<unk>  can be associated with viral exposure and gene mutations. Viral Exposure<unk>  can be associated with exposure to Epstein-Barr virus (EBV) or human T-cell leukaemia virus-1 (HTLV-1). About 30% of PTCL-NOS patients exhibit EBV-infected cancerous T<unk> s, leading to the classification of Epstein-Barr virus-associated peripheral T<unk>  lymphoma not otherwise specified. However, the relationship between EBV and the progression of PTCL-NOS is still under research. About 5% of HTLV-1 carriers would develop the uncommon adult T-cell leukaemia/lymphoma after a long latent period upon infection. HTLV-1 encodes viral proteins to facilitate the proliferation of HTLV-1 infected<unk> s. In the latent period, accumulation of abnormal<unk> s is allowed, leading to adult T-cell leukaemia/lymphoma. Gene Mutations Recent researches identified recurrent mutations that are possibly linked to certain subtypes of<unk> . For example, in patients with AITL, mutations in the Ten Eleven-Translocation 2 (TET2) gene and isocitrate dehydrogenase 2 (IDH2) gene were identified. Inactivation of TET2 gene caused by loss-of-function mutations in mice leads to abnormal haematopoiesis, as well as abnormalities in lymphoid and myeloid lineages. IDH2 mutations alter the function of IDH enzyme, leading to the production of a rare metabolite D-2-hydroxyglutarate, which may drive tumour progression upon accumulation to high level in<unk> s. TET2 and IDH2 mutations can be found in lymphoid tumour<unk> s from some AITL patients, indicating possible linkage between the mutations and that subtype of lymphoma.
Mature T-cell lymphoma
Aggressive lymphoma
Anaplastic large-cell lymphoma
Mixed-cell lymphoma
Pleomorphic T-cell lymphoma
Angioimmunoblastic T-cell lymphoma
Indolent lymphoma
Mantle cell lymphoma