidemiology * 7 History * 8 Society and culture * 9 Research directions * 10 Pregnancy * 11 See also * 12 References * 13 External links
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Classification[edit] Four major kinds of leukemia | Cell type | Acute | Chronic | Lymphocytic leukemia
(or "lymphoblastic") | Acute lymphoblastic leukemia (ALL) | Chronic lymphocytic leukemia (CLL) | Myelogenous leukemia
(also "myeloid" or "nonlymphocytic") | Acute myelogenous leukemia (AML)
(or myeloblastic) | Chronic myelogenous leukemia (CML) |
Clinically and pathologically, leukemia is subdivided into a variety of large groups. The first division is between its acute and chronic forms: * Acute leukemia is characterized by a rapid increase in the number of immature blood cells. Crowding due to such cells makes the bone marrow unable to produce healthy blood cells. Immediate treatment is required in acute leukemia due to the rapid progression and accumulation of themalignant cells, which then spill over into the bloodstream and spread to other organs of the body. Acute forms of leukemia are the most common forms of leukemia in children. * Chronic leukemia is characterized by the excessive build up of relatively mature, but still abnormal, white blood cells. Typically taking months or years to progress, the cells are produced at a much higher rate than normal, resulting in many abnormal white blood cells. Whereas acute leukemia must be treated immediately, chronic forms are sometimes monitored for some time before treatment to ensure maximum effectiveness of therapy. Chronic leukemia mostly occurs in older people, but can theoretically occur in any age group.
Additionally, the diseases are subdivided according to which kind of blood cell is affected. This split divides leukemias into lymphoblastic or lymphocytic leukemias and myeloid or myelogenous leukemias: * In lymphoblastic or lymphocytic leukemias, the cancerous change takes place in a type of marrow cell that normally goes on to form lymphocytes, which are infection-fighting immune system cells. Most lymphocytic leukemias involve a specific subtype of lymphocyte, the B cell. * In myeloid or myelogenous leukemias, the cancerous change takes place in a type of marrow cell that normally goes on to form red blood cells, some other types of white cells, andplatelets.
Combining these two classifications provides a total of four main categories. Within each of these four main categories, there are typically several subcategories. Finally, some rarer types are usually considered to be outside of this classification scheme. * Acute lymphoblastic leukemia (ALL) is the most common type of leukemia in young children. This disease also affects adults, especially those age 65 and older. Standard treatments involve chemotherapy and radiotherapy. The survival rates vary by age: 85% in children and 50% in adults.[4] Subtypes include precursor B acute lymphoblastic leukemia, precursor T acute lymphoblastic leukemia, Burkitt's leukemia, and acute biphenotypic leukemia. * Chronic lymphocytic leukemia (CLL) most often affects adults over the age of 55. It sometimes occurs in younger adults, but it almost never affects children. Two-thirds of affected people are men. The five-year survival rate is 75%.[5] It is incurable, but there are many effective treatments. One subtype is B-cell prolymphocytic leukemia, a more aggressive disease. * Acute myelogenous leukemia (AML) occurs more commonly in adults than in children, and more commonly in men than women. AML is treated with chemotherapy. The five-year survival rate is 40%, except for APL (Acute Promyelocytic Leukemia), which is over 90%.[6] Subtypes of AML include acute promyelocytic leukemia, acute myeloblastic leukemia, and acute megakaryoblastic leukemia. * Chronic myelogenous leukemia (CML) occurs mainly in adults; a very small number of children also develop this disease. Treatment is with imatinib (Gleevec in United States, Glivec in Europe) or other drugs.[7] The five-year survival rate is 90%.[8][9] One subtype is chronic myelomonocytic leukemia. * Hairy cell leukemia (HCL) is sometimes considered a subset of chronic lymphocytic leukemia, but does not fit neatly into this pattern. About 80% of affected people are adult men. No cases in children have been reported. HCL is incurable, but easily treatable. Survival is 96% to 100% at ten years.[10] * T-cell prolymphocytic leukemia (T-PLL) is a very rare and aggressive leukemia affecting adults; somewhat more men than women are diagnosed with this disease.[11] Despite its overall rarity, it is also the most common type of mature T cell leukemia;[12] nearly all other leukemias involve B cells. It is difficult to treat, and the median survival is measured in months. * Large granular lymphocytic leukemia may involve either T-cells or NK cells; like hairy cell leukemia, which involves solely B cells, it is a rare and indolent (not aggressive) leukemia.[13] * Adult T-cell leukemia is caused by human T-lymphotropic virus (HTLV), a virus similar to HIV. Like HIV, HTLV infects CD4+ T-cells and replicates within them; however, unlike HIV, it does not destroy them. Instead, HTLV "immortalizes" the infected T-cells, giving them the ability to proliferate abnormally. Human T cell lymphotropic virus types I and II (HTLV-I/II) are endemic in certain areas of the world.
