Acute Lymphoblastic Leukemia Medication
- Author: Karen Seiter, MD; Chief Editor: Emmanuel C Besa, MD more...
Medication Summary
The medications used to treat acute leukemia cause severe bone marrow depression. Only physicians specifically trained in their use should administer these medications. In addition, access to appropriate supportive care is required.
A regimen of fludarabine and cyclophosphamide and rituximab (FCR) is commonly used. This combination of 3 of the most active drugs is a good example of a synergistic combination of drugs with different mechanisms. Different forms of the FCR combination are used; therefore, the dosing plays a big role in results. FCR provides a cyclical form of treatment, rather than a 1-time, transplant-conditioning regimen followed by stem cells. In a study by Matutes et al, the FCR regimen did not quite overcome fludarabine resistance, which remains probably the single most important hurdle in long-term term outcomes for patients with acute lymphoblastic leukemia (ALL).[45]
Corticosteroids
Class Summary
Corticosteroids may be used during induction, consolidation, and/or maintenance therapy for acute lymphoblastic leukemia (ALL).
Prednisone
Prednisone is a corticosteroid that has a wide range of activities. In ALL, this agent is used because of its direct antileukemic effects.
Dexamethasone (Baycadron, Maxidex, Ozurdex)
Dexamethasone is another corticosteroid that acts as an important chemotherapeutic agent in the treatment of ALL. Like prednisone, this agent is used in induction and reinduction therapy and is also given as intermittent pulses during continuation therapy.
Antineoplastics
Class Summary
Antineoplastic agents are used for induction, consolidation, maintenance, and central nervous system (CNS) prophylaxis.
Cancer chemotherapy is based on an understanding of tumor cell growth and how drugs affect this growth. After cells divide, they enter a period of growth (ie, phase G1), followed by DNA synthesis (ie, phase S). The next phase is a premitotic phase (ie, G2), then, finally, a mitotic cell division (ie, phase M).
Cell-division rates vary for different tumors. Most common cancers grow slowly compared with normal tissues, and the rate may be decreased in large tumors. This difference allows normal cells to recover from chemotherapy more quickly than malignant ones and is the rationale behind current cyclic dosage schedules.
Antineoplastic agents interfere with cell reproduction. Some agents act at specific phases of the cell cycle, whereas others (ie, alkylating agents, anthracyclines, cisplatin) are not phase specific. Cellular apoptosis (ie, programmed cell death) is another potential mechanism of many antineoplastic agents.
Vincristine (Vincasar PFS)
Vincristine is a vinca alkaloid agent that acts by arresting cells in metaphase.
Asparaginase (Elspar)
Asparaginase breaks down extracellular asparagine into aspartic acid and ammonia. Normal cells are capable of synthesizing their own asparagine, but many malignant cells are not.
Asparaginase Erwinia chrysanthemi (Erwinaze)
Catalyzes deamidation of asparagine to aspartic acid and ammonia, thereby reducing circulating levels of asparagine. Lack of asparagine synthetase activity results in cytotoxicity specific for leukemic cells that depend on an exogenous source of the amino acid asparagine. Indicated as part of a multiagent chemotherapeutic regimen for patients with acute lymphoblastic leukemia (ALL) who have developed hypersensitivity to E coli –derived asparaginase. It is estimated that 15-20% of patients with ALL develop a hypersensitivity to E coli –derived asparaginase, which extrapolates to approximately 450-600 children in the United States annually.
Methotrexate (Trexall)
Methotrexate is an antimetabolite of the folic acid analogue type. This agent inhibits dihydrofolate reductase, resulting in inhibition of DNA synthesis, repair, and cellular replication.
Mercaptopurine (Purinethol)
Mercaptopurine is antimetabolite of the purine analogue type. Its primary effect is inhibition of DNA synthesis.
Cyclophosphamide
Cyclophosphamide is an alkylating agent of the nitrogen mustard type that acts by inhibiting cell growth and proliferation.
Cytarabine
Cytosine arabinoside is an antimetabolite that induces activity as a result of activation to cytarabine triphosphate and includes inhibition of DNA polymerase and incorporation into DNA and RNA.
Daunorubicin (Cerubidine)
Daunorubicin is an anthracycline that inhibits topoisomerase II. This agent also inhibits DNA and RNA synthesis by intercalating between DNA base pairs.
Idarubicin (Idamycin)
Idarubicin is a topoisomerase II inhibitor that inhibits cell proliferation by inhibiting DNA and RNA polymerase.
Mitoxantrone (Novantrone)
Mitoxantrone is also a topoisomerase II inhibitor. This agent inhibits cell proliferation by intercalating DNA and inhibiting topoisomerase II.
Dasatinib (Sprycel)
Dasatinib is a multiple tyrosine kinase inhibitor that inhibits the growth of cell lines overexpressing BCR-ABL. This agent is indicated for Philadelphia chromosome–positive acute lymphoblastic leukemia (Ph+ ALL) in individuals with resistance to or who were intolerant of previous therapy.
Nelarabine (Arranon)
Nelarabine is a prodrug of the deoxyguanosine analogue 9-beta-D-arabinofuranosylguanine (ara-G) that is converted to the active 5'-triphosphate, ara-GTP, a T-cell–selective nucleoside analogue. Leukemic blast cells accumulate ara-GTP, which allows for incorporation into DNA, leading to inhibition of DNA synthesis and cell death.
