Acute Myelogenous (Myeloid) Leukemia

Acute myelogenous leukemia (AML) is a fast-growing blood and bone-marrow cancer. It starts when a single early “myeloid” stem cell in the marrow develops harmful genetic changes and loses control of growth and maturity. The cell divides rapidly and makes large numbers of immature white cells called “blasts.” These blasts crowd out normal blood-forming cells. As normal red cells, platelets, and healthy white cells drop, people develop tiredness, infections, bleeding, and other problems in weeks to a few months. Doctors diagnose AML by blood tests, a bone-marrow exam, and genetic tests that look for chromosome and gene changes that define the AML type and guide treatment. NCBICancer.gov

Acute myelogenous leukemia (AML) is a fast-growing blood cancer that starts in the bone marrow—the soft inner part of bones where new blood cells are made. In AML, very early cells meant to become healthy white blood cells (myeloblasts) grow out of control. These immature cells crowd the marrow and spill into the blood. Because they do not work like normal cells, the body becomes low on healthy red cells (causing tiredness and shortness of breath), normal white cells (causing infections), and platelets (causing bruising and bleeding). AML is an emergency because it progresses quickly. Doctors confirm AML by blood tests, bone marrow tests, and genetic tests that guide treatment. Treatment depends on age, general health, and the leukemia’s genetic markers. Standard care uses strong chemotherapy or targeted drugs; some people also need a stem-cell (bone-marrow) transplant for the best chance of cure. The goal is complete remission, then consolidation to keep leukemia away.

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Other names

AML is also called acute myelogenous leukemia, acute myeloid leukemia, or the older term acute non-lymphocytic leukemia (ANLL). Subtype names often reflect the exact genetic change, such as core-binding-factor AML (with RUNX1::RUNX1T1 or CBFB::MYH11), NPM1-mutated AML, FLT3-mutated AML, TP53-mutated AML, or AML, myelodysplasia-related when it arises from prior marrow problems. One special subtype is acute promyelocytic leukemia (APL), driven by a PML::RARA fusion; it is an emergency at diagnosis because of severe bleeding risk, but it is highly curable with specific medicines once recognized quickly. PMCCollege of American PathologistsNCBI

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Types of AML

Doctors now classify AML mainly by genetic features, because these features strongly shape treatment choices and outlook. In modern systems (WHO 2022 and ICC), many AML categories can be diagnosed even if blasts are under 20% when a defining genetic change is present; otherwise, AML usually requires ≥20% blasts. Below are the broad groups you will hear about in simple language: PMCCollege of American Pathologists

1. AML with defining chromosome fusions (“rearrangements”)
   Examples include RUNX1::RUNX1T1 and CBFB::MYH11 (called core-binding-factor AML). These often have better responses to standard chemotherapy compared with many other types. ASH Publications

2. Acute promyelocytic leukemia (APL, PML::RARA)
   A distinct emergency at diagnosis due to severe bleeding tendency (DIC). Treated with all-trans retinoic acid (ATRA) and arsenic trioxide rather than standard chemotherapy and is often highly curable when treated fast. NCBIACEP

3. AML with specific gene mutations
   Common ones include NPM1, FLT3-ITD/TKD, IDH1/IDH2, TP53, and others. Testing all these genes is now standard because they guide targeted drugs and risk grouping. PMC

4. AML, myelodysplasia-related (MR)
   AML that arises from previous marrow disease (like MDS) or carries particular “MR” mutations or cytogenetic patterns. It tends to have a tougher course. PMC

5. Therapy-related AML (t-AML)
   AML that develops after prior chemotherapy or radiation for another illness. It often carries high-risk genetics. American Cancer Society

6. Myeloid sarcoma (“chloroma”)
   A tumor mass of myeloid blasts in tissues outside the marrow, sometimes with or without AML in the blood/marrow. It is treated as AML. Cancer.gov

7. AML not otherwise specified (NOS)
   Used when no defining genetic or clinical category fits; even here, molecular testing still guides care. NCCN

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Causes and risk factors

A “cause” in AML is often a mix of genetic accidents inside marrow stem cells plus exposures or conditions that raise the chance of those accidents. Most people will have no clear single cause.

1. Older age – DNA repair weakens over time; AML is most common in older adults. American Cancer Society

2. Male sex – Slightly higher risk in males for reasons not fully clear. American Cancer Society

3. Smoking – Tobacco toxins damage marrow DNA. American Cancer Society

4. Benzene exposure – A chemical in some workplaces and fuels that injures marrow DNA. American Cancer Society

5. High-dose radiation exposure – Past radiation accidents or intensive medical radiation can increase risk. American Cancer Society

6. Prior chemotherapy – Some drugs (like alkylators, topoisomerase II inhibitors) can later lead to therapy-related AML. American Cancer Society

