Aliases & Classifications for Leukemia

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Summaries for Leukemia

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MedlinePlus:32 Leukemia is cancer of the white blood cells. white blood cells help your body fight infection. your blood cells form in your bone marrow. in leukemia, the bone marrow produces abnormal white blood cells. these cells crowd out the healthy blood cells, making it hard for blood to do its work. there are different types of leukemia, including acute lymphocytic leukemia acute myeloid leukemia chronic lymphocytic leukemia chronic myeloid leukemia leukemia can develop quickly or slowly. chronic leukemia grows slowly. in acute leukemia, the cells are very abnormal and their number increases rapidly. adults can get either type; children with leukemia most often have an acute type. some leukemias can often be cured. other types are hard to cure, but you can often control them. treatments may include chemotherapy, radiation and stem cell transplantation. even if symptoms disappear, you might need therapy to prevent a relapse. nih: national cancer institute

MalaCards based summary: Leukemia is related to myeloid leukemia and chronic lymphocytic leukemia. An important gene associated with Leukemia is RUNX1 (runt-related transcription factor 1), and among its related pathways are Signaling by Robo receptor and Endometrial cancer. The drugs methotrexate and methotrexate sodium and the compounds megapoietin and anagrelide have been mentioned in the context of this disorder. Affiliated tissues include myeloid, t cells and b cells, and related mouse phenotypes are normal and liver/biliary system.

Disease Ontology:8 A cancer that affects the blood or bone marrow characterized by an abnormal proliferation of blood cells.

Wikipedia:64 Leukemia (American English) or leukaemia (British English) /lu??ki?mi??/ is a group of cancers that... more...

Related Diseases for Leukemia

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Diseases in the Leukemia family:

Acute Leukemia Chronic Leukemia
Subacute Leukemia

Diseases related to Leukemia via text searches within MalaCards or GeneCards Suite gene sharing:

(show top 50)    (show all 1137)
idRelated DiseaseScoreTop Affiliating Genes
1myeloid leukemia33.0MPL, KMT2A, ABL1, RUNX1, THPO, PICALM
2chronic lymphocytic leukemia32.8KMT2A, BCL3, TRIM13
3acute leukemia32.5ZBTB16, KMT2A, LYL1, MPL, RUNX1, PML
4chronic myelomonocytic leukemia32.2RUNX1, MPL
5myelodysplastic syndrome32.2ABL1, MLF1, THPO, MPL, KMT2A, RUNX1
6acute myelomonocytic leukemia32.2KMT2A, RUNX1
7megakaryocytic leukemia31.9RUNX1, THPO, MKL1, KMT2A
8wilms tumor31.7ABL1, KMT2A, MME
9refractory anemia31.7RUNX1, MPL, THPO
10precursor b-cell acute lymphoblastic leukemia31.5MME, KMT2A, ABL1
11leukemia, acute myeloid31.5RUNX1, MLF1, SH3GL1
12myelofibrosis31.5MPL, THPO
13leukemia, acute promyelocytic31.5RUNX1, KMT2A, PML, ZBTB16
14breast cancer31.5MME, BCL3, RUNX1, ABL1, KMT2A, PML
15leukemia, acute lymphoblastic31.5MME, KMT2A, MPL, PML, PICALM, ABL1
16acute erythroid leukemia31.4MPL, THPO, MLF1
17leukemia, chronic myeloid31.4RUNX1, ABL1, KMT2A, THPO, MPL, PML
18thrombocytopenia31.4RUNX1, MPL, THPO
19precursor t-cell acute lymphoblastic leukemia31.3LYL1, RUNX1, ABL1, KMT2A, PICALM
20essential thrombocythemia31.3MPL, THPO
21pancytopenia31.3KMT2A, MPL, THPO
22acute myeloid leukemia, adult31.2KMT2A, RUNX1
23b-cell lymphomas31.2MME, KMT2A, BCL3
24prostate cancer31.2ARHGEF12, ABL1, ZBTB16, PML, KMT2A, MME
25purpura31.2THPO
26polycythemia31.2MPL, THPO
27follicular lymphoma31.1KMT2A, MME, BCL3
28acute lymphoblastic leukemia, childhood31.1KMT2A, ABL1, RUNX1, MME
29splenomegaly31.0MPL, THPO
30burkitt lymphoma31.0RUNX1, ABL1, MME
31chronic myeloproliferative disease30.9MPL, THPO
32hematologic cancer30.3THPO, PICALM, MPL, KMT2A, RUNX1, ABL1
33lymphoblastic leukemia11.4
34t-cell leukemia11.3
35adult t-cell leukemia11.1
36childhood leukemia11.1
37monocytic leukemia11.0
38human t-cell leukemia virus type 111.0
39prolymphocytic leukemia11.0
40plasma cell leukemia11.0
41acute monocytic leukemia10.9
42large granular lymphocyte leukemia10.9
43hematopoietic stem cell transplantation10.8
44myeloma10.8
45sarcoma10.7
46chronic neutrophilic leukemia10.7
47lymphoid leukemia10.7
48endotheliitis10.7
49multiple myeloma10.7
50lymphoblastic lymphoma10.7

Graphical network of the top 20 diseases related to Leukemia:



Diseases related to leukemia

Symptoms for Leukemia

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Drugs & Therapeutics for Leukemia

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FDA approved drugs:

