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Patho > Ch 10- Biology of Cancer > Flashcards

Ch 10- Biology of Cancer Flashcards

1
Q

what is cancer?

A

the leading cause of suffering and death in the world, a collection of more than 100 different diseases, each caused by a specific and often age related accumulation of genetic and epigenetic alteration. Environment, heredity and behaviour interact to modify risk of developing cancer and response to treatment.

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2
Q

what does epigenetic mean?

A

study of how behaviours and environment cause changes that affect gene function

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3
Q

what does neoplasm mean?

A

a new/abnormal growth

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4
Q

what is a benign tumour?

A

encapsulated and contain well-differentiated cells/ well organized stroma. Retain normal tissue structure/don’t invade beyond capsule. Can still be dangerous/benign meningioma at base of skull can compress local brain tissue

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5
Q

what is a well differentiated tumour?

A

cells and tissue structures that are like normal tissues and tend to grow and spread slowly

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6
Q

what is an undifferentiated tumour?

A

made up of cells that look very abnormal and often grow and spread quickly

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7
Q

what is a malignant tumour?

A
  • they progress to cancer.
  • rapid growth rates/abnormal organization
  • hallmark of cancer: anaplasia= loss of cellular differentiation= undifferentiated
  • pleomorphic: variability in size and shape
  • large stroma but disorganized with abnormal structure
  • metastasis: ability to spread far beyond tissue of origin/ most deadly characteristic of malignant tumours
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8
Q

what is a carcinomas?

A

cancers arising from epithelial tissue

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9
Q

what is a adenocarcinomas?

A

cancers arising form ductal or glandular structures

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10
Q

what is a carcinoma in situ?

A
  • preinvasive epithelial tumours of glandular or squamous cells origin
  • cancers develop incrementally as they accumulate specific genic lesions
  • they have not broken through basement membrane or invaded surrounding stroma therefore not considered malignant
  • they vary from low-grade to high grade dysplasia (abnormal growth)
  • high grade lesions have highest likelihood of becoming invasive carcinoma
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11
Q

what are the 3 fates of CIS?

A
  1. remain stable for a long time
  2. progress to invasive/metastatic cancers
  3. regress and disappear
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12
Q

what does situ mean?

A

in natural or original place

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13
Q

where does mutation come in for cancer?

A

multiple mutations are required before cancer can develop
- cell aquires characteristics that provide advantage over neighbouring cells
- common advantages: increased growth rate and/or decreased apoptosis

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14
Q

what is the result of mutations in cancer cells?

A
  • decreased need for growth factors to multiply
  • lack contact inhibition
  • anchorage independence to disseminate through body (metastasis)
  • immortality: no apoptosis
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15
Q

what are the two fundamental cancer concepts?

A
  1. cancer is a genetic disease arising from multiple mutations
  2. The tumour microenvironment is a mixture of cells (cancerous and benign) as well as their secretion
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16
Q

what is the stage 1 of cancer?

A

tumour initiation: producing initial cancer cell/ first stage of cancer development/ dependent on specific mutations

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17
Q

what is stage 2 of cancer?

A

tumour promotion: population of cancer cells expands with diversity of phenotypes/additional mutations

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18
Q

what is stage 3 of cancer?

A

tumour progression: spread of tumour to adjacent (invasion) and distal sites (metastasis)/ governed by more mutations and changing microenvironments

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19
Q

what is a small scale mutation?

A

point mutations: alteration of one or a few mucleotide base pairs/can have prodound effects on activity of resultant proteins

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20
Q

what are some types of point mutations?

A

Driver mutations: mutations that “drive” progression of cancer
Passenger mutations: mutations that don’t contribute to malignant phenotype. some are just random events and referred to as “passenger mutations”

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21
Q

what are large scale mutations

A
  1. Chromosome translocations: large changes in chromosome structure. section of one chromosome is translocated to another chromosome
  2. gene amplification: instead of normal two copies of gene, tens or even hundreds of copies are present
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22
Q

what is the clonal proliferation model?

A

selective advantage cancer cell has over neighbouring cells/it can replicate faster than non-mutant neighbours
- increasingly rapid cell division and impaired DNA repair mechanisms of cancer cells= continuing accumulation of mutations throughout progression to most aggressive metastatic lesion

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23
Q

what does tranformation mean?

A

process by which a normal cell becomes a cancer cell

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24
Q

what is transformation directed by?

A

progressive accumulation of genetic changes that alter basic nature of cell and drive it to malignancy

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25
Q

what is the result of mutations?

A
  • genomically heterogeneous mixture of cells
  • where subsets accumulate more and more mutations which increases cell’s malignant potential
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26
Q

how are cells similar to wound healing?

