Molecular Biology Genetics and Immunology of Cancer Flashcards Preview

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Flashcards in Molecular Biology Genetics and Immunology of Cancer Deck (27):
1

DNA is composed of what 4 bases? RNA?

Briefly describe how DNA becomes proteins.

DNA: Adenine, thymine, guanine, cytosine

RNA: Adenine, uracil, guanine, cytosine


DNA...transcription via RNA polymerase...RNA.... translation via ribosome... protein.

2

What is terminal differentiation? where do these cells originate from?

example of terminally differentiated cells.

Describe stem cells.

Terminal differentiation: cells that have lost the ability to proliferate, they have a finite lifespan andd are replaced with new cells produced from stem cells.

Examples: neurons, muscle cells, cardiac cells

Stem Cells: capable of self renewal; cells divide without undergoing terminal differentiation.

3

Describe each of the cell cycle phases.

G0 = resting phase, cell has left the cycle and has stopped dividing

G1= cells increase size, ensures everything is ready for DNA synthesis.

S = DNA replication

G2 = gap between DNA synthesis and mitosis, cell continues to grow.

M = cell growth stops at this stage, beginning of cell division.

4

What are the phases of mitosis?

Interphase, Prophase, metaphase, anaphase, telophase, cytokinesis

5

What are the 2 categories of cancer genes?

Cancer cells contain genetically altered DNA, they can be either hereditary or somatic, which mutation type correlates with each?

Dominant and recessive:

-dominant from proto-oncogenes
-recessive from tumor suppressor


Hereditary - germline

Somatic - spontaneous

5

What are the 2 categories of cancer genes?

Cancer cells contain genetically altered DNA, they can be either hereditary or somatic, which mutation type correlates with each?

Dominant and recessive:

-dominant from proto-oncogenes
-recessive from tumor suppressor


Hereditary - germline

Somatic - spontaneous

6

What is:
-gain-of-function mutations
-loss-of-function mutations


Describe mutation event that must occur for overactivity mutation/gain of function to occur and underactivity mutation/loss of function.

Gain of function: altered or unregulated activity of a proto-oncogene leads to tumorigenesis

Loss of function: loss of activity in tumor suppressors results in unregulated pathways and tumorigenesis.


Overactivity mutation:
-single mutation event creates oncogene, activating mutation enables oncogene to stimulate cell proliferation

Underactivity mutation:
-mutation event inactivates tumor suppressor gene, no effect of mutation (b/c only affects one gene copy). Second mutation event inactivates second tumor suppressor gene copy, these two inactivating mutations functionally eliminate the tumor suppressor gene stimulating cell proliferation of mutated genes.

6

What is:
-gain-of-function mutations
-loss-of-function mutations


Describe mutation event that must occur for overactivity mutation/gain of function to occur and underactivity mutation/loss of function.

Gain of function: altered or unregulated activity of a proto-oncogene leads to tumorigenesis

Loss of function: loss of activity in tumor suppressors results in unregulated pathways and tumorigenesis.


Overactivity mutation:
-single mutation event creates oncogene, activating mutation enables oncogene to stimulate cell proliferation

Underactivity mutation:
-mutation event inactivates tumor suppressor gene, no effect of mutation (b/c only affects one gene copy). Second mutation event inactivates second tumor suppressor gene copy, these two inactivating mutations functionally eliminate the tumor suppressor gene stimulating cell proliferation of mutated genes.

7

What are the 8 hallmarks of CA?

self-sufficiency in growth signals

insensitivity to anti-growth signals

evading apoptosis

limitless reproductive potential

capacity to evade other tissues

sustained angiogenesis

tissue invasion and metastases

genomic instability

7

What are the 8 hallmarks of CA?

self-sufficiency in growth signals

insensitivity to anti-growth signals

evading apoptosis

limitless reproductive potential

capacity to evade other tissues

sustained angiogenesis

tissue invasion and metastases

genomic instability

8

Cancer cells invade nearby tissues in many ways, one of which is invadopodia. What is this?

Invadopodia are actin-rich protrusions of the plasma membrane that are associated with degradation of the extracellular matrix in cancer invasiveness and metastasis.

8

Cancer cells invade nearby tissues in many ways, one of which is invadopodia. What is this?

Invadopodia are actin-rich protrusions of the plasma membrane that are associated with degradation of the extracellular matrix in cancer invasiveness and metastasis.

