Presentation on theme: " Since the cell cycle is known, now we must ask what controls it Noted that healthy cells in contact will not divide ◦ Essentially, this is how our."— Presentation transcript:
Since the cell cycle is known, now we must ask what controls it Noted that healthy cells in contact will not divide ◦ Essentially, this is how our skin heals But what drives the cycle? Sequential control? Experiments have shown that proteins control it
Experiment 1 Experiment 2 S S S G1G1 G1G1 M M M When a cell in the M phase was fused with a cell in G 1, the G 1 cell immediately began mitosis—a spindle formed and chromatin condensed, even though the chromosome had not been duplicated. Something in M phase induced interphase cells to divide. When a cell in the S phase was fused with a cell in G 1, the G 1 cell immediately entered the S phase—DNA was synthesized. S cells contained something that induced regulation in G 1 cells.
Conclusion: the S phase proteins work on G 1 nuclei, M phase works on everything Biologists named these proteins “cyclins” These are used in all three portions of interphase Each is referred to as a “checkpoint” Collectively, they are called growth factors The cell has mechanisms that ensure each phase is complete before moving onto the next We have seen this already with the possibility of a cell entering G 0
G1G1 G 1 checkpoint G1G1 G0G0 If a cell receives a go- ahead signal at the G 1 checkpoint, the cell continues on in the cell cycle. If a cell does not receive a go-ahead signal at the G 1 checkpoint, the cell exits the cell cycle and goes into G 0, a nondividing state.
Overall, it appears as though there are many factors, internal and external that control the cell cycle Ex. Kinetochores not attached to microtubules Ex. Density dependent inhibition Ex. Anchorage dependence, where cells have to be attached to a substratum (solid surface) to divide
Cells anchor to dish surface and divide (anchorage dependence). When cells have formed a complete single layer, they stop dividing (density-dependent inhibition). If some cells are scraped away, the remaining cells divide to fill the gap and then stop (density-dependent inhibition). 25 µm Normal mammalian cells
Cancer can be thought of as uncontrolled growth of cells ◦ They can lack the mechanisms, do not respond properly to them, or have an error in the pathways If they stop, it is at a random point
Cancer cells do not exhibit anchorage dependence or density-dependent inhibition. Cancer cells 25 µm
A mass of cancer cells is known as a tumor ◦ If this tumor stays in the original site – benign ◦ If it spreads to surrounding tissue - malignant A individual tumor cell can break free from the group and invade other organs ◦ It is said to have metastasized ◦ Unfortunately, these cells can continue to grow if supplied with nutrients ◦ Normal cells divide before dying
Cancer cell Blood vessel Lymph vessel Tumor Glandular tissue Metastatic tumor A tumor grows from a single cancer cell. Cancer cells invade neighboring tissue. Cancer cells spread through lymph and blood vessels to other parts of the body. A small percentage of cancer cells may survive and establish a new tumor in another part of the body. Cancer
The two most common treatments we have are chemotherapy and radiation treatments Chemotherapy By definition, treatment of any condition via chemicals Our focus is on antineoplastic drugs – cancer fighters Act by targeting rapidly dividing cells ◦ However, this also includes healthy cells such as bone marrow (blood cells), hair follicles, and sex cells
Common side effects – hair loss and an compromised immune system Essentially theory is the drugs will kill the cancer faster than the patient If not discovered soon enough, treatment would take too long Radiation Therapy Beam of subatomic particles that damages DNA Has to focus on a tumor
With more knowledge on mechanisms of cancer, new treatments are being proposed Viruses are being designed to specifically target cancer cells