Acute M7 Myeloid Leukemia

Acute M7 myeloid leukaemia is a fast-growing blood cancer. It starts in the bone marrow, the soft centre of bones where blood cells are made. In M7, the cancer cells come from very early megakaryoblasts. These are baby cells that normally grow into megakaryocytes, which make platelets. In M7, these blasts grow out of control. They crowd out normal cells. This causes anaemia (low red cells), infections (low white cells), and bleeding or bruising (low platelets). M7 can happen at any age, but it is more common in infants and children. It can also occur with Down syndrome (called ML-DS), which has special features and often responds to gentler therapy. Doctors diagnose it with blood tests, bone-marrow tests, and special markers on the leukaemia cells. Treatment is urgent and planned by specialists. It may include chemotherapy, targeted drugs, and sometimes stem-cell transplant.

Acute M7 myeloid leukaemia—also called acute megakaryoblastic leukemia (AMKL)—is a rare, fast-growing blood cancer. It starts in very early cells in the bone marrow that should mature into megakaryocytes, the cells that make platelets. In AMKL these starter cells become cancer cells called blasts. The blasts crowd out normal marrow, so red cells, white cells, and platelets all fall. People can feel tired, bruise or bleed easily, and get infections. Doctors confirm AMKL by looking at blood and bone marrow, by testing for special surface proteins of megakaryocytes, and by checking chromosomes and gene changes that drive this disease. Some forms are linked to Down syndrome in young children. PMC+1Nature

---

Another names

Acute M7 myeloid leukaemia; Acute megakaryoblastic leukemia (AMKL); AML-M7 (French-American-British/FAB M7); Megakaryocytic acute myeloid leukaemia; Megakaryoblastic AML; Myeloid leukemia associated with Down syndrome (when megakaryoblastic); AML with t(1;22)(p13;q13) RBM15::MKL1 (a distinct molecular subtype often megakaryoblastic); Pediatric AMKL; Non-Down-syndrome AMKL (non-DS-AMKL); Down-syndrome–associated AMKL (DS-AMKL, ML-DS). These names reflect either the cell type (megakaryocyte), the older FAB category (M7), or modern genetic/clinical groupings used in WHO/ICC classifications. College of American PathologistsNaturePMC

---

Types

1. AMKL associated with Down syndrome (DS-AMKL / ML-DS). Happens in children with trisomy 21, almost always carries a GATA1 mutation, and often follows a transient newborn condition called transient abnormal myelopoiesis (TAM). Prognosis and treatment approach differ from other AMKL. NaturePMC+1

2. Non-Down-syndrome pediatric AMKL. Occurs in infants and young children without trisomy 21. Biologically diverse and commonly driven by fusion genes such as CBFA2T3::GLIS2, RBM15::MKL1 (t(1;22)), NUP98::KDM5A, or KMT2A rearrangements. Outcomes vary by fusion, with CBFA2T3::GLIS2 generally high-risk. PMC+1ScienceDirect

3. Adult AMKL. Very rare. Shows genetic patterns that differ from children and often arises on top of prior bone-marrow disease or fibrosis. ScienceDirectWiley Online Library

4. Therapy-related / secondary AMKL. Develops after prior chemotherapy/radiation or evolves from MDS/MPN; grouped within secondary AML in modern systems. ASH PublicationsVia Medica Journals

5. WHO/ICC molecular entities with megakaryoblastic features. Modern classifications recognize entities such as AML with RBM15::MKL1 and myeloid proliferations associated with Down syndrome, which frequently show megakaryoblastic differentiation. College of American Pathologists

---

Causes

Each item explains what it is and why it matters.