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Signs and symptoms[edit]

Common symptoms of chronic or acute leukemia[14]
Damage to the bone marrow, by way of displacing the normal bone marrow cells with higher numbers of immature white blood cells, results in a lack of blood platelets, which are important in the blood clotting process. This means people with leukemia may easily become bruised, bleed excessively, or develop pinprick bleeds (petechiae).
White blood cells, which are involved in fighting pathogens, may be suppressed or dysfunctional. This could cause the patient's immune system to be unable to fight off a simple infection or to start attacking other body cells. Because leukemia prevents the immune system from working normally, some patients experience frequent infection, ranging from infected tonsils, sores in the mouth, or diarrhea to life-threatening pneumonia or opportunistic infections.
Finally, the red blood cell deficiency leads to anemia, which may cause dyspnea and pallor.
Some patients experience other symptoms, such as feeling sick, having fevers, chills, night sweats, feeling fatigued and other flu-like symptoms. Some patients experience nausea or a feeling of fullness due to an enlarged liver and spleen; this can result in unintentional weight loss. Blasts affected by the disease may come together and become swollen in the liver or in the lymph nodes causing pain and leading to nausea.[15]
If the leukemic cells invade the central nervous system, then neurological symptoms (notably headaches) can occur. Uncommon neurological symptoms like migraines, seizures, or coma can occur as a result of brain stem pressure. All symptoms associated with leukemia can be attributed to other diseases. Consequently, leukemia is always diagnosed through medical tests.
The word leukemia, which means 'white blood', is derived from the disease's namesake high white blood cell counts that most leukemia patients have before treatment. The high number of white blood cells are apparent when a blood sample is viewed under a microscope. Frequently, these extra white blood cells are immature or dysfunctional. The excessive number of cells can also interfere with the level of other cells, causing a harmful imbalance in the blood count.
Some leukemia patients do not have high white blood cell counts visible during a regular blood count. This less-common condition is called aleukemia. The bone marrow still contains cancerous white blood cells which disrupt the normal production of blood cells, but they remain in the marrow instead of entering the bloodstream, where they would be visible in a blood test. For an aleukemic patient, the white blood cell counts in the bloodstream can be normal or low. Aleukemia can occur in any of the four major types of leukemia, and is particularly common in hairy cell leukemia.[16]
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Causes[edit]
There is no single known cause for any of the different types of leukemia. The few known causes, which are not generally factors within the control of the average person, account for relatively few cases.[17] The cause for most cases of leukemia is unknown. The different leukemias likely have different causes.
Leukemia, like other cancers, results from mutations in the DNA. Certain mutations can trigger leukemia by activating oncogenes or deactivating tumor suppressor genes, and thereby disrupting the regulation of cell death, differentiation or division. These mutations may occur spontaneously or as a result of exposure to radiation or carcinogenic substances.
