Table 1.
Human cancer cell-derived iPSC lines.
| CANCER TYPES | CELL LINE OR PRIMARY CELLS | REPROGRAMMING METHOD | CELLULAR PHENOTYPES | REFERENCE |
|---|---|---|---|---|
| Melanoma | Colo | Retroviral mir-302s | Reduced migration ability in iPSCs; reduced cell cycle-related gene expression in iPSCs | 15 |
| Prostate cancer | PC-3 | |||
| Melanoma | R545 | Lentiviral OCT4, KLF4, and c-MYC | SOX2 was dispensable for reprogramming melanocytes and melanoma cells | 16 |
| Chronic myeloid leukemia (blast crisis stage) | KBM7 | Retroviral OSKM | Acquired insensitivity to imatinib; loss of BCR-ABL dependency in iPSCs but restored after differentiation | 18 |
| Colorectal cancer | DLD-1, HT-29 | Combination of retroviral or lentiviral OSKM, NANOG, LIN28, BCL2, KRAS, and shRNA for tumor suppressors optimized for each cell line | Acquired sensitivity to chemotherapy in embryoid body cells; reduced invasion and tumorigenicity of embryoid body cells; higher expression of p16 and p53 of embryoid body cells compared to the parental cells | 17 |
| Esophageal cancer | TE-10 | |||
| Gastric cancer | MKN45 | |||
| Hepatocellular cancer | PLC | |||
| Pancreatic cancer | MIAPaCa-2, PANC-1 | |||
| Cholangiocellular cancer | HuCC-T1 | |||
| Chronic myeloid leukemia (chronic phase) | Patient-derived bone marrow cells | Episomal OSKM, NANOG, LIN28, SV40 LT | BCR–ABL fusion iPSCs maintained patient-specific complex karyotype | 24 |
| Lung cancer | A549 | Lentiviral OSNL and nondegradable HIFα | Increase tumorigenic properties of iPSCs in mice; more aggressive and invasive iPSCs | 19 |
| Chronic myeloid leukemia (chronic phase) | Patient-derived bone marrow cells | Retroviral OSKM | CML-iPSCs were insensitive to imatinib but still expressed BCR–ABL; recovered imatinib sensitivity after hematopoietic differentiation | 25 |
| Breast cancer | MCF-7 | Retroviral OSKM | MCF-7/Rep iPSCs did not fully reprogram, and overexpressed Sox2; displayed cancer stem cell features such as high ALDH activity and CD44 expression | 20 |
| Juvenile myelomonocytic leukemia (JMML) | Patient-derived mononuclear cells with E76K missense in PTPN11 gene | Lentiviral OSKM | Increased proliferative capacity, constitutive activation of GM-CSF, enhanced STAT5/ERK phosphorylation in myeloid cells differentiated from JMML iPSCs | 26 |
| Pancreatic ductal adenocarcinoma (PDAC) | Patient-derived pancreatic ductal adenocarcinoma | Lentiviral OSKM | Teratomas from PDAC iPSC-like cells undergo early to invasive stages of human cancer | 27 |
| Glioblastoma multiforme (GBM) | GBM neural stem (GNS) cell lines | PiggyBac driving OCT4 and KLF4 | GNS-iPSCs differentiated to neural progenitors displayed widespread resetting of GBM-associated epigenetic changes, but still remained malignant upon xenotransplantation | 21 |
| Osteosarcoma | SAOS2, HOS, MG63 | Lentiviral OSKM, NANOG, LIN28 | Sarcoma-iPSCs were less tumorigenic compared to parental sarcoma cell lines and could be terminally differentiated into mature connective tissue and red blood cells; terminal differentiation irreversibly abolished their tumorigenic potential | 22 |
| Liposarcoma | SW872 | |||
| Ewing’s sarcoma | SKNEP | |||
| Myelodysplastic syndromes (MDS) | Two patients with del(7q)-MDS | Lentiviral OSKM | MDS-iPSCs recapitulated disease-associated phenotypes, including impaired hematopoietic differentiation | 28 |
| Li Fraumeni syndrome (LFS) | Three patients with G245D missense in p53 gene | Sendai viral OSKM | LFS-iPSCs recapitulated features of osteosarcoma associated with LFS, including defective osteoblastic differentiation as well as tumorigenic ability | 29 |
| Ewing sarcoma (EWS) | CHLA-10 | Episomal OKSM | EWS-iPS cells sustained expression of the EWS-FLI1 fusion transcript; gave rise to tumors with characteristic Ewing histopathology and demonstrated recovery of drug sensitivity following differentiation | 30 |