1. Trisomy 21 (Down syndrome). Trisomy 21 changes fetal blood formation and raises AMKL risk dramatically in early childhood. ASH Publications

2. GATA1 mutation (in DS). A truncating mutation in GATA1 cooperates with trisomy 21; it appears in TAM and persists in many ML-DS cases. NaturePMC

3. Transient abnormal myelopoiesis (TAM). A newborn pre-leukemia in DS; a minority later progress to AMKL. PMCNature

4. CBFA2T3::GLIS2 fusion. A cryptic inversion that creates a fusion gene in infants/young children and is linked with aggressive disease. PMCScienceDirect

5. RBM15::MKL1 fusion (t(1;22)(p13;q13)). A hallmark of some infant AMKL; defines a WHO entity. PMC

6. NUP98::KDM5A fusions. Recurrent in pediatric AMKL; associated with poor outcomes in some cohorts. PMC

7. KMT2A (MLL) rearrangements. Common across infant AML; also seen in non-DS AMKL subsets. PMC

8. HOX-gene–related fusions/programs. HOX pathway dysregulation contributes to leukemic self-renewal in subsets of AMKL. PMC

9. RUNX1 germline variants (familial platelet disorder). Inherited RUNX1 changes predispose to myeloid cancers, sometimes with megakaryocytic features. NCBICancer.gov

10. GATA2 deficiency (germline). A bone-marrow failure/predisposition syndrome that can progress to AML. (Broader AML data; mechanism fits megakaryocyte biology.) MDPI

11. ETV6-related thrombocytopenia (germline). Another inherited platelet disorder that increases AML risk. MDPI

12. TP53/Li-Fraumeni spectrum. Germline TP53 variants increase myeloid cancer risk in some families. MDPI

13. Fanconi anaemia. DNA-repair disorder with strong AML predisposition. MDPI

14. Shwachman–Diamond syndrome. Ribosomopathy linked to marrow failure and AML evolution. MDPI

15. Neurofibromatosis type 1 (NF1) and RAS-pathway syndromes. Altered RAS signaling can predispose to myeloid leukemia. MDPI

16. Prior myelodysplastic syndrome (MDS) or myeloproliferative neoplasm (MPN). Evolution to secondary AML can include megakaryoblastic morphology. Via Medica Journals

17. Therapy-related exposure (alkylators, radiation). Prior cytotoxic therapy increases risk of secondary AML. PMC

18. Benzene/industrial toxins (probable). Environmental DNA-damaging agents contribute to AML risk in general populations. MDPI

19. Bone-marrow fibrosis context. AMKL frequently presents with fibrotic marrow, which reflects disease biology and may complicate sampling. PLOS

20. Age-specific hematopoiesis in infancy. The unique fetal/infant marrow environment appears permissive to AMKL-specific fusions and programs. Frontiers

---

Symptoms

1. Easy bruising and skin spots (petechiae). Low platelets mean very small skin bleeds and frequent bruises.

2. Nosebleeds or gum bleeding. Platelet failure and fragile vessels cause mucosal bleeding.

3. Prolonged bleeding from small cuts. Clotting takes longer when platelets are low or dysfunctional.

4. Fatigue and weakness. Fewer red cells carry less oxygen, so daily tasks feel hard.

5. Pale skin or lips. Anaemia reduces normal pink colour.

6. Fever and repeated infections. Normal white cells are crowded out; immunity drops.

7. Bone or joint pain. Marrow packed with blasts pushes on bone linings.

8. Fullness in the left upper belly. A big spleen from blood cell breakdown or blast infiltration can cause this.

9. Swollen liver. The liver may enlarge for similar reasons.

10. Shortness of breath or chest discomfort. Anaemia or very high blast counts can strain the heart and lungs.

11. Headache, confusion, or vision changes. Very high counts can slow blood flow (leukostasis) or bleeding can occur.

12. Poor appetite and weight loss. Cancer-related inflammation and big organs reduce appetite.

13. Skin nodules or rash (leukaemia cutis). Blasts can settle in the skin.

14. Swollen lymph nodes. Less common but can appear with extramedullary spread.

15. Night sweats. Inflammatory signals from cancer can disturb body temperature.

(These are general AML/AMKL symptoms; each person differs.)

---

Diagnostic Tests

A) Physical examination (bedside observations)

1. Vital signs and general look. Pulse, blood pressure, temperature, and how ill the person appears help judge urgency (fever, sepsis risk, bleeding risk).

