Habitat : Myrica heterophylla is native to Southeastern N. America – New Jersey to Florida, west to Louisiana. It grows on bogs, stream, pond and lake margins, moist regions of mixed deciduous forests, pine flatlands near pitcher-plant bogs, swamps from sea level to 250 metres.
Myrica heterophylla is an evergreen Shrub growing to 3 m (9ft 10in). It is often forming rhizomatous colonies of much-branched specimens, to 3 m. Branchlets appearing black, glabrous to densely pilose; glands sparse or dense, yellow-orange. Leaf blade aromatic when crushed, oblanceolate to elliptic, occasionally obovate, 3-12.4(-14.2) × 1-5.2 cm, sometimes membranous, more often leathery, base cuneate to attenuate, margins entire or serrate distal to middle, apex rounded to acute, apiculate; surfaces abaxially pilose (especially on major veins) or glabrate, densely glandular, adaxially pilose or glabrous, lacking glands or very sparsely glandular; glands yellow. Inflorescences: staminate 0.5-1.8 cm; pistillate 0.3-1.1 cm. Flowers unisexual, staminate and pistillate on different plants. Staminate flowers: bract of flower shorter than staminal column, margins opaque, ciliate, especially at apex and laterally, abaxially glabrous or with few glands; stamens 3-5(-7). Pistillate flowers: bracteoles persistent in fruit, 4, not accrescent or adnate to fruit wall, abaxially pilose, usually along midrib, lacking glands; ovary glabrous or sparsely glandular, not pubescent. Fruits globose-ellipsoid, 3-4.5 mm; fruit wall glabrous or sparsely glandular, obscured by enlarged protuberances (± glandular) and thin to thick coat of gray to white wax.
It is in leaf 12-Jan It is in flower in May, and the seeds ripen in September.
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The flowers are dioecious (individual flowers are either male or female, but only one sex is to be found on any one plant so both male and female plants must be grown if seed is required) and are pollinated by Wind.The plant is not self-fertile.
It can fix Nitrogen.
Suitable for: light (sandy), medium (loamy) and heavy (clay) soils and prefers well-drained soil. Suitable pH: acid, neutral and basic (alkaline) soils. It can grow in semi-shade (light woodland) or no shade. It prefers dry or moist soil. The plant can tolerate maritime exposure.
Prefers a moist soil. Grows well in an open position in a well-drained soil in sun or light shade. Thrives in any ordinary garden soil according to one report whilst another says that it thrives in an acid soil. Prefers a lime-free loamy or peaty soil. Succeeds in dry and maritime climates. Closely related to M. pensylvanica and M. cerifera. Dioecious, male and female plants must be grown if seed is required. Plants in this genus are notably resistant to honey fungus. Many species in this genus have a symbiotic relationship with certain soil micro-organisms, these form nodules on the roots of the plants and fix atmospheric nitrogen. Some of this nitrogen is utilized by the growing plant but some can also be used by other plants growing nearby. Propagation:
Seed – best sown as soon as it is ripe in the autumn in a cold frame. Stored seed germinates more freely if given a 3 month cold stratification and then sown in a cold frame. Germination is usually good. Prick out the seedlings into individual pots when they are large enough to handle and grow on in a cold frame for the first winter. Plant out in late spring or early summer. Cuttings of half-ripe wood, 5 – 8cm with a heel, July/August in a frame. Pot up and overwinter in a cold frame then plant out in late spring or early summer. Fair to good percentage. Layering in spring.
Edible Uses: Condiment; Tea.
The following notes are for the closely related M. cerifera. It is assumed that they also apply to this species. Fruit – raw or cooked. The fruit is about 2 – 4mm in diameter with a single large seed. There is very little edible flesh and this is of poor quality. Leaves and berries are used as a food flavouring. An attractive and agreeable substitute for bay leaves, used in flavouring soups, stews etc. The dried leaves are brewed into a robust tea.
The following notes are for the closely related M. cerifera. It is assumed that they also apply to this species. The root bark is astringent, emetic (in large doses), sternutatory, stimulant and tonic. It is harvested in the autumn, thoroughly dried then powdered and kept in a dark place in an airtight container. It is used internally in the treatment of diarrhoea, jaundice, fevers, colds, influenza, catarrh, excessive menstruation, vaginal discharge etc. Externally, it is applied to indolent ulcers, sore throats, sores, itching skin conditions, dandruff etc. The wax is astringent and slightly narcotic. It is regarded as a sure cure for dysentery and is also used to treat internal ulcers. A tea made from the leaves is used in the treatment of fevers and externally as a wash for itchy skin. Other Uses:
Dye; Hedge; Hedge; Wax; Wood.
The following notes are for the closely related M. cerifera. It is assumed that they also apply to this species. A wax covering on the fruit is extracted by scalding the fruit with boiling water and immersing them for a few minutes, the wax floats to the surface and is then skimmed off. The fruit is then boiled in water to extract the wax from the pulp and once more the wax is skimmed off. It is then strained through a muslin cloth and can be used to make aromatic candles, sealing wax etc. Candles made from this wax are quite brittle but are less greasy in warm weather. They are slightly aromatic, with a pleasant balsamic odour, and do not smoke when put out, making them much more pleasant to use that wax or tallow candles. The wax is also used in making soaps. About 1 kilo of wax can be obtained from 4 kilos of berries. A blue dye is obtained from the fruit. The plant can be grown as an informal hedge, succeeding in windy sites. Wood – light, soft, brittle, fine-grained. The wood weighs 35lb per cubic foot. It is of no commercial value
Known Hazards : Although no reports of toxicity have been seen for this species, there is a report for some members of this genus that some of the constituents of the wax might be carcinogenic.
Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider. Resources:
Botanical Name : Viola adunca Family: Violaceae Genus: Viola Species: V. adunca Kingdom:Plantae Order: Malpighiales
Synonyms : Lophion aduncum. Viola bellidifolia. Viola clarkiae. Viola cordulata. Viola desertorum. Common Names: Hookedspur violet, Early blue violet, Sand violet, and Western dog violet, Kirk’s violet, Hooked Spur violet
Habitat: Viola adunca is native to Eastern and Western N. America – Alaska to California, also Ontario to Quebec and New Brunswick. It grows on damp banks and edges of meadows in most forest communities, 1500 – 2400 metres from Alaska to N. California. Description:
Viola adunca is a perennial plant growing to 0.1 m (0ft 4in). This is a hairy, compact plant growing from a small rhizome system. The leaves are spade- or heart-shaped, sometimes with broadly wavy margins. They are generally 1 to 4 centimeters long. The single-flowered inflorescence grows at the end of a long, very thin peduncle. The nodding flower is a violet with five purple petals, the lower three with white bases and purple veining. The two side petals are white-bearded near the throat. The upper two petals may have hooked spurs at their tips.
It is in flower from Apr to May. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Insects, cleistogamous.The plant is self-fertile.
Suitable for: light (sandy), medium (loamy) and heavy (clay) soils and prefers well-drained soil. Suitable pH: acid and neutral soils. It can grow in semi-shade (light woodland) or no shade. It prefers moist soil.
Prefers a cool moist well-drained humus-rich soil in partial or dappled shade and protection from scorching winds. Tolerates sandstone and limestone soils but becomes chlorotic if the pH is too high. Prefers a pH between 6 and 6.5. All members of this genus have more or less edible leaves and flower buds, though those species with yellow flowers can cause diarrhoea if eaten in large quantities. There is at least one named form selected for its ornamental value. ‘Alba’ has white flowers. Flowers formed late in the season are cleistogamous (lacking petals, the flowers do not open but are self-pollinated).
Seed – best sown in the autumn in a cold frame. Sow stored seed in early spring in a cold frame. Prick out the seedlings into individual pots when they are large enough to handle and plant them out in the summer. Division in the autumn or just after flowering. Larger divisions can be planted out direct into their permanent positions, though we have found that it is best to pot up smaller divisions and grow them on in light shade in a greenhouse or cold frame until they are growing away well. Plant them out in the summer or the following spring. Edible Uses: Young leaves and flower buds – raw or cooked. When added to soup they thicken it in much the same way as okra. A tea can be made from the dried leaves. Medicinal Uses:
Early blue violet was used medicinally mostly by the Blackfoot and Bella Coola Indians. An infusion of the leaves and roots has been used to treat stomach problems and asthma in children, and also as a wash and poultice on sore and swollen joints. The roots and leaves have been chewed by women during childbirth. A poultice of the chewed leaves was applied to sore eyes. A poultice of the crushed flowers was applied to the side or chest in the treatment of pain.
Other Uses : A blue dye can be obtained from the flower.
Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider. Resources:
The myelodysplastic syndromes (MDS, formerly known as “preleukemia”) are a group of disorders caused by poorly formed or dysfunctional blood cells.Myelodysplastic syndromes occur when something goes wrong in your bone marrow — the spongy material inside our bones where blood cells are made.
Patients with MDS often develop severe anemia and require frequent blood transfusions. In most cases, the disease worsens and the patient develops cytopenias (low blood counts) due to progressive bone marrow failure. In about one third of patients with MDS, the disease transforms into acute myelogenous leukemia (AML), usually within months to a few years.
The myelodysplastic syndromes are all disorders of the stem cell in the bone marrow. In MDS, hematopoiesis (blood production) is disorderly and ineffective. The number and quality of blood-forming cells decline irreversibly, further impairing blood production.
There is no cure for myelodysplastic syndromes. Treatment for myelodysplastic syndromes usually focuses on reducing or preventing complications of the disease and of treatments. In certain cases, myelodysplastic syndromes are treated with a bone marrow transplant, which may help prolong life.
The median age at diagnosis of a MDS is between 60 and 75 years; a few patients are younger than 50; MDS diagnoses are rare in children. Males are slightly more commonly affected than females.
The exact number of people with MDS is not known because it can go undiagnosed and there is no mandated tracking of the syndrome. Some estimates are on the order of 10,000 to 20,000 new cases each year in the United States alone. The incidence is probably increasing as the age of the population increases, and some authors propose that the incidence in patients over 70 may be as high as 15 cases per 100,000 per year
Myelodysplastic syndromes rarely cause signs or symptoms in the early stages of the disease.The symptoms are nonspecific and generally related to the blood cytopenias:
In time, myelodysplastic syndromes may cause:
*Anemia—chronic tiredness,fatigue, shortness of breath, chilled sensation, sometimes chest pain
*Neutropenia (low neutrophil count) —increased susceptibility to frequent infections
*Pinpoint-sized red spots just beneath the skin caused by bleeding (petechiae)
*Thrombocytopenia (low platelet count) —increased susceptibility to bleeding and ecchymosis (bruising), as well as subcutaneous hemorrhaging resulting in purpura or petechia.
