User:Manl2895/sandbox

Cancer Research
A common issue with cancer is that it is invasive. The term invasive refers to that fact that tumor cells overrun a host’s cell and destroy it. Once cancer cells become malignant, the cells begin to spread to other organs in the body. Many studies have been created in order to better understand cancer cells which one day may lead to a cure. One way to study cancer cells is to understand them. In order to study the communication between a tumor cell and a host’s cell an in vitro assay is created. This allows us to conduct studies under reasonable conditions in the lab. In one such study the objective was to see how the tumor cell would communicate with the host cells metabolism. In other words, the purpose of this experiment is to view the gap junction between the host cell and the tumor cell.

In this study tumor cells were grown on assays that were later individually mixed with a host cell, the cell of a chicken’s heart. The assay that was used was created by Holtfreter who developed an assay that would allow for the cells not to stick to the Petri dish. Cultures of heart fragments from a chicken were pre made in order for the cancer cells to have something to attach to or in this case invade. These fragmented chicken heart cells were a learning tool developed by Mareel in order to see the effectiveness of invasion in vitro. The cells were grown in wells which were called PHF or pre cultured heart fragments. Five cancer cell lines were used BICR/M1Rk, C6, EMT6/Ro, L, and HeLa. The different cell lines were put through a series of tests including electrophysiological measurements, a light microscopical histology, and ultrastructural data were collected. In the multicell tumor spheroids most of the tumor cell lines showed tight packing except for BICR/M1Rk-MTS (multicell tumor spheroids). BICR/M1Rk-MTS cells appeared to be loosely packed and large in size. Once the tumor cells were mixed with the PHF all that was left was to wait and see if and how long the cells took to invade.

Some of the cells took no time at all to invade the host, some took a little bit longer, and some did not destroy the host cell at all .After the timed incubation periods BICR/M1Rk, C6, and EMT6/Ro showed invasion of PHF within a short period of time via gap junctions. Each cancer cell was able to invade the host’s cell and destroy it. In the case of the HeLa cells and L cells there were no advancement into the PHF, except after a few days HeLa cells were able to invade and destroy the host cell. Though the host cell was not destroyed the cancer cells each surrounded the host’s cell, but only after many hours. This means that it is possible for the process of tumor cell invasion due to heterologous intercellular communication. The HeLa cells took a long time to invade the cell. This could be due to the over growth of HeLa cells created over time. Since there were so many HeLa cells surrounding the PHF Gabbert believes that the lack of space created a competition for nutrients. Thus allowing the HeLa cells to, in a sense win, and over take the PHF. In the case of the L tumor cells, they were not able to invade the PHF. Though HeLa cells were able to accomplish invasion after several hours the L cells are structurally different rendering them inadequate. The L cells have much more intercellular free space and do not surround the host cell as tightly as Hela cells. It is concluded that with a tight gap junction nutrients cannot enter the cell allowing the cancer cells to invade.