2. Skin and mucosa check. Doctors look for petechiae, bruises, gum bleeding, and pallor to estimate platelet and red cell failure.

3. Spleen and liver exam. Gentle palpation can detect enlargement, which suggests blood cell breakdown or leukemic infiltration.

4. Lymph-node exam and skin survey. Nodes and skin nodules may indicate disease outside the marrow.

5. Neurologic screen. A quick check for headaches, confusion, weakness, or vision changes flags possible leukostasis or bleeding that needs urgent imaging.

B) “Manual” tests (hands-on clinic maneuvers and quick point-of-care checks)

6. Orthostatic blood-pressure test. Drop in pressure or rise in pulse when standing hints at volume loss from bleeding.

7. Bedside capillary refill and nail-bed pressure test. Slow refill may go with anaemia or shock.

8. Bedside haemoglobin by finger-prick (HemoCue). A rapid manual estimate of anaemia to triage care.

9. Manual spleen percussion/palpation mapping. Tracks size change across visits when ultrasound is not immediately available.

10. Bedside neurological maneuvers. Simple vision and limb strength checks to decide if urgent brain imaging is needed.

C) Laboratory and pathological tests (core of diagnosis)

11. Complete blood count (CBC) with differential. Shows anaemia, low platelets, and circulating blasts.

12. Peripheral blood smear (human-reviewed). A specialist views cell shapes; AMKL blasts can show cytoplasmic blebs and platelet-like features.

13. Coagulation panel (PT/INR, aPTT, fibrinogen, D-dimer). Detects DIC or bleeding risk common in acute leukaemias.

14. Serum chemistries, uric acid, LDH, phosphorus, potassium, creatinine. Look for tumour lysis and organ strain.

15. Bone-marrow aspiration and trephine biopsy with reticulin stain. Confirms marrow involvement and assesses fibrosis, which is frequent in AMKL and may make aspiration “dry taps.” PLOS

16. Flow cytometry immunophenotyping. AMKL blasts show platelet/megakaryocytic markers CD41, CD42b, CD42a, CD61, often with myeloid immaturity markers; this is a key criterion. PMC+1

17. Cytogenetics (karyotype) and FISH. Detects t(1;22) and other rearrangements or monosomies that guide classification and risk. PMC

18. Molecular testing (RT-PCR/NGS). Finds fusions like CBFA2T3::GLIS2, NUP98::KDM5A, KMT2A-r, and other drivers; guides trials and prognosis. PMC+1

19. GATA1 mutation testing (in children with Down syndrome). Confirms ML-DS biology and helps separate ML-DS from other AMLs. Nature

20. Minimal residual disease (MRD) assessment by flow or molecular assays. Tracks how much leukemia remains after treatment and predicts relapse risk (method depends on the immunophenotype/fusion). PMC

Non-pharmacological treatments

Physiotherapy & physical rehabilitation

1) Supervised low-intensity aerobic walking
Description: 10–20 minutes of easy walking most days, adjusted for counts and fatigue. Purpose: reduce fatigue and deconditioning during chemo. Mechanism: gentle aerobic work improves mitochondrial function and blood flow. Benefits: better energy, mood, and sleep; maintains independence.
Safety: stop with fever, dizziness, chest pain, or very low counts as advised.

2) Light resistance training with bands
Description: 2–3 sessions/week using elastic bands for major muscle groups. Purpose: preserve muscle mass. Mechanism: small mechanical load signals muscle protein synthesis. Benefits: strength for daily tasks and fall prevention.
Safety: avoid Valsalva; adjust when platelets are low.

3) Balance and gait training
Description: simple heel-to-toe, side steps, and sit-to-stand under supervision. Purpose: cut fall risk when anaemic or weak. Mechanism: improves proprioception and neuromuscular control. Benefits: fewer injuries and confidence in walking.

4) Range-of-motion and flexibility work
Description: daily gentle stretches of neck, shoulders, hips, ankles. Purpose: prevent stiffness from bed rest. Mechanism: keeps joint capsule and muscle fibres supple. Benefits: less pain, easier dressing and bathing.

