| Cancer has been present throughout human history. In 1900, cancer was the eighth leading cause of death in America. But it has become the second leading cause of death in the last half of the twentieth century, accounting for approximately one in every four deaths in America. Over the last 30 years, the number of cancer deaths has doubled. Cancer deaths now exceed 550,000 per year, of which 80%~90% were due to invasion and metastasis. Though we have made great efforts in the battle against cancer, we are still not able to conquer cancer. This is due to the limited knowledge about neoplasm, especially on etiology.In 1829, Lobstein and Recamier put forward the hypothesis that neoplasm originated from embryos. With the development of cellular biology, molecular oncology, experimental embryology, experimentaloncology, and immunoembryology, more and more researches have been carried out concerning comparative studies between neoplasm progression and normal embryonic development. Striking similarities present between neoplasm progression and embryonic development have been found: being "young" cells in growth and development, having great potential of proliferation, growth, and differentiation, expressing similar genes (oncogenes/anti-oncogenes, ecto-hormone, ecto-isoenzymes, embryonic antigens), possessing similar mechanisms of angiogenesis and immunological escaping, and especially possessing similarities in invasive behavior and mechanism. These findings suggest there exists homogeneity between neoplasm and embryo. Studies on homogeneity between neoplasm and embryo were focused on the intersection of oncology and embryology. An appreciation of the mechanisms to control "limited" trophoblast cells invasion may likewise lead to insights of "uncontrolled" invasion and metastasis in malignant cells and lead to efficient approach to control their growth and spread within host tissues.Part OneExperiments of Trophoblast Cells from Mouse Ectoplacental Cone Invading Neoplasm Cells in vitroObjective: To determine that the invasiveness of trophoblast cells, being separated from the whole embryonic regulation, is stronger than that of neoplasm cells in vitro.Methods: Pure trophoblast cells of ectoplacental cones from D8.5 mouse embryos were co-cultured with malignant neoplasm cells from various histological source (Human hepatocarcinoma cell line HepG2 and SMMC-7721, Human breast cancer cell line MDA-MB-231 and Bcap-37, Human ovarian cancer cell line SK0V3, Human gastric cancer cell line SGC-7901, Human cervical cancer cell line Hela, Human endometrial cancer cell line RL95-2, Human osteosarcoma cell line ROS17/2.8, Rat breast cancer cell line SHZ-88, Rat osteosarcoma cell line LM8, Human nasopharyngeal cancer cell line HNEl, and Mouse melanoma cell line B16) and normal cells (mouse fibroblast cell line NIH3T3 and L929, human umbilical vein endothelial cell line ECV304, and human tracheal epithelial cell line 9HTE) in vitro. When these two types of invasive cells directly contacted, the capability of invasion and the whole biological characteristics were observed.Results: Mouse ectoplacental cones attached on the co-cultured cells and outgrew in co-cultured system in vitro. At the periphery of mouse ectoplacental cones, trophoblast cells were seen growing toward cancer cells. During the period of 48h-96h after co-culture, trophoblast cellsexhibited the fastest outgrowth rate; while around 144h, outgrowth area was increased to the most, forming an "S" shape of outgrowth area curve. At 72h and 144h of co-culture, there was larger outgrowth area of trophoblast cells in cancer cells co-cultured group than in normal cells co-cultured group (P<0.05). Cancer cells surrounding trophoblast cells altered the patterning of growth direction and appeared round or oval. There was a clear borderline between trophoblast and cancer cells.Conclusion: Trophoblast cells of mouse embryo, possessed stronger invasiveness than cancer cells in vitro. Trophoblast cells displayed a self-limited invasive be...
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