(show all 26)
id Drug Name Active Ingredient(s)13 Pharmaceutical Company Approval Date
1
Arranon13 38 NELARABINE GlaxoSmithKline Approved October 2005
FDA Label: Arranon
Malady that Drug Treats: Lymphoblastic Leukemia
Indications and Usage:13 ARRANON is a nucleoside metabolic inhibitor indicated for the treatment of; patients with T-cell acute lymphoblastic leukemia and T-cell lymphoblastic; lymphoma whose disease has not responded to or has relapsed following; treatment with at least two chemotherapy regimens. This use is based on the; induction of complete responses. Randomized trials demonstrating increased; survival or other clinical benefit have not been conducted. (1)
DrugBank Targets:11 DNA
Mechanism of Action:13 
Target: DNA synthesis
Action: disruptor --> apoptosis
FDA: Nelarabine is a pro-drug of the deoxyguanosine analogue 9-²-D-arabinofuranosylguanine; 266 (ara-G), a nucleoside metabolic inhibitor. Nelarabine is demethylated by adenosine deaminase; 267 (ADA) to ara-G, mono-phosphorylated by deoxyguanosine kinase and deoxycytidine kinase, and; 268 subsequently converted to the active 5 -triphosphate, ara-GTP. Accumulation of ara-GTP in; 269 leukemic blasts allows for incorporation into deoxyribonucleic acid (DNA), leading to inhibition; 270 of DNA synthesis and cell death. Other mechanisms may contribute to the cytotoxic and; 271 systemic toxicity of nelarabine.
2
Arzerra13 38 OFATUMUMAB GlaxoSmithKline Approved October 2009
FDA Label: Arzerra
Malady that Drug Treats: chronic lymphocytic leukemia
Indications and Usage:13 ARZERRA (ofatumumab) is a CD20-directed cytolytic monoclonal antibody; indicated:; in combination with chlorambucil, for the treatment of previously; untreated patients with chronic lymphocytic leukemia (CLL) for whom; fludarabine-based therapy is considered inappropriate. (1.1); for the treatment of patients with CLL refractory to fludarabine and; alemtuzumab. (1.2)
DrugBank Targets:11 -
Mechanism of Action:13 
Target: B-cell
Action: promotes lysis
FDA: Ofatumumab binds specifically to both the small and large extracellular loops of the CD20; 402 molecule. The CD20 molecule is expressed on normal B lymphocytes (pre-B- to mature; 403 B-lymphocyte) and on B-cell CLL. The CD20 molecule is not shed from the cell surface and is; 404 not internalized following antibody binding.; 405; 406 The Fab domain of ofatumumab binds to the CD20 molecule and the Fc domain mediates; 407 immune effector functions to result in B-cell lysis in vitro. Data suggest that possible; 408 mechanisms of cell lysis include complement-dependent cytotoxicity and antibody-dependent,; 409 cell-mediated cytotoxicity.
3
Blincyto13 38 BLINATUMOMAB Amgen Approved December 2014
FDA Label: Blincyto
Malady that Drug Treats: Philadelphia chromosome-negative relapsed /refractory B cell precursor acute lymphoblastic leukemia
Indications and Usage:13 BLINCYTO is a bispecific CD19-directed CD3 T-cell engager indicated for; the treatment of Philadelphia chromosome-negative relapsed or refractory Bcell; precursor acute lymphoblastic leukemia (ALL). This indication is; approved under accelerated approval. Continued approval for this indication; may be contingent upon verification of clinical benefit in subsequent trials. (1)
DrugBank Targets:11 1. B-lymphocyte antigen CD19; 2. T-cell surface glycoprotein CD3 delta chain
Mechanism of Action:13 
Target: CD19-directed CD3 T-cell
Action: engager
FDA: Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on the; surface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenous; T cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant B; cells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell,; upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatory; cytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells.
4
Bosulif13 38 BOSUTINIB MONOHYDRATE Pfizer Approved September 2012
FDA Label: Bosulif
Malady that Drug Treats: Ph+ chronic myelogenous leukemia
Indications and Usage:13 BOSULIF is a kinase inhibitor indicated for the treatment of adult patients; with chronic, accelerated, or blast phase Ph+ chronic myelogenous leukemia; (CML) with resistance or intolerance to prior therapy. (1)
DrugBank Targets:11 1. Breakpoint cluster region protein; 2. Tyrosine-protein kinase ABL1; 3. Tyrosine-protein kinase Lyn; 4. Tyrosine-protein kinase HCK; 5. Proto-oncogene tyrosine-protein kinase Src; 6. Cyclin-dependent kinase 2; 7. Dual specificity mitogen-activated protein kinase kinase 1; 8. Dual specificity mitogen-activated protein kinase kinase 2; 9. Mitogen-activated protein kinase kinase kinase 2; 10. Calcium/calmodulin-dependent protein kinase type II subunit gamma
Mechanism of Action:13 
Target: tyrosine kinase/ Src-family kinases including Src, Lyn, and Hck
Action: inhibitor
FDA: Bosutinib is a tyrosine kinase inhibitor. Bosutinib inhibits the Bcr-Abl kinase that promotes CML; it is also an; inhibitor of Src-family kinases including Src, Lyn, and Hck. Bosutinib inhibited 16 of 18 imatinib-resistant forms of; Bcr-Abl expressed in murine myeloid cell lines. Bosutinib did not inhibit the T315I and V299L mutant cells. In mice,; treatment with bosutinib reduced the size of CML tumors relative to controls and inhibited growth of murine myeloid; tumors expressing several imatinib-resistant forms of Bcr-Abl.
5
Busulfex13 38 BUSULFAN Orphan Medical Approved February 1999
FDA Label: Busulfex
Malady that Drug Treats: leukemia
Indications and Usage:13 BUSULFEX is an alkylating drug indicated for:; Use in combination with cyclophosphamide as a conditioning regimen; prior to allogeneic hematopoietic progenitor cell transplantation for; chronic myelogenous leukemia (CML) (1)
DrugBank Targets:11 DNA
Mechanism of Action:13 
Target: DNA
Action: alkylyzer
FDA: Busulfan is a bifunctional alkylating agent in which two labile methanesulfonate groups are attached to opposite ends of a; four-carbon alkyl chain. In aqueous media, busulfan hydrolyzes to release the methanesulfonate groups. This produces; reactive carbonium ions that can alkylate DNA. DNA damage is thought to be responsible for much of the cytotoxicity of; busulfan.
6
Campath13 38 ALEMTUZUMAB Berlex Laboratories Approved May 2001
FDA Label: Campath
Malady that Drug Treats: Leukemia
Indications and Usage:13 LEMTRADA is a CD52-directed cytolytic monoclonal antibody indicated dizziness, abdominal pain, flushing, and vomiting. (6.1) for the treatment of patients with relapsing forms of multiple sclerosis; (MS).
DrugBank Targets:11 1. CAMPATH-1 antigen; 2. Low affinity immunoglobulin gamma Fc region receptor III-B; 3. Complement C1r subcomponent; 4. Complement C1q subcomponent subunit A; 5. Complement C1q subcomponent subunit B; 6. Complement C1q subcomponent subunit C; 7. Low affinity immunoglobulin gamma Fc region receptor III-A; 8. High affinity immunoglobulin gamma Fc receptor I; 9. Low affinity immunoglobulin gamma Fc region receptor II-a; 10. Low affinity immunoglobulin gamma Fc region receptor II-b; 11. Low affinity immunoglobulin gamma Fc region receptor II-c; ;
Mechanism of Action:13 
Target: CD52 antigen
Action: after binding, induces cell lysis
FDA: The precise mechanism by which alemtuzumab exerts its therapeutic effects in multiple; 490 sclerosis is unknown but is presumed to involve binding to CD52, a cell surface antigen; 491 present on T and B lymphocytes, and on natural killer cells, monocytes, and; 492 macrophages. Following cell surface binding to T and B lymphocytes, alemtuzumab; 493 results in antibody-dependent cellular cytolysis and complement-mediated lysis.
7
Clolar13 38 CLOFARABINE Genzyme Approved December, 2004
FDA Label: Clolar
Malady that Drug Treats: Lymphoblastic Leukemia
Indications and Usage:13 Clolar (clofarabine) injection is a purine nucleoside metabolic inhibitor; indicated for the treatment of pediatric patients 1 to 21 years old with relapsed; or refractory acute lymphoblastic leukemia after at least two prior regimens.; This indication is based upon response rate. There are no trials verifying an; improvement in disease-related symptoms or increased survival with Clolar.; (1)
DrugBank Targets:11 1. DNA polymerase alpha catalytic subunit; 2. Ribonucleoside-diphosphate reductase large subunit; 3. DNA
Mechanism of Action:13 
Target: ribonucleotide reductase
Action: inhibitor
FDA: Clofarabine is sequentially metabolized intracellularly to the 5 -monophosphate metabolite by; deoxycytidine kinase and mono- and di-phospho-kinases to the active 5 -triphosphate metabolite.; Clofarabine has affinity for the activating phosphorylating enzyme, deoxycytidine kinase, equal; to or greater than that of the natural substrate, deoxycytidine. Clofarabine inhibits DNA synthesis; by decreasing cellular deoxynucleotide triphosphate pools through an inhibitory action on; ribonucleotide reductase, and by terminating DNA chain elongation and inhibiting repair through; incorporation into the DNA chain by competitive inhibition of DNA polymerases. The affinity of; clofarabine triphosphate for these enzymes is similar to or greater than that of deoxyadenosine; triphosphate. In preclinical models, clofarabine has demonstrated the ability to inhibit DNA; repair by incorporation into the DNA chain during the repair process. Clofarabine 5 -; triphosphate also disrupts the integrity of mitochondrial membrane, leading to the release of the; pro-apoptotic mitochondrial proteins, cytochrome C and apoptosis-inducing factor, leading to; programmed cell death.; Clofarabine is cytotoxic to rapidly proliferating and quiescent cancer cell types in vitro.
8
Elitek13 38 RASBURICASE sanofi-aventis Approved October 2009
FDA Label: Elitek
Malady that Drug Treats: management of plasma uric acid levels in adults with malignancies
Indications and Usage:13 Elitek is a recombinant urate-oxidase indicated for initial management of; plasma uric acid levels in pediatric and adult patients with leukemia,; lymphoma, and solid tumor malignancies who are receiving anti-cancer; therapy expected to result in tumor lysis and subsequent elevation of plasma; uric acid (1).; Limitation of use: Elitek is indicated only for a single course of treatment (1).
DrugBank Targets:11 1. Uric acid
Mechanism of Action:13 
Target: uric acid
Action: converter to alantoin
FDA: In humans, uric acid is the final step in the catabolic pathway of purines. Rasburicase catalyzes; enzymatic oxidation of poorly soluble uric acid into an inactive and more soluble metabolite; (allantoin).
9
Elliotts B Solution13 CALCIUM CHLORIDE; DEXTROSE; MAGNESIUM SULFATE; POTASSIUM CHLORIDE; SODIUM BICARBONATE; SODIUM CHLORIDE; SODIUM PHOSPHATE, DIBAS Orphan Medical Approved October 1996
FDA Label: -
Malady that Drug Treats: meningeal leukemia or lymphocytic lymphoma
Indications and Usage:13 -
DrugBank Targets: -
Mechanism of Action:13 
Target: cerebrospinal fluid
Action: comparable in pH, electrolyte composition, glucose content, and osmolarity
FDA: -
10
Erwinaze13 38 asparaginase Erwinia chrysanthemi Eusa Pharma Approved November of 2011
FDA Label: Erwinaze
Malady that Drug Treats: acute lymphoblastic leukemia
Indications and Usage:13 ERWINAZE (asparaginase Erwinia chrysanthemi) is an asparagine specific; enzyme indicated as a component of a multi-agent chemotherapeutic regimen; for the treatment of patients with acute lymphoblastic leukemia (ALL) who; have developed hypersensitivity to E. coli-derived asparaginase. (1)
DrugBank Targets:11 -
Mechanism of Action:13 
Target: deamidation of asparagine to aspartic acid and ammonia
Action: catalyzer
FDA: Asparaginase Erwinia chrysanthemi catalyzes the deamidation of asparagine to aspartic acid and ammonia, resulting; in a reduction in circulating levels of asparagine. The mechanism of action of ERWINAZE is thought to be based on; the inability of leukemic cells to synthesize asparagine due to lack of asparagine synthetase activity, resulting in; cytotoxicity specific for leukemic cells that depend on an exogenous source of amino acid asparagine for their; protein metabolism and survival.
11
Gazyva13 38 OBINUTUZUMAB Genentech Approved October of 2013
FDA Label: Gazyva
Malady that Drug Treats: previously untreated chronic lymphocytic leukemia
Indications and Usage:13 GAZYVA (obinutuzumab) is a CD20-directed cytolytic antibody and is; indicated, in combination with chlorambucil, for the treatment of patients with; previously untreated chronic lymphocytic leukemia. (1, 14)
DrugBank Targets:11 1. B-lymphocyte antigen CD20
Mechanism of Action:13 
Target: CD20 antigen expressed on the surface of pre B- and mature B-lymphocytes
Action: engager of immune cells and/or activator of intracellular death signaling pathways and/or activator of the complement cascade
FDA: Obinutuzumab is a monoclonal antibody that targets the CD20 antigen expressed on the surface; of pre B- and mature B-lymphocytes. Upon binding to CD20, obinutuzumab mediates B-cell; lysis through (1) engagement of immune effector cells, (2) by directly activating intracellular; death signaling pathways and/or (3) activation of the complement cascade. The immune effector; cell mechanisms include antibody-dependent cellular cytotoxicity and antibody-dependent; cellular phagocytosis.
12
Gleevec13 38 IMATINIB MESYLATE Novartis Approved May 2001
FDA Label: Gleevec
Malady that Drug Treats: chronic myeloid leukemia/Gastrointestinal stromal tumors (GISTs)
Indications and Usage:13 Gleevec"! (imatinib mesylate) is indicated for the treatment of newly diagnosed adult; patients with Philadelphia chromosome positive chronic myeloid leukemia (CML) in chronic; phase. Follow-up is limited. ; Page 10; Gleevec is also indicated for the treatment of patients with Philadelphia chromosome; positive chronic myeloid leukemia (CML) in blast crisis, accelerated phase, or in chronic; phase after failure of interferon-alpha therapy. Gleevec is also indicated for the treatment of; pediatric patients with Ph+ chronic phase CML whose disease has recurred after stem cell; transplant or who are resistant to interferon alpha therapy. There are no controlled trials; demonstrating a clinical benefit, such as improvement in disease-related symptoms or; increased survival.; Gleevec is also indicated for the treatment of patients with Kit (CD117) positive; unresectable and/or metastatic malignant gastrointestinal stromal tumors (GIST). (See; CLINICAL STUDIES: Gastrointestinal Stromal Tumors.) The effectiveness of Gleevec in; GIST is based on objective response rate (see CLINICAL STUDIES). There are no controlled; trials demonstrating a clinical benefit, such as improvement in disease-related symptoms or; increased survival.
DrugBank Targets:11 1. BCR/ABL fusion protein isoform X9; 2. Mast/stem cell growth factor receptor Kit; 3. RET proto-oncogene; 4. High affinity nerve growth factor receptor; 5. Macrophage colony-stimulating factor 1 receptor; 6. Platelet-derived growth factor receptor alpha; 7. Epithelial discoidin domain-containing receptor 1; 8. Tyrosine-protein kinase ABL1; 9. Platelet-derived growth factor receptor beta
Mechanism of Action:13 
Target: protein-tyrosine kinase
Action: inhibitor
FDA: Imatinib mesylate is a protein-tyrosine kinase inhibitor that inhibits the Bcr-Abl tyrosine; kinase, the constitutive abnormal tyrosine kinase created by the Philadelphia chromosome; abnormality in chronic myeloid leukemia (CML). It inhibits proliferation and induces; apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia; chromosome positive chronic myeloid leukemia. In colony formation assays using ex vivo; peripheral blood and bone marrow samples, imatinib shows inhibition of Bcr-Abl positive; colonies from CML patients.; In vivo, it inhibits tumor growth of Bcr-Abl transfected murine myeloid cells as well; as Bcr-Abl positive leukemia lines derived from CML patients in blast crisis.; Imatinib is also an inhibitor of the receptor tyrosine kinases for platelet-derived; growth factor (PDGF) and stem cell factor (SCF), c-kit, and inhibits PDGF- and; SCF-mediated cellular events. In vitro, imatinib inhibits proliferation and induces apoptosis in; gastrointestinal stromal tumor (GIST) cells, which express an activating c-kit mutation.
13
Iclusig13 38 PONATINIB HYDROCHLORIDE Ariad Pharmaceuticals Approved December 2012
FDA Label: Iclusig
Malady that Drug Treats: chronic myeloid leukemia and Philadelphia chromosome positive acute lymphoblastic leukemia
Indications and Usage:13 Iclusig is a kinase inhibitor indicated for the:; Treatment of adult patients with T315I-positive chronic myeloid; leukemia (chronic phase, accelerated phase, or blast phase) or T315Ipositive; Philadelphia chromosome positive acute lymphoblastic; leukemia (Ph+ ALL).; Treatment of adult patients with chronic phase, accelerated phase, or; blast phase chronic myeloid leukemia or Ph+ ALL for whom no other; tyrosine kinase inhibitor (TKI) therapy is indicated. (1); These indications are based upon response rate. There are no trials verifying an; improvement in disease-related symptoms or increased survival with Iclusig.
DrugBank Targets:11 1. Tyrosine-protein kinase ABL1; 2. Breakpoint cluster region protein; 3. Mast/stem cell growth factor receptor Kit; 4. Proto-oncogene tyrosine-protein kinase receptor Ret; 5. Angiopoietin-1 receptor; 6. Receptor-type tyrosine-protein kinase FLT3; 7. Fibroblast growth factor receptor 1; 8. Fibroblast growth factor receptor 2; 9. Fibroblast growth factor receptor 3; 10. Fibroblast growth factor receptor 4; 11. Tyrosine-protein kinase Lck; 12. Proto-oncogene tyrosine-protein kinase Src; 13. Tyrosine-protein kinase Lyn; 14. Vascular endothelial growth factor receptor 2; 15. Platelet-derived growth factor receptor alpha
Mechanism of Action:13 
Target: tyrosine kinase activity of ABL and T315I mutant ABL
Action: inhibitor
FDA: Ponatinib is a kinase inhibitor. Ponatinib inhibited the in vitro tyrosine kinase activity of ABL and T315I mutant ABL with; IC50 concentrations of 0.4 and 2.0 nM, respectively. Ponatinib inhibited the in vitro activity of additional kinases with IC50; concentrations between 0.1 and 20 nM, including members of the VEGFR, PDGFR, FGFR, EPH receptors and SRC; families of kinases, and KIT, RET, TIE2, and FLT3. Ponatinib inhibited the in vitro viability of cells expressing native or; mutant BCR-ABL, including T315I. In mice, treatment with ponatinib reduced the size of tumors expressing native or; T315I mutant BCR-ABL when compared to controls.
14
Imbruvica13 38 IBRUTINIB Pharmacyclics Approved November of 2013/Approved February 2014
FDA Label: Imbruvica
Malady that Drug Treats: mantle cell lymphoma/chronic lymphocytic leukemia
