Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cancer Biology > Exam 1 > Flashcards

Exam 1 Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

local cancer, not metastasizing, likely won’t metastasize, less problematic

A

benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

starting to spread or already spread to another site in body, problematic, kills

A

malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

endoderm

A

epithelial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

mesoderm

A

connective tissues, muscles, WBC, RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ectoderm

A

nervous, skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

why do epithelial cells often become cancer?

A

replicate a lot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

cancer of epithelial cells that don’t secrete things

A

squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cancer of epithelial cells that do secrete things

A

adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

tumor characteristics

A

progressive, monoclonal, and altered metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

explain how tumors can be progressive

A

normal –> hyper or metaplastic –> dyplsatic –> neoplastic –> metastatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

tissue with excessive number of cells

A

hyperplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

tissue with cells in the wrong place

A

metaplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

individual cells appear abnormal but basement membrane still intact

A

dysplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what falls between dysplastic and neoplastic?

A

adenoma, polyp, papiloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

invasive and cells spread

A

neoplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

cells move to a new tissue

A

metastatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

monoclonal

A

single cells becomes cancerous and replicates into whole tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe the experiment that explained why cancer is monoclonal and not polyclonal

A

only 1 band showing that only 1 type of Ig was present (all cells genetically identical and making exact same proteins versus if polyclonal would have multiple Ig

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

normal metabolism

A

glucose (anaerobic glycolysis) –>pyruvate (aerobic with O2)–> 36 ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hypoxia and metabolism

A

low O2- glucose –> pyruvate –> lactate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

tumor metabolism

A
  • not adequate blood supply
  • hypoxic
  • use a lot of glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

warburg effect

A

cancer cells limit themselves to glycolysis even when O2 abundant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

protooncogene

A

reg, normal gene has potential to turn into oncogene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

oncogene

A

gene/protein that causes/drives cancer and prolif

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

mechanisms to activate a protooncogene to oncogene

A

1) retrovirus
2) point mutations
3) copy # increase
4) chromosomal translocations
5) miRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

tumor suppressor genes functions

A

1) inhibitor of cell cycle
2) activators of apoptosis
3) inhibitors of protooncogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

tumor suppressor gene losing function

A

LOH

1) mitotic recombination
2) during DNA replication
3) chromosomal nondisjunction
4) deletion of portion of chromosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

growth factor

A

protein made/secreted by one cell to tell another to prolif/mitosis/rep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

paracrine growth factor signaling

A

2 cells near neighbors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

endocrine growth factor signaling

A

2 cells not near neighbors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

autocrine growth factor signaling

A

one cell makes own GF, telling to prolif

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does GF act as oncoprotein?

A

autocrine signaling- one cell makes own GF, telling to prolif (epithelial cell expressing GF receptor and due to mutation, expresses ligand)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

EGFR

A

tyrosine kinase that tells cells to prolif ONLY when it binds EGF

34
Q

describe EGFR/EGF in normal cell

A

EGF binds to 2 copies of EGFR, forces EGFR to homodimerize and turn on kinase activity (alone, EGFR can’t phosphorylate itself, but if close to another, can start phosphorylating)

35
Q

autophosphorylation vs transphosphorylation

A

EGFR p EGFR but not itself so trans

36
Q

ligand independent firing

A

even without EGF, EGFR can dimerize and turn on kinase activity through 5 mechanisms which result in losing ligand binding domain and locking into dimerization shape)

37
Q

Why is having signaling evolutionarily favorable?

A
  • regulation
  • redundancy –> safety in having a lot of steps in case something goes wrong
  • signal amplification
38
Q

Ras signaling protogene to oncogene ex

A

mutations

  • switch glycine to valine in Ras protein making Ras always on by abolishing GTPase fun
  • miRNA mut, lose ability to reg Ras protein levels and inhibit Ras transcription (more Ras protein in cell)
  • glycine to arginine making PI3K better at P PIP2
39
Q

integrin signaling in normal cells

A

need 2 signals to prolif

1) GF signaling
2) integrin signaling

*gets survival signal by attaching to ECM, only prolif if ECM and GF present

40
Q

ECM limits

A

number cells in body, attach or die

41
Q

integrin signaling in cancer cells

A

anchorage independent growth so only need GF signaling

*gets survival and prolif signals without ECM

42
Q

when integrins bind to ECM…

A

integrins cluster at focal adhesions occur so FAK can do transphosphorylation

43
Q

integrin signaling steps

A

1) integrin clustering at a focal adhesion
2) focal adhesion kinase (FAK) will transphosphorylate
3) P FAK can bind to GRB2/SOS
4) Ras gets phosphorylated and activated by GRB2/SOS