Many individuals are asymptomatic, and blood cytopenia or other problems are identified as a part of a routine blood count:
*neutropenia, anemia and thrombocytopenia (low cell counts of white and red blood cells, and platelets, respectively);
*splenomegaly or rarely hepatomegaly;
*abnormal granules in cells, abnormal nuclear shape and size; and/or
*chromosomal abnormalities, including chromosomal translocations and abnormal chromosome number.
Although there is some risk for developing acute myelogenous leukemia, about 50% of deaths occur as a result of bleeding or infection. Leukemia that occurs as a result of myelodysplasia is notoriously resistant to treatment.
Myelodysplastic syndromes occur when something happens to disrupt the orderly and controlled production of blood cells. People with myelodysplastic syndromes have blood cells that are immature and defective, and instead of developing normally, they die in the bone marrow or just after entering your bloodstream. Over time, the number of immature, defective cells begins to surpass that of healthy blood cells, leading to problems such as anemia, infections and excess bleeding.
Doctors divide myelodysplastic syndromes into two categories based on their cause:
*Myelodysplastic syndromes with no known cause. Called de novo myelodysplastic syndromes, doctors don’t know what causes these. De novo myelodysplastic syndromes are often more easily treated than are myelodysplastic syndromes with a known cause.
*Myelodysplastic syndromes caused by chemicals and radiation. Myelodysplastic syndromes that occur in response to cancer treatments, such as chemotherapy and radiation, or in response to chemical exposure are called secondary myelodysplastic syndromes. Secondary myelodysplastic syndromes are often more difficult to treat.
Types of myelodysplastic syndromes:
The World Health Organization divides myelodysplastic syndromes into subtypes based on the type of cells involved. Myelodysplastic syndrome subtypes include:
*Refractory cytopenia with unilineage dysplasia. In this type, one or two blood cell types are low in number — most commonly, the red blood cells are affected. Also, one type of blood cell appears abnormal under the microscope.
*Refractory anemia with excess blasts— types 1 and 2. In both these syndromes, any of the three types of cells — red blood cells, white blood cells or platelets — may be low in number and appear abnormal under a microscope.
*Myelodysplastic syndrome, unclassified. In this uncommon syndrome, there are reduced numbers of one of the three types of mature blood cells, and either the white blood cells or platelets look abnormal under a microscope.
*Older age. Most people with myelodysplastic syndromes are adults older than 60. Anyone can develop myelodysplastic syndromes, but they’re rare in younger people.
*Being male. Myelodysplastic syndromes occur more frequently in men than in women.
*Treatment with chemotherapy or radiation. Your risk of myelodysplastic syndromes is increased if you received chemotherapy or radiation, both of which are commonly used to treat cancer.
*Exposure to certain chemicals. Chemicals linked to myelodysplastic syndromes include tobacco smoke, pesticides and industrial chemicals, such as benzene.
*Exposure to heavy metals. Heavy metals linked to myelodysplastic syndrome include lead and mercury.
Complications: Complications of myelodysplastic syndromes include:
*Anemia. Reduced numbers of red blood cells can cause anemia, which can make you feel tired.
*Recurrent infections. Having too few white blood cells increases your risk of serious infections.
*Bleeding that won’t stop. Lacking platelets in your blood to stop bleeding can lead to excessive bleeding that won’t stop.
*Increased risk of cancer. Some people with myelodysplastic syndromes may eventually develop leukemia, a cancer of the blood cells.
MDS must be differentiated from anemia, thrombocytopenia, and/or leukopenia. Usually, the elimination of other causes of these cytopenias, along with a dysplastic bone marrow, is required to diagnose a myelodysplastic syndrome.
A typical investigation includes: *Full blood count and examination of blood film. The blood film morphology can provide clues about hemolytic anemia, clumping of the platelets leading to spurious thrombocytopenia, or leukemia.
*Blood tests to eliminate other common causes of cytopenias, such as lupus, hepatitis, B12, folate, or other vitamin deficiencies, renal failure or heart failure, HIV, hemolytic anemia, monoclonal gammopathy. Age-appropriate cancer screening should be considered for all anemic patients.
*Bone marrow examination by a hematopathologist. This is required to establish the diagnosis, since all hematopathologists consider dysplastic marrow the key feature of myelodysplasia.
*Cytogenetics or chromosomal studies. This is ideally performed on the bone marrow aspirate. Conventional cytogenetics requires a fresh specimen, since live cells are induced to enter metaphase to enhance chromosomal staining. Alternatively, virtual karyotyping can be done for MDS, which uses computational tools to construct the karyogram from disrupted DNA. Virtual karyotyping does not require cell culture and has dramatically higher resolution than conventional cytogenetics, but cannot detect balanced translocations.
*Flow cytometry is helpful to establish the presence of any lymphoproliferative disorder in the marrow.
Anemia dominates the early course. Most symptomatic patients complain of the gradual onset of fatigue and weakness, dyspnea, and pallor, but at least half the patients are asymptomatic and their MDS is discovered only incidentally on routine blood counts. Previous chemotherapy or radiation exposure is an important historic fact. Fever and weight loss should point to a myeloproliferative rather than myelodysplastic process. Children with Down syndrome are susceptible to MDS, and a family history may indicate a hereditary form of sideroblastic anemia or Fanconi anemia.
