Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Molecular biology of Cancer > Lecture Glossary 1&2 > Flashcards

Lecture Glossary 1&2 Flashcards

(81 cards)

Start Studying
1
Q

Oncogenes

A

Mutant alleles of proto-oncogenes; involves gain of function

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

TSG

A

Tumor Suppressor Genes

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

Tumor Suppressor Gene Types

A

1 - Promoters; 2 - Caretaker Genes; mutations involve loss of function

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

Promoter mutation

A

leads to transformation by directly releasing the brakes on cellular proliferation (ie traditional tumor suppressors p53 and pRb)

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

Caretaker mutation

A

no longer able to ensure the integrity of the genome ie those involved in DNA repair; said to have a mutator phenotype

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

Hallmark 1

A

Sustaining poliferative signalling; Therapeutic approach: EGFR inhibitors

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

Oncogene products for proliferative signalling (5)

A

Growth factors; growth factor receptors; signal transduction proteins; nuclear regulatory proteins; cell cycle regulators

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

Oncogenic Growth Factors (2 ie)

A

platelet-derived growth factor (PDGF); transforming growth factor alpha (TGF-a)

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

Oncogenic Growth Factor Receptors (3 Tyrosine Kinase Receptors ie)

A

ERythroBlastic oncogene B ERBB1 (Epithelial Growth Factor Receptor EGFR); ERBB2 (Human Epidermal gf Receptor 2 HER2); Anaplastic Lymphoma Kinase ALK

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

Common 2nd Messenger Oncoproteins

A

RAS; RAF; Pl3K; MYC; D cyclins

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

Hallmark 2

A

Evading Growth Suppressors; insensitivity to anti-growth signals; Therapeutic approach: Cyclin-dependant kinase inhibitors

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

p53

A

Guardian of the Genome; accumulates and binds to damaged DNA; alt senescence; G1 arrest and succesful repair else apoptosis

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

pRb (protein); RB (gene) RetinoBlastoma

A

Governor of Proliferation (cell cycle); hypophosphorylated pRb blocks transcription; subject to cyclin D (eg) phosphorylation; loss of gene RB = loss of pRb

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

Hallmark 3

A

resisting cell death; evading apoptosis; Therapeutic approach: proapoptotic BH3 mimetics

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

apoptosis

A

apo=from + ptosis=falling; programmed cell death

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

Loss of p53

A

mutagenic pathway (Hallmark 2); reduced function of pro-apoptotic factors such as BAX (Hallmark 3); NHEJ pathway (Hallmark 4); loss of synthesis of thrombospondin-1 leading to loss of inhibition of angiogenesis (Hallmark 5)

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

Reduced egress of cytochrome c from mitochondria

A

upregulation of anti-apoptotic factors such as BCL2 BCL-XL MCL-1; loss of Apoptotic Peptidase Activating Factor 1 (APAF-1) which activates caspase 9

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

Upregulation of Inhibitors of ApoPtosis (IAP)

A

inhibit Caspase 9

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

Reduced CD95

A

receptor for FasL enabling Fas-Associated via Death Domain (FADD) leads to Death-induced signalling complex

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

Inactivation of Death-induced signalling complex

A

DISC leads to caspase 8

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

Hallmark 4

A

Limitless replicative potential; Therapeutic approach: Telomerase inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Immortality

A

acquired lesions that inactivate senescence signals and reactivate telomerase which together convey limitless replicative potential

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

Evasion of mitotic crisis

A

Non-Homologous End Joining pathway (NHEJ) after loss of p53 (evasion of senscence) leads to dicentric chromosomes leads to double-stranded breaks (DSB) without telomerase ends in mitotic catastrophe but with telomerase yields cancer

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

Cancer Stem Cells (CSC)

