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Patho > Q2 Cancer > Flashcards

Q2 Cancer Flashcards

1
Q

Cell cycle phases in order
Acronym?

A

G0 - rest
G1 - RNA and protein synthesis. Restriction point included here prior to next stage
S - DNA synthesis (doubled) RNA and proteins synth continues.
G2 - proof reading, RNA/protein synth continues
M - Mitosis (nuclear division) and cytokinesis (cell divison)

G0 1 Step forward until you Get 2 the Mall.

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2
Q

Where are the 3 cell cycle check points?

A

End of G1, early S and end of G2 prior to M.

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3
Q

Regulators of cell cycle have 2 main functions:

A

Suppression - TSGs = inhibiting progression if things don’t check out - allows for DNA repair, pauses and induction of apoptosis
Drive - Proto-oncogenes = growth, survival and proliferation

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4
Q

Rb, TP53, BRCA1/2 are all examples of _____
cycling, c-myc, EGFR, RAS and RAF are all _____

A

TSGs
Proto-oncogenes

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5
Q

T/F: Your patient has a mutated proto-oncogene. This will not disrupt cell regulation since they still have the other one.

A

FALSE. One mutated photo-oncogene will disrupt cell regulation.
One disrupted TSG will not cause issues - only 1 functioning gene is needed to guard DNA.

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6
Q

Only 1 ______ is needed to guard DNA, however if one ______ has a mutation, then cell regulation will be disrupted.

A

TSG
proto-oncogene.

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7
Q

In a health cell, there is a balance of _______ and _________ for quality control

A

TSGs inhibiting cell cycle
proto-oncogenes pushing cell through.

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8
Q

With out _______ cyclins cannot function. What is their purpose?

A

CDK (cyclin dependent kinase)
This pair is a photo-oncogene, so it helps the cell progress through the cycle.

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9
Q

What inhibits CDK/cyclin pairs?

A

Inhibitory proteins (like TSGs)

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10
Q

Tell me about p53

A

This is a TSG that proof reads DNA. If an issue is detected, it sends p21 to inhibit CDK at the G1 cycle. This pauses the cycle and allows GADD45 to repair the DNA. If DNA repair is successful, the cell re-enters the cycle and continues with proliferation, however if repair is unsuccessful, Bax triggers apoptosis.

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11
Q

What damages DNA?

A

Oxidative stress, Nitrosative stress, inflammation, radiation and UV.

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12
Q

How is Rb TSG MOA different from p53?

A

Rb is bound to E2F (elongation factor) which keeps it inactive. E2F’s job is to elongate DNA to assist cell in progressing to S phase. If all is well, CDK4/6 phosphorylates RB which pays E2F to detach and do it’s job. If all is NOT well, no phosphorylation happens which means DNA is not elongated and cell arrests and cannot progress to S phase.

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13
Q

What happens when both TSG p53 are mutated.
Both or 1 Rb mutated?

A

P53 proof reads DNA. Since little or no proofreading happens, there is no input from p21 or other CDK inhibitors, so the cycle continues and assumes all is well. The end result is cells with damaged DNA are allowed to replicate and in doing so gain mutations. This results in cancer.
Nothing to ‘dock” or hold back the E2F so it goes to work elongating DNA and pushing the cell to S phase despite potential mutations.

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14
Q

What happens when CDKs are mutated?

A

The control proteins (p53, p21, etc) don’t fit and can’t control them anymore, so the cell cycle progresses despite potential mutations.

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15
Q

In normal Growth Factor release, _________is present to control it.

A

Negative feedback mechanism.

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16
Q

What does consitutively active mean?

A

The gas pedal is stuck. There is a mutation which knocks out the negative feedback loop, so GF receptor genes are allowed to be extra active all the time with no inhibition.

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17
Q

What are 2 causes of constituteivly active cell?

A

Mutation in GF receptor or mutation in RAS protein.

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18
Q

What mutation is most likely responsible for lung ca development in never smoker women?

A

EGFR mutation.
Especially Asian women

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19
Q

What does it mean that a drug is cell cycle independent?

A

The drug is active during 2 or more phases of the cell cycle.

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20
Q

If a patient has an EGFR mutation, then they can receive ______ for their ca treatment.

A

TKIs

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21
Q

How does estrogen affect the cell cycle?