5) Breathing training and incentive spirometry
Description: deep breathing, pursed lips, and spirometer use after hospital stays. Purpose: prevent atelectasis and infections. Mechanism: inflates alveoli and clears secretions. Benefits: easier breathing, fewer complications.

6) Energy-conservation and pacing plan
Description: plan chores in small blocks with rest breaks; sit for tasks. Purpose: manage cancer-related fatigue. Mechanism: balances activity with recovery. Benefits: more control over the day; less crash fatigue.

7) Neuropathy-safe foot care and proprioceptive drills
Description: tactile stimulation, towel scrunches, ankle alphabet. Purpose: support nerves affected by chemo (e.g., vinca-like agents in some AML regimens). Mechanism: enhances sensory-motor feedback. Benefits: steadier gait; fewer foot injuries.

8) Gentle yoga chair poses
Description: seated spinal twists, cat-cow, ankle rolls; 10–15 minutes. Purpose: reduce stiffness and anxiety. Mechanism: parasympathetic activation; gentle muscle stretch. Benefits: calmer mood and better flexibility.
Safety: avoid inversions and straining.

9) Postural training for bone-marrow biopsy soreness
Description: heat/ice per team advice; scapular setting; thoracic extension drills. Purpose: reduce local pain and guarding. Mechanism: improves muscle balance and circulation. Benefits: faster return to normal posture.

10) Oedema and bruising-aware limb care
Description: elevation, gentle active pumping, protective sleeves when advised. Purpose: limit swelling and protect fragile skin. Mechanism: aids venous/lymph return. Benefits: comfort and fewer skin tears.

11) Pelvic floor and core activation for cough/strain
Description: diaphragmatic breathing with light pelvic floor engagement. Purpose: support trunk when coughing/vomiting. Mechanism: coordinated pressure management. Benefits: less back pain and strain.

12) Hospital mobility pathway
Description: sit up for meals, short corridor walks with staff. Purpose: prevent deconditioning. Mechanism: interrupts bed-rest cascade. Benefits: maintains independence and appetite.

13) Occupational therapy for ADLs
Description: adaptive tools, shower seats, grab bars, clothing hacks. Purpose: safe self-care with low energy. Mechanism: reduces effort and risk. Benefits: dignity, safety, and less caregiver burden.

14) Oral-mucositis comfort routine
Description: bland rinses (salt/bicarbonate), ice chips during certain infusions per team protocol, soft toothbrush. Purpose: ease mouth sores. Mechanism: reduces local inflammation/nociception. Benefits: better eating and hydration.

15) Sleep hygiene programme
Description: fixed sleep/wake times, dim lights, no screens late, quiet routine. Purpose: improve sleep in hospital/home. Mechanism: resets circadian cues. Benefits: less fatigue and better mood.

Mind-body, “gene/molecular education,” and educational therapy

16) Mindfulness-based stress reduction
Description: 10 minutes/day of guided breath awareness. Purpose: lower anxiety and pain. Mechanism: down-regulates HPA axis; improves attentional control. Benefits: calmer coping and better treatment adherence.

17) Cognitive-behavioural therapy (brief)
Description: short CBT modules for fear of relapse, guilt, and insomnia. Purpose: reshape unhelpful thoughts. Mechanism: cognitive restructuring + behavioural activation. Benefits: better mood and function.

18) Guided imagery for procedures
Description: audio scripts before bone-marrow tests or lumbar puncture. Purpose: reduce procedure distress. Mechanism: shifts attentional focus; lowers sympathetic arousal. Benefits: less pain perception and nausea.

19) Music therapy
Description: patient-chosen relaxing tracks or therapist-led sessions. Purpose: reduce anxiety and improve appetite. Mechanism: limbic modulation; dopamine reward. Benefits: improved quality of life.

20) Psycho-oncology family sessions
Description: brief family meetings about roles, fears, and plans. Purpose: strengthen support network. Mechanism: shared coping strategies. Benefits: fewer conflicts; clearer communication.

