UNIT 2: Cellular Reproduction and Cancer Notes

Predict the result of a mutation that allows a cell to move past checkpoint G2 even though DNA replication has not been completed

-DNA could have errors -resulting cells have more mutations

What is metastasis? Why is it harmful?

-cancer cell spreads from a site of origin to another part of the body through the blood or lymph -----cancer cells do this when they loose their ability to adhere to each other It is difficult to locate/ treat multiple tumors

if cyclin was always available in the cell at high concentrations, what effect would this have on the cell cycle?

-cell cycle does not stop at G2 checkpoint (skip over checkpoints)

Explain the process of angiogenesis (growth of blood vessels into a tumor) and how it allows tumors to grow larger.

-cells starved of O2 deep inside a tumor release VGEF (vascular endothelial growth factor) -VGEF triggers blood vessels to grow into the tumors ---*O2 and sugar riched blood can reach the tumor cells and "feed" them-tumor has the resources to grow bigger* It allows food and O2 to reach the cells on the interior of the tumor

Predict the result of a mutation that allows a cell to move past checkpoint M even though the chromosomes were not prepared for division

-chromosomes won't separate properly -extra or missing chromosomes in daughter cells

How do tumor-suppressor genes regulate the cell cycle?

-inhibit the expression of genes involved in speeding up the cell cycle (a gene that stops the cell cycle) -cell cycle's "brakes" *mutations in tumor-suppressor genes lead to cancer by allowing the cell to evade the checkpoints

predict the result of a mutation that allows a cell to move past checkpoint G1 even though the cell has not grown sufficiently

-may be stopped at G2 checkpoint to fix these issues -may not be big enough to properly divide

What can cause the creation of oncogenes?

-mutations in the proteins involved in the growth control pathway so the proteins work all the time, not just when signaled to do so -translocation (moving pieces of chromosomes): proto-oncogenes is now next to a gene that boosts its expression~becomes an oncogene -duplication of a gene~may result in extra receptors for growth fators

Suggest why the cell cycle is shorter in epithelial cells than in liver or muscle cells

-shorter life span (die due to exposure) so they must divide more often to replace cells -increase chance of cancer in those tissues

Viral Infections also lead to inflammation that contributes to cancer

-when your body experiences infection, the immune system triggers the inflammatory response. This dilates the blood vessels to bring white blood cells to the area to fight infection -free radicals are produced to fight infection, but they can damage DNA -dead and damage cells need to be replaced by mitosis. the inflammatory response promotes tissue repair by stimulating cell division. If the neighboring cells that are called to divide have mutations, the new cells will inherit them -tumor growth leads to more inflammation, further fueling the cell division

How do Viruses infect cells?

1) each type of virus tends to infect only a certain type of cell in the body 2) when in contact with host cell, the virus can insert its genetic material into its host, literally taking over the host's functions. 3) an infected cell produces more viral protein and genetic material instead of its usual products 4) sometimes the new viruses bud off the host cell. Other times the cell bursts open releasing the new viruses (lytic cycle)

How can the Lysogenic Cycle lead to cancer?

1) the viral DNA could be inserted into a gene that regulates the cell cycle ----the shut down of a tumor suppressor gene would take the cell one step closer to becoming cancerous 2) some human genes can be taken out and incorporated into the virus ----when the virus infects a new cell, the cancer-causing gene is transferred to the new cell ----cancer-causing genes include ONCOGENES and INACTIVATED TUMOR SUPPRESSOR GENES *virus cells must take over the host cell in the process. They can activate or inactivate genes involved in the cell cycle. Viruses can integrate their DNA in our chromosomes which a) can alter genes resulting in an increase in susceptibility for cancer or b) activate/inactivate cell cycle genes when turning the host cell into a virus factory*

Describe the characteristics that make cancer cells different from normal cells.

1. increase mutation rate- mutations in genes, extra chromosomes, genes are in the wrong location 2. Loss of cell cycle controls- a) don't stop at checkpoints, b) can divide without receiving a signal to do so 3. differentiated- many extra genes turned on 4. lack contact inhibition- doesn't stop dividing when crowded 5. invasive- cancer grows into surrounding tissues 6. induce local blood vessel formation (angiogenesis)-blood provides oxygen and food to the tumor allowing it to grow bigger 7. less adherent-they can divide when not attached to other cells 8. can spread throughout the body via the bloodstream or through the lymphatic system -metastasizes 9. transplantable 10. heritable-genes that predisposed you to cancer

how do cancer cells differ from normal cells in the following ways?