The average age at diagnosis for MDS is about 65 years, but pediatric cases have been reported. Some patients have a history of exposure to chemotherapy (especially alkylating agents such as melphalan, cyclophosphamide, busulfan, and chlorambucil) or radiation (therapeutic or accidental), or both (e.g., at the time of stem cell transplantation for another disease). Workers in some industries with heavy exposure to hydrocarbons such as the petroleum industry have a slightly higher risk of contracting the disease than the general population. Males are slightly more frequently affected than females. Xylene and benzene exposure has been associated with myelodysplasia. Vietnam veterans that were exposed to Agent Orange are at risk of developing MDS.
The features generally used to define a MDS are: blood cytopenias; ineffective hematopoiesis; dyserythropoiesis; dysgranulopoiesis; dysmegakaropoiesis and increased myeloblast.
Dysplasia can affect all three lineages seen in the bone marrow. The best way to diagnose dysplasia is by morphology and special stains (PAS) used on the bone marrow aspirate and peripheral blood smear. Dysplasia in the myeloid series is defined by:
1.Hypersegmented neutrophils (also seen in Vit B12/Folate deficiency)
2.Hyposegmented neutrophils (Pseudo-Pelger Huet)
3.Hypogranular neutrophils or pseudo Chediak Higashi large granules
4.Auer rods – automatically RAEB II (if blast count <5% in the peripheral blood and <10% in the bone marrow aspirate) also note Auer rods may be seen in mature neutrophils in AML with translocation t(8;21)
5.Dimorphic granules (basophilic and eosinophilic granules) within eosinophils
1.Binucleated erythroid percursors and karyorrhexis
2.Erythroid nuclear budding
3.Erythroid nuclear strings or internuclear bridging (also seen in congenital dyserythropoietic anemias)
4.Loss of E-cadherin in normoblasts is a sign of aberrancy
5.PAS (globular in vacuoles or diffuse cytoplasmic staining) within erythroid precursors in the bone marrow aspirate (has no bearing on paraffin fixed bone marrow biopsy). Note: One can see PAS vacuolar positivity in L1 and L2 blasts (AFB classification; the L1 and L2 nomenclature is not used in the WHO classification)
6.Ringed sideroblasts seen on Prussian blue iron stain (10 or more iron granules encircling 1/3 or more of the nucleus and >15% ringed sideroblasts when counted amongst red cell precursors)
Megakaryocytic series (can be the most subjective)
1.Hyposegmented nuclear features in platelet producing megakaryocytes (lack of lobation)
2.Hypersegmented (osteoclastic appearing) megakaryocytes
3.Ballooning of the platelets (seen with interference contrast microscopy)
Other stains can help in special cases (PAS and napthol ASD chloroacetate esterase positivity) in eosinophils is a marker of abnormality seen in chronic eosinophilic leukemia and is a sign of aberrancy.
On the bone marrow biopsy high grade dysplasia (RAEB-I and RAEB-II) may show atypical localization of immature precursors (ALIPs) which are islands of immature precursors cells (myeloblasts and promyelcytes) localized to the center of intertrabecular space rather than adjacent to the trabeculae or surrounding arterioles. This morphology can be difficult to recognize from treated leukemia and recovering immature normal marrow elements. Also topographic alteration of the nucleated erythroid cells can be seen in early myelodysplasia (RA and RARS), where normoblasts are seen next to bony trabeculae instead of forming normal interstitially placed erythroid islands.
Myelodysplasia is a diagnosis of exclusion and must be made after proper determination of iron stores, vitamin deficiencies, and nutrient deficiencies are ruled out. Also congenital diseases such as congenital dyserythropoietic anemia (CDA I through IV) has been recognized, Pearson’s syndrome (sideroblastic anemia), Jordans anomaly – vacuolization in all cell lines may be seen in Chanarin-Dorfman syndrome, ALA (aminolevulinic acid) enzyme deficiency, and other more esoteric enzyme deficiencies are known to give a pseudomyelodysplastic picture in one of the cell lines, however, all three cell lines are never morphologically dysplastic in these entities with the exception of chloramphenicol, arsenic toxicity and other poisons.
All of these conditions are characterized by abnormalities in the production of one or more of the cellular components of blood (red cells, white cells other than lymphocytes and platelets or their progenitor cells, megakaryocytes).
No definitive cure or treatment for myelodysplastic syndromes exists. Instead, most people receive supportive care to help manage symptoms such as fatigue and to prevent bleeding and infections.
Blood transfusions can be used to replace red blood cells, white blood cells or platelets in people with myelodysplastic syndromes.
Medications used to increase the number of healthy blood cells your body produces include:
*Medications that increase the number of blood cells your body makes. Called growth factors, these medications are artificial versions of substances found naturally in your bone marrow. Some growth factors, such as erythropoietin or darbepoietin, can reduce the need for blood transfusions by increasing red blood cells. Others may help prevent infections by increasing white blood cells in people with certain myelodysplastic syndromes.Medications that stimulate blood cells to mature, rather than remain immature.
*Medications such as azacitidine (Vidaza) and decitabine (Dacogen) may improve the quality of life of people with certain myelodysplastic syndromes and help delay progression to acute myelogenous leukemia. But these drugs aren’t effective in all people, and some can cause further blood cell problems. Medications that suppress your immune system.
*Medications used to suppress the immune system may be used in certain myelodysplastic syndromes.Medication for people with a certain genetic abnormality. If your myelodysplastic syndrome is associated with a genetic abnormality called isolated del(5q), your doctor may recommend lenalidomide (Revlimid). Lenalidomide may reduce the need for blood transfusions in people with this abnormality.