21) Genetic and molecular education session
Description: nurse/doctor explains the patient’s subtype and markers. Purpose: informed consent and realistic expectations. Mechanism: knowledge reduces uncertainty. Benefits: better decisions and adherence.

22) Infection-prevention education
Description: hand hygiene, mask use during neutropenia, food safety, central-line care. Purpose: cut infection risk. Mechanism: interrupts pathogen entry. Benefits: fewer hospitalisations.

23) Treatment roadmap coaching
Description: calendar with chemo cycles, labs, transfusions, and goals. Purpose: reduce surprises. Mechanism: visual planning. Benefits: higher confidence and on-time care.

24) Symptom diary and red-flag checklist
Description: daily record of fever, bruising, bleeding, breathlessness, pain, bowel habits. Purpose: early detection. Mechanism: prompts timely calls. Benefits: faster help; safer care.

25) Return-to-activity plan after counts recover
Description: staged increases in walking, light chores, social time. Purpose: safe rehabilitation. Mechanism: graded exposure. Benefits: smoother recovery without overdoing.

---

Drug treatments

(Descriptions are general. Doses vary by age, subtype, organ function, and protocol; paediatric and Down-syndrome regimens are distinct. Do not use these numbers without your oncology team.)

1) Cytarabine (Ara-C)
Class: antimetabolite. Typical use/dose/time: part of induction and consolidation; dosing ranges from low dose (e.g., 100 mg/m²/day by infusion) to high dose (e.g., 1–3 g/m² every 12 h for several days) depending on protocol. Purpose: kill dividing blasts. Mechanism: cytidine analogue that blocks DNA synthesis. Side effects: low counts, mucositis, nausea, liver enzyme rise; at high dose can cause cerebellar toxicity and conjunctivitis (use eye drops as directed).

2) Daunorubicin
Class: anthracycline. Use/dose: often combined with cytarabine during induction; dosing commonly 45–90 mg/m² total per cycle divided over days, per protocol. Purpose: rapid cytoreduction. Mechanism: intercalates DNA and inhibits topoisomerase II. Side effects: myelosuppression, mucositis, hair loss, and dose-related heart toxicity—requires heart monitoring.

3) Idarubicin
Class: anthracycline (alternative to daunorubicin). Use/dose: used in some induction regimens, dosing varies (e.g., 10–12 mg/m² on several days). Purpose: intensify induction. Mechanism: topoisomerase II inhibition. Side effects: low counts, infection risk, cardiotoxicity, orange/red urine discoloration.

4) Etoposide
Class: topoisomerase II inhibitor. Use/dose: sometimes added to induction or consolidation; dosing per protocol (e.g., 100 mg/m²/day for 3–5 days). Purpose: add a different mechanism to kill blasts. Mechanism: prevents DNA repair and replication. Side effects: myelosuppression, nausea, hair loss; rare secondary leukaemia risk with cumulative exposure.

5) High-dose Cytarabine (HiDAC) consolidation
Class: antimetabolite (dose-intensified). Use/dose: post-remission consolidation (e.g., 1–3 g/m² q12h for 3 days per cycle) tailored to age and risk. Purpose: deepen remission. Mechanism: same as cytarabine with higher intracellular Ara-CTP. Side effects: cerebellar changes, eye irritation, profound neutropenia—requires strict monitoring.

6) FLAG-IDA (Fludarabine + Cytarabine + G-CSF + Idarubicin)
Class: multi-agent. Use: for relapsed/refractory AML/AMKL or high-risk disease. Purpose: salvage to achieve remission. Mechanism: fludarabine enhances Ara-C uptake; combination increases DNA damage. Side effects: severe cytopenias, infections; careful supportive care needed.

7) Gemtuzumab ozogamicin
Class: anti-CD33 antibody-drug conjugate. Use/dose: selected CD33-positive AML; dosing is protocol-based in small fractions to reduce liver toxicity. Purpose: targeted kill of CD33-bearing blasts. Mechanism: delivers calicheamicin toxin into leukaemia cells. Side effects: infusion reactions, low counts, veno-occlusive liver disease risk—strict criteria apply.