9

Molecular Basis of CA

mutations commonly from radiation, chemicals, or viruses may lead to increased synthesis of oncogenes or decreased synthesis of tumor suppressor genes leading to uncontrolled cell growth.

9

Molecular Basis of CA

mutations commonly from radiation, chemicals, or viruses may lead to increased synthesis of oncogenes or decreased synthesis of tumor suppressor genes leading to uncontrolled cell growth.

10

What are proto-oncogenes?

What: normal cell proteins that have the potential to cause cancer when mutated.

10

Describe the grading of each of the following tumors in respect to differentiation, characterisitics, and growth rate.
-I
-II
-III
-IV


Which stages are most likely to be responsive to therapy? Which stage is hardest to get rid of?

I: Well differentiated, looks like tissue of origin, makes proteins like original tissue, slow growing, close to normal cell divison

II. Moderately differentiated, many features like tissue of origin. faster, see occasional mitoses

III. Poorly differentiated, few features of tissue origin, very little organization, see more mitoses

IV. completely undifferentiated anaplastic, has no features to help distinguish its origin, see many mitoses throughout the tissue.


Stages 3 and 4 are most likely to be responsive to therapy

Stage I hardest to get rid of, easiest to treat.

11

What cell type do each of the following tumors originate from?
- carcinoma
- sarcoma
- lymphoma/leukemia
- germ cell tumors
- blastomas

Carcinoma: epithelial cells

Sarcoma: CT cells (including bones)

Lymphoma and leukemia - blood tumors

Germ cell tumors: testicle and ovary

Blastomas: immature cells or embyronic tissue

11

What cell type do each of the following tumors originate from?
- carcinoma
- sarcoma
- lymphoma/leukemia
- germ cell tumors
- blastomas

Carcinoma: epithelial cells

Sarcoma: CT cells (including bones)

Lymphoma and leukemia - blood tumors

Germ cell tumors: testicle and ovary

Blastomas: immature cells or embyronic tissue

12

Are most CA inherited or sporadic?

Most CA are sporadic!

13

Describe metastasis on a cellular level

1. clonal expansion and growth

2. metastatic subclone adheres and invades basement membrane

3. passage through extracellular membrane and intravasation

4. binds to host lymphocyte and platelets forming tumor cell bolus

5. extravasation and metastatic deposit

6. angiogenesis and growth

*may also spread through lymphatic system

14

What is the MC sites of metastases for each of the following?
-breast
-lung
-colorectal
-prostate
-melanoma
-primary brain

Breast: axilla LN, internal mammary LN, bone

Lung: hilar LN, mediastinal LN, supra-clavicular LN

Colorectal: pelvic LN, mesenteric LN, liver

Prostate: Pelvic LN, bone

Melanoma: Regional LN

Brain: brain and peritoneal, pleural CSF

15

Why are some cancers much more aggressive than others?

b/c cancer cells can be aneuploid; more or less than 46 chromosomes

16

Describe the grading of each of the following tumors in respect to differentiation, characterisitics, and growth rate.
-I
-II
-III
-IV


Which stages are most likely to be responsive to therapy? Which stage is hardest to get rid of?

I: Well differentiated, looks like tissue of origin, makes proteins like original tissue, slow growing, close to normal cell divison

II. Moderately differentiated, many features like tissue of origin. faster, see occasional mitoses

III. Poorly differentiated, few features of tissue origin, very little organization, see more mitoses

IV. completely undifferentiated anaplastic, has no features to help distinguish its origin, see many mitoses throughout the tissue.


Stages 3 and 4 are most likely to be responsive to therapy

Stage I hardest to get rid of, easiest to treat.

17

Traditional cancer therapies kill rapidly dividing tumor cells but may spare stem cells, why is this a problem?

This is a problem b/c this may spare abnormal stem cells that can give rise to new tumors.

18

What are properties of cancer stem cells?

abilities to self-renew*

the ability to differentiate into multiple cell types

they form distinct population in tumors that likely causes dz relapse and metastasis.

19

Are most CA inherited or sporadic?

Most CA are sporadic!

20

What are some common hereditary CA syndromes

Hereditary breast/ovarian cancer syndrome

Lynch Syndrome (HNPCC- hereditary non-polyposis colon CA)

Familial Adenomatous polyposis syndrome