[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/) › White-cell neoplasms: causes and translocations

# White-cell neoplasms: causes and translocations

- Mechanism

Leukaemias and lymphomas start with genetic accidents, often swapped chromosome pieces, helped along by genes, viruses, inflammation and past treatment.

Updated Nov 12, 2026

## Key points

- Lymphoma translocations often join an oncogene to an immunoglobulin locus, the result of errors during class switching or somatic hypermutation (the enzyme AID).
- Inherited risk: Down syndrome, Fanconi anaemia, Bloom syndrome, ataxia–telangiectasia and neurofibromatosis type 1.
- Viruses: HTLV-1 (adult T-cell leukaemia/lymphoma), EBV (Burkitt, Hodgkin, immunodeficiency lymphomas, NK/T lymphoma), HHV-8 (primary effusion lymphoma).
- Chronic inflammation: H. pylori and gastric MALT lymphoma, coeliac disease and intestinal T-cell lymphoma, breast implants and an anaplastic T-cell lymphoma.
- Prior alkylating agents or radiation cause therapy-related myeloid neoplasms; smoking modestly increases AML risk.

## What it is

Most white-cell neoplasms carry recurrent genetic lesions, and balanced chromosomal translocations are especially typical. They either block differentiation (transcription factor fusions) or switch on growth and survival signals (tyrosine kinases, MYC, BCL2). Several factors raise the risk: inherited genomic instability or Down syndrome, lymphotropic viruses, chronic antigen stimulation at a tissue site, earlier chemotherapy or radiation, and tobacco smoke.

## Step by step

- A progenitor or lymphocyte acquires a first lesion, often a translocation or a mutation in a transcription factor or epigenetic regulator.
- Differentiation is partly blocked, so the cell keeps dividing at an immature stage.
- A second class of mutation activates signalling (tyrosine kinases, RAS pathway) or blocks apoptosis.
- Viruses or chronic antigen stimulation keep the cell population large, raising the chance of new mutations.
- Immune deficiency removes the T cells that would destroy virus-infected clones.
- A fully transformed clone expands and replaces the marrow or a lymphoid organ.

## Translocations of haematolymphoid neoplasms to know

| Translocation | Genes joined | Effect | Neoplasm |
| --- | --- | --- | --- |
| [t(9;22), the Philadelphia chromosome](https://durgical.com/en/conditions/chronic-myeloid-leukaemia/) | BCR::ABL1 | Constitutive tyrosine kinase | Chronic myeloid leukaemia; a subset of B-ALL |
| [t(12;21)](https://durgical.com/en/conditions/acute-leukaemia/) | ETV6::RUNX1 | Abnormal transcription factor, maturation block | Childhood B-ALL (good prognosis) |
| t(14;18) | IGH::BCL2 | Anti-apoptotic BCL2 overexpressed | Follicular lymphoma |
| [t(8;14)](https://durgical.com/en/conditions/non-hodgkin-lymphoma/) | MYC::IGH | MYC overexpressed, very fast growth | Burkitt lymphoma |
| t(11;14) | CCND1::IGH | Cyclin D1 overexpressed, G1 to S push | Mantle cell lymphoma (also some myelomas) |
| t(11;18) | BIRC3::MALT1 | Constant NF-κB activation | Gastric MALT lymphoma that no longer responds to H. pylori eradication |
| [t(15;17)](https://durgical.com/en/conditions/acute-leukaemia/) | PML::RARA | Retinoic acid receptor blocks maturation | Acute promyelocytic leukaemia |

## Clinical notes

- Translocations are detected by karyotype, FISH or PCR and guide both diagnosis and targeted therapy (kinase inhibitors, retinoic acid).
- HTLV-1 is endemic in parts of the Colombian Pacific coast, the Caribbean basin and southern Japan.

## Memory aid

Nine twenty-two kinases, fourteen eighteen survives, eight fourteen sprints, eleven fourteen cycles, fifteen seventeen bleeds.