8) Azacitidine
Class: hypomethylating agent. Use/dose: cycles (e.g., 75 mg/m²/day for 7 days) in older/unfit patients or with venetoclax; sometimes as bridge therapy. Purpose: re-activate tumour suppressor genes and differentiate blasts. Mechanism: DNA methyltransferase inhibition. Side effects: cytopenias, nausea, injection-site reactions.

9) Decitabine
Class: hypomethylating agent. Use/dose: 5- or 10-day cycles per protocol, often with venetoclax. Purpose: similar to azacitidine. Mechanism: hypomethylation and cytotoxicity in S-phase. Side effects: low counts, fatigue, infections.

10) Venetoclax
Class: BCL-2 inhibitor (targeted). Use/dose: commonly combined with azacitidine/decitabine; dose ramp-up over days; avoid strong CYP3A inhibitors/inducers; grapefruit and Seville oranges interact. Purpose: drive leukaemia cell death by blocking anti-apoptosis protein BCL-2. Mechanism: primes mitochondria for apoptosis. Side effects: tumour lysis risk, profound neutropenia, infections—close lab monitoring.

11) Intrathecal methotrexate ± cytarabine
Class: CNS-directed chemo. Use: prophylaxis or treatment when CNS involvement risk is present (per centre policy). Purpose: protect brain and spinal fluid. Mechanism: direct exposure of blasts to chemo in CSF. Side effects: headache, nausea; rare neurotoxicity.

12) Ruxolitinib (selected ML-DS with JAK pathway lesions, investigational/off-label per trial)
Class: JAK1/2 inhibitor. Use: considered in trials or selected cases guided by genetics. Purpose: target overactive JAK–STAT signalling. Mechanism: blocks cytokine signalling that supports blasts. Side effects: cytopenias, infections, liver enzyme rise; must be specialist-led.

13) FLT3 inhibitors (e.g., midostaurin in induction; gilteritinib in relapse if FLT3+)
Class: kinase inhibitors. Use: only if FLT3 mutation is present. Purpose: block FLT3-driven growth. Mechanism: inhibits mutant tyrosine kinase. Side effects: QT prolongation, cytopenias, GI upset; drug-drug interactions.

14) Menin-pathway inhibitors (trial settings for KMT2A-rearranged leukaemia)
Class: epigenetic/complex-disrupting agents. Use: in clinical trials or per approvals that may evolve; specialist centres only. Purpose: reverse KMT2A-driven transcriptional programme. Mechanism: disrupt menin–KMT2A interaction. Side effects: differentiation syndrome risk, cytopenias—requires experienced teams.

15) Allogeneic haematopoietic stem-cell transplantation (HSCT) conditioning medicines
Class: various (e.g., busulfan, cyclophosphamide, fludarabine) used before donor stem cells. Use: high-risk or relapsed AMKL in remission. Purpose: eradicate residual disease and reset marrow with donor cells. Mechanism: myeloablation/immunoablation followed by graft-versus-leukaemia effect. Side effects: infertility risk, infections, organ toxicities; post-transplant graft-versus-host disease prophylaxis required.

---

Dietary “molecular” supplements

(Use only with your oncology team; some increase bleeding/infection risk or interact with medicines.)

1) Vitamin D (correct deficiency)
Dose: per labs (often 800–2000 IU/day; higher short courses if deficient per doctor). Function/mechanism: supports bone health, immune signalling. Notes: monitor levels; avoid excess.

2) Oral nutritional protein supplement (whey/pea)
Dose: 15–25 g protein serving as needed. Function: maintain lean mass for healing. Mechanism: provides amino acids for muscle repair when appetite is low. Caution: check renal function.

3) Omega-3 fish oil (if platelets adequate and doctor approves)
Dose: often 1 g/day EPA+DHA; avoid if bleeding risk high. Function: anti-inflammatory support. Mechanism: influences eicosanoid pathways. Caution: can increase bleeding tendency—often avoided during thrombocytopenia.

