3.1.3. When Cells Lose Control
How normal cells become cancerous:
In the normal cell cycle, cells go through cell division that is regulated by signals that tell cells when to start and stop dividing. However, in cancer cells, they lack the signal that tells them to stop dividing which leads to them growing uncontrollably. Proto-oncogenes are responsible for regulating cell division and apoptosis. However, when mutations occur they can turn into oncogenes which cause uncontrolled cell growth, cancer. Lucky for us, our body contains a pair of tumor suppressor genes, one from each parent, that limits tumor growth. If the tumor suppressant doesn't work in stopping the cells from dividing, they can metastasize to other areas of the body. This happens when they invade neighboring tissues and blood vessels and their cells travel to other areas of the body and cause harm. |
Cancerous cells:
- Nuclei is nearly as big as the cell itself -The shape of the cells is also abnormal (wavy-outer edges) - There are a lot of cells on the slide |
Normal cells:
- Nuclei size is normal - Fewer cells which indicates normal growth and death rates - Nuclei barely visible (cancerous cell nuclei are darker because there is less DNA) |
3.1.4. DNA Microarray
This is an image of our wet lab results we obtained from the experiment.
3.2.2. Skin Cancer Prevention
When determining whether a mole is normal or malignant you need to consider the ABCDE's. The A stands for asymmetry. This means that if the mole is divided in two and the two halves don't match, then it's a warning sign for a malignant mole. B stands for border. If your mole has an uneven or sculpted border it could be malignant. The C means color. If the mole is the same color throughout (often brown) then it is most likely benign. The D stands for diameter. Malignant moles are usually larger in diameter while benign moles are smaller. Finally, E stands for evolving. If a mole is changing over time then it is most likely malignant.
This is an image of our yeast plate from when we tested the effects on different sunscreen sun protective factors on yeast cell growth and death. The section with 0 SPF had barely any growth because the UV rays killed off the yeast cells. The section with 50 SPF had some growth due to overgrowth from the section with 100 SPF sunscreen that protected the yeast cells from being killed of by the UV rays.
3.2.5. Routine Screenings
This is an image of the timeline I created to show when in life, and how often, you should get routine cancer screenings. For skin cancer you should be tested early on and regularly throughout life by either yourself or a doctor. With lung cancer, if you are high risk, you should begin annual screening at age 55, in both male and females. For colon and rectal cancer, there are various testing options but they should begin at age 55 and vary in how often they should be performed. In males, testicular cancer screening should be performed regularly through self-examination beginning at age 16. Also, prostate cancer screenings should be annual starting at age 45 if you have a family history or of African-American descent. For females, endometrial cancer testing should begin after menopause if symptoms occur. For breast cancer, screening needs to begin at age 45 with breast cancer screening and mammograms annually until age 54. After age 55 mammograms should be scheduled every two years.
3.3.2. Biofeedback Therapy
Biofeedback therapy has the power to control stress in patients receiving cancer treatment. This therapy prevents them from seeing or hearing their treatment so they are less worried about it and can possibly feel less pain.
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3.4.1. Personalized Medicine
In this activity, each of our cancer patients responded differently to the medication they were given. The first patients, Renee, was completely fine after treatment and was doing better than before. Su and Jada are doing a little better but they still need more treatment. Finally, Maggie, was doing a lot worse than before her cancer treatment. To understand why each patient responded differently to their treatment we look at their SNP's. These differences lead us to believe that the reason they were reacting different to the treatment was because of these tiny changes in their DNA that caused their body to have more or less thiopurine methyltransferase (TPMT) which regulates the drug we were giving to them, azathioprine.