Indications and Usage:13 IMBRUVICA is a kinase inhibitor indicated for the treatment of patients with:; Mantle cell lymphoma (MCL) who have received at least one prior; therapy (1.1).; ; Accelerated approval was granted for this indication based on overall; ; response rate. Continued approval for this indication may be contingent; ; upon verification of clinical benefit in confirmatory trials.; ; Chronic lymphocytic leukemia (CLL) who have received at least one; prior therapy (1.2).; Chronic lymphocytic leukemia with 17p deletion (1.3).; Waldenström s macroglobulinemia (WM) (1.4).
DrugBank Targets:11 1. Tyrosine-protein kinase BTK
Mechanism of Action:13 
Target: Bruton's tyrosine kinase (Btk)
Action: selective inhibitor
FDA: Ibrutinib is a small-molecule inhibitor of BTK. Ibrutinib forms a covalent bond with a cysteine; residue in the BTK active site, leading to inhibition of BTK enzymatic activity. BTK is a; signaling molecule of the B-cell antigen receptor (BCR) and cytokine receptor pathways. BTK s; role in signaling through the B-cell surface receptors results in activation of pathways necessary; for B-cell trafficking, chemotaxis, and adhesion. Nonclinical studies show that ibrutinib inhibits; malignant B-cell proliferation and survival in vivo as well as cell migration and substrate; adhesion in vitro.
15
Intron A13 38 INTERFERON ALFA-2B Schering-Plough Approved December 1997/ Approved December 1995/ Approved March 1997
FDA Label: Intron A
Malady that Drug Treats: non-Hodgkin's lymphoma/ malignant melanoma / Hepatitis C
Indications and Usage:13 Hairy Cell Leukemia INTRON® A is indicated for the treatment of patients 18 years of; age or older with hairy cell leukemia.; Malignant Melanoma INTRON A is indicated as adjuvant to surgical treatment in; patients 18 years of age or older with malignant melanoma who are free of disease but; at high risk for systemic recurrence, within 56 days of surgery.; Follicular Lymphoma INTRON A is indicated for the initial treatment of clinically; aggressive (see Clinical Pharmacology) follicular Non-Hodgkin s Lymphoma in; conjunction with anthracycline-containing combination chemotherapy in patients 18; years of age or older. Efficacy of INTRON A therapy in patients with low-grade, lowtumor; burden follicular Non-Hodgkin s Lymphoma has not been demonstrated.; Condylomata Acuminata INTRON A is indicated for intralesional treatment of selected; patients 18 years of age or older with condylomata acuminata involving external; surfaces of the genital and perianal areas (see DOSAGE AND ADMINISTRATION).; The use of this product in adolescents has not been studied.; AIDS-Related Kaposi's Sarcoma INTRON A is indicated for the treatment of selected; patients 18 years of age or older with AIDS-Related Kaposi's Sarcoma. The likelihood; of response to INTRON A therapy is greater in patients who are without systemic symptoms, who have limited lymphadenopathy and who have a relatively intact immune; system as indicated by total CD4 count.; Chronic Hepatitis C INTRON A is indicated for the treatment of chronic hepatitis C in; patients 18 years of age or older with compensated liver disease who have a history of; blood or blood-product exposure and/or are HCV antibody positive. Studies in these; patients demonstrated that INTRON A therapy can produce clinically meaningful effects; on this disease, manifested by normalization of serum alanine aminotransferase (ALT); and reduction in liver necrosis and degeneration.; A liver biopsy should be performed to establish the diagnosis of chronic hepatitis.; Patients should be tested for the presence of antibody to HCV. Patients with other; causes of chronic hepatitis, including autoimmune hepatitis, should be excluded. Prior; to initiation of INTRON A therapy, the physician should establish that the patient has; compensated liver disease. The following patient entrance criteria for compensated liver; disease were used in the clinical studies and should be considered before INTRON A; treatment of patients with chronic hepatitis C:; No history of hepatic encephalopathy, variceal bleeding, ascites, or other; clinical signs of decompensation; Bilirubin Less than or equal to 2 mg/dL; Albumin Stable and within normal limits; Prothrombin Time Less than 3 seconds prolonged; WBC Greater than or equal to 3000/mm3; Platelets Greater than or equal to 70,000/mm3; Serum creatinine should be normal or near normal.; Prior to initiation of INTRON A therapy, CBC and platelet counts should be; evaluated in order to establish baselines for monitoring potential toxicity. These tests; should be repeated at Weeks 1 and 2 following initiation of INTRON A therapy, and; monthly thereafter. Serum ALT should be evaluated at approximately 3-month intervals; to assess response to treatment (see DOSAGE AND ADMINISTRATION).; Patients with preexisting thyroid abnormalities may be treated if thyroidstimulating; hormone (TSH) levels can be maintained in the normal range by medication.; TSH levels must be within normal limits upon initiation of INTRON A treatment and TSH; testing should be repeated at 3 and 6 months (see PRECAUTIONS, Laboratory; Tests).; INTRON A in combination with REBETOL® is indicated for the treatment of; chronic hepatitis C in patients 3 years of age and older with compensated liver disease; previously untreated with alpha interferon therapy and in patients 18 years of age and; older who have relapsed following alpha interferon therapy. See REBETOL prescribing; information for additional information. Chronic Hepatitis B INTRON A is indicated for the treatment of chronic hepatitis B in; patients 1 year of age or older with compensated liver disease. Patients who have been; serum HBsAg positive for at least 6 months and have evidence of HBV replication; (serum HBeAg positive) with elevated serum ALT are candidates for treatment. Studies; in these patients demonstrated that INTRON A therapy can produce virologic remission; of this disease (loss of serum HBeAg) and normalization of serum aminotransferases.; INTRON A therapy resulted in the loss of serum HBsAg in some responding patients.; Prior to initiation of INTRON A therapy, it is recommended that a liver biopsy be; performed to establish the presence of chronic hepatitis and the extent of liver damage.; The physician should establish that the patient has compensated liver disease. The; following patient entrance criteria for compensated liver disease were used in the; clinical studies and should be considered before INTRON A treatment of patients with; chronic hepatitis B:; No history of hepatic encephalopathy, variceal bleeding, ascites, or other; signs of clinical decompensation; Bilirubin Normal; Albumin Stable and within normal limits; Prothrombin Time Adults less than 3 seconds prolonged; Pediatrics less than or equal to 2 seconds prolonged; WBC Greater than or equal to 4000/mm3; Platelets Adults greater than or equal to 100,000/mm3; Pediatrics greater than or equal to 150,000/mm3; Patients with causes of chronic hepatitis other than chronic hepatitis B or chronic; hepatitis C should not be treated with INTRON A. CBC and platelet counts should be; evaluated prior to initiation of INTRON A therapy in order to establish baselines for; monitoring potential toxicity. These tests should be repeated at treatment Weeks 1, 2,; 4, 8, 12, and 16. Liver function tests, including serum ALT, albumin, and bilirubin,; should be evaluated at treatment Weeks 1, 2, 4, 8, 12, and 16. HBeAg, HBsAg, and; ALT should be evaluated at the end of therapy, as well as 3- and 6-months posttherapy,; since patients may become virologic responders during the 6-month period; following the end of treatment. In clinical studies in adults, 39% (15/38) of responding; patients lost HBeAg 1 to 6 months following the end of INTRON A therapy. Of; responding patients who lost HBsAg, 58% (7/12) did so 1 to 6 months post-treatment.; A transient increase in ALT greater than or equal to 2 times baseline value (flare); can occur during INTRON A therapy for chronic hepatitis B. In clinical trials in adults; and pediatrics, this flare generally occurred 8 to 12 weeks after initiation of therapy and; was more frequent in responders (adults 63%, 24/38; pediatrics 59%, 10/17) than in; nonresponders (adults 27%, 13/48; pediatrics 35%, 19/55). However, in adults and; pediatrics, elevations in bilirubin greater than or equal to 3 mg/dL (greater than or equal; to 2 times ULN) occurred infrequently (adults 2%, 2/86; pediatrics 3%, 2/72) during; therapy. When ALT flare occurs, in general, INTRON A therapy should be continued unless signs and symptoms of liver failure are observed. During ALT flare, clinical; symptomatology and liver function tests including ALT, prothrombin time, alkaline; phosphatase, albumin, and bilirubin, should be monitored at approximately 2-week; intervals (see WARNINGS).
DrugBank Targets:11 1. Interferon alpha/beta receptor 2; 2. Interferon alpha/beta receptor 1
Mechanism of Action:13 
Target: intracellular oncogene expression, natural killer and cytotoxic T-cells, microphage, cytokine production
Action: stimulation, induction (unspecified effects on oncogene expression)
FDA: -
16
Marqibo13 38 VINCRISTINE SULFATE Talon Therapeutics Approved August 2012
FDA Label: Marqibo
Malady that Drug Treats: Ph- acute lymphoblastic leukemia
Indications and Usage:13 Marqibo is a vinca alkaloid indicated for the treatment of adult patients with; Philadelphia chromosome-negative (Ph-) acute lymphoblastic leukemia (ALL); in second or greater relapse or whose disease has progressed following two or; more anti-leukemia therapies. This indication is based on overall response; rate. Clinical benefit such as improvement in overall survival has not been; verified (1.1).