Among adults, the known causes are natural and artificial ionizing radiation, a few viruses such as human T-lymphotropic virus, and some chemicals, notably benzene and alkylatingchemotherapy agents for previous malignancies.[18][19][20] Use of tobacco is associated with a small increase in the risk of developing acute myeloid leukemia in adults.[18] Cohort and case-control studies have linked exposure to some petrochemicals and hair dyes to the development of some forms of leukemia. Diet has very limited or no effect, although eating more vegetables may confer a small protective benefit.[17]
Viruses have also been linked to some forms of leukemia. Experiments on mice and other mammals have demonstrated the relevance of retroviruses in leukemia, and human retroviruses have also been identified. The first human retrovirus identified was human T-lymphotropic virus, or HTLV-1, which is known to cause adult T-cell leukemia.[21]
Some people have a genetic predisposition towards developing leukemia. This predisposition is demonstrated by family histories and twin studies.[18] The affected people may have a single gene or multiple genes in common. In some cases, families tend to develop the same kinds of leukemia as other members; in other families, affected people may develop different forms of leukemia or related blood cancers.[18]
In addition to these genetic issues, people with chromosomal abnormalities or certain other genetic conditions have a greater risk of leukemia.[19] For example, people with Down syndrome have a significantly increased risk of developing forms of acute leukemia (especially acute myeloid leukemia), and Fanconi anemia is a risk factor for developing acute myeloid leukemia.[18]
Whether non-ionizing radiation causes leukemia has been studied for several decades. The International Agency for Research on Cancer expert working group undertook a detailed review of all data on static and extremely low frequency electromagnetic energy, which occurs naturally and in association with the generation, transmission, and use of electrical power.[22] They concluded that there is limited evidence that high levels of ELF magnetic (but not electric) fields might cause childhood leukemia. Exposure to significant ELF magnetic fields might result in twofold excess risk for leukemia for children exposed to these high levels of magnetic fields.[22] However, the report also says that methodological weaknesses and biases in these studies have likely caused the risk to be overstated.[22] No evidence for a relationship to leukemia or another form of malignancy in adults has been demonstrated.[22] Since exposure to such levels of ELFs is relatively uncommon, the World Health Organization concludes that ELF exposure, if later proven to be causative, would account for just 100 to 2400 cases worldwide each year, representing 0.2 to 4.9% of the total incidence of childhood leukemia for that year (about 0.03 to 0.9% of all leukemias).[23]
A few cases of maternal-fetal transmission (a baby acquires leukemia because its mother had leukemia during the pregnancy) have been reported.[18]
According to a study conducted at the Center for Research in Epidemiology and Population Health in France, children born to mothers who use fertility drugs to induce ovulation are more than twice as likely to develop leukemia during their childhoods than other children.[24]
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Diagnosis[edit]
Diagnosis is usually based on repeated complete blood counts and a bone marrow examination following observations of the symptoms, however, in rare cases blood tests may not show if a patient has leukemia, usually this is because the leukemia is in the early stages or has entered remission. A lymph node biopsy can be performed as well in order to diagnose certain types of leukemia in certain situations.
Following diagnosis, blood chemistry tests can be used to determine the degree of liver and kidney damage or the effects of chemotherapy on the patient. When concerns arise about visible damage due to leukemia, doctors may use an X-ray, MRI, or ultrasound. These can potentially view leukemia's effects on such body parts as bones (X-ray), the brain (MRI), or the kidneys, spleen, and liver (ultrasound). Finally, CT scans are rarely used to check lymph nodes in the chest.
Despite the use of these methods to diagnose whether or not a patient has leukemia, many people have not been diagnosed because many of the symptoms are vague, unspecific, and can refer to other diseases. For this reason, the American Cancer Society predicts that at least one-fifth of the people with leukemia have not yet been diagnosed.[16]
Mutation in SPRED1 gene has been associated with a predisposition to childhood leukemia.[25] SPRED1 gene mutations can be diagnosed with genetic sequencing.
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Treatment[edit]
Most forms of leukemia are treated with pharmaceutical medication, typically combined into a multi-drug chemotherapy regimen. Some are also treated with radiation therapy. In some cases, abone marrow transplant is effective.