*Bone marrow stem cell transplant
During a bone marrow stem cell transplant, your defective blood cells are destroyed using powerful chemotherapy drugs. Then the abnormal bone marrow stem cells are replaced with healthy, donated cells (allogeneic transplant). Unfortunately, few people are candidates for this procedure because of the high risks involved in transplanting in older adults — those most likely to have myelodysplastic syndromes. Even among young, relatively healthy people, the number of transplant-related complications is high.
Prognosis: Indicators of a good prognosis Younger age; normal or moderately reduced neutrophil or platelet counts; low blast counts in the bone marrow(<20%) and no blasts in the blood; no Auer rods; ringed sideroblasts; normal karyotypes of mixed karyotypes without complex chromosome abnormalities and in vitro marrow culture- non leukemic growth pattern.
Indicators of a poor prognosis Advanced age; Severe neutropenia or thrombocytopenia ; high blast count in the bone marrow (20-29%) or blasts in the blood; Auer rods; absence of ringed sideroblasts; abnormal localization or immature granulocyte precursors in bone marrow section all or mostly abnormal karyotypes or complex marrow chromosome abnormalities and in vitro bone emarrow culture-leukemic growth pattern.
Prognosis and karyotype Good: Normal, -Y, del(5q), del(20q)
Intermediate or variable: +8, other single or double anomalies
Poor; Complex (>3 chromosomal aberrations); chromosome 7 anomalies
The International Prognostic Scoring System (IPSS) is the most commonly used tool in MDS to predict long-term outcome.
Cytogenetic abnormalities can be detected by conventional cytogenetics, a FISH panel for MDS, or Virtual Karyotype.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose
Leukemia or leukaemia (Greek leukos “white”; aima “blood”) is a cancer of the blood or bone marrow and is characterized by an abnormal proliferation (production by multiplication) of blood cells, usually white blood cells (leukocytes). Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader group of diseases called hematological neoplasms.
Leukemia is a type of cancer. Cancer is a group of many related diseases. All cancers begin in cells, which make up blood and other tissues. Normally, cells grow and divide to form new cells as the body needs them. When cells grow old, they die, and new cells take their place.
Sometimes this orderly process goes wrong. New cells form when the body does not need them, and old cells do not die when they should. Leukemia is cancer that begins in blood cells.
Leukemia is a malignant cancer of the blood and bone marrow that affects thousands of children and adults. Acute leukemia progresses quickly while chronic leukemia develops more slowly.
The immune system protects the body from potentially harmful substances. The inflammatory response (inflammation) is part of innate immunity. It occurs when tissues are injured by bacteria, trauma, toxins, heat or any other cause.
Normal blood cells
Blood cells form in the bone marrow. Bone marrow is the soft material in the center of most bones.
Immature blood cells are called stem cells and blasts. Most blood cells mature in the bone marrow and then move into the blood vessels. Blood that flows through the blood vessels and heart is called the peripheral blood.
The bone marrow makes different types of blood cells. Each type has a special function:
In people with leukemia, the bone marrow produces abnormal white blood cells. The abnormal cells are leukemia cells. At first, leukemia cells function almost normally. In time, they may crowd out normal white blood cells, red blood cells, and platelets. This makes it hard for blood to do its work.
Types Of Leukemia:-
The types of leukemia are grouped by how quickly the disease develops and gets worse. Leukemia is either chronic (gets worse slowly) or acute (gets worse quickly): Chronic leukemia—Early in the disease, the abnormal blood cells can still do their work, and people with chronic leukemia may not have any symptoms. Slowly, chronic leukemia gets worse. It causes symptoms as the number of leukemia cells in the blood rises.
Acute leukemia—The blood cells are very abnormal. They cannot carry out their normal work. The number of abnormal cells increases rapidly. Acute leukemia worsens quickly.
The types of leukemia are also grouped by the type of white blood cell that is affected. Leukemia can arise in lymphoid cells or myeloid cells. Leukemia that affects lymphoid cells is called lymphocytic leukemia. Leukemia that affects myeloid cells is called myeloid leukemia or myelogenous leukemia.
There are four common types of leukemia:
1.Chronic lymphocytic leukemia (chronic lymphoblastic leukemia, CLL) accounts for about 7,000 new cases of leukemia each year. Most often, people diagnosed with the disease are over age 55. It almost never affects children.
2.Chronic myeloid leukemia (chronic myelogenous leukemia, CML) accounts for about 4,400 new cases of leukemia each year. It affects mainly adults.
3.Acute lymphocytic leukemia (acute lymphoblastic leukemia, ALL) accounts for about 3,800 new cases of leukemia each year. It is the most common type of leukemia in young children. It also affects adults.
4.Acute myeloid leukemia (acute myelogenous leukemia, AML) accounts for about 10,600 new cases of leukemia each year. It occurs in both adults and children.
Hairy cell leukemiais a rare type of chronic leukemia. This booklet does not deal with hairy cell leukemia or other rare types of leukemia. Together, these rare leukemias account for about 5,200 new cases of leukemia each year. The Cancer Information Service (1-800-4-CANCER) can provide information about these types of leukemia.
No one knows the exact causes of leukemia. Doctors can seldom explain why one person gets this disease and another does not. However, research has shown that people with certain risk factors are more likely than others to develop leukemia. A risk factor is anything that increases a person’s chance of developing a disease.