4) Ginger for nausea (food or capsule)
Dose: 0.5–1 g/day divided. Function: antiemetic support. Mechanism: 5-HT3 and cholinergic modulation in gut. Caution: may interact with anticoagulants; tell your team.

5) Melatonin (sleep aid)
Dose: 1–3 mg at bedtime. Function: sleep quality. Mechanism: circadian signalling. Caution: daytime drowsiness; check interactions.

6) L-glutamine (mucositis support if approved)
Dose: typical 10 g 2–3×/day short courses under supervision. Function: fuel for gut cells. Mechanism: may reduce mucosal injury. Caution: not for everyone; discuss first.

7) Thiamine (B1) if low intake
Dose: per doctor (e.g., 50–100 mg/day if deficient risk). Function: energy metabolism. Mechanism: cofactor for carbohydrate enzymes. Caution: supplement only if indicated.

8) Zinc (only if deficient)
Dose: 8–11 mg/day elemental; short therapeutic courses if low. Function: wound repair and taste recovery. Mechanism: enzyme cofactor. Caution: excess harms copper balance.

9) Prophylactic probiotics – generally avoid in neutropenia
Note: live probiotics can cause bloodstream infection when neutrophils are very low. Safer approach: fermented foods only when counts recover and team approves. Function: gut comfort; Mechanism: microbiome; Caution: often contraindicated during treatment.

10) Multivitamin without iron (if diet poor)
Dose: once daily. Function: broad micronutrient back-up. Mechanism: covers small gaps. Caution: avoid high-dose antioxidants during chemo unless your team agrees.

---

Immunity/regenerative/stem-cell” related medicines

(These are not anti-cancer chemo; they support recovery or are part of transplant care. Use only under specialist care.)

1) Filgrastim (G-CSF)
Dose: weight-based daily injections after chemo as directed. Function: speed neutrophil recovery. Mechanism: stimulates marrow to make neutrophils. Caution: bone pain; rare splenic effects.

2) Pegfilgrastim (long-acting G-CSF)
Dose: single injection per cycle at the right time. Function: same as G-CSF with longer action. Caution: timing matters to avoid worsened cytopenia.

3) Sargramostim (GM-CSF)
Dose: per protocol. Function: broader myeloid recovery. Mechanism: stimulates granulocytes/monocytes. Caution: fever, fluid retention.

4) Intravenous immunoglobulin (IVIG)
Dose: intermittent infusions when recurrent infections and low IgG. Function: passive immunity support. Mechanism: pooled antibodies. Caution: headaches, thrombosis risk; renal monitoring.

5) Plerixafor (mobilisation agent in selected settings)
Function: mobilises stem cells to bloodstream for collection (mostly autologous; AML usually needs allogeneic graft). Mechanism: CXCR4 antagonist. Caution: used rarely in AML; specialist decision.

6) Allogeneic HSCT (donor stem-cell infusion) – cellular therapy
Function: replaces diseased marrow with donor cells; provides graft-versus-leukaemia effect. Mechanism: donor immune system attacks residual blasts. Caution: graft-versus-host disease, infections; long-term follow-up essential.

---

Procedures / “Surgeries

1) Central venous catheter/port placement
Procedure: small operation to place a reliable line. Why: safe chemo, blood draws, transfusions, antibiotics.

2) Bone-marrow aspiration and biopsy
Procedure: needle sample from hip bone. Why: diagnose, measure minimal residual disease, check response.

3) Lumbar puncture ± intrathecal chemo
Procedure: needle into spinal fluid under sterile care. Why: look for CNS disease and give protective chemo.

4) Leukapheresis (selected hyperleukocytosis cases)
Procedure: machine removes excess white cells. Why: reduce viscosity and complications before chemo.

5) Splenectomy (rare, highly selected)
Procedure: remove spleen. Why: only if massive spleen causes pain, rupture risk, or severe cytopenias not otherwise managed; very uncommon in AMKL.