Acute lymphoblastic[edit]
Further information: Acute lymphoblastic leukemia#Treatment
Management of ALL focuses on control of bone marrow and systemic (whole-body) disease. Additionally, treatment must prevent leukemic cells from spreading to other sites, particularly thecentral nervous system (CNS) e.g. monthly lumbar punctures. In general, ALL treatment is divided into several phases: * Induction chemotherapy to bring about bone marrow remission. For adults, standard induction plans include prednisone, vincristine, and an anthracycline drug; other drug plans may include L-asparaginase or cyclophosphamide. For children with low-risk ALL, standard therapy usually consists of three drugs (prednisone, L-asparaginase, and vincristine) for the first month of treatment. * Consolidation therapy or intensification therapy to eliminate any remaining leukemia cells. There are many different approaches to consolidation, but it is typically a high-dose, multi-drug treatment that is undertaken for a few months. Patients with low- to average-risk ALL receive therapy with antimetabolite drugs such as methotrexate and 6-mercaptopurine (6-MP). High-risk patients receive higher drug doses of these drugs, plus additional drugs. * CNS prophylaxis (preventive therapy) to stop the cancer from spreading to the brain and nervous system in high-risk patients. Standard prophylaxis may include radiation of the head and/or drugs delivered directly into the spine. * Maintenance treatments with chemotherapeutic drugs to prevent disease recurrence once remission has been achieved. Maintenance therapy usually involves lower drug doses, and may continue for up to three years. * Alternatively, allogeneic bone marrow transplantation may be appropriate for high-risk or relapsed patients.[26]
Chronic lymphocytic[edit]
Further information: Chronic lymphocytic leukemia#Treatment
Decision to treat[edit]
Hematologists base CLL treatment on both the stage and symptoms of the individual patient. A large group of CLL patients have low-grade disease, which does not benefit from treatment. Individuals with CLL-related complications or more advanced disease often benefit from treatment. In general, the indications for treatment are: * Falling hemoglobin or platelet count * Progression to a later stage of disease * Painful, disease-related overgrowth of lymph nodes or spleen * An increase in the rate of lymphocyte production [27]
Treatment approach[edit]
CLL is probably incurable by present treatments. The primary chemotherapeutic plan is combination chemotherapy with chlorambucil or cyclophosphamide, plus a corticosteroid such asprednisone or prednisolone. The use of a corticosteroid has the additional benefit of suppressing some related autoimmune diseases, such as immunohemolytic anemia or immune-mediated thrombocytopenia. In resistant cases, single-agent treatments with nucleoside drugs such as fludarabine,[28] pentostatin, or cladribine may be successful. Younger patients may considerallogeneic or autologous bone marrow transplantation.[29]
Acute myelogenous[edit]
Further information: Acute myeloid leukemia#Treatment
Many different anti-cancer drugs are effective for the treatment of AML. Treatments vary somewhat according to the age of the patient and according to the specific subtype of AML. Overall, the strategy is to control bone marrow and systemic (whole-body) disease, while offering specific treatment for the central nervous system (CNS), if involved.
In general, most oncologists rely on combinations of drugs for the initial, induction phase of chemotherapy. Such combination chemotherapy usually offers the benefits of early remission and a lower risk of disease resistance. Consolidation and maintenance treatments are intended to prevent disease recurrence. Consolidation treatment often entails a repetition of induction chemotherapy or the intensification chemotherapy with additional drugs. By contrast, maintenance treatment involves drug doses that are lower than those administered during the induction phase.[30]
Chronic myelogenous[edit]
Further information: Chronic myelogenous leukemia#Treatment
There are many possible treatments for CML, but the standard of care for newly diagnosed patients is imatinib (Gleevec) therapy.[31] Compared to most anti-cancer drugs, it has relatively few side effects and can be taken orally at home. With this drug, more than 90% of patients will be able to keep the disease in check for at least five years,[31] so that CML becomes a chronic, manageable condition.
In a more advanced, uncontrolled state, when the patient cannot tolerate imatinib, or if the patient wishes to attempt a permanent cure, then an allogeneic bone marrow transplantation may be performed. This procedure involves high-dose chemotherapy and radiation followed by infusion of bone marrow from a compatible donor. Approximately 30% of patients die from this procedure.[31]
Hairy cell[edit]
Further information: Hairy cell leukemia#Treatment
Decision to treat
Patients with hairy cell leukemia who are symptom-free typically do not receive immediate treatment. Treatment is generally considered necessary when the patient shows signs and symptoms such as low blood cell counts (e.g., infection-fighting neutrophil count below 1.0 K/µL), frequent infections, unexplained bruises, anemia, or fatigue that is significant enough to disrupt the patient's everyday life.