DrugBank Targets:11 1. Tubulin beta chain; 2. Tubulin alpha-4A chain
Mechanism of Action:13 
Target: tubulin
Action: alters polymerization equilibrium
FDA: Marqibo is a sphingomyelin/cholesterol liposome-encapsulated formulation of vincristine sulfate.; Non-liposomal vincristine sulfate binds to tubulin, altering the tubulin polymerization equilibrium, resulting in; altered microtubule structure and function. Non-liposomal vincristine sulfate stabilizes the spindle apparatus,; preventing chromosome segregation, triggering metaphase arrest and inhibition of mitosis.
17
Mylotarg13 38 GEMTUZUMAB OZOGAMICIN Wyeth Approved May 2000
FDA Label: Mylotarg
Malady that Drug Treats: Acute Myeloid Leukemia (AML)
Indications and Usage:13 Mylotarg is indicated for the treatment of patients with CD33 positive acute myeloid leukemia in; first relapse who are 60 years of age or older and who are not considered candidates for other; cytotoxic chemotherapy. The safety and efficacy of Mylotarg in patients with poor performance; status and organ dysfunction has not been established.; The effectiveness of Mylotarg is based on OR rates (see CLINICAL STUDIES section). There; are no controlled trials demonstrating a clinical benefit, such as improvement in disease-related; symptoms or increased survival, compared to any other treatment.
DrugBank Targets:11 1. Myeloid cell surface antigen CD33; 2. Low affinity immunoglobulin gamma Fc region receptor III-B; 3. Complement C1r subcomponent; 4. Complement C1q subcomponent subunit A; 5. Complement C1q subcomponent subunit B; 6. Complement C1q subcomponent subunit C; 7. Low affinity immunoglobulin gamma Fc region receptor III-A; 8. Complement C1s subcomponent; 9. High affinity immunoglobulin gamma Fc receptor I; 10. Low affinity immunoglobulin gamma Fc region receptor II-a; 11. Low affinity immunoglobulin gamma Fc region receptor II-b; 12. Low affinity immunoglobulin gamma Fc region receptor II-c
Mechanism of Action:13 
Target: CD33 antigen expressed by; hematopoietic cells
Action: binds to form complex that then causes a break in the DNA double strand
FDA: Mylotarg is directed against the CD33 antigen expressed by; hematopoietic cells. Binding of the anti-CD33 antibody portion of Mylotarg with the CD33; antigen results in the formation of a complex that is internalized. Upon internalization, the; calicheamicin derivative is released inside the lysosomes of the myeloid cell. The released; calicheamicin derivative binds to DNA in the minor groove resulting in DNA double strand; breaks and cell death.; Gemtuzumab ozogamicin is cytotoxic to the CD33 positive HL-60 human leukemia cell line.; Gemtuzumab ozogamicin produces significant inhibition of colony formation in cultures of adult; leukemic bone marrow cells. The cytotoxic effect on normal myeloid precursors leads to; substantial myelosuppression, but this is reversible because pluripotent hematopoietic stem cells; are spared. In preclinical animal studies, gemtuzumab ozogamicin demonstrates antitumor; effects in the HL-60 human promyelocytic leukemia xenograft tumor in athymic mice.
18
Neupogen13 38 FILGRASTIM Amgen Approval April 1998
FDA Label: Neupogen
Malady that Drug Treats: slow white blood cell recovery following chemotherapy
Indications and Usage:13 NEUPOGEN is a leukocyte growth factor indicated to; Decrease the incidence of infection as manifested by febrile neutropenia ; in patients with nonmyeloid malignancies receiving myelosuppressive anticancer; drugs associated with a significant incidence of severe neutropenia; with fever (1.1); Reduce the time to neutrophil recovery and the duration of fever, following; induction or consolidation chemotherapy treatment of patients with acute; myeloid leukemia (AML) (1.2); Reduce the duration of neutropenia and neutropenia-related clinical; sequelae e.g. febrile neutropenia, in patients with nonmyeloid; malignancies undergoing myeloablative chemotherapy followed by bone; marrow transplantation (BMT) (1.3); Mobilize autologous hematopoietic progenitor cells into the peripheral; blood for collection by leukapheresis (1.4); Reduce the incidence and duration of sequelae of severe neutropenia (e.g. ; fever infections oropharyngeal ulcers) in symptomatic patients with; congenital neutropenia cyclic neutropenia or idiopathic neutropenia (1.5); Increase survival in patients acutely exposed to myelosuppressive doses of; radiation (Hematopoietic Syndrome of Acute Radiation Syndrome) (1.6)
DrugBank Targets:11 1. Granulocyte colony-stimulating factor receptor; 2. Neutrophil elastase
Mechanism of Action:13 
Target: hematopoietic cells
Action: stimulates proliferation/ regulated production of neutophils
FDA: Colony-stimulating factors are glycoproteins which act on hematopoietic cells by binding to specific cell; surface receptors and stimulating proliferation differentiation commitment and some end-cell functional; activation.; Endogenous G-CSF is a lineage-specific colony-stimulating factor that is produced by monocytes ; fibroblasts, and endothelial cells. G-CSF regulates the production of neutrophils within the bone marrow; and affects neutrophil progenitor proliferation differentiation, and selected end-cell functions (including; enhanced phagocytic ability priming of the cellular metabolism associated with respiratory burst ; antibody-dependent killing, and the increased expression of some cell surface antigens). G-CSF is not; species-specific and has been shown to have minimal direct in vivo or in vitro effects on the production or; activity of hematopoietic cell types other than the neutrophil lineage.
19
Revlimid13 38 LENALIDOMIDE Celgene Approved June 2013
FDA Label: Revlimid
Malady that Drug Treats: mantle cell lymphoma
Indications and Usage:13 REVLIMID is a thalidomide analogue indicated for the treatment of patients; with:; Multiple myeloma (MM), in combination with dexamethasone (1.1).; Transfusion-dependent anemia due to low- or intermediate-1-risk; myelodysplastic syndromes (MDS) associated with a deletion 5q; abnormality with or without additional cytogenetic abnormalities (1.2).; Mantle cell lymphoma (MCL) whose disease has relapsed or progressed; after two prior therapies, one of which included bortezomib (1.3).; Limitations of Use:; REVLIMID is not indicated and is not recommended for the treatment; of patients with chronic lymphocytic leukemia (CLL) outside of; controlled clinical trials (1.4).
DrugBank Targets:11 1. Protein cereblon; 2. Tumor necrosis factor ligand superfamily member 11; 3. Cadherin-5; 4. Prostaglandin G/H synthase 2
Mechanism of Action:13 
Target: T cells and natural killer cells/ pro-inflammatory cytokines by monocytes
Action: activator/inhibitor
FDA: Lenalidomide is an analogue of thalidomide with immunomodulatory, antiangiogenic, and antineoplastic properties. Lenalidomide inhibits; proliferation and induces apoptosis of certain hematopoietic tumor cells including multiple myeloma, mantle cell lymphoma, and del (5q); myelodysplastic syndromes in vitro. Lenalidomide causes a delay in tumor growth in some in vivo nonclinical hematopoietic tumor models; including multiple myeloma. Immunomodulatory properties of lenalidomide include activation of T cells and natural killer (NK) cells, increased; numbers of NKT cells, and inhibition of pro-inflammatory cytokines (e.g., TNF-± and IL-6) by monocytes. In multiple myeloma cells, the; combination of lenalidomide and dexamethasone synergizes the inhibition of cell proliferation and the induction of apoptosis.
20
Rituxan13 38 RITUXIMAB Biogen IDEC, Genentech Approved November 1997
FDA Label: Rituxan
Malady that Drug Treats: non-hodgkin's lymphoma
Indications and Usage:13 Rituxan® (rituximab) is a CD20-directed cytolytic antibody indicated for the; treatment of patients with:; Non-Hodgkin s Lymphoma (NHL) (1.1); Chronic Lymphocytic Leukemia (CLL) (1.2); Rheumatoid Arthritis (RA) in combination with methotrexate in adult; patients with moderately-to severely-active RA who have inadequate; response to one or more TNF antagonist therapies (1.3); Granulomatosis with Polyangiitis (GPA) (Wegener s Granulomatosis) and; Microscopic Polyangiitis (MPA) in adult patients in combination with; glucocorticoids (1.4); Limitations of Use: Rituxan is not recommended for use in patients with; severe, active infections (1.5).
DrugBank Targets:11 1. Low affinity immunoglobulin gamma Fc region receptor III-B; 2. Complement C1r subcomponent; 3. Complement C1q subcomponent subunit A; 4. Complement C1q subcomponent subunit B; 5. Complement C1q subcomponent subunit C; 6. Low affinity immunoglobulin gamma Fc region receptor III-A; 7. Complement C1s subcomponent; 8. High affinity immunoglobulin gamma Fc receptor I; 9. Low affinity immunoglobulin gamma Fc region receptor II-a; 10. Low affinity immunoglobulin gamma Fc region receptor II-b; 11. Low affinity immunoglobulin gamma Fc region receptor II-c; 12. B-lymphocyte antigen CD20
Mechanism of Action:13 
Target: CD20 antigen expressed on the surface of; pre-B and mature B-lymphocytes
Action: mediator of B-cell lysis through different possible types of cytotoxicity