## Test yourself

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

## Why are translocations to the immunoglobulin heavy-chain locus so common in B-cell lymphomas?

Class switching and somatic hypermutation deliberately break and mutate DNA at that locus (through AID), so errors can join it to an oncogene.

## Which virus causes adult T-cell leukaemia/lymphoma?

HTLV-1.

## Which translocation underlies acute promyelocytic leukaemia?

t(15;17), forming the PML::RARA fusion gene.

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[More Pathology questions →](https://durgical.com/en/practice/?f=pathology)

## Elsewhere in DurgiPedia

- [B-cell activation, class switching and affinity maturation](https://durgical.com/en/immunology/b-cell-activation-class-switching-and-affinity-maturation/)
- [How HIV destroys CD4 T cells](https://durgical.com/en/immunology/how-hiv-destroys-cd4-t-cells/)

## Connections

## Related 7

- [Translocations, amplifications and epigenetic changes in cancer](https://durgical.com/en/general-pathology/translocations-amplifications-and-epigenetic-changes-in-cancer/)
- [Oncogenic viruses and H. pylori: the table to know](https://durgical.com/en/general-pathology/oncogenic-viruses-and-h-pylori-the-table-to-know/)
- [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/)
- [Tobacco: how smoking injures tissue](https://durgical.com/en/general-pathology/tobacco-how-smoking-injures-tissue/)
- [Radiation and cancer: ultraviolet and ionizing](https://durgical.com/en/general-pathology/radiation-and-cancer-ultraviolet-and-ionizing/)
- [White-cell neoplasms: classification](https://durgical.com/en/general-pathology/white-cell-neoplasms-classification/)
- [Gastrointestinal lymphoma](https://durgical.com/en/general-pathology/gastrointestinal-lymphoma/)

## Related conditions 11

- [Down syndrome (trisomy 21)](https://durgical.com/en/conditions/down-syndrome/)
- [Fanconi anaemia](https://durgical.com/en/conditions/fanconi-anaemia/)
- [Ataxia-telangiectasia](https://durgical.com/en/conditions/ataxia-telangiectasia/)
- [Helicobacter pylori gastritis](https://durgical.com/en/conditions/helicobacter-pylori-gastritis/)
- [Coeliac disease](https://durgical.com/en/conditions/coeliac-disease/)
- [HIV infection and AIDS](https://durgical.com/en/conditions/hiv-infection-and-aids/)
- [Sjögren disease](https://durgical.com/en/conditions/sjogren-disease/)
- [Acute leukaemia (AML and ALL)](https://durgical.com/en/conditions/acute-leukaemia/)
- [Non-Hodgkin lymphoma](https://durgical.com/en/conditions/non-hodgkin-lymphoma/)
- [Chronic myeloid leukaemia](https://durgical.com/en/conditions/chronic-myeloid-leukaemia/)
- [Kaposi sarcoma](https://durgical.com/en/conditions/kaposi-sarcoma/)

## Microorganisms 5

- [Epstein–Barr virus](https://durgical.com/en/microbiology/epstein-barr-virus/)
- [Human T-lymphotropic virus type 1](https://durgical.com/en/microbiology/human-t-lymphotropic-virus-type-1/)
- [Human herpesvirus 8](https://durgical.com/en/microbiology/human-herpesvirus-8/)
- [Helicobacter pylori](https://durgical.com/en/microbiology/helicobacter-pylori/)
- [Human immunodeficiency virus](https://durgical.com/en/microbiology/human-immunodeficiency-virus/)

[← 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: [Non-Hodgkin Lymphoma Treatment (PDQ®)–Patient Version](https://www.cancer.gov/types/lymphoma/patient/adult-nhl-treatment-pdq) (National Cancer Institute (NCI), 2026); [Acute Myeloid Leukemia Treatment (PDQ®)–Patient Version](https://www.cancer.gov/types/leukemia/patient/adult-aml-treatment-pdq) (National Cancer Institute (NCI), 2026).

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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/white-cell-neoplasms-causes-and-translocations/