10 - Cancer (Unfinished) Flashcards

1
Q

Anaplasia

A

Loss of cellular differentiation

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

Pleomorphic

A

Variable in size and shape

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

Stroma

A

General word for “supporting structure”

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

Metastasis

A

Ability to spread beyond tissue of origin, most deadly characteristic of malignant tumors

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

Carcinoma

A

cancer arising from epithelial tissue

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

Adenocarcinoma

A

cancer arising from ductal or glandular structures

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

Carcinoma in situ (CIS)

A

Preinvasive epithelial tumours of glandular or squamous cells origin. Have not yet invaded surrounding stroma, not considered malignant.

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

Contact Inhibition

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

Three stages of Cancer

A
  1. Tumor initiaion (inital cancer cell)
  2. Tumor promotion (population of cancer cells increase, w/ addition mutations
    3.Tumor progression (metastasis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Point Mutations

A

alteration of one or a few
nucleotide base pairs / can have profound effects on activity of resultant proteins

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

Driver mutations

A

Mutations that “drive” the progression of cancer

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

Passenger mutations

A

Mutations that don’t contribute to malignancy, just random events (incidental)

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

Chromosome translocations

A

Section of one chromosome is translocated to another chromosome, large change in chromosome structure

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

Gene amplification

A

Instead of normal two copies of gene, tens or even hundreds of copies are present.
Example: gene expression of HER2 proteins

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

Clonal Proliferation Model

A

Selective advantage cancer cell has over neighboring cells = it can replicate faster than nonmutant neighbors

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

Proto-oncogenes

A

Normal genes that direct protein synthesis and cellular growth

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

Oncogenes

A

Mutated proto-oncogenes cells, operate independent of body regulatory mechanisms, allows uncontrolled growth

18
Q

Burkitt Lymphoma

A

Cancer where translocation changes normal chromosomes to produce oncogenes and abnormal B lymphocytes.

19
Q

Anti-oncogenes

A

Tumour supressing genes, must be inactivated for caner proliferation to occur.

20
Q

P53

A

Referred to as “Guardian of the Genome” Monitors cellular stress and activates caretaker genes to repair genetic damage, inactivation requires at least two mutations

21
Q

Hayflick Limit

A

Limit to cellular division

22
Q

Telomeres

A

Cap on end of chromosome, “ticket” that must be used in order to divide, limits cell division

23
Q

Telomerase

A

Enzyme that maintains telomeres, usually only active in gonads, but is also activated by cancer for unlimited proliferation

24
Q

Angiogenesis

A

Production of new blood vessels.
Cancers secrete angiogenic factors to form vessels that support them.

25
Q

Warburg effect

A

aerobic glycolosis, allows cancer cells to continually produce lactate which is a source of molecular building blocks

26
Q

Intrinsic controlled apoptosis

A

Monitors cellular stress, if cell can recover, activation of BAX. If cell must be destroyed, activation of BAK. (regulate release of pro-apotoptic molecules)

27
Q

Extrinsic controlled apoptosis

A

Dormant until death receptor is activated by BAK

28
Q

Anoikis

A

Induction of apoptosis when a cell has seperated from its ECM attatchment

29
Q

Epithelial-mesenchymal transition (EMT)

A

Model for transition of cancer cells to metastatic cancer cells
-occurs normally in embryonic development and wound healing
1.Transition from epithelial like cells to more undifferentiated cells
2.Undiferentiated cells avoid anoikis, enter circulation and spread,

30
Q

Intravasation

A
31
Q

Extravasation

A
32
Q

Tumour-Initiaitng Cells (TICs)

A
33
Q

Dormancy

A

a stable non-proliferating state that is reversible

34
Q

oncolytic viruses

A

Viruses that specifically attack cancer cells

35
Q

Stage I Cancer

A
36
Q

Stage II Cancer

A
37
Q

Paraneoplastic Syndromes

A
38
Q

Cachexia Syndrome

A
39
Q

leukopenia

A
40
Q

Thrombocytopenia

A
41
Q

Asthenia

A