7. Myelodysplastic syndromes (MDS) – A chronic marrow disorder that can transform to AML. American Cancer Society

8. Myeloproliferative neoplasms (MPN) – Conditions like polycythemia vera or myelofibrosis can evolve to AML. Cancer.gov

9. Inherited predisposition (familial AML) – Rare; certain germline mutations (e.g., CEBPA) raise lifetime risk. Cancer.gov

10. Down syndrome and other genetic syndromes – Some congenital conditions increase risk of myeloid leukemias. Cancer.gov

11. Aplastic anemia with clonal evolution – Damaged marrow that acquires leukemic clones. Cancer.gov

12. Occupational solvent exposure – Long-term exposure to certain solvents is linked to AML in some studies. American Cancer Society

13. Previous radiation therapy – Therapeutic radiation for prior cancers can contribute to t-AML. American Cancer Society

14. Family history of AML – Rare, but risk is higher if a close relative had AML. American Cancer Society

15. Inherited bone-marrow failure syndromes – e.g., Fanconi anemia; higher lifetime AML risk. Cancer.gov

16. Chronic immunosuppression – May allow abnormal clones to grow, though links are less strong. Cancer.gov

17. Prior cytotoxic exposure at younger age – Children treated for cancer can develop AML years later. American Cancer Society

18. Obesity – Associated with a modestly increased leukemia risk in some studies. Cancer.gov

19. Environmental radiation (very high) – Rare events (e.g., nuclear accidents) increase leukemia risk. American Cancer Society

20. Random chance – Many cases arise from spontaneous DNA errors with no identifiable exposure. Cancer.gov

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Common symptoms and signs

1. Tiredness and weakness – Low red cells (anemia) reduce oxygen delivery, causing fatigue and shortness of breath on exertion. Cancer.gov

2. Pale skin – Another sign of anemia noticed by family or clinicians. American Cancer Society

3. Easy bruising and bleeding – Low platelets and clotting problems cause nosebleeds, gum bleeding, or heavy periods. American Cancer Society

4. Frequent or severe infections – Low healthy neutrophils and dysfunctional blasts make it hard to fight germs; fevers are common. American Cancer Society

5. Bone or joint pain – Marrow packed with blasts increases pressure, causing deep aching. American Cancer Society

6. Night sweats and fevers – Inflammation and infection are frequent in AML. Cancer.gov

7. Weight loss or poor appetite – From systemic illness and infections. Cancer.gov

8. Swollen belly from enlarged liver or spleen – Leukemia cells can collect in these organs. American Cancer Society

9. Swollen gums or gum pain – “Gingival infiltration,” especially in some monocytic-type AMLs. Cancer.gov

10. Skin spots (petechiae) or larger bruises (ecchymoses) – From low platelets and fragile capillaries. American Cancer Society

11. Shortness of breath – From anemia, infection, or very high white counts (“leukostasis” in rare cases). Cancer.gov

12. Headaches, confusion, or stroke-like symptoms – Possible with leukostasis or bleeding; urgent care needed. Cancer.gov

13. Lymph node swelling – Less common than in lymphoid cancers but can occur. Cancer.gov

14. Prolonged bleeding after minor cuts or dental work – A platelet/clotting sign. American Cancer Society

15. In APL specifically: sudden severe bleeding or clots – Due to DIC/hyperfibrinolysis; treat as an emergency. NCBI

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Diagnostic tests

A) Physical-exam–based assessments

1. General exam for pallor, bruises, rashes, and fever
   The doctor looks for anemia (pale skin), petechiae, ecchymoses, and fever. These bedside clues point toward bone-marrow failure and infection risk in AML. American Cancer Society

2. Mouth and gum check
   Swollen or bleeding gums can reflect low platelets or direct leukemia cell build-up, especially in monocytic variants. Cancer.gov

3. Abdomen exam for liver and spleen size
   An enlarged spleen or liver suggests leukemia cells have collected there. It also helps explain belly fullness or early satiety. American Cancer Society

4. Lymph-node survey
   While less prominent than in lymphoid leukemias, enlarged nodes may appear with certain AML subtypes and guide biopsy decisions. Cancer.gov

5. Neurologic check (headache, vision, weakness)
   This screens for leptomeningeal spread, leukostasis, hemorrhage, or infection—conditions that require urgent imaging or lumbar puncture later. Cancer.gov

B) Manual/bedside laboratory methods

6. Manual differential and peripheral-smear review
   A trained technologist and hematologist examine blood under the microscope to count blasts, look for Auer rods, assess dysplasia, and guide urgent steps (e.g., APL suspicion). Cancer.gov

7. Manual reticulocyte count (if needed)
   Helps judge bone-marrow red-cell production; a low retic count in anemia supports marrow failure from leukemia. Cancer.gov

8. Bedside capillary smear in unstable patients
   A quick finger-stick smear can reveal blast overload when rapid decisions are needed before full lab results are ready. Cancer.gov

9. Orthostatic vital signs and bleeding assessment
   Simple bedside checks detect volume loss or active bleeding, which is crucial in APL or severe thrombocytopenia. NCBI

