Renal cell carcinoma |
Ongoing clonal evolution; de-differentiation and ploidy status |
Progenitor cells of metastasis and primary tumor cells |
5, 15 |
Oral squamous cell carcinoma |
Drug transporter proteins and ploidy status |
Transient shift between multiple tumorigenic fractions |
16 |
Breast cancer |
Evolution of six distinct PTEN mutations |
Selective enrichment of metastatic, therapy resistant clones |
19 |
Ovarian serous adenocarcinoma |
Mutant mitochondrial DNA profile in tumorigenic CSC clones |
19 immortalized stem and progenitor clones from single tumor sample |
21 |
Colon cancer |
Deletion of APC gene |
Intestinal stem cells form adenomas; transient amplifying cells result in microadenomas |
24 |
Prostate cancer |
MYC amplification and PTEN loss |
Well-differentiated acinar adenocarcinoma, androgen receptor (AR) and prostate-specific antigen (PSA) positive originated from Luminal epithelial cells; Basal epithelial cells generated more aggressive tumors and low/absent AR and PSA expression |
25 |
Papillary thyroid carcinoma |
Senescent-associated secretory phenotype (SASP). |
Promote collective invasion of non-senescent tumor cells |
41 |
Leukemia |
BCR-ABL-independent mechanisms |
Survival of leukemic stem cells (LSCs) Minimal residual disease or Persister cells with increased stem cell characteristics and quiescence |
60 |
Pancreatic ductal adenocarcinoma (PDAC) |
High CD9 expression; high glutamine uptake and cell surface expression of the glutamine transporter ASCT2 |
Tumor-initiating cells (TICs) enhanced tumorigenicity. |
62 |
Ovarian cancer |
Transdifferentiation to tumor-derived endothelial cells, pericytes and lymphatic endothelial cells |
Ovarian CSCs |
63 |
Glioblastoma (GBM) |
Transdifferentiation into Tumor Derived Endothelial Cells (TDEC) |
GBM stem-like cells (GSC) |
64 |