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BGD > Cancer Biodiversity > Flashcards

Cancer Biodiversity Flashcards

1
Q

“growth in the absence of stimulus” defines what?

A

Neoplasia.

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2
Q

Carcinogenesis describes the process by which a group of neoplastic cells of monoclonal origin accumulate genetic chances until a metastatic phenotype is reached.

A

Carcinogenesis describes the process by which a group of neoplastic cells of monoclonal origin accumulate genetic chances until a metastatic phenotype is reached.

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3
Q

“Well differentiated” means

A

cell have differentiated correctly and so they look and behave like surrounding tissue.

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4
Q

What is a defining feature of early G1?

A

Mitogen-dependent. Won’t progress without growth signals.

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5
Q

What do we call the point where mitogens are no longer required, and borders the early and late G1 phases?

A

R point

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6
Q

What cyclin is dominant in early G1?

A

Cyclin D (and CDK4,6)

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7
Q

What’s that concept for when both alleles need to mutate to become carcinogenic?

A

The KNUDSON two-hit hypothesis.

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8
Q

What is the relationship between active cyclin:CDK complexes, RB and E2F?

A

E2F mediates S-phase gene transcription.
Constitutively it is inhibited (bound) by the RB protein, which is active in its hypophosphorylated state.
Cyclin/CDK complexes phosphorylate RB, liberating E2F and progressing toward the S phase.

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9
Q

What is the first cell cycle checkpoint?

A

G1/S - checking integrity before replication.

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10
Q

What happens in the S phase?

A

DNA replication

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11
Q

Is p53 important in the G1/S or the G2/M checkpoint?

A

Trick: BOTH.

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12
Q

The G2/M checkpoint: checking ______

A

for DNA damage in replicated DNA prior to mitosis.

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13
Q

What do Raf and CDKs have in common?

A

They’re both Ser-Thr kinases.

Not to be confused with Ras, a regulatory GTPase.

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14
Q

Apoptosis can be pathological or physiological. How does that contrast with necrosis?

A

Necrosis is ONLY pathological.

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15
Q

What kicks necrosis off?

A

Some irreversible injury like ischaemia, which compromises membrane integrity.

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16
Q

What are 4 apoptosis triggers?

A

DNA beyond repair
Disfunctional proteins
Loss of BM adhesion
Immune-mediated apoptosis

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17
Q

Apoptosis is important to ____________.

A

Homeostasis of total cell population.

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18
Q

How does breakdown occur in apoptosis? Two important features.

A
  1. ATP dependent degradation;

2. Blebbing into apoptotic bodies for phagocytic clearance.

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19
Q

There are two pathways to apoptosis. What is the common feature in both of them?

A

CASPASE activation.

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20
Q

What are the two pathways of apoptosis?

A

Intrinsic - mitochondrial

Extrinsic - death-receptor (e.g. Fas, the TNF receptor)

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21
Q

What triggers intrinsic apoptosis?

A

Cytochrome C leakage from damaged mitochondria triggers caspase activation.

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22
Q

What three processes describe the disordered breakdown of DNA in necrosis?
I lied to Clancy; I didn’t put a hex on you to force you to pick your nose.

A

pyknosis, karyorrhexia, karolysis

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23
Q

What three processes describe the disordered breakdown of DNA in necrosis?

A

pyknosis, karyorrhexia, karyolysis

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24
Q

Apoptotic DNA degradation: chr_________ c_________ followed by _________ into __________ and ______ away.

A

Chromatin condensation and fragmentation into portions and blebbing away in apoptotic bodies.

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25
Q

What two words describe necrosis as a whole process under the microscope?

A

Swelling and rupture.

26
Q

What does apoptosis look like under the microscope?

4 aspects.

A

nuclear shrinkage
chromatin condensation
membrane integrity preserved
blebbing into apoptotic bodies.

27
Q

Describe degradation in necrosis?

A

Rupture and leaking of contents or enzymatic degradation.

28
Q

Ultimately what triggers necrotic cell death?

A

ATP depletion and Ca2+ influx.

29
Q

Name the six aspect headings of Apoptosis/Necrosis differences.

A 
Process (physiological?)
Mechanism/trigger
Degradation and dispersal
Inflammation? 
Microscope appearance
DNA degradation mechanism
30
Q

p53 is pro-apoptotic, an example of an antiapoptotic protein would be ____

A

BCL2

31
Q

Contact inhitition is a _____ ______ ______

A

self-regulatory function.