C) Laboratory and pathological tests

10. Complete blood count (CBC) with automated differential
    Shows anemia, thrombocytopenia, white-cell abnormalities, or very high counts. It is the doorway test that triggers the work-up. Cancer.gov

11. Peripheral blood smear (morphology)
    Confirms blasts, Auer rods, dysplastic cells, or promyelocytes. In suspected APL, immediate action is critical even before genetic confirmation. NCBI

12. Coagulation panel (PT/INR, aPTT, fibrinogen, D-dimer)
    Screens for DIC and bleeding risk, especially in APL. Low fibrinogen and high D-dimer strongly support APL-type coagulopathy. NCBIEMCrit Project

13. Comprehensive metabolic panel and tumor-lysis labs
    Kidney function, uric acid, potassium, phosphate, and calcium help identify tumor lysis syndrome and guide supportive care. Cancer.gov

14. Bone-marrow aspiration and biopsy
    The key test. It measures blast percentage and provides material for all genetic and flow studies that define AML type and risk. Cancer.gov

15. Flow cytometry (immunophenotyping)
    Labels cells with antibodies to show their lineage and maturity (myeloid markers like CD13, CD33; monocytic markers; etc.). Distinguishes AML from ALL or non-leukemic causes. Cancer.gov

16. Cytogenetics (karyotype) and FISH
    Identify chromosome gains, losses, or swaps (translocations). Finding fusions like RUNX1::RUNX1T1 or CBFB::MYH11 can diagnose AML and carry prognostic value. ASH Publications

17. Molecular testing (PCR/NGS panel)
    Looks for mutations (e.g., NPM1, FLT3, IDH1/2, TP53). Modern guidelines recommend broad mutational profiling at diagnosis because results guide targeted therapy and risk grouping. PMC

D) Electrodiagnostic tests

18. Electrocardiogram (ECG)
    Baseline ECG is useful before certain AML drugs (e.g., arsenic trioxide for APL) that can prolong the QT interval, and for evaluating infection-related strain or electrolyte-driven rhythm changes. ACEP

19. Electroencephalogram (EEG) in selected cases
    Used if seizures or altered mental status suggest CNS bleeding, infection, or metabolic problems in severe AML presentations. (Imaging and lumbar puncture usually come first; EEG adds functional information.) Cancer.gov

E) Imaging tests

20. Chest X-ray
    Quick check for pneumonia or fluid overload in febrile, breathless patients. Infections are common and can be life-threatening at AML diagnosis. Cancer.gov

21. CT chest/abdomen/pelvis (as indicated)
    Looks for occult infections, organ enlargement, or masses (myeloid sarcoma) and helps guide urgent antibiotics or procedures. Cancer.gov

22. Brain MRI (or CT) for neuro symptoms
    Detects bleeding, stroke, or leukemic involvement when patients have headache, confusion, or focal deficits. Cancer.gov

23. Echocardiogram
    Assesses heart function before anthracycline chemotherapy and helps manage fluid status during intensive treatment. Cancer.gov

Non-pharmacological treatments

1. Energy conservation & fatigue pacing (Physiotherapy)
   Description. Daily fatigue in AML is profound. Energy conservation means planning tasks, resting before you are exhausted, using tools (stools, grabbers), and breaking activities into short blocks with scheduled naps. Therapists teach “activity pacing” and the “20-20-20” method (20 minutes light task → 20 minutes rest → repeat). Home changes include placing items at waist height, using shower chairs, and sitting for tasks like cooking.
   Purpose. Reduce exhaustion and prevent crashes that delay recovery.
   Mechanism. Low hemoglobin and inflammation reduce oxygen delivery; pacing lowers energy demand and keeps heart rate and breathing steady, leaving more reserve for healing.
   Benefits. Better daily function, fewer falls, improved mood and sleep, more consistent participation in rehab and clinic visits.

2. Graded aerobic training (Physiotherapy)
   Description. Short, low-intensity walking or stationary cycling under therapist guidance, adapted to blood counts and symptoms. Start with 5–10 minutes at comfortable pace, add 1–2 minutes every few days if safe.
   Purpose. Improve stamina without overexertion.
   Mechanism. Gentle aerobic work boosts mitochondrial efficiency, improves circulation, and counteracts deconditioning from bed rest and chemotherapy.
   Benefits. Less shortness of breath with daily tasks, improved sleep and appetite, better mood.

3. Light resistance exercise (Physiotherapy)
   Description. Elastic bands or 0.5–2 kg hand weights for large muscle groups (legs, glutes, back, chest), 1–2 sets of 8–12 reps, 3–4 days/week, adjusted for platelets. Avoid heavy lifting when platelets are low.
   Purpose. Preserve muscle and bone strength.
   Mechanism. Mechanical load stimulates muscle protein synthesis and slows bone loss.
   Benefits. Easier transfers, fewer aches, better balance and independence.