FDA: Rituximab is a monoclonal antibody that targets the CD20 antigen expressed on the surface of; pre-B and mature B-lymphocytes. Upon binding to CD20, rituximab mediates B-cell lysis. Possible; mechanisms of cell lysis include complement dependent cytotoxicity (CDC) and antibody dependent; cell mediated cytotoxicity (ADCC). The antibody induced apoptosis in the DHL 4 human B cell; lymphoma cell line.; B cells are believed to play a role in the pathogenesis of rheumatoid arthritis (RA) and associated; chronic synovitis. In this setting, B cells may be acting at multiple sites in the; autoimmune/inflammatory process, including through production of rheumatoid factor (RF) and; other autoantibodies, antigen presentation, T-cell activation, and/or proinflammatory cytokine; production.
21
Sprycel13 38 DASATINIB Bristol-Myers Squibb Approved June 2006
FDA Label: Sprycel
Malady that Drug Treats: Chronic Myeloid Leukemia
Indications and Usage:13 SPRYCEL is a kinase inhibitor indicated for the treatment of; newly diagnosed adults with Philadelphia chromosome-positive (Ph+); chronic myeloid leukemia (CML) in chronic phase. (1, 14); adults with chronic, accelerated, or myeloid or lymphoid blast phase Ph+; CML with resistance or intolerance to prior therapy including imatinib. (1,; 14); adults with Philadelphia chromosome-positive acute lymphoblastic; leukemia (Ph+ ALL) with resistance or intolerance to prior therapy. (1, 14)
DrugBank Targets:11 1. Tyrosine-protein kinase ABL1; 2. Proto-oncogene tyrosine-protein kinase Src; 3. Ephrin type-A receptor 2; 4. Tyrosine-protein kinase Lck; 5. Tyrosine-protein kinase Yes; 6. Mast/stem cell growth factor receptor Kit; 7. Platelet-derived growth factor receptor beta; 8. Signal transducer and activator of transcription 5B; 9. Abelson tyrosine-protein kinase 2; 10. Tyrosine-protein kinase Fyn
Mechanism of Action:13 
Target: BCR-ABL, SRC family; (SRC, LCK, YES, FYN), c-KIT, EPHA2, and PDGFR² kinases
Action: inhibitor
FDA: Dasatinib, at nanomolar concentrations, inhibits the following kinases: BCR-ABL, SRC family; (SRC, LCK, YES, FYN), c-KIT, EPHA2, and PDGFR². Based on modeling studies, dasatinib is; predicted to bind to multiple conformations of the ABL kinase.; In vitro, dasatinib was active in leukemic cell lines representing variants of imatinib mesylate; sensitive and resistant disease. Dasatinib inhibited the growth of chronic myeloid leukemia; (CML) and acute lymphoblastic leukemia (ALL) cell lines overexpressing BCR-ABL. Under the; conditions of the assays, dasatinib was able to overcome imatinib resistance resulting from BCRABL; kinase domain mutations, activation of alternate signaling pathways involving the SRC; family kinases (LYN, HCK), and multi-drug resistance gene overexpression.
22
Synribo13 38 OMACETAXINE MEPESUCCINATE Teva Pharmaceutical Approved October 2012
FDA Label: Synribo
Malady that Drug Treats: chronic or accelerated phase chronic myeloid leukemia
Indications and Usage:13 SYNRIBO for Injection is indicated for the treatment of adult patients with chronic or accelerated phase chronic myeloid leukemia (CML) with resistance and/or intolerance to two or more tyrosine kinase inhibitors (TKI) (1)
DrugBank Targets:11 1. 50S ribosomal protein L2; 2. 60S ribosomal protein L3
Mechanism of Action:13 
Target: A-site cleft in the peptidyl-transferase center of the; large ribosomal subunit from a strain of archaeabacteria
Action: inhibitor of protein synthesis
FDA: The mechanism of action of omacetaxine mepesuccinate has not been fully elucidated but includes inhibition of protein synthesis and; is independent of direct Bcr-Abl binding. Omacetaxine mepesuccinate binds to the A-site cleft in the peptidyl-transferase center of the; large ribosomal subunit from a strain of archaeabacteria. In vitro, omacetaxine mepesuccinate reduced protein levels of the Bcr-Abl; oncoprotein and Mcl-1, an anti-apoptotic Bcl-2 family member. Omacetaxine mepesuccinate showed activity in mouse models of; wild-type and T315I mutated Bcr-Abl CML.
23
Tasigna13 38 NILOTINIB HYDROCHLORIDE MONOHYDRATE Novartis Approved October 2007
FDA Label: Tasigna
Malady that Drug Treats: chronic myelogenous leukemia
Indications and Usage:13 Tasigna is a kinase inhibitor indicated for:; The treatment of newly diagnosed adult patients with Philadelphia; chromosome positive chronic myeloid leukemia (Ph+ CML) in chronic phase.; The treatment of chronic phase (CP) and accelerated phase (AP) Ph+ CML in; adult patients resistant to or intolerant to prior therapy that included imatinib.; (1.2); --------------
DrugBank Targets:11 1. Tyrosine-protein kinase ABL1; 2. Mast/stem cell growth factor receptor Kit
Mechanism of Action:13 
Target: Bcr-Abl kinase, c-kit and Platelet Derived Growth Factor (PDGF)
Action: inhibitor of signal transduction
FDA: Nilotinib is an inhibitor of the BCR-ABL kinase. Nilotinib binds to and stabilizes the inactive conformation of; the kinase domain of ABL protein. In vitro, nilotinib inhibited BCR-ABL mediated proliferation of murine; leukemic cell lines and human cell lines derived from patients with Ph+ CML. Under the conditions of the; assays, nilotinib was able to overcome imatinib resistance resulting from BCR-ABL kinase mutations, in 32 out; of 33 mutations tested. In vivo, nilotinib reduced the tumor size in a murine BCR-ABL xenograft model.; Nilotinib inhibited the autophosphorylation of the following kinases at IC50 values as indicated: BCR-ABL (20; to 60 nM), PDGFR (69 nM), c-KIT (210 nM), CSF-1R (125 to 250 nM), and DDR1 (3.7 nM).
24
Treanda13 38 BENDAMUSTINE HYDROCHLORIDE Cephalon Approved October 2008
FDA Label: Treanda
Malady that Drug Treats: Chronic lymphocytic leukemia and B-cell non-Hodgkin s lymphoma
Indications and Usage:13 TREANDA is an alkylating drug indicated for treatment of patients with:; Chronic lymphocytic leukemia (CLL). Efficacy relative to first line; therapies other than chlorambucil has not been established. (1.1); Indolent B-cell non-Hodgkin lymphoma (NHL) that has progressed during; or within six months of treatment with rituximab or a rituximab-containing; regimen. (1.2)
DrugBank Targets: -
Mechanism of Action:13 
Target: -
Action: -
FDA: Bendamustine is a bifunctional mechlorethamine derivative containing a purine-like benzimidazole ring.; Mechlorethamine and its derivatives form electrophilic alkyl groups. These groups form covalent bonds with electronrich; nucleophilic moieties, resulting in interstrand DNA crosslinks. The bifunctional covalent linkage can lead to cell; death via several pathways. Bendamustine is active against both quiescent and dividing cells. The exact mechanism of; action of bendamustine remains unknown.
25
Trisenox13 38 ARSENIC TRIOXIDE Cell Therapeutics Approved September 2000
FDA Label: Trisenox
Malady that Drug Treats: Acute Promyelocytic Leukemia
Indications and Usage:13 TRISENOX is an arsenical indicated for induction of remission and; consolidation in patients with acute promyelocytic leukemia (APL) who are; refractory to, or have relapsed from, retinoid and anthracycline chemotherapy,; and whose APL is characterized by the presence of the t(15;17) translocation; or PML/RAR-alpha gene expression.
DrugBank Targets:11 1. Inhibitor of nuclear factor kappa-B kinase subunit beta; 2. Thioredoxin reductase 1, cytoplasmic; 3. Transcription factor AP-1; 4. G1/S-specific cyclin-D1; 5. Mitogen-activated protein kinase 3; 6. Mitogen-activated protein kinase 1; 7. RAC-alpha serine/threonine-protein kinase
Mechanism of Action:13 
Target: DNA/ promyelocytic leukemia (PML)-; retinoic acid receptor (RAR)-alpha
Action: damager
FDA: The mechanism of action of TRISENOX is not completely understood. Arsenic trioxide causes morphological; changes and DNA fragmentation characteristic of apoptosis in NB4 human promyelocytic leukemia cells in; vitro. Arsenic trioxide also causes damage or degradation of the fusion protein promyelocytic leukemia (PML)-; retinoic acid receptor (RAR)-alpha.
26
Zydelig13 38 IDELALISIB Gilead Approved July 2014
FDA Label: Zydelig
Malady that Drug Treats: relapsed CLL, follicular B-cell NHL and small lymphocytic lymphoma
Indications and Usage:13 Zydelig is a kinase inhibitor indicated for the treatment of patients with:; Relapsed chronic lymphocytic leukemia (CLL), in combination with; rituximab, in patients for whom rituximab alone would be considered; appropriate therapy due to other co-morbidities. (1.1); Relapsed follicular B-cell non-Hodgkin lymphoma (FL) in patients; who have received at least two prior systemic therapies. (1.2); Relapsed small lymphocytic lymphoma (SLL) in patients who have; received at least two prior systemic therapies. (1.3); Accelerated approval was granted for FL and SLL based on overall; response rate. Improvement in patient survival or disease related; symptoms has not been established. Continued approval for these; indications may be contingent upon verification of clinical benefit in; confirmatory trials.
DrugBank Targets:11 1. Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta isoform (P110´)
Mechanism of Action:13 
Target: PI3K´ kinase
Action: inhibitor
FDA: Idelalisib is an inhibitor of PI3K´ kinase, which is expressed in normal and malignant Bcells.; Idelalisib induced apoptosis and inhibited proliferation in cell lines derived from; malignant B-cells and in primary tumor cells. Idelalisib inhibits several cell signaling; pathways, including B-cell receptor (BCR) signaling and the CXCR4 and CXCR5; signaling, which are involved in trafficking and homing of B-cells to the lymph nodes and; bone marrow. Treatment of lymphoma cells with idelalisib resulted in inhibition of; chemotaxis and adhesion, and reduced cell viability.