Typical treatment approach
Patients who need treatment usually receive either one week of cladribine, given daily by intravenous infusion or a simple injection under the skin, or six months of pentostatin, given every four weeks by intravenous infusion. In most cases, one round of treatment will produce a prolonged remission.[32]
Other treatments include rituximab infusion or self-injection with Interferon-alpha. In limited cases, the patient may benefit from splenectomy (removal of the spleen). These treatments are not typically given as the first treatment because their success rates are lower than cladribine or pentostatin.[33]
T-cell prolymphocytic[edit]
Further information: T-cell prolymphocytic leukemia#Treatment
Most patients with T-cell prolymphocytic leukemia, a rare and aggressive leukemia with a median survival of less than one year, require immediate treatment.[34]
T-cell prolymphocytic leukemia is difficult to treat, and it does not respond to most available chemotherapeutic drugs.[34] Many different treatments have been attempted, with limited success in certain patients: purine analogues (pentostatin, fludarabine, cladribine), chlorambucil, and various forms of combination chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisoneCHOP, cyclophosphamide, vincristine, prednisone [COP], vincristine, doxorubicin, prednisone, etoposide, cyclophosphamide, bleomycin VAPEC-B). Alemtuzumab (Campath), a monoclonal antibody that attacks white blood cells, has been used in treatment with greater success than previous options.[34]
Some patients who successfully respond to treatment also undergo stem cell transplantation to consolidate the response.[34]
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History of WBC

Rudolf Virchow
Leukemia was first observed by pathologist Rudolf Virchow in 1845. Observing an abnormally large number of white blood cells in a blood sample from a patient, Virchow called the condition Leukämie in German, which he formed from the two Greek words leukos (λευκός), meaning "white", and aima(αίμα), meaning "blood". Around ten years after Virchow's findings, pathologist Franz Ernst Christian Neumann found that one deceased leukemia patient's bone marrow was colored "dirty green-yellow" as opposed to the normal red. This finding allowed Neumann to conclude that a bone marrow problem was responsible for the abnormal blood of leukemia patients.
By 1900 leukemia was viewed as a family of diseases as opposed to a single disease. By 1947 Boston pathologist Sidney Farber believed from past experiments thataminopterin, a folic acid mimic, could potentially cure leukemia in children. The majority of the children with ALL who were tested showed signs of improvement in their bone marrow, but none of them were actually cured. This, however, led to further experiments.
In 1962, researchers Emil J. Freireich Jr. and Emil Frei III used combination chemotherapy to attempt to cure leukemia. The tests were successful with some patients surviving long after the tests.[43]
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Society and culture[edit]
Leukemias are often romanticized in 20th century fiction. It is portrayed as a joy-ending, clean disease whose fair, innocent and gentle victims die young or at the wrong time. As such, it is the cultural successor to tuberculosis, which held this cultural position until tuberculosis was discovered to be an infectious disease.[44] The 1970 romance novel Love Story is an example of this romanticization of leukemia.
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Research directions[edit]
Significant research into the causes, prevalence, diagnosis, treatment, and prognosis of leukemia is being performed. Hundreds of clinical trials are being planned or conducted at any given time.[45] Studies may focus on effective means of treatment, better ways of treating the disease, improving the quality of life for patients, or appropriate care in remission or after cures.
