Table I.
Relevant experimental models and results (literature is presented in chronological order).
| Author's/year | Experimental model | Description and results | (Refs.) |
|---|---|---|---|
| Braun, 1959 | Graft of tumor cells into healthy and/or growing tissues | Succession ofgrafts of plant teratoma clonal cells on healthy tobacco plant. Disappearance of the teratoma and plant generation with seeds capable of giving life to a new plant | (26) |
| Pierce, 1961 | Transplantation of Murine Embryonic Tumor Cells into mice healthy tissues results in cancer cells differentiation re- | (16) | |
| Macpherson, 1965 | Hamster sarcoma cells. Succession of cell cultures and platings. Transformation of 19% of cells, which return to orienting themselves in an orderly manner, as in healthy tissues | (21) | |
| Rose & Wallingford, 1948 | Lucke renal tumor cells. Planting on regenerative salamander limbs. Block of tumor growth and subsequent differentiation of cells. Failed to determine whether the differentiated cells came from cancer cells or healthy tissue | (27,28) | |
| Coleman, 1993 | Liver cancer cells. Injected into liver tissue. Reduction of malignancy and, in some cases, differentiation of cancer cells. | (36) | |
| Brinster, 1974 | Graft of tumor cells into blastocysts/embryos | Murine testicular teratocarcinoma cells. Injection into murine blastocyst implanted in albino femalemice. Development of healthy mice | (17) |
| Mintz & Illmensee, 1974 | Embryonic carcinoma cells from black mice. Blastocyst injection implanted in brown female mice. Normal fetal development; normal newborn mice feature hybrid traits between black and brown mice | (18) | |
| Podesta, 1984 | Neuroblastoma cells. Injected into 8 ½ day old murine blastocyst. Differentiation of tumor cells. | (41,42) | |
| Gootwine, 1982 | Leukemia cells. Injected into 10-day old murine blastocyst. Correct hematopoietic maturation. | (43) | |
| Bissell, 1984 | Rous sarcoma virus. Injected into chicken embryos. No tumor development. | (24) | |
| Gerschenson, 1986 | Mouse melanoma cells. Implanted into embryos in the murine uterus. Cell differentiation and normal embryonic development. Differentiation occurs when cells are implanted into a 14-day embryo. | (44) | |
| Hendrix, 2005 | Human melanoma cells. Implanted in zebrafish embryos in the early stages of development. Suppression of malignant tumor phenotype and birth of healthy fish. | (50) | |
| Gersch, 1951 | Induction of tumors in healthy animal tissues and monitoring of their evolution | Spontaneous tumors in animals. Observations on the rate of onset. Reduced occurrence of tumors in animals with high regenerative capacities | (29) |
| Seilern-Aspang & Kratochwil, 1962 | Triton-induced epithelial tumors. Monitoring the spontaneous evolution of tumors. Tendency to tumor regression in anatomical areas with high regenerative potential. Results confirmed by histological analysis | (32) | |
| DeCosse, 1973 | Exposure of cancer cells to solublefactors of the embryonic microenvironment | Murine breast adenocarcinoma cells. Exposure to diffusible substances of murine embryonic mesenchyme. Differentiation of tumor cells. | (46) |
| Biava, 1988 | Primary murine lung cancer. Administration (in vivo) of homogenates of pregnant murine uteri. Suppression of tumor development | (47) | |
| Biava, 2001; 2002 | Glioblastoma, melanoma, renal adenocarcinoma, breast cancer, and lymphoblastic leukemia cells. Exposure to embryonic extracts of zebrafish taken before gastrulation. Reduction of cell proliferation rates. | (48,49) | |
| Bizzarri, 2006 | Human colon cancer cells. Exposure to factors extracted from zebrafish embryos prior to gastrulation. Reduced rate of cell proliferation. In addition, the activation of p53, of the cell cycle blocking system pRb/E2F1, and of a synergistic effect with 5FU was observed. | (51) | |
| Allegrucci, 2011 | Breast cancer cells. Exposure to axolotl, frog, and mouse embryonic cell extracts. Stable reversal of malignant phenotype (confirmed with subsequent implantation of reprogrammed cells in immunosuppressed mice). | (97) | |
| Saad, 2018 | Breast cancer cells. Exposure to axolotl oocyte extracts. Stable reversal of cancer phenotype, cell cycle arrest mediated by upregulation of p27 and reduction of RB phosphorylation, induction of tumor dormancy. | (98) | |
| Bizzarri, 2019 | Breast cancer cells. Exposure to embryonic extracts of zebrafish taken at different times of embryogenesis. Reduction of invasiveness, migration, and proliferation parameters; action on cytoskeleton and TCTP downregulation. An activation method of reversion was identified, implying the down-regulation of TCTP by exposing the cells to a specific embryonic microenvironment composition that corresponds to a specific phase of embryogenesis. | (82) | |
| Henrix, 2007 Postovit, 2008 | Exposure of cancer cells to soluble factors secreted by embryonic stem cells | Melanoma cells and breast cancer cells. Exposed to embryonic stem cell factors. Reversal of the malignant phenotype and activation of apoptotic processes (nodal signal inhibition was also observed). If cells are exposed to factors extracted from umbilical cord and bone marrow stem cells, then no phenotypic reversion is observed. | (84, 86) |
| Giuffrida, 2009 | Ovarian, prostate, and breast cancer cells. Microenvironmental exposure of human embryonic stem cells. Reversion of malignant phenotype block of cancer cells in phase G1 | (94) | |
| Costa, 2009 | Melanoma cells. Microenvironmental exposure of human embryonic stem cells. Reversion of malignant phenotype. The study identified some mRNAs involved in these cellular reprogramming processes. | (90) |