The Molecular Biology of Cancer: Questions

Part A: Multiple Choice

1. What is the progression of a normal cell into a lethal tumor?

a. tumor -> transformation -> benign tumor -> malignant tumor

b. transformation -> tumor -> malignant tumor -> benign tumor

c. normal cell -> transformation -> cancer cell -> tumor -> benign tumor -> malignant tumor

d. normal cell -> transformation -> tumor -> malignant tumor

2. One example of a growth factor is:

a. G0

b. p53

c. oncogene

d. PDFG

3. Which of the following is not a way for a proto-oncogene to become an oncogene?

a. chromosomes that are broken or rejoined incorrectly

b. a proto-oncogene that lies adjacent to an especially active promoter

c. point mutations

d. more Ras genes than p53 genes

4. In the typical stimulatory pathway, the sequence of events is:

a. growth factor binds to a tyrosine-kinase receptor, the signal is relayed to Ras, which then passes the signal to a series of protein kinases and the last one activates a transcription factor

b. growth factor binds to a G protein, the signal is relayed to p53, which passes the signal to a series of protein kinases and the last one activates a transcription factor

c. G protein attaches to the tyrosine-kinase receptor, the signal is relayed to Ras, which then passes the signal to another growth factor that activates a transcription factor

d. growth factor attaches to an activator of a transcription factor, which releases Ras and thus instigating the creation of the protein that stimulates the cell cycle

5. Which of the following statements is true?

a. Cancer results from an accumulation of mutations, which occur only later in life.

b. An oncogene protein that is a hyperactive version of a protein in the cell cycle can increase cell division even in the absence of a growth factor.

c. A malignant tumor is also known as an adenoma.

d. A tumor is a mass of abnormal cells within an otherwise normal tissue.

6. The most easily spread of all cancers is/are:

a. Blood

b. Lung

c. Lung and Lymph

d. Lung, Blood, and Lymph

7. Cell division can be controlled by all of the following except:

a. translocation

b. cells going from the G1 phase to the G0 phase

c. PDFG

d. cyclin

8. Attributes of normal cells include:

a. cell anchorage

b. proto-oncogene, cell anchorage, density dependent inhibition

c. density dependent inhibition, cell anchorage

d. cell anchorage, density independent inhibition

9. Because mutant tumor-suppressor alleles are usually recessive:

a. mutations must knock out one allele in a cell’s genome to block tumor suppression

b. mutations must cause dominant alleles to be turned into recessive ones

c. mutations must knock out both alleles in a cell’s genome to block tumor suppression

d. mutations must make any recessive alleles in a cell’s genome to become dominant

10. Viruses contribute to cancer development by:

a. creating epithelial cells

b. causing cell lysis

c. disintegrating DNA

d. integrating their genetic material into the DNA of infected cells

Part B: Diagrams/Pictures

1. The picture to the side shows the growth of normal cells and cancerous cells in a culture. Name two factors that cancer cells do not have that are present in normal cells displayed here.

2. This picture shows the growth of cancer cells in the body. Name what is occurring in this picture and through what system the cancer moves.

3. Based on the picture, what is the function of p53?

Part C: Short Answer

List the main components of both growth-stimulating and growth inhibiting pathways

Part D: Reaction/Thinking/Reflection/Abstract Question

If cells can become cancerous from a variety of mutations, such as by having a hyperactive version of a protein in a stimulatory pathway like Ras, what are possible, if hypothetical, ways that scientists can attempt to rid a human of cancer?

Answers

Part A

  1. C
  2. D
  3. D
  4. A
  5. B
  6. D
  7. A
  8. B
  9. C
  10. D

Part B

  1. cell-cell adhesion, anchorage dependency, density dependent inhibition
  2. metastasis; circulatory system
  3. activates transcription factors which can repair damaged DNA; if DNA is irreparable p53 activates suicide genes which cause cell death by apoptosis

Part C

Growth factors, membrane receptors, G proteins (such as Ras), protein kinases, and transcription activators

Part D

Through gene therapy, scientists can possibly cause cells to cease overexpressing proteins that overstimulate the cell cycle. Viruses are estimated to contributing to 15% of human cancer cases worldwide, so if inoculations for preventable diseases are available cancer cases will likely decrease. Onco-genes are more likely to appear as a person ages due to an accumulation of mutations in DNA; therefore, those who are older should be screened for cancers in order to catch changes that could lead to cancer. Cancer can be caused by having too much of a protein, so perhaps if a person received injections of a protein that signals cell inhibition rather than the continuation of the cell cycle the uncontrollable growth could be controlled.