4. Range-of-motion & gentle stretching (Physiotherapy)
   Description. Daily shoulder, hip, knee, ankle ROM; hold easy stretches 15–30 seconds, repeat 2–3 times.
   Purpose. Prevent stiffness from hospital bed rest and IV lines.
   Mechanism. Maintains joint capsule length and tendon glide.
   Benefits. Less pain, smoother movement, easier dressing and hygiene.

5. Balance & fall-prevention training (Physiotherapy)
   Description. Sit-to-stand drills, tandem stance near support, home safety set-up (no loose rugs, night lights).
   Purpose. Reduce fall risk, especially when anemic or dizzy.
   Mechanism. Rehearses protective reactions; environmental changes remove hazards.
   Benefits. Fewer injuries and emergency visits.

6. Breathing exercises & inspiratory muscle training (Physiotherapy)
   Description. Diaphragmatic breathing, incentive spirometer use, and short sessions with a threshold device when prescribed.
   Purpose. Prevent atelectasis and support oxygenation.
   Mechanism. Recruits alveoli and strengthens respiratory muscles.
   Benefits. Less shortness of breath, better cough clearance, fewer chest infections.

7. Neuropathy-friendly movement (Physiotherapy)
   Description. If chemo causes tingling/numb feet, use wider-base stance, ankle-strength drills, and textured insoles.
   Purpose. Maintain mobility despite sensory change.
   Mechanism. Proprioceptive training improves joint-position awareness.
   Benefits. Fewer stumbles, more confident walking.

8. Lymphedema and edema self-care (Physiotherapy/OT)
   Description. Elevation, ankle pumps, and compression if prescribed.
   Purpose. Control swelling from fluids/meds.
   Mechanism. Aids venous/lymph return.
   Benefits. Comfort, easier shoe wear.

9. Oral care routine (Supportive)
   Description. Soft brush, bland rinses (salt/baking soda), alcohol-free mouthwash; avoid flossing when platelets are very low.
   Purpose. Prevent mouth sores and infections.
   Mechanism. Lowers bacterial load and protects mucosa.
   Benefits. Less pain, improved eating.

10. Skin & catheter care education (Supportive/Educational)
    Description. Daily inspection, gentle washing, sterile dressing changes for central lines as instructed.
    Purpose. Prevent line infections.
    Mechanism. Breaks biofilm formation and contamination.
    Benefits. Fewer fevers and hospitalizations.

11. Sleep hygiene coaching (Mind-body)
    Description. Consistent bedtime, cool/dark room, no screens 60 minutes before bed, relaxation audio.
    Purpose. Restore sleep disrupted by steroids/anxiety.
    Mechanism. Resets circadian cues and lowers arousal.
    Benefits. Better energy, mood, pain tolerance.

12. Mindfulness-based stress reduction (Mind-body)
    Description. Brief (5–10 min) daily mindfulness or guided imagery using apps.
    Purpose. Reduce anxiety/depression, improve coping.
    Mechanism. Lowers sympathetic drive and cortisol.
    Benefits. Better quality of life and pain control. TIME

13. Yoga or tai chi (Mind-body/Movement)
    Description. Chair or mat-based gentle flows, 1–3 times/week, adapted to counts.
    Purpose. Combine movement with calm focus.
    Mechanism. Enhances flexibility, balance, parasympathetic tone.
    Benefits. Less fatigue and stress; improved balance. TIME

14. Music therapy or art therapy (Mind-body)
    Description. Guided sessions to express feelings and distract from symptoms.
    Purpose. Reduce distress and pain.
    Mechanism. Cognitive/emotional reframing and attention diversion.
    Benefits. Better mood, engagement with care. TIME

15. Cognitive-behavioral therapy (CBT) brief modules (Mind-body)
    Description. Short, structured sessions (in person or telehealth) focused on coping with uncertainty, sleep, and symptom-related thoughts.
    Purpose. Reduce anxiety/insomnia.
    Mechanism. Replaces unhelpful thoughts; builds skills.
    Benefits. Better adherence to treatment; lower distress. TIME

16. Genetic counseling & education (“Gene/Educational therapy”)
    Description. A counselor explains your leukemia’s gene changes (e.g., FLT3, IDH1/2), how they guide therapy and transplant decisions, and family risk where relevant.
    Purpose. Informed consent and realistic expectations.
    Mechanism. Translates complex reports into practical choices.
    Benefits. Better shared decision-making; timely testing. NCCN

17. Clinical-trial education (Educational therapy)
    Description. Review trial options (new targeted drugs/menin inhibitors), eligibility, visits, and risks.
    Purpose. Expand access to cutting-edge care.
    Mechanism. Matching biomarkers to investigational agents.
    Benefits. Potential for better outcomes and future access. U.S. Food and Drug AdministrationAML Hub

18. Fertility preservation counseling (Educational)
    Description. Early discussion of sperm banking or oocyte/embryo cryopreservation when safe to delay treatment briefly.
    Purpose. Preserve future family options.
    Mechanism. Banking gametes before gonadotoxic chemo.
    Benefits. Protects quality-of-life goals.

