bio midterm quiz 2

cancer

- biggest risk factor: age

cell growth factors

- chemical signals that tell a cell to divide

DNA

- constantly mutating

smart design drugs

- in use or in development that respond to specific mutant proteins common in some cancers - show some promise - often unaffordable, not covered adequately by many insurance plans

BRCA1 + BRACA2

- proteins that recognize mutated/damaged DNA & initiate DNA repair - 10% of women develop breast cancer, but 60% of women with a mutation in the genes for BRCA1 or 2 develop breast cancer - mutations are also risk factors for ovarian cancers & other cancers

HeLa cells

- unique cancer cells - developed bc of different, rare mutations - most common tested-on cells - there was a search for a human cell line to grow in lab, then Henriette Lacks - she went to John Hopkins hospital bc she had a rare kind of cervical cancer - cells still growing today - in 1952, a factory made a polio vaccine with HeLa cells - used around world in labs for diseases, vaccines, etc. - other cell lines in same room would be contaminated bc so aggressive - testing with these = * - used for testing bc easy to take care of, they keep growing - her family not told - alias: Helen Lane

2.) Distinguish between a familial and a sporadic cancer.

A familial cancer occurs more frequently than expected within a family but does not demonstrate any observable pattern of inheritance. It usually affects those over the age of sixty. A sporadic cancer occurs usually as a result of environmental or unknown factors, and does not have any observable pattern of inheritance within the family. Sporadic cancer cannot be passed on, there is no predisposition to a type of cancer because mutations are acquired only in the tissues that develop the cancer. It's also not present in higher than expected levels in three family generations.

9.) What is the difference between a proto-oncogene and a tumor-suppressor gene?

A proto-oncogene encodes for proteins that start or maintain cell growth and division. A tumor-suppressor gene turns off or decreases the rate of cell division.

p53

A tumor suppressor protein. "Guardian of the genome." - gene for p53 is mutated in >50% of human cancers - inactive: nothing - active: cell cycle arrest → DNA repair → cell cycle restart → cellular & genetic stability - active: apoptosis (program cell death) → death & elimination of damaged cells → cellular & genetic stability

stem cells

Add back telomerase.

hipylori

Bacteria for stomach ulcers.

CHAPTER 12 TEXTBOOK QUESTIONS

CHAPTER 12 TEXTBOOK QUESTIONS

CHAPTER 13 TEXTBOOK QUESTIONS

CHAPTER 13 TEXTBOOK QUESTIONS

14.) What are the roles of cellular proto-oncogenes, and how are these roles consistent with their implication in oncogenesis?

Cellular proto-oncogenes encodes proteins that normally start or maintain cell growth and division. If they're mutated or misexpressed, they become oncogenes and lead to aberrant cell cycle control. Furthermore, if inactivated, this leads to oncogenesis; normal cells stop dividing and cancerous cells are switched on to divide permanently.

20.) Can you postulate a reason or reasons why children with Down syndrome are 20 times more likely to develop leukemia than children in the general population?

Children with Down syndrome are at times up to 20 times more likely to develop leukemia because they experience more x-rays during medical treatment than the general population does. Also, early lifetime infections are a possible cause that would make these children more prone to leukemia.

12.) Briefly describe how to clone a segment of DNA. Start with cutting the DNA of interest with a restriction enzyme.

Cloning DNA requires three things. One, a way to cut the DNA at specific sites to produce consistent, manageable pieces. Two, a carrier molecule to hold the DNA for transfer to a host cell for cloning. Three, a host cell in which many copies of the selected DNA molecule can be produced. Now, how it's cloned. First, the DNA to be cloned is cut with a restriction enzyme. Then, a plasmid vector is cut with that same enzyme. Both types of DNA that are cut with said enzyme have complementary sticky ends. Next, when the DNA fragments and the cut plasmids are mixed, they can bind together by their sticky ends and link to form recombinant DNA molecules by DNA ligase. Lastly, the recombinant plasmids are transferred to bacterial host cells. At each bacterial cell division, the plasmid is replicated, producing many clones of the foreign DNA.

cancer cells

Created by accumulation of mutations to oncogenes & tumor suppressor genes. - add back telomerase - carry mutations & genetic abnormalities of all type - damaged, but not enough to die

18.) You are in charge of a new gene therapy clinic. Two cases have been referred to you for review and possible therapy. Case 1: A mutation in the promoter of a proto-oncogene causes the gene to make too much of its normal product, a receptor protein that promotes cell division. The uncontrolled cell division has caused cancer. Case 2: A mutation in an exon of a tumor-suppressor gene makes this gene nonfunctional. The product of this gene normally suppresses cell division. The mutant gene cannot suppress cell division, and this had led to cancer. What treatment options can you suggest for each case?

