Chapter 17: Cancer Flashcards
There are several ways that a protooncogene can be activated to become an oncogene. Consider these possibilities: I. Loss of function of mutation Il. Gain of function or constitutively active mutation III. Gene amplification IV. Chromosomal translocation leading to increased or ectopic gene expression.
Answer: II, III, and IV
Three genetic mechanisms that cause genetic changes to cellular proto-oncogenes and the resulting activation of oncogenes are; mutation, gene amplification, and chromosome rearrangements.
Which of the following statements is the most likely explanation for a specific cancer ( eg colon cancer) appearing in several memebres of the same family?
a- Affected individuals have inherited a deletion of a proto-oncogene that was mutated in the ancestors germline cells.
b- affected individuals have inherited a deletion of a tumor suppressor gene that was mutated in the ancesters somatic cells
c- Affected individuals have inherited a deletion of a tumor suppressor gene that was mutated in the ancestors germline cells
d- affected individuals have inherited a defective gene whose product interferes with a mismatch repair
c- Affected individuals have inherited a deletion of a tumor suppressor gene that was mutated in the ancestors germline cells
Cancer is considered a progressive multi-step disease, why is this?
Tumor development arises from the accumulation of 4-6 different mutations in cells over the course of many years.
- What are the 4 major group of tumors?
carcinoma
sarcoma
leukemia/lymphoma
neuroblastoma
a. Carcinomas : transformation of epithelial cells lining various organs (lung, colon, breast,
prostate)
b. Sarcomas : mesenchymal tissue, includes tumor of bone and muscle
c. Hematopoietic : (blood forming) these organs represent frequent targets for oncogene
events and malignant transformation of associated cells leads to leukemias, lymphomas,
myelomas
d. Neuroectodermal : Included in these are neuroblastomas, gliostomas, neuromas,
neurofibrosarcomas, and melanomas.
- Tumors are said to be “monoclonal.” What does this mean?
a. “All cells within a cancer descend from a single common progenitor cell. Sometimes termed the cell of origin.
All cells within a cancer descend from a single common progenitor cell. aka. cell of origin
- List the three genetic modifications that convert proto-oncogenes into oncogene.
translocation/transposition
gene amplification and over expression
point mutation
- Define dysplasia.
abnormal development of cells within tissue or organs
Cells forming marginally abnormal epithelium including relatively undeveloped polyps.
- How may cancer cells achieve immortalization?
a. Overexpression of a gene regulation
b. Change in protein structure
c. Translocations
1- gene amplification and over expression
2- point mutation
- How may cancer cells achieve immortalization?
- Once adapted to a culture, cancer calls can proliferate without limit, this causes the cancer cell to become immortalized.
- All transformed cells cells that emerge/survive from a crisis
- List at least four phenotypic characteristics of cancer cells.
a. Anchorage dependent : don’t require attachment to a physical substrate
b. Reduced requirement for growth factors to sustain proliferation
c. Don’t stop dividing when contact is made with neighboring cell in petri dish
d. Once adapted to culture they can proliferate without limit (immortalized).
- do not stop dividing when they contact neighboring cell
- cancer cells often have chromosomal abnormalities
- cancer cells have a greatly reduced requirement for growth factors to sustain growth and proliferation
- cancer cells are anchorage independent
- What does the term metastasis mean?
- Malignant tumors become established in distant organs.
- Spread of cancer to a distant site.
- What is loss of heterozygosity?
- Cross chromosomal events that result in the loss of the entire gene and the surrounding chromosomal region.
- Loss of normal function in one allele of a gene in which the other allele was already inactivated
- How can a mutation in a single gene target multiple phenotypic characteristic at the same time?
- A mutation on a single gene can target multiple phenotypic characteristics due to pleiotropy. [Pleiotropy occurs when one gene influences two or more seemingly unrelated phenotypic traits.]
- Mutation in a pleiotropic gene
- Pleiotropy: Pleiotropy refers to the phenomenon where a single gene mutation affects multiple seemingly unrelated traits or phenotypic characteristics. This occurs when the gene in question plays a role in different biological processes or is involved in the regulation of multiple pathways. For example, a gene involved in embryonic development may also have effects on organ formation, immune function, and cognitive abilities. As a result, a mutation in that gene can lead to abnormalities or changes in multiple phenotypic traits.
- What is a “magic bullet” in cancer? Is p53 a “magic bullet”?
-A magic bullet is a drug that would kill cancer cells by specifically targeting only the difference between cancer cells and their normal counterparts.
- Substance or therapy capable of destroying pathogens, provides remedy for disease. P53 allows cells to cell cycle arrest and go through apoptosis.
The idea behind a magic bullet is to develop a treatment that specifically targets the unique characteristics or vulnerabilities of cancer cells, such as specific proteins or genetic mutations that drive their growth and survival. By selectively targeting cancer cells, a magic bullet could potentially minimize the side effects and toxicity often associated with traditional cancer treatments like chemotherapy and radiation therapy.
Now, regarding p53, it is not considered a “magic bullet” in the context of cancer treatment. p53 is a protein known as the “guardian of the genome” due to its crucial role in regulating cell division and preventing the formation of cancerous cells. Mutations in the p53 gene are among the most common genetic alterations found in various types of cancer.
- How is apoptosis modified in a cancer cell?
- Apoptosis refers to cell death, besides unregulated growth, cancer also hijacks cellular death pathways. Cancer cells can compromise the activity of P53 by increasing the inhibitors of P53, or silencing the activators of P53, disabling the gatekeepers.
- Increasing inhibitors of p53, or silencing the activators