This agent is approved by the US Food and Drug Administration (FDA) as an orphan drug to treat persons with T-cell ALL whose disease has not responded to or which has relapsed with at least 2 chemotherapy regimens.
Clofarabine (Clolar)
Clofarabine is a purine nucleoside antimetabolite that inhibits DNA synthesis and is indicated for relapsed or refractory acute lymphoblastic leukemia in pediatric patients. Pools of cellular deoxynucleotide triphosphate are decreased by inhibiting ribonucleotide reductase and terminating DNA chain elongation and repair. This agent also disrupts mitochondrial membrane integrity. It is indicated for the treatment of patients aged 1-21 years who have relapsed or refractory acute ALL. For adults older than 21 years, base dosing on surface area as in pediatrics. Clofarabine is not indicated for adults older than 21 years.
Colony-Stimulating Factors
Class Summary
Colony-stimulating factors (CSF) act as hematopoietic growth factors that stimulate THE development of granulocytes. These agents are used to treat or prevent neutropenia when patients receive myelosuppressive cancer chemotherapy and to reduce the period of neutropenia that is associated with bone marrow transplantation (BMT). Colony-stimulating factors are also used to mobilize autologous peripheral blood progenitor cells for BMT and in management of chronic neutropenia.
Filgrastim (Neupogen)
Filgrastim is a granulocyte colony-stimulating factor (G-CSF) that activates and stimulates the production, maturation, migration, and cytotoxicity of neutrophils.
Pegfilgrastim (Neulasta)
Pegfilgrastim is a long-acting filgrastim created by the covalent conjugate of recombinant G-CSF (ie, filgrastim) and monomethoxypolyethylene glycol. As with filgrastim, this agent acts on hematopoietic cells by binding to specific cell surface receptors, thereby activating and stimulating production, maturation, migration, and cytotoxicity of neutrophils.
Antimicrobials
Class Summary
Prophylactic antimicrobial drugs are given to prevent infection in patients receiving chemotherapy.
Trimethoprim-sulfamethoxazole (Septra, Bactrim)
Trimethoprim-sulfamethoxazole (TMP-SMZ) inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. All immunocompromised patients should be treated with TMP-SMZ to prevent Pneumocystis carinii pneumonia (PCP).
Antifungals
Class Summary
These agents may change the permeability of the fungal cell, resulting in a fungicidal effect.
Nystatin
Nystatin is used to prevent fungal infections in mucositis. This agent is a fungicidal and fungistatic antibiotic from Streptomyces noursei that is effective against various yeasts and yeastlike fungi. Nystatin acts by changing the permeability of the fungal cell membrane after binding to cell membrane sterols, causing cellular contents to leak.
Treatment with this agent should continue until 48 hours after the symptoms disappear. Nystatin is not substantially absorbed from the gastrointestinal tract.
Clotrimazole
Clotrimazole may be used instead of nystatin to prevent fungal infections. It is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing death of fungal cells.
Itraconazole (Sporanox)
Itraconazole has fungistatic activity and is used to prevent fungal infections in high-risk patients. This drug is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting CYP-dependent synthesis of ergosterol, a vital component of fungal cell membranes. The bioavailability of this drug is greater in the oral solution compared with the capsule formulation.
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| Chromosome Number | 3-Year Event-Free Survival |
| Near tetraploidy | 46-56% |
| Normal karyotype | 34-44% |
| Hyperdiploidy >50 | 32-59% |
| Hyperdiploidy 47-50 | 21-53% |
| Pseudodiploidy | 12-25% |
| Hypodiploidy | 11% |
| Abnormality | Genes Involved | 3-Year Event-Free Survival |
| t(10;14)(q24;q11) | HOX11/TCRA | 75% |
| 6q | Unknown | 47% |
| 14q11 | TCRA/TCRD | 42% |
| 11q23 | MLL | 18-26% |
| 9p | Unknown | 22% |
| 12 | TEL | 20% |
| t(1;19)(q23;p13) | PBX1/E2A | 20% |
| t(8;14)(q24;q32) t(2;8)(p12;q24) t(8;22)(q24;q11) | c-myc/IGH IGK/c-myc c-myc/IGL | 17%* 80%† |
| t(9;22)(q34;q11) | bcr-abl | 5-10%* 66%‡ |
| t(4;11)(q21;q23) | AF4-MLL | 0-10% |
| * Traditional regimens. † Hyper-CVAD (cyclophosphamide, vincristine, doxorubicin [Adriamycin], dexamethasone) with rituxan. ‡ Hyper-CVAD with imatinib. | ||
| ALL Cells | TdT | CD19 | CD10 | CyIg | SIg |
| Early B-precursor ALL | + | + | - | - | - |
| Pre–B-cell ALL (see the image below) | + | + | + | + | - |
| B-cell ALL | - | + | +/- | +/- | + |
| ALL = acute lymphoblastic leukemia; Cylg = Cytoplasmic immunoglobulin; SIg =Surface immunoglobulin; TdT = terminal deoxynucleotidyl transferase. | |||||
| ALL Cells | TdT | Surface CD3 | CD4/CD8 |
| Early T-precursor ALL | + | - | +/+ or -/- |
| T-cell ALL | + | + | +/- or -/+ |
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