19. Infection-prevention coaching (Educational)
    Description. Hand hygiene, safe food handling, mask use in crowds, pet/litter precautions, and vaccination planning with the team.
    Purpose. Reduce infections during neutropenia.
    Mechanism. Cuts exposure pathways.
    Benefits. Fewer fevers/hospital stays. Infectious Diseases Society of America

20. Nutrition counseling
    Description. Registered dietitian helps maintain calories/protein with taste changes and nausea; focuses on cooked, safe foods during neutropenia.
    Purpose. Prevent weight and muscle loss.
    Mechanism. Meets protein/energy needs without unsafe foods.
    Benefits. Better treatment tolerance.

21. Nausea self-management training
    Description. Ginger tea, slow sips, small frequent meals; use prescribed anti-nausea medicines correctly.
    Purpose. Keep nutrition/hydration steady.
    Mechanism. Settles stomach; anticipatory coping.
    Benefits. Fewer ER visits for dehydration.

22. Constipation/diarrhea self-care plan
    Description. Stool softeners when on opioids; fiber and fluids; call if severe diarrhea/fever.
    Purpose. Avoid complications.
    Mechanism. Supports bowel regularity.
    Benefits. Comfort and safety.

23. Safe physical activity plan during low counts
    Description. Activity thresholds: avoid impact if platelets very low; avoid crowded gyms when neutropenic.
    Purpose. Move safely while protecting from bleeding/infection.
    Mechanism. Risk-stratified movement.
    Benefits. Continues rehab without harm. PMC

24. Caregiver training
    Description. Teach family how to help transfers, meds, appointments, and watch for red-flags.
    Purpose. Shared safety net.
    Mechanism. Early detection and support.
    Benefits. Fewer complications at home.

25. Advance care planning conversation
    Description. Discuss values, emergency preferences, and transplant choices early.
    Purpose. Aligns care with your goals.
    Mechanism. Formal documentation of wishes.
    Benefits. Peace of mind; clear guidance for the team.

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Drug treatments

1) Cytarabine (Ara-C) – antimetabolite chemotherapy
Dose/time. In standard “7+3” induction, continuous IV infusion daily for 7 days (common dose 100–200 mg/m²/day), paired with an anthracycline for days 1–3; high-dose cytarabine may be used later for consolidation. Englishchemoexperts.com
Purpose. Core backbone to kill leukemia blasts and induce remission.
Mechanism. Mimics a DNA building block and blocks DNA synthesis, causing cell death in rapidly dividing blasts.
Key side effects. Low blood counts, infection, mouth sores, nausea; with high doses—cerebellar toxicity and conjunctivitis (prevent with steroid eye drops as directed).

2) Daunorubicin – anthracycline chemotherapy
Dose/time. Given IV on days 1–3 with cytarabine in “7+3” (common dose 60–90 mg/m²/day); liposomal daunorubicin is part of CPX-351 (see below). chemoexperts.com
Purpose. Synergizes with cytarabine to clear blasts.
Mechanism. Intercalates DNA and inhibits topoisomerase II, causing breaks.
Side effects. Low counts, mucositis, hair loss; potential heart toxicity—your team monitors heart function.

3) Idarubicin – anthracycline
Dose/time. Often used instead of daunorubicin (e.g., days 1–3). chemoexperts.com
Purpose. Alternative anthracycline in induction.
Mechanism/side effects. Similar to daunorubicin; heart monitoring is important.

4) CPX-351 (Vyxeos®: liposomal daunorubicin + cytarabine) – fixed-dose liposomal chemo
Dose/time. For therapy-related AML or AML with myelodysplasia-related changes: 44/100 mg/m² IV over 90 minutes on days 1, 3, 5 (induction); 29/65 mg/m² on days 1, 3 for consolidation. U.S. Food and Drug Administrationaccp1.orgPubMed
Purpose. Improved outcomes in these poor-risk subtypes.
Mechanism. Delivers drugs together in a 1:5 ratio liposome for longer exposure to blasts.
Side effects. Prolonged low counts, infections; similar anthracycline risks.

5) Gemtuzumab ozogamicin (Mylotarg®) – CD33-targeted antibody-drug conjugate
Dose/time. In some newly diagnosed adults, 3 mg/m² IV on days 1, 4, 7 added to induction; also used in certain relapse settings. U.S. Food and Drug AdministrationPMC
Purpose. Targets CD33-positive blasts to deepen responses.
Mechanism. Antibody binds CD33 and delivers calicheamicin toxin into leukemia cells.
Side effects. Low counts, liver toxicity (including veno-occlusive disease), infusion reactions.