32
Q

Name 8 cancer hallmarks

I can’t get on the phone to Ms Hewitt - she’s gonna help me invase this castle when I can find the philosphophers stone. Once I have that I won’t need anyone’s help. I can avoid any fear of death. I promise I won’t go crazy.

A 
Immortality
Loss of contact inhibition
Tissue invasion/metastasis
Genomic instability
Angiogenesis
Growth factor self-sufficiency
Poor differentiation (and pleiomorphism)
Evasion of apoptosis.

Growth suppressor evasion
Immune evasion

33
Q

What process is overcome to achieve immortality?

A

p53 can sense shortened telomeres and halt cell cycle. This doesn’t happen in cancer.

34
Q

How might cancer overcome telomere-related senescence?

A

Ectopic activation of stem cell telomerases (which lengthen telomeres)

35
Q

What are three methods a cancer can become self-sufficient from growth factors?

A
  1. constitutively active GF receptors.
  2. autocrine GF expression
  3. overexpression of receptors
36
Q

What are two growth factor receptors famously overexpressed in cancer?

A

HER2

EGFR

37
Q

What must a cell be able to do to be metastatic?

A

De-adhere from other cells and migrate through the basement membrane.

38
Q

What is 1) the molecular and 2) the microscopic hallmarks of a ‘mutator’ phenotype?

A

checkpoint dysregulation

abnormal karyotype

39
Q

List 6 cancer risk factors

A 
Diet
Viral infection
UV radiation
ionising radiation
cigarette smoke
environmental pollution

Asbestos

40
Q

List 3 work-related carcinogens

A

Cadmium
Aromatic amines - RUBBER workers, DYE workers - bladder
polycyclic hydrocarbons - COAL GAS workers - skin/lung

41
Q

Aromatic amines. Who’s job is risky?

A

Rubber and dye workers

42
Q

Polycyclic hydrocarbons. Who’s problem?

A

Coal gas manufacturers.

43
Q

List two non-genetically based risk factors for cancer susceptibility

A

AGE and GEOGRAPHY

e.g. melanoma in australia

44
Q

What do coal gas manufacturers need to watch out for?

A

polycyclic hydrocarbons.

45
Q

PHRASES loss-of-function; gain-of-function; loss-of-inhibition

A

augmentation of endogenous function

46
Q

PHRASES proteins whose activities counteract the hallmarks of cancer, generally related to the cell cycle and cell death.

A

qualitative or quantitative changes

47
Q

PHRASES inhibit neoplastic growth; constitutive activation

A

GF, GFr, signal transducers and transcription factors

48
Q

Oncogenes ___ ___ ___ or ___ ___ ___

A

stimulate cell division or prevent cell death

49
Q

NB Oncogene vs proto-oncogene

A

NB Oncogene vs proto-oncogene

Unmutated endogenous version

50
Q

Inheretence patterns:
Oncogenes
TS genes

A

autosomal dominant

autosomal recessive

51
Q

List three growth factor receptors

A

RET, EGFR, HER2

52
Q

Transcription factor oncogene

A

Myc

53
Q

Two ser-thr kinases (oncogenes)

A

CDKs; Raf

54
Q

Three signal transducing oncogenes

A

Ras;
PI3K
Atk

55
Q

What’s a GF oncogene?

A

Gene for PDGF platelet derived growth factor

56
Q

Five TS genes

A 
BRCA1 
BRCA2 
PTEN 
RB 
P53
57
Q

Five non-cancer functions. p53 will have a role in them because p53 has a role in damn well everything.

A 
cell cycle
apoptosis
checkpoints
senescent 
Genome integrity
58
Q

In order, the type of cell as it progresses through teh carcinogenesis stages.

A
  1. normal cell
  2. cell with stem cell like properties
  3. mutator phenotype
  4. cancer cell monoclonal founder
59
Q

Put the four stages of carcinogenesis in order

A
  1. Initiating mutation
  2. Aquisitoin of genetic instability
  3. Acquisition of cancer hallmarks
  4. Further genetic evolution
60
Q

_____ are constitutively expressed and are activated by ______, which aren’t constitutively expressed.

A

CDK; cyclins

BGD (7 decks)

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