In general, there are two types of leukemia research: clinical or translational research and basic research. Clinical/translational research focuses on studying the disease in a defined and generally immediately patient-applicable way, such as testing a new drug in patients. By contrast, basic science research studies the disease process at a distance, such as seeing whether a suspected carcinogen can cause leukemic changes in isolated cells in the laboratory or how the DNA changes inside leukemia cells as the disease progresses. The results from basic research studies are generally less immediately useful to patients with the disease.[46]
Treatment through gene therapy is currently being pursued. One such approach turns T cells into cancer-targeting attackers. As of August 2011, a year after treatment, two of the three patients are cancer-free.[47][48] In addition to this identifying stem cells that cause different types of leukaemia is being researched.[49]
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Pregnancy[edit]
Leukemia is rarely associated with pregnancy, affecting only about 1 in 10,000 pregnant women.[50] How it is handled depends primarily on the type of leukemia. Nearly all leukemias appearing in pregnant women are acute leukemias.[51] Acute leukemias normally require prompt, aggressive treatment, despite significant risks of pregnancy loss and birth defects, especially if chemotherapy is given during the developmentally sensitive first trimester.[50] Chronic myelogenous leukemia can be treated with relative safety at any time during pregnancy with Interferon-alpha hormones.[50]Treatment for chronic lymphocytic leukemias, which are rare in pregnant women, can often be postponed until after the end of the pregnancy.[50][51]
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See also[edit] * Acute erythroid leukemia * Antileukemic drugs, medications used to kill leukemia cells * Hematologic diseases, the large class of blood-related disorders, including leukemia * Cancer-related fatigue
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References[edit] 1. ^ Jump up to:a b c d Mathers, Colin D, Cynthia Boschi-Pinto, Alan D Lopez and Christopher JL Murray (2001). "Cancer incidence, mortality and survival by site for 14 regions of the world".Global Programme on Evidence for Health Policy Discussion Paper No. 13 (World Health Organization). 2. Jump up^ "SEER Stat Fact Sheets: Leukemia". National Cancer Institute. 2011. "Approximately 10.8% were diagnosed under age 20" 3. Jump up^ "Leukemia". Mosby’s Medical, Nursing &Allied Health Dictionary (Fourth ed.). Mosby-YearBook. 1994. p. 903. 4. Jump up^ Jameson, J. N. St C.; Dennis L. Kasper; Harrison, Tinsley Randolph; Braunwald, Eugene; Fauci, Anthony S.; Hauser, Stephen L; Longo, Dan L. (2005). Harrison's principles of internal medicine. New York: McGraw-Hill Medical Publishing Division. ISBN 0-07-140235-7. 5. Jump up^ Finding Cancer Statistics » Cancer Stat Fact Sheets »Chronic Lymphocytic Leukemia National Cancer Institute. 6. Jump up^ Colvin G. A., Elfenbein G. J. (2003). "The latest treatment advances for acute myelogenous leukemia". Medicine and Health, Rhode Island 86 (8): 243–6. PMID 14582219. 7. Jump up^ Novartis 8. Jump up^ Patients with Chronic Myelogenous Leukemia Continue to Do Well on Imatinib at 5-Year Follow-Up Medscape Medical News 2006. 9. Jump up^ Updated Results of Tyrosine Kinase Inhibitors in CMLASCO 2006 Conference Summaries. 10. Jump up^ Else, M., Ruchlemer, R., Osuji, N. (2005). "Long remissions in hairy cell leukemia with purine analogs: a report of 219 patients with a median follow-up of 12.5 years".Cancer 104 (11): 2442–8. doi:10.1002/cncr.21447.PMID 16245328. 