6) Midostaurin (Rydapt®) – FLT3 inhibitor
Dose/time. 50 mg orally twice daily with food on days 8–21 during each induction and consolidation cycle; sometimes continued as single-agent maintenance. For newly diagnosed FLT3-mutated AML with 7+3. U.S. Food and Drug AdministrationFDA Access Data
Purpose. Improves survival in FLT3-mutated AML when added to chemo.
Mechanism. Blocks FLT3 signaling that drives blast growth.
Side effects. Nausea, vomiting, low counts; drug–drug interactions via CYP3A4 require careful review. Cancer Network

7) Quizartinib (Vanflyta®) – FLT3-ITD inhibitor
Dose/time. Oral once daily with standard anthracycline/cytarabine induction and cytarabine consolidation; also as maintenance after consolidation (per FDA label). Stop 7 days before conditioning if proceeding to transplant; not indicated as post-transplant maintenance. U.S. Food and Drug Administrationvanflytahcp.comdaiichisankyo.com
Purpose. Specifically for newly diagnosed FLT3-ITD-positive AML.
Mechanism. Potently inhibits FLT3-ITD signaling.
Side effects. QT prolongation, low counts; ECG monitoring needed.

8) Gilteritinib (Xospata®) – FLT3 inhibitor
Dose/time. 120 mg orally once daily for relapsed/refractory FLT3-mutated AML. U.S. Food and Drug AdministrationPMCFDA Access Data
Purpose. Treats relapse with FLT3 mutation.
Mechanism. Inhibits FLT3 and related kinases.
Side effects. Transaminitis, differentiation syndrome, QT prolongation—your team monitors closely.

9) Ivosidenib (Tibsovo®) – IDH1 inhibitor
Dose/time. With azacitidine for newly diagnosed IDH1-mutated AML in older/unfit adults; also used alone in some settings. Dosing per label and team. U.S. Food and Drug Administration+1
Purpose. Targets IDH1-mutant AML to induce differentiation.
Mechanism. Blocks mutant IDH1 and lowers oncometabolite 2-HG, allowing blasts to mature.
Side effects. Differentiation syndrome, QT prolongation, liver enzyme changes.

10) Olutasidenib (Rezlidhia®) – IDH1 inhibitor
Dose/time. 150 mg orally twice daily until progression or toxicity for relapsed/refractory IDH1-mutated AML. U.S. Food and Drug AdministrationFDA Access Data
Purpose. Option after relapse with IDH1 mutation.
Mechanism. Lowers 2-HG, promotes differentiation.
Side effects. Differentiation syndrome, liver tests changes, fatigue.

11) Enasidenib (Idhifa®) – IDH2 inhibitor
Dose/time. 100 mg orally once daily for relapsed/refractory IDH2-mutated AML. U.S. Food and Drug AdministrationFDA Access DataOncology Nursing Society
Purpose. Treats relapse with IDH2 mutation.
Mechanism. Inhibits mutant IDH2 → reduces 2-HG → differentiation.
Side effects. Differentiation syndrome, indirect hyperbilirubinemia, GI upset.

12) Venetoclax (Venclexta®) – BCL-2 inhibitor (targeted)
Dose/time. In older/unfit newly diagnosed AML, combined with azacitidine or decitabine; FDA granted accelerated approval (2018) and later regular approval for combinations in untreated AML (2020). Grapefruit, Seville orange, and starfruit can dangerously raise drug levels—avoid these foods. U.S. Food and Drug Administration+1 Drugs.com+1
Purpose. Deep responses without intensive chemo.
Mechanism. Blocks BCL-2, making blasts ready to undergo apoptosis.
Side effects. Tumor lysis (needs careful ramp-up), low counts, infections; major interactions with azoles/CYP3A inhibitors. venclexta+1

13) Azacitidine – hypomethylating agent
Dose/time. Given in cycles (often 7 days each month) alone or with venetoclax, or with ivosidenib when IDH1-mutated and unfit for intensive therapy. U.S. Food and Drug Administration+1
Purpose. For people who cannot tolerate intensive chemo; also platform for targeted combos.
Mechanism. Restores normal gene expression by hypomethylation, nudging blasts to mature.
Side effects. Low counts, GI upset, injection-site reactions.

14) Decitabine – hypomethylating agent
Dose/time. Given IV on 5- or 10-day schedules; commonly combined with venetoclax in older/unfit AML. U.S. Food and Drug Administration
Purpose. As above, alternative HMA.
Mechanism/side effects. Similar to azacitidine.

15) All-trans retinoic acid (ATRA, tretinoin) & Arsenic trioxide (ATO) – differentiation therapy for APL (a special AML subtype)
Dose/time. ATRA plus ATO is standard and can cure most people with APL; exact doses are protocol-based. New England Journal of MedicinePMCASH Publications
Purpose. Rapidly treats APL, which is a medical emergency due to bleeding risk.
Mechanism. Forces promyelocytes to mature and lose their harmful properties.
Side effects. Differentiation syndrome, QT prolongation (ATO), liver tests changes; very careful monitoring is required.