A

Estrogen increases expression of CCND1 (cyclin D1) which codes for CDK 4/6 which allows for phosphorylation of Rb and E2F to elongate DNA and push forward to the S phase of cell cycle. Inhibiting estrogen synthesis will reduce CCND1 and CDK 4 levels, preventing DNA elongation.

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22
Q

What are DNA Adducts? Examples?

A

Strand breaks or mutations caused by carcinogens binding to DNA
Monoalkyllation
Intercalating (chemotherapy and industrial dyes), inter strand crosslinked (ionizing radiation)
Double/single strand break
Intrastrand Crosslink (UV light)

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23
Q

Why are DNA adducts bad?

A

They’re like a piece of string caught in a zipper - makes the DNA helix difficult to unzip and therefore more likely to fracture/be damaged or mutated during replication.

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24
Q

What is the most important risk factor for cancer in the WORLD?

A

Tobacco

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25
Q

What mutation does Aflatoxin cause and which cancer is this associated with?

A

It’s a fungus mutagen that causes G249T mutation in the RAS proto-oncogene
Hepatocellular cancer.

26
Q

The only instance where anti-oxidants have been studied to have improvement?

A

Letting/zeaxanthin and vitamin e/c in reduced progression of age related macular degeneration.

27
Q

What are some key signs of genetic cancer causing defects?

A

Multiple persons within a generation and multiple generations with cancer
Cancer dx prior to age 50
More than 1 cancer in the same person
Family hx of rare cancers.

28
Q

People with BRCA1/2 mutations are _______ more likely to develop breast ca

A

38-63%

29
Q

Match the infectious agent to the type of cancer they cause:
H Pylori
HPV
HBV
HCV
EBV
KSHV
Plasmodium falciparum
Schistosome
Clonorcchis sinensis

A

H pylori - MALT and gastric cancer
HPV - cervical, reproductive, anal, oral cancer
HBV/HCV - hepatocellular cancer and lymphoma
EBV - lymphoma
KSHV - Kaposi sarcoma
Plasmodium - Burkett lymphoma
Schistosome - bladder ca
Clonorchis - cholangiocarcinoma.

30
Q

Leading cause of infectious cancer in men? Women?

A

men - H.pylori
Women - HPV

31
Q

Patho Phys of H pylor induced oncogenesis

A

Oxidative damage causes acid glands in the stomach to atrophy and go away. This leads to intestinal Metaplasia then dysplasia and finally carcinoma.

32
Q

The cellular destruction of H. Pylori is reversible up until low grade dysplasia. After low grade dysplasia, it WILL progress to cancer.

A
33
Q

Which of the below histological samples taken from a patient with H pylori is still reversible?
A. Low grade dysplasia/adenoma
B. Gastric adenocarcenoma in distal stomach
C. High grade dysplasia/adenoma.

A

A.
B + C are not reversible.

34
Q

T/F: a patient with Grade 1 (low grade) cervical episomal cells is reversible. what is the patho behind this?

A

True. After episomal cells become integrated, it is irreversible

Normally, E2 controls the bad boys (E7 and E6). HPV integrates E2 altering its struction so control over E6/7 is lost. E6 binds to and blocks Rb fxn and E6 binds to and blocks p53fxn.

35
Q

How is obesity and increased levels of insulin associated with cancer?

A

Increased levels of insulin and ILGF1 promote growth, proliferation and angiogenesis and inhibition of apoptosis

36
Q

How is obesity ad high levels of lepton tied to malignancy?

A

Increased levels of lepton = increased growth signals via RAS and PI3K

37
Q

How is obesity and low levels of adipokine tied to malignancy?

A

Low adipokine = less tumor suppressor function, more angiogenesis and more cell cycle promotion.

38
Q

How is immune deficiency tied to malignancy?

A

Decrease in T and B cells can decrease the body’s ability to neutralize/kill abnormal cells.

39
Q

Why does HIV have such a high rate of cancer?

A

Imagine a picket fence where each steak is a group of specialized T and B cells who have memory to attack different viruses/bacteria. As HIV kills off these cells, there may be whole pickets killed off and now no memory exists on how to fight that specific pathogen.

40
Q

How does the HIV Tat gene promote oncogenesis?