11. Jump up^ Matutes, Estella. (1998) "T-cell prolymphocytic leukemia, a rare variant of mature post-thymic T-cell leukemias, has distinct clinical and laboratory characteristics and a poor prognosis." Cancer Control Journal Volume 5 Number 1. 12. Jump up^ Valbuena JR, Herling M, Admirand JH, Padula A, Jones D, Medeiros LJ (March 2005). "T-cell prolymphocytic leukemia involving extramedullary sites". American Journal of Clinical Pathology 123 (3): 456–64. doi:10.1309/93P4-2RNG-5XBG-3KBE. PMID 15716243. 13. Jump up^ Elaine Sarkin Jaffe, Nancy Lee Harris, World Health Organization, International Agency for Research on Cancer, Harald Stein, J. W. Vardiman (2001). Pathology and genetics of tumours of haematopoietic and lymphoid tissues. World Health Organization Classification of Tumors 3. Lyon: IARC Press. ISBN 92-832-2411-6. 14. Jump up^ Reference list is found at image description page in Wikimedia Commons 15. Jump up^ "Leukemia". Columbia Electronic Encyclopedia, 6th Edition. Retrieved 4 November 2011. 16. ^ Jump up to:a b American Cancer Society (2010). "How is Leukemia Diagnosed?". Detailed Guide: Leukemia – Adult Chronic. American Cancer Society. Retrieved 4 May 2010.[dead link] 17. ^ Jump up to:a b Ross JA, Kasum CM, Davies SM, Jacobs DR, Folsom AR, Potter JD (August 2002). "Diet and risk of leukemia in the Iowa Women's Health Study". Cancer Epidemiol. Biomarkers Prev. 11 (8): 777–81. PMID 12163333. 18. ^ Jump up to:a b c d e f Wiernik, Peter H. (2001). Adult leukemias. New York: B. C. Decker. pp. 3–15. ISBN 1-55009-111-5. 19. ^ Jump up to:a b Robinette, Martin S.; Cotter, Susan; Van de Water (2001). Quick Look Series in Veterinary Medicine: Hematology. Teton NewMedia. p. 105. ISBN 1-893441-36-9. 20. Jump up^ Stass, Sanford A.; Schumacher, Harold R.; Rock, William R. (2000). Handbook of hematologic pathology. New York, N.Y: Marcel Dekker. pp. 193–194. ISBN 0-8247-0170-4. 21. Jump up^ Leonard, Barry (1998). Leukemia: A Research Report. DIANE Publishing. p. 7. ISBN 0-7881-7189-5. 22. ^ Jump up to:a b c d Non-Ionizing Radiation, Part 1: Static and Extremely Low-Frequency (ELF) Electric and Magnetic Fields (IARC Monographs on the Evaluation of the Carcinogenic Risks). Geneva: World Health Organisation. 2002. pp. 332–333, 338. ISBN 92-832-1280-0. 23. Jump up^ "WHO | Electromagnetic fields and public health". Retrieved 2009-02-18. 24. Jump up^ Rudant, Jérémie; Alicia Amigou, Laurent Orsi, Thomas Althaus, Guy Leverger, André Baruchel, Yves Bertrand, Brigitte Nelken, Geneviève Plat, Gérard Michel, Nicolas Sirvent, Pascal Chastagner, Stéphane Ducassou, Xavier Rialland, Denis Hémon, Jacqueline Clavel (2012). "Fertility treatments, congenital malformations, fetal loss, and childhood acute leukemia: The ESCALE study (SFCE)".Pediatric Blood & Cancer 60 (2): 301–8.doi:10.1002/pbc.24192. ISSN 1545-5009.PMID 22610722. Lay summary. 25. Jump up^ Pasmant E, Ballerini P, Lapillonne H et al. SPRED1 disorder and predisposition to leukemia in children. Blood 2009; 114:1131. 26. Jump up^ Hoffbrand AV, Moss PAH, and Pettit JE, "Essential Haematology", Blackwell, 5th ed., 2006. 27. Jump up^ National Cancer Institute. "Chronic Lymphocytic Leukemia (PDQ) Treatment: Stage Information". Retrieved 2007-09-04. 28. Jump up^ Eichhorst BF, Busch R, Hopfinger G, Pasold R, Hensel M, Steinbrecher C, Siehl S, Jäger U, Bergmann M, Stilgenbauer S, Schweighofer C, Wendtner CM, Döhner H, Brittinger G, Emmerich B, Hallek M, German CLL Study Group. (2006). "Fludarabine plus cyclophosphamide versus fludarabine alone in first-line therapy of younger patients with chronic lymphocytic leukemia". Blood 107 (3): 885–91.doi:10.1182/blood-2005-06-2395. PMID 16219797. 