Also emerging: Revumenib (Revuforj®) – a menin inhibitor now FDA-approved for relapsed/refractory acute leukemia with KMT2A translocation, including AML; trials and priority reviews are expanding its use (e.g., NPM1-mutant R/R AML). Discuss eligibility with your team. U.S. Food and Drug AdministrationReutersAML Hub

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Dietary “molecular” supplements

Talk to your oncology team before any supplement. Many are not recommended during active chemo; some increase bleeding or interact with drugs. General guidance stresses getting nutrients from food first and using supplements only for clear deficiencies. ScienceDirectAmerican Cancer Society

1. Vitamin D (e.g., 800–2000 IU/day if deficient) – supports bone and immune function; monitor levels to avoid excess.

2. Protein/whey isolate (10–20 g with meals) – helps maintain lean mass when appetite is low.

3. Omega-3 (EPA/DHA) (≈1 g/day with meals) – may help inflammation and appetite; stop before procedures if advised due to bleeding concerns. Evidence in oncology is mixed; food sources preferred. MDPI

4. Glutamine (used for mucositis in some settings; dosing varies like 10 g TID) – benefits are inconsistent; only use if your team recommends.

5. Zinc (RDA 8–11 mg/day; higher only if deficient) – supports taste and wound healing; excess can harm copper balance.

6. Selenium (≤200 mcg/day if deficient) – antioxidant role; avoid high doses during chemo without approval.

7. Ginger (capsules/tea per label) – can ease nausea; watch bleeding risk if combined with anticoagulants.

8. Curcumin/turmeric – anti-inflammatory in lab studies but may interact with chemo/drug metabolism; usually not started during active treatment without approval.

9. Probiotics – generally avoid during neutropenia due to rare bloodstream infections and uncertain benefit in AML. PMCjhoponline.comScienceDirect

10. Electrolyte solutions – for hydration on nausea/diarrhea days; choose low-sugar formulas.

Important food–drug interaction: Avoid grapefruit, Seville oranges, and starfruit with venetoclax (and discuss with other targeted drugs) due to strong interaction risk. Drugs.com+1

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Immunity/regen/stem-cell–related” supportive drugs

(These are supportive, not leukemia killers. Use only when your team prescribes.)

1. Filgrastim (G-CSF) – boosts neutrophils during profound neutropenia; typical dosing ~5 mcg/kg/day SC. Helps shorten infection risk windows (team-directed). Infectious Diseases Society of America

2. Pegfilgrastim – single fixed dose per chemo cycle in some settings to sustain neutrophil recovery; timing around chemo is critical. Infectious Diseases Society of America

3. Sargramostim (GM-CSF) – sometimes used for count recovery or after transplant; dosing is protocol-based. Infectious Diseases Society of America

4. Plerixafor – CXCR4 antagonist used primarily to mobilize stem cells for collection in transplant pathways; dose ~0.24 mg/kg SC per protocol.

5. Eltrombopag / Romiplostim – platelet growth agents used selectively for thrombocytopenia (often off-label in AML; specialist decision).

6. IVIG (intravenous immunoglobulin) – may be used in recurrent, documented infections with low IgG levels after transplant; individualized.

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Procedures/surgeries

1. Allogeneic hematopoietic stem-cell transplant (allo-HSCT)
   Procedure. High-dose chemo (± radiation) to wipe out leukemia and immune cells, then infusion of donor stem cells.
   Why done. Offers the best chance of long-term control/cure for many intermediate/high-risk AML profiles by adding graft-versus-leukemia effect.

2. Leukapheresis (therapeutic apheresis)
   Procedure. Blood runs through a machine that removes excess white cells and returns the rest.
   Why done. Temporary emergency measure for hyperleukocytosis with leukostasis symptoms, while definitive chemo starts; benefit is debated and guideline support is weak-to-conditional, so decisions are individualized. PMC+2PMC+2

3. Central venous catheter/port placement
   Procedure. Small surgery to place a long-term line in a large vein.
   Why done. Allows safe delivery of chemo, transfusions, and blood draws.

4. Lumbar puncture ± intrathecal chemo
   Procedure. Needle into spinal canal to check/ treat CNS involvement when indicated.
   Why done. Diagnose or prevent leukemia in the central nervous system in selected cases.

5. Splenectomy (rare)
   Procedure. Surgical removal of the spleen.
   Why done. Considered in unusual cases of massive splenomegaly causing pain or cytopenias not responding to other treatments.

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Prevention & safety tips

1. Wash hands often; avoid sick contacts and crowded indoor spaces during neutropenia. Infectious Diseases Society of America

2. Follow central-line care exactly.

3. Food safety: eat thoroughly cooked meats/eggs; avoid unpasteurized dairy; rinse produce well.

4. Stay up to date on vaccines as advised by your team (no live vaccines during neutropenia). Infectious Diseases Society of America

5. Use a soft toothbrush; avoid flossing when platelets are very low; report mouth sores early.

6. Move daily but respect count-based activity limits to prevent bleeding or falls.

7. Tell your team about every supplement and over-the-counter drug. American Cancer Society

8. Avoid grapefruit/Seville oranges/starfruit with venetoclax and discuss interactions for other targeted drugs. Drugs.com

9. Keep a fever kit: thermometer at home; know your emergency plan for fever ≥38.0 °C. UpToDate

10. Attend all scheduled blood tests and transfusions.

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When to see a doctor

• Fever ≥38.0 °C (100.4 °F) or chills—this is an emergency during neutropenia. UpToDate

• New bleeding, black stools, blood in urine, nosebleeds that won’t stop.