---

Preventions (practical)

1. Hand hygiene and mask use during neutropenia.

2. Food safety: fully cook meats/eggs; avoid unpasteurised dairy and raw sprouts.

3. Central-line care: clean technique, daily check for redness.

4. Oral care: soft brush, bland rinses; avoid alcohol mouthwashes.

5. Vaccines: family members up to date; patient vaccines timed per oncology plan after therapy.

6. Avoid crowds and sick contacts when counts are low.

7. Sun protection (some drugs increase sensitivity).

8. Fertility counselling and contraception before and during therapy.

9. Smoking cessation and alcohol minimisation.

10. Medication list review: avoid interactions (e.g., with venetoclax, azoles, grapefruit).

---

When to see doctors urgently

• Fever ≥ 38.0 °C (100.4 °F) once, or any chills.

• New bleeding, nosebleeds that will not stop, black/tarry stools, or red urine.

• Shortness of breath, chest pain, severe headache, confusion, new weakness, or fainting.

• Rapid belly swelling, severe left-upper-abdomen pain (spleen), or sudden severe bone pain.

• Central-line redness, pus, or pain.

• Little urine, dizziness, or swelling after starting potent drugs (tumour lysis signs).

• Any symptom your team said is a “red flag”.

---

What to eat and what to avoid

Eat: soft, cooked foods; tender meats, eggs well cooked, fish well cooked; mashed potatoes, rice, pasta; cooked vegetables and peeled/cooked fruits; yoghurt that is pasteurised; soups and stews; nut butters; oatmeal; plenty of safe fluids. Small frequent meals help. Use oral nutrition drinks if appetite is low (team-approved).

Avoid (especially during neutropenia): raw or undercooked meats, fish, or eggs; sushi; unpasteurised milk/cheese/juice; raw sprouts; salad bars; mould-ripened cheeses; well water unless boiled; alcohol beyond small amounts; grapefruit/Seville oranges with venetoclax or some targeted drugs; large herbal or antioxidant megadoses without approval; live probiotics during severe neutropenia.

---

Frequently asked questions

1) Is M7 different from other AML?
Yes. It starts from megakaryoblasts (platelet-making cells). It behaves differently and needs expert care.

2) Is M7 curable?
Many patients reach remission, and some are cured, especially with good-risk biology or with transplant when indicated. Results vary by age and subtype.

3) Why do people with Down syndrome get special treatment plans?
Their blasts are more sensitive to some drugs, and they may have higher side-effect risks, so gentler regimens can still work well.

4) How do doctors choose my plan?
They look at age, fitness, genetics of the leukaemia, and early treatment response. Plans follow protocols tested in trials.

5) Will I need a transplant?
Only if risk is high, disease comes back, or your team believes it gives the best chance of cure. Not everyone needs one.

6) What are the biggest dangers during treatment?
Infections, bleeding, and organ toxicities. Quick reporting of fever or bleeding saves lives.

7) Can exercise help?
Yes—gentle, supervised activity can reduce fatigue and keeps you stronger. Only do what your team allows.

8) What about vitamins or herbs?
Use only what your team approves. Some supplements raise bleeding risk or block your cancer drugs.

9) Why so many blood tests?
They track counts, kidney/liver function, and signs of tumour lysis or drug effects so the team can adjust care quickly.

10) What is “minimal residual disease” (MRD)?
Very small amounts of leukaemia left after treatment, found by sensitive tests. MRD helps guide next steps.

11) Will my hair fall out?
Many AML drugs cause hair loss. It usually grows back after treatment ends.

12) Can I get vaccines?
Timing matters. Inactivated vaccines are given at specific times; live vaccines are delayed. Your team will schedule them.

13) What is tumour lysis syndrome?
When many cancer cells die quickly and spill contents into blood. It can harm kidneys and heart. Labs and fluids prevent it.

14) How long is treatment?
Induction is weeks; consolidation cycles may take months. Transplant adds more time. Plans are personalised.

15) How can family help?
Help with transport, meals, infection control, and emotional support. Learn the red-flags and the medication schedule.

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 06, 2025.

PDF Documents For This Disease Condition References