A

cells within a tumor that can self-renew and drive tumorigenesis; each renewal one daughter remains stem cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Hallmark 5
Sustained angiogenesis; Therapeutic approach: inhibitors of VEGF signalling
26
angiogenesis
the formation of new blood vessels from pre-existing vessels
27
Angiogenic activation
RAS MYC and MAPK signalling upregulate Vascular Endothelial Growth Factor (VEGF) expression and stimulate angiogenesis
28
Hallmark 6
Tissue invasion and metastasis; Therapeutic approach: inhibitors of HGF/c-Met
29
EMT-MET
Epithelial-mesenchymal transition & reverse
30
mesenchyme
from mesos=middle + enkhuma=infusion; undifferentiated mesodermal cells that give rise to such structures as connective tissues & blood & lymphatics & bone and cartilage
31
Tissue Invasion
Tumor moves to neighbouring differentiated cells ie from epithelial to basement membrane
32
Intravasation
down regulation of adhesion molecules like E-cadherin enables tumorous cells to detach from primary tumor and enter blood stream
33
Extravasation
Tumorous cells leave blood stream and attach to distant arteriole
34
Micrometastasis
Tumor cell division begins in new location
35
Metastasis
Occurs when colonization takes and tumor angiogenesis promotes growth
36
matrix metalloproteases
a group of enzymes that in concert are responsible for the degradation of most extracellular matrix proteins during organogenesis growth and normal tissue turnover
37
chemotaxis
movement of a cell in response to chemical signals
38
Metastatic process
Tumor and recruited stromal cells secrete proteolytic enzymes (eg metalloproteases & cathepsins) that degrade basement membranes and ECM & release growth factors and generate chemotactic and angiogenic fragments from cleavage of ECM glycoproteins
39
ECM
Extra Cellular Matrix
40
Hallmark 7
Avoiding Immune destruction; Therapeutic approach: Immune activating anti-CTLA4 mAb
41
Immune surveillance
the normal function of the immune system is to constantly scan the body for emerging malignant cells and destroy them
42
Cancer Immunoediting
The ability of tumors to change the immunogenic properties of cells that ultimately leads to the darwenian selection of subclones that are best able to avoid immune deletion
43
immune evasion mechnism 1
selective outgrowth of antigen-negative variants
44
immune evasion mechnism 2
Secretion of immuno-suppressive factors (TGF-ß galectins; sugar-rich lectin-like factor IL-10; prostaglandin E2; metabolites derived from tryptophan; VEGF)
45
immune evasion mechnism 3
Engaging normal immune regulation pathways that serve as checkpoints in immune response (ie upregulating PD-L1&2 cell surface proteins that active the Programmed Death-1 (PD-1) receptor on effector T cells and inhibit T cell activiaton)
46
immune evasion mechnism 4
Induction of regulatory T cells
47
Hallmark 8
altered tumor metabolism; Therapeutic approach: aerobic glycolysis inhibitors
48
Warburg effect
aerobic glycolysis
49
aerobic glycolysis benefit
provides rapidly dividing tumor with metabolic intermediates required for synthesis of cellular components (through PI3K/Akt pathway) not available through mitochondrial oxidative phosphorylation
50
VEGF
Vascular Endothelial Growth Factor
51
Ras
small GTP-binding protein when activated proceeds to stimulate cascade of protein kinases important in a myriad of growth factor responses
52
Myc
transcripton regulator of genes responsible for cell growth and proliferation
53
PI3K
Phosphotidyl Inositol 3 Kinase
54
Akt
Protein Kinase B
55
Autophagy
From auto=self + phagos=eating; 4 steps—vesicle nucleation; vesicle elongation (becomes autophagosome); autophagosome & lysosome docking and fusion (becomes autolysosome); vesicle breakdown and degradation
56
Autophagy progression
In early stages inhibits tumor formation; in late stages promotes tumor formation
57
Hallmark 9
Cancer-enabling inflammation; Therapeutic approach: selective anti-inflammatory drugs
58
Hallmark 10
Genomic Instability; Therapeutic approach: PARP inhibitors
59
Causes of Genomic Damage (5)
inherited germline mutations; environmental factors; loss of function in genome maintenance/repair; infections; intracellular DNA damage
60
Inherited Germline Mutation predispositions
Rb; p53; APC; CDKN2A; BRCA1&2
61
Carcinogenic Environmental Factors
Carcinogens; UV & other irradiation; chemotherapeutic agents
62
Genome Maintenance LoF targets
BRCA; XRCC; MSH; p53
63
BRCA
BReast CAncer gene
64
APC
Adenomatous Polyposis Coli; the APC protein is a negative regulator of ß-catenin concentrations and interacts with E-cadherin in cell adhesion
65
CDKN2a
Cyclin Dependant Kinase iNhibitor 2A; gene encodes at least two proteins responsible for cell cycle regulation
66
XRCC
X-ray Repair Cross Complementing; protein involved in DNA SS break repair
67
MSH
MutS Homolog; protein involved in DNA repair complex
68
Infectious causes of cancer
Viral: HPV–cervical cancer; Bacterial: H Pylori–stomach cancer
69
Carcinogenic Intracellular DNA damage
Spontaneous de-amination; Reactive Oxygen Species (ROS); replicative accidents (ie anaphase bridges)
70
Heriditary Cancers
Genomic instability and mutation primary event
71
Sporadic Cancers
Genetic instability and mutation secondary to sustained proliferative signalling OR evading growth suppressors; followed by resisting cell death
72
PARP
Poly (Adp-Ribose) Polymerase; a family of proteins involvedin DNA repair & genomic stability and programmed cell death
73
BH3
One of the members of the Bcl-2 Homology domain which only has an apoptotic role
74
CTLA4
Cytotoxic T-lymphocyte-Associated protein 4; a protein receptor functioning as immune checkpoint downregulating immune response
75
TNM
Tumor (0-4) indicates primary size; Nodes (lymph) (0-3) degree of spread to lymph nodes; Metastasis (0-1) has cancer spread to distant site
76
anaplasia
ana=backward + plasis= formation; cells with a loss of morphological characteristics and orientation
77
hyperplasia
hyper=over + plasis=formation; cell overgrowth
78
dysplasia
dys=bad + plasis=formation; abnormal growth or development ie enlarged nucleus; cytologically different
79
metaplasia
meta=beyond + plasis=formation; one type of normal cell is replaced by a cell of another type not normally present at the site; 'invaders' appear normal; ie squamous cells replaced by secretory cells
80
adenomas
pedunculated polyps (pre-invsive stalk like growths) in the colon
81
Tumor progression
Normal –> hyperplastic –> dysplastic –> neoplastic –>

Molecular biology of Cancer (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions