Handorf Cancer Flashcards by Alex Maxted

2 heritable properties defining cancer cells:

1) they reproduce in defiance of the normal restraints on cell division
2) they invade and colonize territories normally reserved for other cells

How well did you know this?

Not at all

Perfectly

Adenoma

neoplastic, benign glandular tissue

fibrous CT capsule

How well did you know this?

Not at all

Perfectly

Adenocarcinoma

invasive, cancerous gland tissue

How well did you know this?

Not at all

Perfectly

Cancers have a ________ origin

monoclonal

How well did you know this?

Not at all

Perfectly

How does cancer incidence correlate with age?

Increased incidence

How well did you know this?

Not at all

Perfectly

How does the timing of cancer incidence correlate with carcinogen exposure?

“Delayed onset of cancer after exposure to a carcinogen”

How well did you know this?

Not at all

Perfectly

T/F: According to Dr. Handorf’s lecture, it’s often one mutation responsible for cancer.

F: “multiple mutations in genes associated with cancer” and animal models indiciate that multiple mutations are needed to induce cancer

How well did you know this?

Not at all

Perfectly

T/F: Cancer occurs often in certain families, seemingly due to genetic predisposition

How well did you know this?

Not at all

Perfectly

Cancer cells have a shared ______ in their DNA.

“abnormality”

How well did you know this?

Not at all

Perfectly

What characteristic determines if a cell if malignant?

the ability to metastasize

How well did you know this?

Not at all

Perfectly

Tumor progression involves successive rounds of:

mutation and selection

How well did you know this?

Not at all

Perfectly

What is involves in cancer cell success?

“immortality”

How well did you know this?

Not at all

Perfectly

Indefinite cell growth

Immortalization

How well did you know this?

Not at all

Perfectly

Independence of growth factors in tumors

Transformation

How well did you know this?

Not at all

Perfectly

Invasion and growth at distant site

Metastasis

How well did you know this?

Not at all

Perfectly

Genes the help in cancer avoidance

Tumor Suppressor Genes

How well did you know this?

Not at all

Perfectly

Genes involved in cancer cell predisposition

Oncogenes (Tumor Promoter Genes)

How well did you know this?

Not at all

Perfectly

Genes that directly regulate tumor cell growth

Gatekeepers

How well did you know this?

Not at all

Perfectly

Genes involved in repairing DNA damage or maintaining genomic integrity

Caretakers

How well did you know this?

Not at all

Perfectly

BRCA is a type of ________ gene

Caretaker

How well did you know this?

Not at all

Perfectly

Non-hereditary retinoblastoma arises from

point mutation

How well did you know this?

Not at all

Perfectly

Loss of activity of what genes promote cancer formation?

tumor suppressor genes

How well did you know this?

Not at all

Perfectly

Condition in which a ton of colon polyps develop by age 20 due to an inherited, inactivated susceptibility gene

Familial Polyposis Coli

familial adenomatous polyposis

How well did you know this?

Not at all

Perfectly

T/F: Cells usually arise from one cancerous cell.

How do cancers progress (in general terms)?

In stages (via clonal expansion)

What contributes to the progression of a single cancer cell?

Growth advantage over the surrounding cells

T/F: As mutant cells proliferate, they continue to accumulate mutations.

T (according to one of the pictures in the lecture)

What are 5 general characteristics of cancerous cells?

1. Avoidance of apoptosis 2. Genetic instability 3. Invasiveness (ability to escape home tissue) 4. Metastasis (ability to survive/prolif in other sites) 5. Loss of normal regulation of cell proliferation

Gain of function mutations activate:

oncogenes

Genes that behave in a dominant fashion to stimulate or sustain replication

oncogenes

Loss of function mutations are associated with:

tumor suppressor genes

Genes that act in a recessive manner

Tumor suppressor genes

Loss of function mutations may result what 2 cellular problems?

1. increased/sustained proliferation | 2. decreased DNA repair

How many inactivating mutations are usually required to eliminate the action of p53 genes?

2 | p53 = tumor suppressor gene

First discovered human oncogene

ras

Onocgenes' normal cellular counterpart

proto-oncogenes

What are the different outcomes for one versus two oncogenes present?

1: sporadic tumors 2: MORE sporadic tumors at an earlier age

What are 3 ways that proto-oncogenes become oncogenic? What results from each?

1. chromosome rearrangement = -nearby regulatory DNA sequence results in overproduction of normal protein -fusion to another (more active) gene results in overproduction of normal protein or hyperactive protein 2. gene amplification = normal protein overproduced 3. mutation in coding sequence = hyperactive protein is made in normal amounts

What happens when you fuse normal cells and tumor cells?

Your get cells with a normal phenotype (this suggests that there are tumor suppressors in the normal cells

APC (adenomatous polyposis coli gene) is an example of what type of tumor suppressor gene?

gatekeeper (which directly regulates cell growth)

Childhood tumor that arises in neural precursor cells in the immature retina (What is defective?)

Inherited Retinoblastoma | Rb

The loss of _____ will drive excessive epithelial proliferation.

tumor suppressor gene

The loss of __________ drives the excessively proliferating epithelium towards small tumor formation.

activation of oncogene (which encourages unrestricted growth)

Once a small tumor has formed, what event will result in this tumor becoming larger?

loss of a second tumor suppressor gene | the assumption is that loss of the first one led to the tumor

Once a tumor has become invasive, what is likely to occur?

mutations will begin to accumulate rapidly, resulting in metastasis

An inherited (active/inactive) APC gene causes cancer susceptibility.

inactivated (it's a gatekeeper)

What type of cellular structure is p53?

transcription factor

What is the result of p53 inactivation?

genome instability

3 things that p53 is responsible for in the cell:

1. Induction of cell cycle arrest (G1checkpoint) in response to DNA damage (p21 induction) 2. Induction of apoptosis (excessive mitogenic stimulation or if damage cannot be repaired) 3. Induction of genes required for DNA repair

What causes cancer by binding and inactivating p53?

E6 protein of Human Papillomavirus

What causes Li-Fraumeni Syndrome?

defective p53

Hereditary Nonpolyposis Colorectal Cancer is caused by:

mutations in one of five DNA repair genes involved in DNA mismatch repair

What is the function of the complex containing BRCA1 and 2?

homologous recombination repair | tumor suppression

3 Characteristics of Stem cells:

1. Relatively undifferentiated 2. capacity for unlimited or prolonged self renewal 3. can produce at least one highly differentiated cell type

What abilities do stem cells and cancer cells have in common?

1. extensive ability to proliferate | 2. can give rise to abnormal tissues

T/F: Most tumors have a clonal origin.

Explain why tumors and stem cells are both considered to be heterogenous.

different phenotypic characteristics different proliferative potentials (tumor cells have these characteristics because they have a clonal origin)

What suggests that tumor and stem cells undergo analogous processes?

Because most tumors have a clonal origin, tumorigenic cancer cells must give rise to phenotypically diverse progeny, including cancer cells with different ranges of proliferative potential. (this needs more clarification)

Why are stem cells targets of transformation?

already actively proliferating (other cells would have to develop self-renewal potential, in addition to whatever other mutations)