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? asked in HealthDiseases & ConditionsCancer · 1 decade ago

do people ALWAYS die when they have leukemia?

all i know about it is that its a cancer.

how ad is it, and how bad does it feel?

does everyone die who gets it?

6 Answers

  • Panda
    Lv 7
    1 decade ago
    Favorite Answer

    Leukemia is cancer of the blood. There are four major types of leukemia and many subtypes . . some of these leukemia's are more aggressive, thus more deadly than others. Survival from leukemia depends on many different factors . . not all leukemia is the same, the type a person gets is often age specific . . children are more likely to get certain types of cancer that older adults almost never get. A great deal of research in childhood leukemia has resulted in higher survival rates . . children still die from leukemia, but not as many as in the past because treatment is more effective.

    Surviving leukemia or any cancer depends on the type, the stage at diagnosis, the patients age, overall health, and the patients response to first line treatment. The good news is that more people are surviving cancer including leukemia than they did in the past, the bad news is that there is still no cure for the disease and people including children can still die from it.

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  • 1 decade ago

    Yes Leukemia is a type of cancer and no not everyone dies from it. Im 17 years old and was diagnosed when i was 7 - I survived it!

    I had a total of 3 years chemotherapy to help fight it.

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  • Cydney
    Lv 5
    1 decade ago

    Leukemia is a type of cancer that can be treated and a good number of people do survive.

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  • 1 decade ago

    Not everyone dies from it. I had a little 3 year old cousin who survived it.

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  • 1 decade ago

    Chronic myelogenous leukemia

    From Wikipedia, the free encyclopedia

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    Chronic myelogenous leukemia

    Classification and external resources

    The Philadelphia chromosome as seen by metaphase FISH.

    ICD-10 C92.1

    ICD-9 205.1

    ICD-O: M9875/3

    DiseasesDB 2659

    MedlinePlus 000570

    eMedicine med/371

    MeSH D015464

    Chronic myelogenous (or myeloid) leukemia (CML), also known as chronic granulocytic leukemia (CGL), is a form of leukemia characterized by the increased and unregulated growth of predominantly myeloid cells in the bone marrow and the accumulation of these cells in the blood. CML is a clonal bone marrow stem cell disorder in which proliferation of mature granulocytes (neutrophils, eosinophils, and basophils) and their precursors is the main finding. It is a type of myeloproliferative disease associated with a characteristic chromosomal translocation called the Philadelphia chromosome. Historically, it has been treated with chemotherapy, interferon and bone marrow transplantation, although targeted therapies introduced at the beginning of the 21st century have radically changed the management of CML.



    * 1 Signs and symptoms

    * 2 Diagnosis

    * 3 Pathophysiology

    * 4 Classification

    o 4.1 Chronic phase

    o 4.2 Accelerated phase

    o 4.3 Blast crisis

    * 5 Treatment

    o 5.1 Chronic phase

    * 6 Prognosis

    * 7 Epidemiology

    * 8 References

    * 9 External links

    [edit] Signs and symptoms

    Patients are often asymptomatic at diagnosis, presenting incidentally with an elevated white blood cell count on a routine laboratory test. In this setting, CML must be distinguished from a leukemoid reaction, which can have a similar appearance on a blood smear. Symptoms of CML may include: malaise, low-grade fever, gout, increased susceptibility to infections, anemia, and thrombocytopenia with easy bruising (although an increased platelet count (thrombocytosis) may also occur in CML). Splenomegaly may also be seen.[1][2]

    [edit] Diagnosis

    CML is often suspected on the basis on the complete blood count, which shows increased granulocytes of all types, typically including mature myeloid cells. Basophils and eosinophils are almost universally increased; this feature may help differentiate CML from a leukemoid reaction. A bone marrow biopsy is often performed as part of the evaluation for CML, but bone marrow morphology alone is insufficient to diagnose CML.[2][3]

    Ultimately, CML is diagnosed by detecting the Philadelphia chromosome. This characteristic chromosomal abnormality can be detected by routine cytogenetics, by fluorescent in situ hybridization, or by PCR for the bcr-abl fusion gene.[2]

    Controversy exists over so-called Ph-negative CML, or cases of suspected CML in which the Philadelphia chromosome cannot be detected. Many such patients in fact have complex chromosomal abnormalities which mask the (9;22) translocation, or have evidence of the translocation by FISH or RT-PCR in spite of normal routine karyotyping.[4] The small subset of patients without detectable molecular evidence of bcr-abl fusion may be better classified as having an undifferentiated myelodysplastic/myeloproliferative disorder, as their clinical course tends to be different from patients with CML.[5]

    [edit] Pathophysiology

    CML was the first malignancy to be linked to a clear genetic abnormality, the chromosomal translocation known as the Philadelphia chromosome. This chromosomal abnormality is so named because it was first discovered and described in 1960 by two scientists from Philadelphia, Pennsylvania: Peter Nowell of the University of Pennsylvania and David Hungerford of the Fox Chase Cancer Center. [6]

    In this translocation, parts of two chromosomes (the 9th and 22nd by conventional karyotypic numbering) switch places. As a result, part of the BCR ("breakpoint cluster region") gene from chromosome 22 is fused with the ABL gene on chromosome 9. This abnormal "fusion" gene generates a protein of p210 or sometimes p185 weight (p is a weight measure of cellular proteins in kDa). Because abl carries a domain that can add phosphate groups to tyrosine residues (a tyrosine kinase), the bcr-abl fusion gene product is also a tyrosine kinase.[1][3]

    The fused bcr-abl protein interacts with the interleukin 3beta(c) receptor subunit. The bcr-abl transcript is continuously active and does not require activation by other cellular messaging proteins. In turn, bcr-abl activates a cascade of proteins which control the cell cycle, speeding up cell division. Moreover, the bcr-abl protein inhibits DNA repair, causing genomic instability and making the cell more susceptible to developing further genetic abnormalities. The action of the bcr-abl protein is the pathophysiologic cause of chronic myelogenous leukemia. With improved understanding of the nature of the bcr-abl protein and its action as a tyrosine kinase, targete

    Source(s): Chronic myelogenous leukemia From Wikipedia, the free encyclopedia
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  • Anonymous
    1 decade ago

    ummm....its a treatment for cancer...and it I think it deals with radiation.....oh and not all of em die...just most of em.

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