For case 1, I would suggest drug therapy. The overactive proto-oncogene is caused by a mutated promoter receptor protein of a proto-oncogene. Drug therapy can be used to target the mutated receptor of the proto-oncogene. A drug with a molecule targets and binds to the promoter protein will silence the gene. With a blocked promoter receptor, transcription rates will drop for that gene. For case 2, drug therapy can also be used. It's believed to stop the growth of cancer cells. It's done by selectively blocking the action of oncogene proteins on the growth and the division of cancer cells.

proto-oncogenes

Genes that code for proteins that make cell divide.

tumor suppressors

Genes that code for proteins that prevent a cell from dividing or fix mutations.

cancer immunotherapies

Harnessing the immune system to fight cancer.

27.) 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?

I believe there could be certain environmental factors that make them more susceptible to colon cancer than other ethnic groups. I also believe it could be due to genetics of ancestry. Furthermore, this is all about variation in gene composition.

11.) In cloning human DNA, why is it necessary to insert the DNA into a vector such as a bacterial plasmid?

In recombinant DNA technology, the vector is what carries the foreign DNA molecule. With our human DNA, it cannot be done simply. A bacterial plasmid is able to do this easily.

4.) What does it mean to have a malignant tumor?

It means to have a tumor that is made of cancer cells. This kind of tumor grows rapidly, invades and infiltrates nearby tissues and spreads to other parts of the body. These are involved in metastasis.

DNA repair enzymes

Needed to prevent cancerous mutations.

RAS

Protein that normally encourages cell division when a cell comes in contact with a growth factor.

oncogenes

Proto-oncogenes when mutated.

24.) What are some factors that epidemiologists have associated with a relatively high risk of developing cancer?

Smoking has been determined to be one of the major risk factors that epidemiologists have associated with high risks from developing cancer. This is due to the constant inflammation that can be seen in the body when a person smokes, leading the increased numbers in cell mutations.

7.) It is often the case that a predisposition to certain forms of cancer is inherited. An example is familial retinoblastoma. What does it mean to have inherited an increased probability of acquiring a certain form of cancer? What subsequent event(s) must occur?

Some people inherit a mutant allele that causes a predisposition to cancer, which is present in the germ cells and all the somatic cells of these people in a heterozygous condition. They already have one hit, so if they develop a mutation in the other normal allele, the cell can become cancerous

mutations to proto-oncogenes (oncogenes)

These can create proteins that lead to uncontrolled cell division

tumor suppressor genes

These code for proteins which prevent a cell from dividing.

mutated RAS

This could send signals that the cell should divide even in absence of growth factors. Gain of function.

3.) Dolly made headlines in 1997 when her birth was revealed. Why was cloning Dolly so important, considering that cattle and sheep were already being cloned through embryo splitting?

This is because the way Dolly was cloned was different from embryo splitting. She was cloned by taking a cell from a specific adult animal and then using that cell to make a genetic copy of that adult animal. This also suggested that it might one day be possible to clone humans.

1.) Cloning is a general term used for whole organisms and DNA sequences. Define what we mean when we say we have a clone.

When we say that we have a clone, we mean that we have someone who looks exactly like we do and acts exactly like we do. These clones are molecules, cells, individuals derived from a single ancestor. For example, identical twins are clones because they are derived from a single ancestral cell (fertilized egg).

15.) Which of the following mutations will result in cancer? a. Homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein b. Dominant mutation in a tumor-suppressor gene in which the normal protein product is overexpressed c. Homozygous recessive mutation in which there is a deletion in the coding region of a prot-oncogene, leaving it nonfunctional d. Dominant mutation in a proto-oncogene in which the normal protein product is overexpressed

a. Homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein d. Dominant mutation in a proto-oncogene in which the normal protein product is overexpressed

3.) Benign tumors: a. are noncancerous growths b. do not contain mutations c. are malignant and clonal in origin d. metastasize to other tissues e. none of these

a. are noncancerous growths

4.) What is meant by the term recombinant DNA? a. DNA from bacteria and viruses b. DNA from different sources that normally are not found together c. DNA from restriction-enzyme digestions d. DNA that can make RNA and proteins e. None of these

b. DNA from different sources that normally are not found together

10.) Which enzyme is responsible for covalently linking DNA strands together? a. DNA polymerase b. DNA ligase c. ecoRI d. Restriction enzymes e. RNA polymerase

b. DNA ligase

5.) Metastasis refers to the process in which: a. Tumor cells can die b. Tumor cells detach and move to secondary sites c. Cancer does not spread to other tissues d. Tumors become benign e. Cancer can be cured

b. Tumor cells detach and move to secondary site

8.) A proto-oncogene is a gene that: a. Normally causes cancer b. Normally suppresses tumor formation c. Normally functions to promote cell division d. Is involved in forming only benign tumors e. Is expressed only in blood cells

c. Normally functions to promote cell division

5.) Restriction enzymes: a. Recognize specific nucleotide sequences in DNA b. Cut both strands of DNA c. Often produce single0stranded tails d. Do all of these e. None of these

d. Do all of these

proteins coded for by proto-oncogenes

encourage cell division