Leukaemia (Leukemia)
Leukaemia — Cancer of the Blood-Forming System
From the Philadelphia chromosome to imatinib, BTK inhibitors, venetoclax, and CAR-T — eight integrating modules in molecular haematology.
Why a course on leukaemia?
Leukaemia is the prototype of malignancy as a clonal, molecularly-driven disease. With roughly 470,000 new cases each year worldwide, it is not the largest cancer by incidence — but it has driven a wildly disproportionate share of the field’s conceptual revolutions. The Philadelphia chromosome (1960) was the first cancer-specific genetic lesion ever identified. Imatinib (2001) was the first rationally-designed targeted oncology drug. Tisagenlecleucel (2017) was the first FDA-approved CAR-T cell therapy. Venetoclax was the first BCL2-selective therapeutic.
The course traces the four classical leukaemias — AML, ALL, CML, CLL — from their cells of origin in the haematopoietic hierarchy through their molecular drivers to modern targeted therapy and stem-cell transplant. It cross-references Cancer, Cancer / genetic basis, DNA repair, Cancer therapy, Pharmacology, and Cell Physiology.
Course Parts
Overview & Epidemiology
Cancer of haematopoietic cells; the four major types (AML, ALL, CML, CLL); ~470,000 new cases/year globally; pediatric ALL peak, adult AML at median 70, elderly CLL; Bennett & Virchow 1845.
Normal Haematopoiesis
HSC hierarchy, myeloid vs lymphoid commitment, the marrow niche, growth factors (G-CSF, EPO, TPO, IL-3), key TFs (RUNX1, GATA1, PU.1, CEBPA).
Acute Leukaemias (AML & ALL)
Blast morphology, FAB and 2022 WHO/ICC classification, FLT3-ITD/NPM1/IDH1/2 in AML, Ph+ and Ph-like ALL, BCR-ABL1, ETV6-RUNX1, KMT2A rearrangements.
Chronic Leukaemias (CML & CLL)
CML — t(9;22), BCR-ABL fusion, three phases, the imatinib revolution. CLL — IGHV mutated/unmutated, ZAP-70, del 17p, Rai/Binet staging.
Genetics & Molecular Drivers
Cytogenetics, the Philadelphia chromosome (Nowell & Hungerford 1960), translocations and fusion proteins, TET2/DNMT3A/ASXL1/NOTCH1/TP53, clonal haematopoiesis (CHIP).
Diagnosis
Peripheral blood smear, bone-marrow biopsy, flow-cytometry immunophenotyping, FISH, NGS panels, qPCR for BCR-ABL, MRD by flow / ddPCR / NGS.
Therapy
7+3 induction, midostaurin/gilteritinib, venetoclax + azacitidine, BFM ALL regimens, TKIs through ponatinib, BTKi, anti-CD20, blinatumomab, inotuzumab, CAR-T (tisagenlecleucel).
Stem-Cell Transplant & MRD
HLA matching, allo vs auto, conditioning intensity, GvHD vs GvL, MRD as the new endpoint, "operational cure" in CML, MRD-guided therapy.
What you’ll learn
- Distinguish AML, ALL, CML, and CLL clinically and morphologically.
- Trace the haematopoietic hierarchy from HSC to mature blood cells.
- Read flow-cytometry plots and immunophenotyping reports.
- Reason about FLT3-ITD, NPM1, BCR-ABL1, IGHV, TP53 risk stratification.
- Apply WHO/ICC 2022 classification of myeloid and lymphoid neoplasms.
- Counsel a CML patient on imatinib vs second-generation TKI choice.
- Interpret MMR, MR4, MR4.5 monitoring milestones in CML.
- Anticipate cytokine release syndrome and ICANS after CAR-T infusion.
Prerequisites
Working knowledge of basic immunology, cell-cycle and apoptosis biology, and core cancer genetics. The course cross-references Cancer, Cell Physiology, and Pharmacology.