Studies have found the following risk factors for leukemia:
Very high levels of radiation —People exposed to very high levels of radiation are much more likely than others to develop leukemia. Very high levels of radiation have been caused by atomic bomb explosions (such as those in Japan during World War II) and nuclear power plant accidents (such as the Chernobyl [also called Chornobyl] accident in 1986).
Medical treatment that uses radiation can be another source of high-level exposure. Radiation used for diagnosis, however, exposes people to much lower levels of radiation and is not linked to leukemia.
Working with certain chemicals—Exposure to high levels of benzene in the workplace can cause leukemia. Benzene is used widely in the chemical industry. Formaldehyde is also used by the chemical industry. Workers exposed to formaldehyde also may be at greater risk of leukemia. *Chemotherapy—Cancer patients treated with certain cancer-fighting drugs sometimes later develop leukemia. For example, drugs known as alkylating agents are associated with the development of leukemia many years later. *Down syndrome and certain other genetic diseases—Some diseases caused by abnormal chromosomes may increase the risk of leukemia. *Human T-cell leukemia virus-I (HTLV-I)—This virus causes a rare type of chronic lymphocytic leukemia known as human T-cell leukemia. However, leukemia does not appear to be contagious. *Myelodysplastic syndrome—People with this blood disease are at increased risk of developing acute myeloid leukemia.
Like all blood cells, leukemia cells travel through the body. Depending on the number of abnormal cells and where these cells collect, patients with leukemia may have a number of symptoms.
Common symptoms of leukemia:
*Fevers or night sweats
*Feeling weak or tired *Headache
*Bleeding and bruising easily (bleeding gums, purplish patches in the skin, or tiny red spots under the skin)
*Pain in the bones or joints
*Swelling or discomfort in the abdomen (from an enlarged spleen)
*Swollen lymph nodes, especially in the neck or armpit *Weight loss
Such symptoms are not sure signs of leukemia. An infection or another problem also could cause these symptoms. Anyone with these symptoms should see a doctor as soon as possible. Only a doctor can diagnose and treat the problem.
In the early stages of chronic leukemia, the leukemia cells function almost normally. Symptoms may not appear for a long time. Doctors often find chronic leukemia during a routine checkup—before there are any symptoms. When symptoms do appear, they generally are mild at first and get worse gradually.
In acute leukemia, symptoms appear and get worse quickly. People with this disease go to their doctor because they feel sick. Other symptoms of acute leukemia are vomiting, confusion, loss of muscle control, and seizures. Leukemia cells also can collect in the testicles and cause swelling. Also, some patients develop sores in the eyes or on the skin. Leukemia also can affect the digestive tract, kidneys, lungs, or other parts of the body. Click to see :->Tips to know the symptoms of Leukemia
If a person has symptoms that suggest leukemia, the doctor may do a physical exam and ask about the patient’s personal and family medical history. The doctor also may order laboratory tests, especially blood tests.
The exams and tests may include the following:
*Physical exam—The doctor checks for swelling of the lymph nodes, spleen, and liver.
*Blood tests—The lab checks the level of blood cells. Leukemia causes a very high level of white blood cells. It also causes low levels of platelets and hemoglobin, which is found inside red blood cells. The lab also may check the blood for signs that leukemia has affected the liver and kidneys.
*Biopsy—The doctor removes some bone marrow from the hipbone or another large bone. A pathologist examines the sample under a microscope. The removal of tissue to look for cancer cells is called a biopsy. A biopsy is the only sure way to know whether leukemia cells are in the bone marrow.
There are two ways the doctor can obtain bone marrow. Some patients will have both procedures:
*Bone marrow biopsy: The doctor uses a very thick needle to remove a small piece of bone and bone marrow.
Local anesthesia helps to make the patient more comfortable.
*Cytogenetics—The lab looks at the chromosomes of cells from samples of peripheral blood, bone marrow, or lymph nodes.
*Spinal tap—The doctor removes some of the cerebrospinal fluid (the fluid that fills the spaces in and around the brain and spinal cord). The doctor uses a long, thin needle to remove fluid from the spinal column. The procedure takes about 30 minutes and is performed with local anesthesia. The patient must lie flat for several hours afterward to keep from getting a headache. The lab checks the fluid for leukemia cells or other signs of problems.
Chest x-ray—The x-ray can reveal signs of disease in the chest.
A person who needs a bone marrow aspiration or bone marrow biopsy may want to ask the doctor the following questions:-
*Will you remove the sample of bone marrow from the hip or from another bone?
*How long will the procedure take? Will I be awake? Will it hurt?
*How soon will you have the results? Who will explain them to me?
*If I do have leukemia, who will talk to me about treatment? When?
Many people with leukemia want to take an active part in making decisions about their medical care. They want to learn all they can about their disease and their treatment choices. However, the shock and stress after a diagnosis of cancer can make it hard to think of everything to ask the doctor. Often it helps to make a list of questions before an appointment. To help remember what the doctor says, patients may take notes or ask whether they may use a tape recorder. Some also want to have a family member or friend with them when they talk to the doctor—to take part in the discussion, to take notes, or just to listen.
The doctor may refer patients to doctors who specialize in treating leukemia, or patients may ask for a referral. Specialists who treat leukemia include hematologists, medical oncologists, and radiation oncologists. Pediatric oncologists and hematologists treat childhood leukemia.
