Table 2. Examples of mouse models underscoring telomere dysfunction as either a driving force in cancer development or as a cancer suppressor
GenotypeCancer phenotypeReference
Terc−/− p53−/−      Earlier onset lymphoma/sarcoma, epithelial carcinomaChin et al., 1999
Terc−/− Msh2−/−      Lymphoma/carcinomaMartinez et al., 2009a
Trf1lox/lox K5-cre p53−/−      Squamous cell carcinomaMartínez et al., 2009b
Pot1alox/lox p53lox/lox hCD2-iCre      T cell lymphomasPinzaru et al., 2016
Pot1alox/lox p53lox/lox Sprr2f-Cre      Endometrial adenocarcinomasAkbay et al., 2013
Tpp1Acd p53−/−      CarcinomasElse et al., 2009
Tpp1lox/lox K5-cre p53−/−      Cancer suppressorTejera et al., 2010
Terc−/− Ink4a/Arf−/−      Delayed lymphoma/fibrosarcoma onsetKhoo et al., 2007
Trf1lox/lox p53−/− K-RasLSLG12V      Growth impairment of lung carcinomaGarcía-Beccaria et al., 2015

The effects of telomere dysfunction in cancer-prone mouse models depend on the status of DNA damage surveillance mechanisms, acting oncogenes, and tissue-specific factors.