cancerlotsofcancerness

Cancer Article SCI Human Biology - 1 Assigned: 11/10 Due: 11/11

1. The article begins by mentioning two important people with cancer. Who is Elizabeth Edwards? Who is Tony Snow? (This article was written 03/07/07. As a part of this question find out what has happened in the year and a half since this article was written with respect to the cancer of Ms. Edwards and Mr. Snow. Include a link to your sources.) Mrs. Edwards, the 57-year-old wife of the presidential candidate John Edwards, and Mr. Snow, the 51-year-old press secretary to President Bush, announced that the cancers for which they had previously been treated had returned and metastasized: in her case, spreading from breast to bone, in his, from colon to liver. 2. What is a metastatic cancer cell? When a type of cancer spreads from one area, to a different area of the body. 3. Why does the author call cancer cells barbarians and cannibals? They are barbarians because the colonist cells co-opt all nutrients in their adopted organ and starving their normal neighbors of air, sugar and salts, and blocking traffic and clogging conduits, and finally, when their greed exceeds their easy grab, tearing open surrounding cells and feasting like cannibals on the meat of their fellows.

4. What do we know about the events that transform a normal cell to a cancer cell? They have identified genetic mutations and chromosomal aberrations that prompt cells to think they are being stimulated by growth hormones when they are not, that stifle safety signals meant to keep cell division in check, and that shore up the tips of chromosomes and so immortalize cells that otherwise would be slated to die. 5. Why is harder to study metastatic cancer cells? Because they cant be studied in vitro, they must be analyzed in vivo. 6. How many cells do primary tumors shed each day (in a rodent)? Yet how many metastatic tumors do these rodents have? They only shed about 5 each day but have like a million. 7. Describe two ways metastatic cells can travel through the body avoiding detection from our immune system. To survive the journey, malignant cells must reinvent themselves as parasites. A few manage to slim down to almost bacterial dimensions by pinching off unnecessary hanks of their cytoplasm. Others take on what Dr. Weinberg calls “hitchhikers,” attracting an entourage of platelets and red blood cells to their surface “to escort them through the rapids into safe pools within tissues.” 8. Where is the first site (oasis for the cancer cell) that metastasis generally occurs? Why? Why is it an oasis? (What is an oasis?) Such oases might be wound sites to which the chaperone platelets handily stick, enabling their companion cancer cells to gain their first toehold in virgin terrain — and to begin feeding on the rich broth of growth hormones and factors with which wound sites typically teem. 9. What is a dormant micrometastasis? Why are they relevant to human health? appear to either die or lapse into dormancy. Patients may harbor thousands or millions of these dormant micrometastases without suffering a fatal relapse of the disease. They are non active for long periods of time and go unnoticed. 10. What evidence do we have that metastasis occurs in organs that are similar to the organ of the primary tumor? Give two examples. primary tumors tend to metastasize to their “preferred” organ: cells learn a skill set from their tissue of origin, and some lessons are more easily applied to one novel setting than to another. Breast tumors, for example, are known to metastasize to bone tissue, where the invasive cells perversely take advantage of their ability to gather calcium ions for breast milk and apply it to the rampant dissolution of calcium-rich bone. Malignant melanoma spreads readily to the brain, presumably because neural tissue and the melanocytes that give rise to melanoma both arise from the same class of cells during gestation.

11. The gene and its protein, both called RBM3, are vital for cell division in normal cells. In cancers, low oxygen levels in the tumors cause the amount of this protein to go up dramatically. This causes cancer cells to divide uncontrollably, leading to increased tumor formation. Researchers used new powerful technology to genetically "silence" the protein and reduce the level of RBM3 in cancerous cells. The approach stopped cancer from growing and led to cell death. The new technique has been tested successfully on several types of cancers - breast, pancreas, colon, lung, ovarian and prostate. http://www.medicalnewstoday.com/articles/106919.php