44
Q

PI3K is what type of signal

A

anti-apoptotic

45
Q

Jak/Stat is a signaling pathway for

A

circulating cells

46
Q

proteins involved in Jak/Stat pathway

A

GF cytokines, transmembrane receptor, Jak, STAT

47
Q

Jak proteins

A

class of kinases that bind to transmembrane receptors, transphosphorylate when dimerization happens, P transmembrane receptor

48
Q

STAT proteins

A

bind to P transmembrane receptor, get P, dimerize, go to nucleus to turn on expression of genes for proliferation

49
Q

Beta catenin is involved in

A

GF signaling and binding cadherin

50
Q

Wnt

A

type of GF that uses Beta catenin to turn on prolif (APC tumor repressor)

51
Q

APC mutation

A

out of control proliferation in colon

52
Q

no APC present

A

transcription ON all the time

53
Q

colon cancer

A
  • shed epithelial cells.. need to be repopulated
  • stem cells located in crypts of colon
  • stromal cells secrete Wnt GF to drive prolif of stem cells
54
Q

Beta catenin in colon cancer

A

B-catenin off, prolif off

55
Q

what happens if Wnt is not present?

A
  • Wnt doesn’t bind frizzled receptor
  • APC and friends bind P Beta catenin
  • Beta catenin degraded and not acting as transcription factor
56
Q

what happens if Wnt is present?

A
  • Wnt binds frizzled receptor
  • APC and friends bind frizzled
  • Beta catenin enters nucleus and turns on transcription of genes for prolif
57
Q

why is the cancer phenotype recessive?

A

need 2 mutated copies, multiple issues accumulate for normal to cancer

58
Q

Rb is a

A

tumor suppressor gene associated with retinoblastoma

59
Q

familial retinoblastoma

A

usually both eyes affected, multiple tumors, slightly younger avg age of onset

60
Q

familial retinoblastoma genetics

A

at birth, one inherited mutated RB gene and one WT –> LOH –> disease

61
Q

sporadic retinoblastoma

A

usually one eye

62
Q

sporadic retinoblastoma genetics

A

at birth both WT –> random de novo mut –> LOH–> disease

63
Q

LOH ways

A

1) mitotic recombination
2) during DNA replication
3) chromosomal nondisjunction
4) deletion of portion of chromosome

64
Q

mitotic recombination

A

during mitosis, homologous chromosomes swap “homologous” genetic info

65
Q

during DNA replication

A

sometimes DNA poly will “jump” from one homologous chromosome to another (part of mut copied into WT)

66
Q

chromosomal nondisjunction

A

unequal pulling of chromosomes, possible for cell to get 2 mut copies of chromosomes

67
Q

deletion of portion of chromosome

A

part of WT randomly deleted + mut —> missing WT copy of gene + mut version (2 mut in end)

68
Q

VHL

A

ubiquitin ligase, kidneys and blood vessels

69
Q

pVHL

A

involved in sensing O2 levels

70
Q

H1F1a

A

transcription factor, turns on VEGF exp if O2 levels low

71
Q

VEGF

A

tells blood vessel cells to prolif

72
Q

problems with VEGF and HIFIa

A

cancer mut in pVHL that causes more VEGF

73
Q

normoxia conditions and HIFIa

A

-HIFIa gets hydroxyl groups added
-pVHL can bind to HIFIa with hydroxyl groups
-pVHL adds ubiquitin to HIFIa
HIFIa gets degraded

74
Q

normal cell cycle

A
  • end M to R- cell taking in signals from environment and using signals to decide prolif or not
  • R to M, cell no longer pays attention to external signals (committed)
75
Q

cancer cell cycle

A

prolif without proper signals

76
Q

cyclin/CDK levels

A

CDK proteins stable and cyclin fluctuate

77
Q

external signals (integrin/GF) control which cyclin

A

D

78
Q

cyclin + CDK required for

A

kinase activity

79
Q

cyclin/CDK are proteins related to

A

DNA rep and mitosis

  • P of histones –> loosening chromatin structure for DNA rep
  • P of DNA poly subunits –> need for DNA rep
  • P nuclear mem proteins –> lead to destruction –> allow M
80
Q

no Rb is like

A

hyper P Rb (not bound DNA, transcription of cell cycle genes)

81
Q

HPV causes

A

cervical cancer

  • E7 protein from HPV adds ubiquitin to Rb –> degrade
  • cell will then transcribe its cell cycle genes

Cancer Biology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions