Claim: Discovery offers prospect of shorter treatment and cure for chronic myelogenous leukemia
Verdict: REFUTES

Retrieved passages:
title: Chronic myelogenous leukemia
text: of leukemogenic effects and hence the relative lack of potential for secondary hematologic malignancies to result from treatment. IRIS, an international study that compared interferon/cytarabine combination and the first of these new drugs imatinib, with long-term follow up, demonstrated the clear superiority of tyrosine-kinase-targeted inhibition over existing treatments. The first of this new class of drugs was imatinib mesylate (marketed as Gleevec or Glivec), approved by the U.S. Food and Drug Administration (FDA) in 2001. Imatinib was found to inhibit the progression of CML in the majority of patients (65–75%) sufficiently to achieve regrowth of their normal bone marrow stem

title: Chronic myelogenous leukemia
text: present in a patient with CML: The only curative treatment for CML is a bone marrow transplant or an allogeneic stem cell transplant. Other than this there are four major mainstays of treatment in CML: treatment with tyrosine kinase inhibitors, myelosuppressive or leukopheresis therapy (to counteract the leukocytosis during early treatment), splenectomy and interferon alfa-2b treatment. Due to the high median age of patients with CML it is relatively rare for CML to be seen in pregnant women, despite this, however, chronic myelogenous leukemia can be treated with relative safety at any time during pregnancy with Interferon-alpha hormones. In the

title: Myeloid sarcoma
text: chronic myelogenous leukemia (CML), polycythemia vera, essential thrombocytosis, or myelofibrosis). The detection of a chloroma is considered "de facto" evidence these premalignant conditions have transformed into an acute leukemia requiring appropriate treatment. For example, presence of a chloroma is sufficient to indicate chronic myelogenous leukemia has entered its 'blast crisis' phase. At least one case of "FIP1L1-PDGFRA" fusion gene-induced eosinophilic leukemia presenting with myeloid sarcoma and eosinophilia has been reported. This form of myeloid sarcoma is distinguished by its highly successful treatment with imatinib (the recommended treatment for "FIP1L1-PDGRGA" fusion gene-induced eosinophilic leukemia) rather than more aggressive and toxic therapy.

title: Chronic myelogenous leukemia
text: Chronic myelogenous leukemia Chronic myeloid leukemia (CML), also known as chronic myelogenous leukemia, is a cancer of the white blood cells. It is a form of leukemia characterized by the increased and unregulated growth of 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 a proliferation of mature granulocytes (neutrophils, eosinophils and basophils) and their precursors is found. It is a type of myeloproliferative neoplasm associated with a characteristic chromosomal translocation called the Philadelphia chromosome. CML is largely treated with targeted drugs called

title: Chronic myelogenous leukemia
text: 4, 2012 and 27 March 2013 respectively for the treatment of adult patients with Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) with resistance, or intolerance to prior therapy. While capable of producing significantly improved responses compared with the action of imatinib, neither dasatinib nor nilotinib could overcome drug resistance caused by one particular mutation found to occur in the structure of BCR-ABL1 known as the T315I mutation (i.e. where the 315th amino acid is mutated from a threonine residue to an isoleucine residue). Two approaches were developed to the treatment of CML as a result: In 2007, Chemgenex released results

title: Leukemia
text: of patients will be able to keep the disease in check for at least five years, 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. Decision to treat Patients with hairy cell leukemia who are symptom-free typically do not receive immediate treatment. Treatment is generally

title: Chronic myelogenous leukemia
text: cell population (a cytogenetic response) with stable proportions of maturing white blood cells. Because some leukemic cells (as evaluated by RT-PCR) persist in nearly all patients, the treatment has to be continued indefinitely. Since the advent of imatinib, CML has become the first cancer in which a standard medical treatment may give to the patient a normal life expectancy. To overcome imatinib resistance and to increase responsiveness to TK inhibitors, four novel agents were later developed. The first, dasatinib, blocks several further oncogenic proteins, in addition to more potent inhibition of the BCR-ABL protein, and was initially approved in 2007

title: Atypical chronic myeloid leukemia
text: molecular pathogenesis of this disease has remained elusive and the outcome dismal (median survival 37 months) with no improvement over the last 20 years. This sharply contrasts with the outcome for CML, for which the prognosis was dramatically improved by the development of imatinib as a specific inhibitor of the BCR-ABL protein and in particular for CML. In 2012 "SETBP1" was identified as a novel oncogene in aCML; specific somatic mutations of this gene were discovered in people with aCML and related diseases. These mutations, which are identical to the ones present in SGS as germline mutations, impair the degradation

title: Chronic myelogenous leukemia
text: inhibitors, survival rates have improved dramatically. A 2006 followup of 553 patients using imatinib (Gleevec) found an overall survival rate of 89% after five years. A 2011 followup of 832 patients using imatinib who achieved a stable cytogenetic response found an overall survival rate of 95.2% after 8 years, which is similar to the rate in the general population. Fewer than 1% of patients died because of leukemia progression. CML accounts for 8% of all leukaemias in the UK, and around 680 people were diagnosed with the disease in 2011. The American Cancer Society estimates that in 2014, about 5,980

title: Chronic myelogenous leukemia
text: tyrosine-kinase inhibitors (TKIs) which have led to dramatically improved long-term survival rates since 2001. These drugs have revolutionized treatment of this disease and allow most patients to have a good quality of life when compared to the former chemotherapy drugs. In Western countries, CML accounts for 15–25% of all adult leukemias and 14% of leukemias overall (including the pediatric population, where CML is less common). The way CML presents depends on the stage of the disease at diagnosis as it has been known to skip stages in some cases. Most patients (~90%) are diagnosed during the chronic stage which is

title: Fanconi anemia
text: be interpreted as a reflection of premature aging of stem cells. The first line of therapy is androgens and hematopoietic growth factors, but only 50-75% of patients respond. A more permanent cure is hematopoietic stem cell transplantation. If no potential donors exist, a savior sibling can be conceived by preimplantation genetic diagnosis (PGD) to match the recipient's HLA type. Many patients eventually develop acute myelogenous leukemia (AML). Older patients are extremely likely to develop head and neck, esophageal, gastrointestinal, vulvar and anal cancers. Patients who have had a successful bone marrow transplant and, thus, are cured of the blood problem

title: Clonal hypereosinophilia
text: a patient with "SPTBN1-FLT3"-related disease had findings of chronic myelogenous leukemia. Two patients with "ETV6-FLT3"-related disease experienced complete hematologic remissions when treated with a multi-kinase inhibitor, sunitinib, that has inhibitory activity against FLT3 protein. However, these remissions were short-lived. A third patient with "ETV6-FLT3"-related disease was treated with a similarly active kinase inhibitor, sorafenib. This patient achieved a complete hematological response and was then given a hematopoietic stem cell transplantation. The latter treatment regimen, FLT3 inhibitor followed by hematopoietic stem cell transplantation, may be the best approach currently available for treating "FLT3"-releated hematological disease. The "ETV6" gene (also known as

title: Chronic myelogenous leukemia
text: having an undifferentiated myelodysplastic/myeloproliferative disorder, as their clinical course tends to be different from patients with CML. CML must be distinguished from a leukemoid reaction, which can have a similar appearance on a blood smear. CML is often divided into three phases based on clinical characteristics and laboratory findings. In the absence of intervention, CML typically begins in the "chronic" phase, and over the course of several years progresses to an "accelerated" phase and ultimately to a "blast crisis". Blast crisis is the terminal phase of CML and clinically behaves like an acute leukemia. Drug treatment will usually stop this

title: Chronic myelogenous leukemia
text: past, antimetabolites (e.g., cytarabine, hydroxyurea), alkylating agents, interferon alfa 2b, and steroids were used as treatments of CML in the chronic phase, but since the 2000s have been replaced by Bcr-Abl tyrosine-kinase inhibitors drugs that specifically target BCR-ABL, the constitutively activated tyrosine kinase fusion protein caused by the Philadelphia chromosome translocation. Despite the move to replacing cytotoxic antineoplastics (standard anticancer drugs) with tyrosine kinase inhibitors sometimes hydroxyurea is still used to counteract the high leukocyte counts encountered during treatment with tyrosine kinase inhibitors like imatinib; in these situations it may be the preferred myelosuppressive agent due to its relative lack

title: Acute myeloid leukemia
text: "IDH1", "IDH2") is less clear. Cure rates in clinical trials have ranged from 20–45%; although clinical trials often include only younger people and those able to tolerate aggressive therapies. The overall cure rate for all people with AML (including the elderly and those unable to tolerate aggressive therapy) is likely lower. Cure rates for promyelocytic leukemia can be as high as 98%. Relapse is common, and the prognosis is poor. Long-term survival after a relapse is so rare that the only known case was submitted to the Catholic Church as evidence of a miracle attributed to Marie-Marguerite d'Youville. Acute myeloid

title: Chronic myelogenous leukemia
text: progression if started early. One of the drivers of the progression from chronic phase through acceleration and blast crisis is the acquisition of new chromosomal abnormalities (in addition to the Philadelphia chromosome). Some patients may already be in the accelerated phase or blast crisis by the time they are diagnosed. Approximately 85% of patients with CML are in the chronic phase at the time of diagnosis. During this phase, patients are usually asymptomatic or have only mild symptoms of fatigue, left side pain, joint and/or hip pain, or abdominal fullness. The duration of chronic phase is variable and depends on

title: Chronic myelogenous leukemia
text: new cases of chronic myeloid leukemia were diagnosed, and about 810 people died of the disease. This means that a little over 10% of all newly diagnosed leukemia cases will be chronic myeloid leukemia. The average risk of a person getting this disease is 1 in 588. The disease is more common in men than women, and more common in whites than African-Americans. The average age at diagnosis is 64 years, and this disease is rarely seen in children. Chronic myelogenous leukemia Chronic myeloid leukemia (CML), also known as chronic myelogenous leukemia, is a cancer of the white blood cells.

title: Acute myeloid leukemia
text: and IDH2, which lead to the generation of a novel oncometabolite, "D"-2-hydroxyglutarate, which inhibits the activity of epigenetic enzymes such as TET2. The hypothesis is that such epigenetic mutations lead to the silencing of tumor suppressor genes and/or the activation of proto-oncogenes. First-line treatment of AML consists primarily of chemotherapy, and is divided into two phases: induction and postremission (or consolidation) therapy. The goal of induction therapy is to achieve a complete remission by reducing the number of leukemic cells to an undetectable level; the goal of consolidation therapy is to eliminate any residual undetectable disease and achieve a cure.

title: Chronic myelomonocytic leukemia
text: is 91%, 52% and 9%; and risk of AML transformation is 0%, 19% and 54% respectively. The treatment of CMML remains challenging due to the lack of clinical trials investigating the disease as its own clinical entity. It is often grouped with MDS in clinical trials, and for this reason the treatment of CMML is very similar to that of MDS. Most cases are dealt with as supportive rather than curative because most therapies do not effectively increase survival. Indications for treatment include the presence of B symptoms, symptomatic organ involvement, increasing blood counts, hyperleukocytosis, leukostasis and/or worsening cytopaenias. Blood

title: Acute myeloid leukemia
text: courses of intensive chemotherapy, known as consolidation chemotherapy. For people at high risk of relapse (e.g. those with high-risk cytogenetics, underlying MDS, or therapy-related AML), allogeneic stem cell transplantation is usually recommended if the person is able to tolerate a transplant and has a suitable donor. The best postremission therapy for intermediate-risk AML (normal cytogenetics or cytogenetic changes not falling into good-risk or high-risk groups) is less clear and depends on the specific situation, including the age and overall health of the person, the person's values, and whether a suitable stem cell donor is available. For people who are not