Appearance: cancer cells are abnormally shaped- large nucleus, smaller cytoplasm Genetic Contents: cancer cells consist of extra chromosomes ---dedifferentiated, mutation in proto-oncogenes and tumor suppresor genes, extended telomeres (telomerase is activated) Behavior: -proliferation, metastasizes, avoids apoptosis, lacks contact inhibition and anchorage dependence

What is the normal function of BRCA 1 and BRCA 2 genes

BRCA 1 and BRCA 2 genes are tumor suppressor genes that normally repair DNA damage *When mutated, the DNA isn't repaired at checkpoints and the damage cells can divide

The genetic material could be ___________ or _____________

DNA or RNA

viral E6 Oncoprotein in HPV

E6 protein binds to p53 and inactivates it. ---p53 is a tumor suppressor gene that stops the cell cycle and apoptosis when there is too much DNA damage ---infected cells (HPV) divide with damage DNA E6 protein activates telomerase (extends the telomeres) which causes the cell to become immortal

What "phase" of the cell cycle are cells said to be in when they are not dividing or planning to divide

G0

the cell grows by producing more proteins and organelles

G1

there is ample supply of energy and raw materials available

G1 and G2 checkpoint

there is adequate room in the environment for more cells

G1 checkpoint

which checkpoint appears to regulate whether the cell is in G0 or not?

G1 checkpoint

Name the three checkpoints

G1, G2, M

the cell prepares for cell division with the appearance of centrosomes

G2

The DNA has been completely replicated and checked for errors

G2 checkpoint

Examples of Viruses and Their associated cancers

Human Papilloma Virus (HPV), Types 16 and 18: cervical cancer Epstein Bar Virus (Mono): Lymphoma Hepatitis B or C: liver cancer Human T-Lymphotropic Virus (HTLV): adult T-cell Leukemia

Mitosis and cytokinesis

M

all chromosomes are attached to the spindles

M checkpoint

Which checkpoint in the cell cycle is regulated by the concentation of MPF

MPF peaks right before Mitosis. when the cell is in G2 phase

Why does cancer often take years to develop?

Multiple mutations must occur for cancer cells to develop ways of evading cell cycle control and gain other traits that allow it to become invasive

Explain why cancer cells often have to have multiple mutations in both proto-oncogenes and tumor-suppressor genes

Need to cut the breaks (mutate tumor suppressor genes) and press down on the gas pedal (oncogenes) to make the cell cycle go out of control.

can the change in cyclin concentration during mitosis be explained by the fact that the cell divides in two and thus divides the material in the cell into two smaller volumes? If no, propose an explanation for the change in concentration that is seen.

No- cyclin concentration drops to zero not half. Cyclin is degraded in mitosis (CDK is an enzyme that stays constant because it remains unchanged through the reaction. Cyclin is CDK's substrate. It is catalyzed by CDK)

Does inheriting a mutation in a cancer gene, such as BRCA 1, guarantee the development of a cancerous tumor? Why or why not?

No- only inheriting a susceptibility (higher chance of developing cancer) ----it takes multiple mutations to develop cancer

DNA replication occurs

S

What are the two main causes of cancer? How do these behaviors contribute to the development of the disease?

Two main causes: smoking and dieting -Smoking: chemicals damage DNA -Dieting: a poor diet leads to a lack of antioxidants that destroy free radicals. Free radicals can damage DNA. Fatty foods move slower through digestive system giving them time for mutated cells to develop

Radiation

UV lights and X-rays, radioisotopes exposure

Biopsy

a diagnostic tool that removes tumor cells, often with a needle for examination by a pathologist

MRI

a diagnostic tool that uses magnetic waves to create images

Ultrasound

a diagnostic tool that uses sound waves to create images

Mammogram

a diagnostic tool that uses x-rays to create images

Chemotherapy

a treatment that destroys cells with anticancer drugs

Radiation Therapy

a treatment that destroys cells with internal or external radiation

hormone therapy

a treatment that prevents cancer cells from getting or using the hormones they needed

surgery

a treatment that removes all of the tumor and surrounding tissues

biological therapy

a treatment whose drugs bind to sites on cells and block proteins that allow cancer cells to grow