Whenever possible, patients should be treated at a medical center that has doctors experienced in treating leukemia. If this is not possible, the patient’s doctor may discuss the treatment plan with a specialist at such a center.
Getting a second opinion
Sometimes it is helpful to have a second opinion about the diagnosis and the treatment plan. Some insurance companies require a second opinion; others may cover a second opinion if the patient or doctor requests it. There are a number of ways to find a doctor for a second opinion:
The patient’s doctor may be able to suggest a doctor who specializes in adult or childhood leukemia. At cancer centers, several specialists often work together as a team.
The Cancer Information Service, at 1-800-4-CANCER, can tell callers about nearby treatment centers.
A local or state medical society, a nearby hospital, or a medical school can usually provide the names of specialists.
The American Board of Medical Specialties (ABMS) has a list of doctors who have met certain education and training requirements and have passed specialty examinations. The Official ABMS Directory of Board Certified Medical Specialists lists doctors’ names along with their specialty and their educational background. The directory is available in most public libraries. Also, ABMS offers this information on the Internet .
Preparing for treatment
The doctor can describe treatment choices and discuss the results expected with each treatment option. The doctor and patient can work together to develop a treatment plan that fits the patient’s needs.
Treatment depends on a number of factors, including the type of leukemia, the patient’s age, whether leukemia cells are present in the cerebrospinal fluid, and whether the leukemia has been treated before. It also may depend on certain features of the leukemia cells. The doctor also takes into consideration the patient’s symptoms and general health.
These are some questions a person may want to ask the doctor before treatment begins:
*What type of leukemia do I have?
*What are my treatment choices? Which do you recommend for me? Why?
*What are the benefits of each kind of treatment?
*What are the risks and possible side effects of each treatment?
*If I have pain, how will you help me?
*What is the treatment likely to cost?
*How will treatment affect my normal activities?
*Would a clinical trial (research study) be appropriate for me? Can you help me find one?
People do not need to ask all of their questions or understand all of the answers at one time. They will have other chances to ask the doctor to explain things that are not clear and to ask for more information.
Methods of treatment:-
The doctor is the best person to describe the treatment choices and discuss the expected results. Depending on the type and extent of the disease, patients may have chemotherapy, biological therapy, radiation therapy, or bone marrow transplantation. If the patient’s spleen is enlarged, the doctor may suggest surgery to remove it. Some patients receive a combination of treatments.
People with acute leukemia need to be treated right away. The goal of treatment is to bring about a remission. Then, when signs and symptoms disappear, more therapy may be given to prevent a relapse. This type of therapy is called maintenance therapy. Many people with acute leukemia can be cured.
Chronic leukemia patients who do not have symptoms may not require immediate treatment. The doctor may suggest watchful waiting for some patients with chronic lymphocytic leukemia. The health care team will monitor the patient’s health so that treatment can begin if symptoms occur or worsen. When treatment for chronic leukemia is needed, it can often control the disease and its symptoms. However, chronic leukemia can seldom be cured. Patients may receive maintenance therapy to help keep the cancer in remission.
A patient may want to talk to the doctor about taking part in a clinical trial, a research study of new treatment methods. The section on “The Promise of Cancer Research” has more information about clinical trials.
In addition to anticancer therapy, people with leukemia may have treatment to control pain and other symptoms of the cancer, to relieve the side effects of therapy, or to ease emotional problems. This kind of treatment is called symptom management, supportive care, or palliative care.
Most patients with leukemia receive chemotherapy. This type of cancer treatment uses drugs to kill leukemia cells. Depending on the type of leukemia, the patient may receive a single drug or a combination of two or more drugs.
People with leukemia may receive chemotherapy in several different ways:
*By mouth *By injection directly into a vein (IV or intravenous)
*Through a catheter (a thin, flexible tube) placed in a large vein, often in the upper chest—A catheter that stays in place is useful for patients who need many IV treatments. The health care professional injects drugs into the catheter, rather than directly into a vein. This method avoids the need for many injections, which can cause discomfort and injure the veins and skin.
*By injection directly into the cerebrospinal fluid—If the pathologist finds leukemia cells in the fluid that fills the spaces in and around the brain and spinal cord, the doctor may order intrathecal chemotherapy. The doctor injects drugs directly into the cerebrospinal fluid. This method is used because drugs given by IV injection or taken by mouth often do not reach cells in the brain and spinal cord. (A network of blood vessels filters blood going to the brain and spinal cord. This blood-brain barrier stops drugs from reaching the brain.) The patient may receive the drugs in two ways:
*Injection into the spine: The doctor injects the drugs into the lower part of the spinal column.
*Ommaya reservoir: Children and some adult patients receive intrathecal chemotherapy through a special catheter called an Ommaya reservoir. The doctor places the catheter under the scalp. The doctor injects the anticancer drugs into the catheter. This method avoids the discomfort of injections into the spine.
Patients receive chemotherapy in cycles: a treatment period, then a recovery period, and then another treatment period. In some cases, the patient has chemotherapy as an outpatient at the hospital, at the doctor’s office, or at home. However, depending on which drugs are given, and the patient’s general health, a hospital stay may be necessary.
Some people with chronic myeloid leukemia receive a new type of treatment called targeted therapy. Targeted therapy blocks the production of leukemia cells but does not harm normal cells. Gleevec, also called STI-571, is the first targeted therapy approved for chronic myeloid leukemia.
People with some types of leukemia have biological therapy. This type of treatment improves the body’s natural defenses against cancer. The therapy is given by injection into a vein.
