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- Which of the following factors contributes to angiogenesis as a result of a tumor growth? Select all that apply: a. Increasing tumor's access to oxygen and nutrients b. Increasing tumor's ability for growth, invasion, and metastasis c. Increasing expression of proto-oncogenes for cancer cells d. Increasing expression of tumor-suppressor genes for cancer cellsLooking at Figure 1, what did Romansik et al. (2007) find regarding the relationship between the mitotic index and tumor grades. Explain their findings in your own words. Use specific details from Figure 1. The research paper is here: https://journals.sagepub.com/doi/10.1354/vp.44-3-335Although cancer is not a contagious disease in humans or other vertebrates, there have been rare cases in which cancers have spread from one organism to another. Describe three cases of these contagious cancers and what conditions might have led to their appearance. For an introduction to this topic, see http:// www.cancer.org/cancer/cancerbasics/is-cancer-contagious.
- Excessive angiogenesis and reduced apoptosis are two of the six characteristics that define cancerous tumors. Discuss how developing treatments for these two conditions might prevent the development of cancer altogether from pre-malignant tumors.Which of the following statements are correct about tumor cell masses (select all that apply)? A. Stromal cells of tumor masses are generally just contaminants and play no role in tumor progression B. Most stromal cells are of mesenchymal origin C. Fibroblasts, macrophages and lymphocytes are commonly found in the stroma of tumor masses D. In Hodgkin's Lymphoma, the majority of cells in the tumor mass are neoplastic E. In carcinomas, neoplastic and stromal cells are present at similar numbersWhich of the following statements are correct about tumors and metastasis (select all that apply)? A. The majority of cancer deaths are due to primary tumor B. Loss of basement membrane by tumor mass is strong predictor of metastasis potential C. The tissue stroma contributes to whether a tumor cell will metastasize D. The majority of life threatening tumors occur in epithelial tissues E. The tendency of a primary tumor to metastasize is similar across different tissue types
- Which of the following steps are correct about multistep tumorigenesis (select all that apply)? A. Mutations in progenitor cells are more likely to develop a neoplastic state compared to mutations in stem cells B. Driver mutations give a cell clone a proliferative advanage C. The rate of mutation /genetic change is constant during tumor progression D. Nutrition/diet may effect rate of tumorigenesis E. All cells within a tumor are biologically equivalent and equally capable of high levels proliferationDiscuss the principles that govern the presence and maintenance of stem cells both in vivo and in vitro? What is the current status of the technology, and its possible applications? What are the pros and cons of the technology, and how do these issues personally affect people?Another model, the random model, proposes that any cell in a malignant tumor has the potential to form a new tumor. Does the cancer stem cell hypothesis contradict this idea?
- Studies have shown that there are significant differences in cancer rates among different ethnic groups. For example, the Japanese have very high rates of colon cancer but very low rates of breast cancer. It has also been demonstrated that when members of low-risk ethnic groups move to high-risk areas, their cancer risks rise to those of the high-risk area. For example, Japanese who live in the United States, where the risk of breast cancer is high, have higher rates of breast cancer than do Japanese who live in Japan. What are some of the possible explanations for this phenomenon? What factors may explain why the Japanese have higher rates of colon cancer than do other ethnic groups?how are the hallmarks resisting cell death and enabling replicative immortality essential for cancer development. explain each in 3-5 sentences.The Human papillomavirus (HPV) has been linked to an increased risk of cervical cancer. The HPV E6 and E7 proteins govern the cell via altering cellular proteins. The E6 protein interacts with the tumor suppressor protein p53 and directs its ubiquitin-mediated destruction. Can you elaborate about the P63 gene: its function and if it can be altered/mutated by HPV? If it does, what is the relationship between P53 and P63? Thank you!