29. Jump up^ Gribben JG (January 2008). "Stem cell transplantation in chronic lymphocytic leukemia". Biol. Blood Marrow Transplant. 15 (1 Suppl): 53–8.doi:10.1016/j.bbmt.2008.10.022. PMC 2668540.PMID 19147079. 30. Jump up^ American Cancer Society (22 March 2012). "Typical treatment of acute myeloid leukemia (except promyelocytic M3)". Detailed Guide: Leukemia – Acute Myeloid (AML). American Cancer Society. Retrieved 31 Oct 2012. 31. ^ Jump up to:a b c Fausel C (October 2007). "Targeted chronic myeloid leukemia therapy: seeking a cure". J Manag Care Pharm13 (8 Suppl A): 8–12. PMID 17970609. 32. Jump up^ "Cladribine in a weekly versus daily schedule for untreated active hairy cell leukemia: final report from the Polish Adult Leukemia Group (PALG) of a prospective, randomized, multicenter trial – Robak et al. 109 (9): 3672 – Blood". Retrieved 2007-09-10. 33. Jump up^ "Filgrastim for Cladribine-Induced Neutropenic Fever in Patients With Hairy Cell Leukemia – Saven et al. 93 (8): 2471 – Blood". Retrieved 2007-09-10. 34. ^ Jump up to:a b c d Dearden CE, Matutes E, Cazin B (September 2001)."High remission rate in T-cell prolymphocytic leukemia with CAMPATH-1H". Blood 98 (6): 1721–6.doi:10.1182/blood.V98.6.1721. PMID 11535503. 35. Jump up^ "JMMLfoundation.org". JMMLfoundation.org. Retrieved 2010-08-29.[dead link] 36. Jump up^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved 2009-11-11. 37. Jump up^ Lozano, R (Dec 15, 2012). "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet 380 (9859): 2095–128.doi:10.1016/S0140-6736(12)61728-0. PMID 23245604. 38. ^ Jump up to:a b c "Leukemia Facts & Statistics." The Leukemia & Lymphoma Society. Retrieved 2009-07-02. 39. Jump up^ Horner MJ, Ries LAG, Krapcho M, Neyman N, et al. (eds)."SEER Cancer Statistics Review, 1975–2006".Surveillance Epidemiology and End Results (SEER). Bethesda, MD: National Cancer Institute. Retrieved 2009-11-03. "Table 1.4: Age-Adjusted SEER Incidence and U.S. Death Rates and 5-Year Relative Survival Rates By Primary Cancer Site, Sex and Time Period" 40. ^ Jump up to:a b James G. Gurney, Malcolm A. Smith, Julie A. Ross (1999) Cancer Incidence and Survival among Children and Adolescents, United States SEER program 1975–1995, chapter on Leukemia Cancer Statistics Branch, National Cancer Institute, available online from the SEER web site 41. Jump up^ Childhood Blood Cancers | The Leukemia & Lymphoma Society 42. Jump up^ Facts 2012 from The Leukemia & Lymphoma Society 43. Jump up^ Patlak, Margie. "Targeting Leukemia: From Bench to Bedside". Breakthroughs in Bioscience. The Federation of American Societies for Experimental Biology. Retrieved 20 May 2010. 44. Jump up^ Sontag, Susan (1978). Illness as Metaphor. New York: Farrar, Straus and Giroux. p. 18. ISBN 0-374-17443-1. 45. Jump up^ Search of: leukemia – List Results – ClinicalTrials.gov 46. Jump up^ "Understanding Clinical Trials for Blood Cancers". Leukemia and Lymphoma Society. Retrieved 19 May 2010. 47. Jump up^ Jaslow, Ryan. "New Leukemia Therapy Destroys Cancer by Turning Blood Cells into "Assassins"". CBSnews.com HealthPop section. Retrieved 11 August 2011. 48. Jump up^ Coghlan, Andy (26 March 2013)Gene therapy cures leukaemia in eight days The New Scientist, Retrieved 15 April 2013 49. Jump up^ "How we're beating leukaemia". Retrieved 24 September 2013. 50. ^ Jump up to:a b c d Shapira T, Pereg D, Lishner M (September 2008). "How I treat acute and chronic leukemia in pregnancy".Blood Rev. 22 (5): 247–59.doi:10.1016/j.blre.2008.03.006. PMID 18472198. 51. ^ Jump up to:a b Koren G, Lishner M (2010). "Pregnancy and commonly used drugs in hematology practice". Hematology Am Soc Hematol Educ Program 2010: 160–5.doi:10.1182/asheducation-2010.1.160.PMID 21239787.