[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [General pathology](https://durgical.com/en/general-pathology/) › [White cells, lymph nodes, spleen and thymus](https://durgical.com/en/general-pathology/areas/hematolymphoid/) › Chronic myeloid leukaemia

# Chronic myeloid leukaemia

- Lesion

One swapped chromosome makes a kinase that never switches off. The blood fills with granulocytes, the spleen swells, and tablets now control it.

Updated Nov 12, 2026

## Key points

- t(9;22)(q34;q11) BCR::ABL1; the CML protein is usually 210 kDa, while many Ph-positive ALLs carry a smaller, stronger 190 kDa form.
- Blood: marked leukocytosis with granulocytes at every stage (myelocytes and neutrophils most), basophilia and eosinophilia, blasts few.
- Huge spleen with extramedullary haematopoiesis and subcapsular infarcts.
- Blast crisis: about two-thirds myeloid, most of the rest pre-B lymphoid.
- Leukaemoid reaction lacks basophilia and BCR::ABL1.

On this page

- The basics Key points
- What it is
- Structure
- Step by step
- CML vs leukaemoid reaction
- Markers
- Memory aid
- Elsewhere in DurgiPedia

- Clinical Clinical notes

- Study Test yourself

- Connections Connections

## What it is

Chronic myeloid leukaemia (CML) arises in a pluripotent stem cell carrying the Philadelphia chromosome, t(9;22), which creates the BCR::ABL1 fusion tyrosine kinase. The kinase drives growth-factor-independent proliferation, mostly of granulocytic and megakaryocytic progenitors, with release of immature forms. Untreated, a chronic phase lasting a few years gives way to an accelerated phase and blast crisis, which can be myeloid or lymphoid because the disease starts in a stem cell. Kinase inhibitors have transformed the outlook.

## Structure

- Marrow: close to 100% cellular, mostly maturing granulocytes; megakaryocytes increased, often small; scattered sea-blue histiocytes.
- Spleen: red pulp full of granulocytic precursors, resembling marrow; infarcts are common.
- Blood smear: the whole granulocytic maturation sequence plus basophils.

## Step by step

- A stem cell acquires t(9;22), forming BCR::ABL1.
- The fusion kinase activates RAS–MAPK, PI3K–AKT and STAT pathways without growth factors.
- Granulocytic and megakaryocytic output rises; immature cells leave the marrow early.
- Extramedullary haematopoiesis enlarges spleen and liver.
- Additional mutations block differentiation: accelerated phase, then blast crisis.

## CML vs leukaemoid reaction

| Feature | Chronic myeloid leukaemia | Leukaemoid reaction |
| --- | --- | --- |
| Basophils and eosinophils / BCR::ABL1 | Increased basophils and eosinophils; BCR::ABL1 present | Not increased; BCR::ABL1 absent |
| Cause and course | Clonal stem cell neoplasm; progressive | Severe infection or tumour; resolves with the cause |

## Markers

- BCR::ABL1 by PCR or FISH
- Philadelphia chromosome on karyotype

## Clinical notes

- Fatigue, weight loss, left upper quadrant dragging from a big spleen in a middle-aged adult.
- Daily oral BCR::ABL1 kinase inhibitors give long survival; resistance comes from kinase mutations, handled with later-generation inhibitors.
- Molecular monitoring of BCR::ABL1 transcripts tracks response; some patients in deep remission can stop treatment.

## Memory aid

Philadelphia, nine twenty-two: a kinase that never sleeps, a spleen that never stops growing, and a pill that finally tames it.

## Test yourself

Think of the answer, then tap the question to see it.

## Why can CML blast crisis be lymphoid?

The disease starts in a pluripotent stem cell that can give rise to both myeloid and lymphoid cells.

## Which blood finding helps separate CML from a leukaemoid reaction?

Basophilia (and eosinophilia), together with the BCR::ABL1 fusion.

## Which phase follows untreated chronic phase CML?

An accelerated phase and then blast crisis, an acute leukaemia.

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## Elsewhere in DurgiPedia

- [White blood cells: types and functions](https://durgical.com/en/physiology/white-blood-cells-types-and-functions/)

## Connections

## Related 5

- [Oncogenes: RAS, MYC, HER2, BCR-ABL and the table to know](https://durgical.com/en/general-pathology/oncogenes-ras-myc-her2-bcr-abl-and-the-table-to-know/)
- [Myeloproliferative neoplasms: overview](https://durgical.com/en/general-pathology/myeloproliferative-neoplasms-overview/)
- [Reactive leukocytosis](https://durgical.com/en/general-pathology/reactive-leukocytosis/)
- [Acute lymphoblastic leukaemia/lymphoma](https://durgical.com/en/general-pathology/acute-lymphoblastic-leukaemia-lymphoma/)
- [Splenomegaly and hypersplenism](https://durgical.com/en/general-pathology/splenomegaly-and-hypersplenism/)

## Related conditions 2

- [Chronic myeloid leukaemia](https://durgical.com/en/conditions/chronic-myeloid-leukaemia/)
- [Acute leukaemia (AML and ALL)](https://durgical.com/en/conditions/acute-leukaemia/)

[← All of general pathology](https://durgical.com/en/general-pathology/)

Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: [Chronic Myeloid Leukemia Treatment (PDQ®)–Patient Version](https://www.cancer.gov/types/leukemia/patient/cml-treatment-pdq) (National Cancer Institute (NCI), 2026); [Chronic myeloid leukemia: MedlinePlus Genetics](https://medlineplus.gov/genetics/condition/chronic-myeloid-leukemia/) (MedlinePlus, US National Library of Medicine, 2026).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/general-pathology/chronic-myeloid-leukaemia/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/chronic-myeloid-leukaemia/