Chemical agents

alcohol, tobacco smoke, chemicals

proto-oncogenes

are the accelerator: increase in cyclin and control pathways that stimulate cell cycle

propose an explanation for the change in the maturation promoting factor concentration throughout the cell cycle based on your knowledge of the concentration of CDK and cyclin

as cyclin increases in interphase, it can combine with CDK to form MPF. That's why its concentration increases as cyclin increases

treatment of therapeutic Vaccines (Biological therapy)

boost the body's immune system so it can fight off cancer that has already developed.

tumor suppressor gene

brake: stops cell division when cells: are crowded, DNA needs to be repaired, or if apoptosis should occur ---regulates many checkpoints

describe the changes in the concentration of CDK as the cell moves through different phases of the cell cycle

constant because enzymes stay unchanged

identify the three parts of the maturation promoting factor (MPF)

cyclin, CDK, and phosphate group (energy needed)

Explain how mutagens causes mutations

damage DNA -if not repaired, it can alter gene function and lead to cancer

Distinguish between gametic and somatic mutations

gametic: inherited in sperm/egg somatic: (body cells) occur in organism's lifetime

Examples of DNA viruses include

herpes, epstein bar (mono), chicken pox, HPV

describe the changes in the concentration of cyclin as the cell moves through different phases of the cell cycle

increase in interphase and decrease in mitosis

Explain the difference between inherited and sporadic cancer

inherited cancer: cancer causing mutation occurs in the embryo (the embryo received it from its parents) so every cell in the embryo contains that mutation and is one step closer to becoming cancerous (predisposition) (ex: BRCA1 gene in breast cancer) sporadic cancer: cancer causing mutations occur in body cells during lifetime (most common)

Vaccines

injection used to boost your immune system

how might a cell be affected by the development of a degradation-resistant cyclin mutant?

it is continually stimulatated to go through G2 checkpoint and divide with any damaged DNA

Why is cancer often referred to as a "disease of old age"?

it takes multiple mutations to accumulate before the cell can become cancerous

Examples of RNA viruses include

measles, mumps, rabies, ebola, influenza, flu

suggest two or more combinations of mutations that would tend to allow the cell cycle to become unregulated

mutation in a proto-oncogene (speed up cell division) and mutation in tumor suppressor so it doesn't work (does not stop cell division)

Explain how a mutation in a tumor suppressor gene can contribute to cancer

p53: normally decides if the cell repairs its DNA or undergoes apoptosis at the cell cycle checkpoints ---if mutated, mutated cells with damaged DNA don't stop at the checkpoints and continue to be copied BRCA 1 and 2 genes: normally repair damaged DNA ---if mutated, chromosomes are more likely to break

Preventative vaccines

prevent infection of cancer causing viruses

All viruses consist of a ___________________ , called a _______ and ______________.

protein coat, capsid, genetic material

How do proto-oncogenes and oncogenes differ?

proto-oncogenes: normal genes that trigger cell division oncogenes: mutation in proto-oncogene ---boots cells division ---cell cycle's "gas pedal" is stuck

Persistent Viral Infections: The Lysogenic Cycle

sometimes the viral genome becomes incorporated into the host cell's genome, where it remains dormant

What are telomeres? How does the loss of control over telomere length contribute to cancer?

telomeres (normal functioning): repeating segments at the end of chromosomes and they shorten with every cell division, eventually leading to cell death (limits the number of cell division) telomeres (cancerous): some cancer cells have the enzyme telomerase activated. -- Telomerase's job is to extend the length of the telomeres -------telomeres never shorten, leading the cell to become immortal

What is a tumor? What is the difference between benign and malignant tumors?

tumor: a growth that contains cells that have escaped the controls of the cell cycle benign tumor: grows in place and doesn't invade surrounding tissues (in-situ) malignant tumors: cancer, tumor invades surrounding tissues

can infection increase your risk of cancer?

virus cells must take over the host cell. In the process, they can activate or inactivate genes involved in the cell cycle.

Describe another situation in which the cell cycle shortens to allow rapid cell division before returning to normal

when tissues are damaged and need repair or the body needs to grow