Drug clinical trials:

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Inferred drug relations via UMLS61/NDF-RT40:

Cell-based therapeutics:


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Data from LifeMap, the Embryonic Development and Stem Cells Database
Read about Leukemia cell therapies at LifeMap Discovery.

Genetic Tests for Leukemia

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Anatomical Context for Leukemia

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MalaCards organs/tissues related to Leukemia:

31
Myeloid, T cells, B cells, Bone, Bone marrow, Monocytes, Neutrophil, Endothelial, Breast, Lung, Skin, Testes, Liver, Colon, Prostate, Nk cells, Brain, Lymph node, Thyroid, B lymphoblasts, Spleen, Kidney, Pituitary, Testis, Heart, Smooth muscle, Thymus, Placenta, Spinal cord, Skeletal muscle, Tonsil, Whole blood, Cortex, Adipocyte, Eye, Retina, Pancreas, Uterus, Small intestine, Cervix, Tongue, Fetal liver, Adrenal cortex, Pineal, Cardiac myocytes, Cerebellum, Adrenal gland, Fetal brain, Temporal lobe, Atrioventricular node, Appendix

Animal Models for Leukemia or affiliated genes

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Publications for Leukemia

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Articles related to Leukemia:

(show top 50)    (show all 24667)
idTitleAuthorsYear
1
Mast cell leukemia with prolonged survival on PKC412/midostaurin. (25031773)
2014
2
Intraventricular hemorrhage in a patient with chronic myeloid leukemia and anterior communicating artery aneurysm. (23860156)
2013
3
MicroRNA profiling reveals aberrant microRNA expression in adult ETP-ALL and functional studies implicate a role for miR-222 in acute leukemia. (23522449)
2013
4
Reply to myelosuppression after frontline fludarabine, cyclophosphamide, and rituximab in patients with chronic lymphocytic leukemia: Analysis of Persistent and New-Onset Cytopenia. (24151154)
2013
5
Renal Infarction Secondary to Invasive Aspergillosis in a 5-Year-Old Girl With Acute Lymphoblastic Leukemia. (24136022)
2013
6
Characterization of bone marrow mast cells in acute myeloid leukemia with t(8;21) (q22;q22); RUNX1-RUNX1T1. (24035334)
2013
7
Treatment-, patient-, and disease-related factors and the emergence of adverse events with tyrosine kinase inhibitors for the treatment of chronic myeloid leukemia. (23553655)
2013
8
Defining consensus leukemia-associated immunophenotypes for detection of minimal residual disease in acute myeloid leukemia in a multicenter setting. (23912609)
2013
9
Prognostic value of plasma levels of thrombomodulin and von Willebrand factor in Egyptian children with acute lymphoblastic leukemia. (24243921)
2013
10
Wiskott-Aldrich syndrome with unusual clinical features similar to juvenile myelomonocytic leukemia. (22736231)
2012
11
Mogamulizumab for the treatment of adult T-cell leukemia/lymphoma. (23110261)
2012
12
CD117 expression is a sensitive but nonspecific predictor of FLT3 mutation in T acute lymphoblastic leukemia and T/myeloid acute leukemia. (22261446)
2012
13
Rapid screening of ASXL1, IDH1, IDH2, and c-CBL mutations in de novo acute myeloid leukemia by high-resolution melting. (22929312)
2012
14
MLL-AF9 and MLL-ENL alter the dynamic association of transcriptional regulators with genes critical for leukemia. (20854876)
2011
15
DNMT3A mutations are rare in childhood acute myeloid leukemia. (21685466)
2011
16
Treatment of therapy related acute promyelocytic leukemia with the combination of all trans retinoic acid and arsenic trioxide without chemotherapy: a series of three patients. (20350274)
2010
17
TP53 mutation profile in chronic lymphocytic leukemia: evidence for a disease specific profile from a comprehensive analysis of 268 mutations. (20861914)
2010
18
An unusual case of febrile neutropenia: acute myeloid leukemia presenting as myeloid sarcoma of the spleen. (18717148)
2008
19
Concomitant EBV-related B-cell proliferation and juvenile myelomonocytic leukemia in a 2-year-old child. (17618684)
2008
20
Cardiac involvement with human T-cell lymphotrophic virus type-1-associated adult T-cell leukemia/lymphoma: The NIH experience. (18297519)
2008
21
Fludarabine induces apoptosis of human T-cell leukemia virus type 1-infected T cells via inhibition of the nuclear factor-kappaB signal pathway. (17344917)
2007
22
The role of WWP1-Gag interaction and Gag ubiquitination in assembly and release of human T-cell leukemia virus type 1. (17609263)
2007
23
Expression of CLLU1 in patients with chronic lymphocytic leukemia and its prognostic significance]. (18457263)
2007
24
Troglitazone inhibits cell growth and induces apoptosis of B-cell acute lymphoblastic leukemia cells with t(14;18). (16809887)
2006
25
Purine nucleoside analogues and combination therapies in B-cell chronic lymphocytic leukemia: dawn of a new era. (15068894)
2004
26
Prognostic factors in myelodysplastic and myeloproliferative types of chronic myelomonocytic leukemia: a retrospective analysis of 83 patients from a single institution. (15257942)
2004
27
Recent progress in the protein-tyrosine phosphatase SHP1 gene: the significant correlation of the SHP1 gene silencing with the onset of lymphomas/leukemias]. (14619449)
2003
28
Hodgkin's type of Richter's syndrome in familial chronic lymphocytic leukemia treated with cladribine and cyclophosphamide. (12802926)
2003
29
Phase I trial of a novel diphtheria toxin/granulocyte macrophage colony-stimulating factor fusion protein (DT388GMCSF) for refractory or relapsed acute myeloid leukemia. (12006512)
2002
30
Preferential expression of the transcription coactivator HTIF1alpha gene in acute myeloid leukemia and MDS-related AML. (11986951)
2002
31
Cytotoxic efficacy of bendamustine in human leukemia and breast cancer cell lines. (12029443)
2002
32
Homologous recombinational repair vis-A -vis chlorambucil resistance in chronic lymphocytic leukemia. (12007561)
2002
33
Activity and expression of the multidrug resistance proteins P-glycoprotein, MRP1, MRP2, MRP3 and MRP5 in de novo and relapsed acute myeloid leukemia. (11587212)
2001
34
Cytokine expression of T cells in chronic myeloid leukemia. (11775253)
2000
35
Identification of a human T-cell leukemia virus type I tax peptide in contact with DNA. (10567395)
1999
36
Acute dacryocystitis as a presenting sign of pediatric leukemia. (10372893)
1999
37
Okadaic acid-induced apoptosis of HL60 leukemia cells is preceded by destabilization of bcl-2 mRNA and downregulation of bcl-2 protein. (9762907)
1998
38
Myeloperoxidase gene expression in infant leukemia: a Pediatric Oncology Group Study. (9638984)
1998
39
Generation of reactive oxygen intermediates after treatment of blasts of acute myeloblastic leukemia with cytosine arabinoside: role of bcl-2. (8683994)
1996
40
Life-threatening hyperleukocytosis and pulmonary compromise after priming with recombinant human granulocyte-macrophage colony-stimulating factor in a patient with acute myelomonocytic leukemia. (7799037)
1995
41
Hypercalcemia associated with all-trans-retinoic acid in the treatment of acute promyelocytic leukemia. (8501972)
1993
42
Chemotherapy-related side effects in children with acute lymphocytic leukemia in Taiwan: a nursing perspective. (1514401)
1992
43
Amplification of ETS2 oncogene in acute nonlymphoblastic leukemia with t(6;21;18). (1728954)
1992
44
Hairy cell leukemia: splenectomy after alpha 2b-interferon therapy. (1878598)
1991
45
Results of the vincristine, doxorubicin, and dexamethasone regimen in adults with standard- and high-risk acute lymphocytic leukemia. (2189958)
1990
46
Effects of the antisense v-myb' expression on K562 human leukemia cell proliferation and differentiation. (1979645)
1990
47
Acute non-lymphoblastic leukemia. Correlation between clinical and hematological parameters in 87 adult patients. (3121464)
1987
48
An intensive care chemo- or chemoimmunotherapy regimen for patients with intermediate and poor-prognosis acute lymphatic leukemia and leukemic lymphoblastic lymphosarcoma: preliminary results with 14-month median follow-up. (6949235)
1982
49
Myeloblastic leukemia and congenital hemihypertrophy. (192872)
1977
50
Periarteritis nodosa simulating eosinophilic leukemia; a case report. (14771060)
1950