A

Activates proto-oncogenes like c-my which promote angiogenesis, inhibit p53 and support inflammation by activating cytokines.
Enhances E6/7 expression which leads to rapid progression of cervical cancer.

41
Q

What is the tie between HIV and lymphoma?

A

In HIV, there is more frequent replication of B cells since they’re being killed by the virus. Greater replication = greater chance of genetic error.

42
Q

In order for a Tcell to activate it needs:

A

2 factor authentication: MHC-TCR AND CD28-B7-1

43
Q

In order to regulate the immune response, the APC’s B7-1 stops engaging with the T-cell ______ and instead engages with _______

A

CD28
CTLA-4

44
Q

An APC is engaging with a T-cells CD28. This is ___________(activating or deactivating) the T-cell.

A

CD28 -ACtivate! (Rhymes with 8)
CTLA-4 - deactivate (“hit the floor” go to sleep)

45
Q

What do you do If you want a T-cell to STAY turned on?

A

If you want him to STAY activated, then you use an antibody to bind/block CTLA-4 so that CD28 stays open and continues to activate Tcells

46
Q

If a APC PDL1 ligand binds to a Tcell PD1 receptor, what happens?
In a NORMAL body, is this good or bad? Is it good or bad with cancer?

A

Programmed cell death of the immune Tcell is initiated because PD1 activation blocks B7-1/CD28 interaction.
NORMALLy this is good because it prevents the immune system from becoming overexuberant. Keeps it in check.
With cancer, some cancer cells have evolved to display PDL1 which allows them to blunt/turn off the immune response by binding to PD1 on the Tcell.

47
Q

How can we combat cancer cells who have evolved to display the PDL1 ligand?

A

AntiPD1 and antiPDL1 antibodies can block the binding of the cancer PDL1 and Tcell PD1 receptor, leaving the immune system on, increasing T cell proliferation and allowing continued tumor destruction.

48
Q

What kind of tumors benefit most from check point inhibitor treatment?

A

Any tumor that has a DNA repair deficit.

49
Q

Check point inhibitors are a type of immune therapy.

A
50
Q

What is a large caveat with immune therapy such as checkpoint inhibitors?

A

-itis of everything! It ramps up the immune response to the point where the body may start attacking itself. -Itis of any organ in the body can occur and can be very severe/fatal.

51
Q

What does it mean if a certain type of cancer has a B-RAF mutation? What type of meds help in this situation?

A

Negative feedback for GF is inhibited so proliferation, survival, growth and angiogenesis continue unabated.
TKI (tyrosine kinase inhibitors) - block the signal transduction from BRAF to MEK and ERK, Turing in off those pro-survival signals

52
Q

How do TKI meds work?

A

Block signal transduction from BRAF - MEK-ERK turning off pro-survival signals

53
Q

If a cancer is expressing PDL1, is this good or bad?

A

Good sign - it means it will be more responsive to tx.

54
Q

How does CAR-T work?

A

Chimeric Antigen Receptor T cells
Patient’s lymphocytes are collected and modified in the lab to have a receptor that will bind to Leukemia cell CD19. These modified T cells are then reinfused to the patient and attack leukemia cells by binding to them and releasing performing and granzyme.

55
Q

What is the caveat to CAR-T treatment?

A

It is extremely cytotoxic.
Best results seen in children with refractory acute lymphoblastic leukemia.

56
Q

CDKs work with _______ to guard each phase of the cell cycle. They are controlled by _______

A

TSGs
CDKis.

57
Q

T/F: When TSGs become constitutively active, they allow for constant signals for growth, proliferation and survival.

A

False. Proto-oncogenes.
TSGs are inhibitory.

58
Q

You can treat a presence of ______ but not an absence of _______

A

Proto-oncogenes but not an absence of TSGs.

59
Q

Targeted therapies are good for ________ not ________

A

Gain of function mutations (overactive proteins) not loss of function (TSG mutations)

60
Q

What other cells could CAR-T cells potentially start killing?

A

CAR-T cells attack CD19 on the leukemia cells. B lymphocytes are the only other cell in the body with CD19, so they could also be attacked.

61
Q

A patient is deemed a “survivor” from the moment _______ until ________

A

They are diagnosed with cancer until they die

Patho (18 decks)

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