• Sudden shortness of breath, chest pain, severe headache, confusion, fainting.

• Rapidly rising swelling, pain, or redness around your catheter.

• Little or no urine, severe vomiting/diarrhea, or signs of dehydration.

• Any new rash, yellowing eyes/skin, or severe right-upper-abdominal pain (possible drug toxicity).

• New weakness/numbness, trouble speaking, or severe visual changes.

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What to eat & what to avoid

1. Aim for protein each time you eat: eggs, cooked fish/chicken, legumes, tofu.

2. Choose cooked foods when counts are low; avoid raw/undercooked meats, runny eggs, unpasteurized dairy.

3. Hydrate with water or oral rehydration drinks; sip often if nauseated.

4. Small, frequent meals to fight early fullness and taste changes.

5. Soften foods (soups, yogurt, smoothies) when mouth sores are present.

6. Add calories safely: nut butters, olive oil, avocado (washed, peeled).

7. Limit alcohol—it can worsen low platelets and drug interactions.

8. Avoid grapefruit/Seville oranges/starfruit on venetoclax; discuss for other targeted drugs. Drugs.com

9. Be cautious with herbal supplements—many interact or increase bleeding. American Cancer Society

10. See a dietitian for a personalized plan.

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Frequently Asked Questions

1) Is AML curable?
Yes—many people, especially those who can receive intensive chemo and, when indicated, an allogeneic stem-cell transplant, are cured. Others can live longer with targeted drugs and lower-intensity regimens.

2) What is “7+3” induction?
Seven days of continuous cytarabine plus three days of an anthracycline (like daunorubicin)—the long-standing standard remission-induction for many fit adults. chemoexperts.comEnglish

3) What if my leukemia has FLT3 mutation?
Your team may add a FLT3 inhibitor such as midostaurin (newly diagnosed with 7+3), quizartinib (newly diagnosed FLT3-ITD), or gilteritinib (relapsed/refractory). U.S. Food and Drug Administration+2U.S. Food and Drug Administration+2

4) What if I have an IDH1 or IDH2 mutation?
Ivosidenib (IDH1) with azacitidine in older/unfit newly diagnosed AML, olutasidenib (IDH1) for R/R AML, and enasidenib (IDH2) for R/R AML are approved options. U.S. Food and Drug Administration+2U.S. Food and Drug Administration+2

5) I’m older or cannot tolerate intensive chemo—what then?
Venetoclax plus azacitidine/decitabine is a widely used regimen that improves responses in untreated AML not eligible for intensive induction. U.S. Food and Drug Administration

6) What is APL and why is it special?
Acute promyelocytic leukemia is a distinct AML subtype treated with ATRA + arsenic trioxide, often achieving very high cure rates when managed urgently. New England Journal of Medicine

7) What is differentiation syndrome?
A sudden inflammatory reaction that can occur with IDH inhibitors, ATRA/ATO, or gilteritinib—causes fever, fluid in lungs, low blood pressure. It’s treatable if recognized early; call immediately.

8) Will I need a transplant?
Depends on your genetic risk group, response to treatment, and health. Doctors review transplant risks/benefits after induction results.

9) How are very high white counts handled at diagnosis?
Doctors lower counts quickly using hydroxyurea, urgent chemo, and sometimes leukapheresis for symptoms; the apheresis benefit remains debated and is individualized. PMC+1

10) What infections am I protected against?
Teams use antibacterial/antifungal/antiviral prophylaxis in high-risk neutropenia (per IDSA guidance) and treat any fever immediately with antibiotics. Infectious Diseases Society of AmericaUpToDate

11) Are supplements safe during chemo?
Often not during active treatment—some increase bleeding or block drugs. Always clear supplements with your team first. American Cancer Society

12) Can I exercise?
Yes—gentle, guided exercise is encouraged and improves fatigue and mood. Use platelet and neutrophil-aware safety rules.

13) What about diet?
Aim for cooked, protein-rich meals; safe food handling; and hydration. Avoid grapefruit/Seville oranges/starfruit with venetoclax. Drugs.com

14) What is a menin inhibitor?
A newer class (e.g., revumenib) that targets leukemias with KMT2A rearrangement and is FDA-approved in that setting; trials are expanding to other mutations. U.S. Food and Drug AdministrationReuters

15) What if I cannot tolerate side effects?
Tell your team early. Many side effects are manageable with dose changes, supportive meds, growth factors, transfusions, and rehab.

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: September 07, 2025.

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