Variations for Leukemia

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Expression for genes affiliated with Leukemia

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Search GEO for disease gene expression data for Leukemia.

Pathways for genes affiliated with Leukemia

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Compounds for genes affiliated with Leukemia

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Compounds related to Leukemia according to GeneCards Suite gene sharing:

(show all 19)
idCompoundScoreTop Affiliating Genes
1megapoietin4410.7THPO, MPL
2anagrelide44 1111.6MPL, THPO
3af 104410.6KMT2A, PICALM
4etoposide44 50 60 1113.5RUNX1, THPO, PML, KMT2A
5imatinib44 50 1112.5RUNX1, ABL2, ABL1, THPO
6cytarabine44 50 1112.4MME, ABL1, THPO
7actinomycin d4410.4KMT2A, THPO, MME, PML
8h2o24410.4ABL2, THPO, PML, MME, ABL1
9oligonucleotide4410.4KMT2A, ARHGEF12, THPO, ABL1, RUNX1
10vegf4410.4ABL1, THPO, MPL, MME, RUNX1
11zinc44 2411.3MME, KMT2A, MPL, PML, ABL1, ZBTB16
12gtp44 2811.3KMT2A, ARHGEF12, MPL, ABL1
13dmso4410.3THPO, RUNX1, ABL1
14proline4410.3ABL1, PML, KMT2A, RUNX1
15retinoic acid44 2411.3PML, THPO, ABL1, ZBTB16, RUNX1, KMT2A
16lysine4410.2MME, MPL, PML, THPO
17tyrosine4410.1THPO, RUNX1, ZBTB16, ABL2, ABL1, MPL
18leucine4410.1PICALM, MME, PML, KMT2A
19cysteine449.9ABL1, MPL, THPO, MME, PML

GO Terms for genes affiliated with Leukemia

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Cellular components related to Leukemia according to GeneCards Suite gene sharing:

idNameGO IDScoreTop Affiliating Genes
1histone methyltransferase complexGO:003509710.3KMT2B, KMT2A
2nucleusGO:00056349.6BCL3, RUNX1, ZBTB16, ABL1, PICALM, MLF1
3cytoplasmGO:00057379.5PML, MKL1, MLF1, ABL1, SH3GL1, KMT2A

Biological processes related to Leukemia according to GeneCards Suite gene sharing:

(show all 21)
idNameGO IDScoreTop Affiliating Genes
1myeloid progenitor cell differentiationGO:000231810.7MLF1, RUNX1
2hemopoiesisGO:003009710.6ZBTB16, PICALM, RUNX1
3regulation of histone H3-K4 methylationGO:005156910.6KMT2A, KMT2B
4myeloid cell differentiationGO:003009910.6PML, THPO, ZBTB16, RUNX1
5positive regulation of oxidoreductase activityGO:005135310.6ABL2, ABL1
6regulation of endocytosisGO:003010010.6ABL1, ABL2, PICALM
7regulation of actin cytoskeleton reorganizationGO:0200024910.6ABL1, ABL2
8negative regulation of viral release from host cellGO:0190218710.6TRIM13, PML
9maintenance of protein location in nucleusGO:005145710.6BCL3, PML
10histone H3-K4 trimethylationGO:008018210.6KMT2B, KMT2A
11definitive hemopoiesisGO:006021610.5RUNX1, LYL1
12regulation of cell motilityGO:0200014510.5ABL1, ABL2
13central nervous system developmentGO:000741710.5RUNX1, ZBTB16, SH3GL1
14positive regulation of transcription, DNA-templatedGO:004589310.4KMT2A, BCL3, LYL1, PICALM, ZBTB16, RUNX1
15protein complex assemblyGO:000646110.4KMT2A, PML, PICALM
16histone H3-K4 methylationGO:005156810.4KMT2A, KMT2B
17intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorGO:004277110.3PML, BCL3
18regulation of autophagyGO:001050610.3ABL2, ABL1
19transcription, DNA-templatedGO:000635110.3BCL3, LYL1, KMT2B, RUNX1, PML, MKL1
20embryonic hemopoiesisGO:003516210.2RUNX1, KMT2A
21response to gamma radiationGO:001033210.0PML, TRIM13

Molecular functions related to Leukemia according to GeneCards Suite gene sharing:

idNameGO IDScoreTop Affiliating Genes
1histone methyltransferase activity (H3-K4 specific)GO:004280010.3KMT2B, KMT2A
2actin monomer bindingGO:000378510.3ABL2, ABL1, MKL1
3DNA bindingGO:00036779.8RUNX1, ZBTB16, ABL1, MLF1, PML, KMT2B
4sequence-specific DNA binding transcription factor activityGO:00037009.8RUNX1, ZBTB16, MKL1, KMT2A, KMT2B, BCL3
5protein bindingGO:00055159.4ARHGEF12, RUNX1, ZBTB16, ABL2, ABL1, PICALM

Sources for Leukemia

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2CDC
12ExPASy
13FDA
14FMA
22GTR
23HGMD
24HMDB
25ICD10
26ICD10 via Orphanet
27ICD9CM
28IUPHAR
29KEGG
33MeSH
34MESH via Orphanet
35MGI
38NCI
39NCIt
40NDF-RT
43NINDS
44Novoseek
46OMIM
47OMIM via Orphanet
51PubMed
52QIAGEN
57SNOMED-CT via Orphanet
61UMLS
62UMLS via Orphanet