For some patients with chronic lymphocytic leukemia, the type of biological therapy used is a monoclonal antibody. This substance binds to the leukemia cells. This therapy enables the immune system to kill leukemia cells in the blood and bone marrow.
For some patients with chronic myeloid leukemia, the biological therapy is a natural substance called interferon. This substance can slow the growth of leukemia cells.
Patients may want to ask these questions about chemotherapy or biological therapy:-
*Why do I need this treatment?
*What drugs will I get?
*Should I see my dentist before treatment begins?
*What will the treatment do?
*Will I have to stay in the hospital?
*How will we know the drugs are working?
*How long will I be on this treatment?
*Will I have side effects during treatment? How long will they last? What can I do about them?
*Can these drugs cause side effects later on?
*How often will I need checkups?
Radiation therapy (also called radiotherapy) uses high-energy rays to kill leukemia cells. For most patients, a large machine directs radiation at the spleen, the brain, or other parts of the body where leukemia cells have collected. Some patients receive radiation that is directed to the whole body. (Total-body irradiation usually is given before a bone marrow transplant.) Patients receive radiation therapy at a hospital or clinic.
These are some questions a person may want to ask the doctor before having radiation therapy:-
*Why do I need this treatment?
*When will the treatments begin? How often will they be given? When will they end?
*How will I feel during therapy? Will there be side effects? How long will they last? What can we do about them?
*Can radiation therapy cause side effects later on?
*What can I do to take care of myself during therapy?
*How will we know if the radiation is working?
*Will I be able to continue my normal activities during treatment?
*How often will I need checkups?
Stem cell transplantation:-
Some patients with leukemia have stem cell transplantation. A stem cell transplant allows a patient to be treated with high doses of drugs, radiation, or both. The high doses destroy both leukemia cells and normal blood cells in the bone marrow. Later, the patient receives healthy stem cells through a flexible tube that is placed in a large vein in the neck or chest area. New blood cells develop from the transplanted stem cells.
There are several types of stem cell transplantation:-
*Bone marrow transplantation—The stem cells come from bone marrow.
*Peripheral stem cell transplantation—The stem cells come from peripheral blood.
*Umbilical cord blood transplantation—For a child with no donor, the doctor may use stem cells from umbilical cord blood. The umbilical cord blood is from a newborn baby. Sometimes umbilical cord blood is frozen for use later. Stem cells may come from the patient or from a donor: –
*Autologous stem cell transplantation—This type of transplant uses the patient’s own stem cells. The stem cells are removed from the patient, and the cells may be treated to kill any leukemia cells present. The stem cells are frozen and stored. After the patient receives high-dose chemotherapy or radiation therapy, the stored stem cells are thawed and returned to the patient.
*Allogeneic stem cell transplantation—This type of transplant uses healthy stem cells from a donor. The patient’s brother, sister, or parent may be the donor. Sometimes the stem cells come from an unrelated donor. Doctors use blood tests to be sure the donor’s cells match the patient’s cells.
*Syngeneic stem cell transplantation—This type of transplant uses stem cells from the patient’s healthy identical twin.
After a stem cell transplant, patients usually stay in the hospital for several weeks. The health care team protects patients from infection until the transplanted stem cells begin to produce enough white blood cells.
These are some questions a person may want to ask the doctor before having a stem cell transplant:-
*What kind of stem cell transplant will I have? If I need a donor, how will we find one?
*How long will I be in the hospital? What care will I need when I leave the hospital?
*How will we know if the treatment is working?
*What are the risks and the side effects? What can we do about them?
*What changes in normal activities will be necessary?
*What is my chance of a full recovery? How long will that take?
*How often will I need checkups?
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
In a major breakthrough that could help devise better treatment for blood cancer and aid the development of drugs that would stop the process before it advances, Canadian scientists have for the first time converted normal human blood cells to leukemia stem cells in the lab.
The team then transplanted the converted cells into lab mice and watched it replicate the entire disease process, from the very moment it begins. Till now, most human leukemia research involved studying a patient’s diseased cells. But because cancer takes months to develop, “just studying the cells at the end of the process does not tell us the series of changes that caused the cells to become leukemic and when they happened. We have now duplicated the natural process of cell death, as it happens. This will help us understand how cancer begins,” Dr John Dick at Ontario Cancer Institute said.
According to Dick, this peek into leukemia’s development will allow scientists to ask questions that include: Is the childhood disease different from that in adults? In which cell type does leukemia arise? And which genes are involved and in which order do they have to operate?
Reacting to the study, former head of Rajiv Gandhi Cancer Institute Dr Y P Bhatia told TOI, “Once the basic cellular structure is known, better treatment solutions can be devised. This is a major breakthrough. Scientists can now see the first cells that will give birth to leukemia and then watch as the disease as it slowly progresses.”
The groundbreaking research involved infecting cells from umbilical cord blood with a virus engineered to carry one of the genes known to cause certain types of leukemia. Dr Dick’s team introduced a specific leukemia gene into normal stem cells and injected the genetically altered cells into mice that lacked immune systems. This resulted in the mices developing leukemia, displaying the same characteristics and patterns of human disease.
He said, “We are studying how leukemia arises in the first place. We found that with the leukemia gene we were using, the disease only arose from immature stem and progenitor cells. The leukemic stem cells that were created seemed to change as the human leukemia was grown for longer times in a series of transplanted mice.”