A

because initial cancer cell proliferation triggers a typical proinflammatory response by itself and adjacent nonmalignant cells
- as with wound healing, mediators recruit inflammatory or immune cells and cells associated with tissue repair

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27
Q

what happens when there is abnormal wound healing?

A
  • recruited cells form a stroma
  • stroma surrounds and infliltrates tumour/stroma cells can make up 90% of tumour mass
  • stroma growth not just affected by rapid cancer cell proliferation but also various cell additions to stroma
  • extensive paracrine signaling among stromal and cancer cells affects both populations
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28
Q

what is the effect of abnormal wound healing?

A
  • cancer cells increase proliferation and become more heterogeneous
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29
Q

what is the process of abnormal wound healing?

A

= great deal of cancer cell death
- surviving cells are more aggressive
- many take on a metastatic phenotype

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30
Q

WHICH MECHANISM?
Cancer cell: I need the ability of uncontrolled growth

A

Sustained proliferation signals
- Pro-oncogene control this
- Oncogene= mutations
- Result: blocking of body’s mechanism to stop uncontrolled growth

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31
Q

how do normal cells normally enter proliferative phases?

A

in response to growth factors

32
Q

how do growth factors work?

A

by binding to specific receptors on cell surface and activate intracellular signaling pathways affecting DNA synthesis and cellular growth

33
Q

what are proto-oncogenes?

A

normal genes that direct protein synthesis and cellular growth

34
Q

what are oncogenes?

A

mutated proto-oncogenes cells
- they are independent of normal regulatory mechanisms
- mutations produce them allowing uncontrolled growth
- various stromas produce their own growth factors that contribute

35
Q

what do translocations do in terms of signaling?

A

can cause excessive and inappropriate production of oncogenes

36
Q

WHICH MECHANISM?
Cancer cell: I need to stop tumour suppressor genes

A

Evading growth suppressor
- 2 mutations required
- Result: inactivation of tumour suppressor genes

37
Q

what needs to occur for cancer proliferation to occur?

A

tumour suppressor genes must be inactivated

38
Q

what do normal tumour-suppressor genes do?

A
  • inhibit proliferation
  • stop cell division when cells
    are damaged
  • prevent mutations
39
Q

what is P53?

A

it is a classical tumour suppressor gene
- monitors cellular stress and activates “caretaker genes” to repair genetic damage
- also controls cellular apoptosis
- inactivation requires at least 2 mutations

40
Q

WHICH MECHANISM?
Cancer cell: there appears to be a limit to how many times i can divide. Must stop that

A

Telomeres control this
- cancer activates telomeres to provide unlimited tickets to divide

41
Q

what are telomeres?

A

protective caps on each chromosome

42
Q

what happens to telomeres when cells proliferate?

A

the caps shorten with each divison

43
Q

what happens when telomeres run out?

A

the cell can no longer divide= cell dies (apoptosis)

44
Q

what is telomerase?

A

enzyme that maintains telomeres= they dont decrease in number with cell division. usually are only active in ovaries and testes and stem cells

45
Q

how to cancer cells manipulates telomerase?

A

they activate telomerase which = unlimited telomeres= unlimited proliferation= immortality

46
Q

WHICH MECHANISM?
Cancer cell: We need our own blood supply if we are going to move around the body

A

Angiogenesis
- Irregular development of vessels
- Increased risk of hemorrhage
- Result: cancer has access to systemic blood system

47
Q

what is angiogenesis?

A
  • cancer cells can activate production of new blood vessels
  • advanced cancers secrete angiogenic factors
  • GF= growth factor
  • Vascular endothelial GF
  • Platelet derived GF
  • Basic fibroblast GF
48
Q

how does angiogenesis work?

A
  • vessels formed within tumours differ from healthy vessels
  • perform irregular branching from existing capillaries, rather than regular branching seen in healthy tissue
  • cell contact between endothelial cells is less tight= vessels more porous and prone to hemorrhage
  • tumor created vessels allow passage of tumour cells into vascular system= metastasize
49
Q

WHICH MECHANISM?
Cancer cell: We need more building blocks to build more cells

A

Programming energy metabolism
- Warburg effect/lactic acid
- Increased risk of hemorrhage
- Result: rapid cellular growth

50
Q

how do normal cells reprogram energy metabolism?

A
  • with oxygen use aerobic metabolism
  • with limited oxygen, use gylcolysis (and produce lactic acid)
51
Q

how do cancer cells reprogram energy metabolism?

A

even in presence of adequate oxygen, use only glycolysis.

52
Q

what is the warburg effect?

A

aerobic glycolysis

53
Q

how does cancer benefit from the warburg effect?

A
  • shift to glycolysis allows continual production of lactate
  • lactate used for production of lipids, nucleosides, amino acids, and other molecular building blocks needed for rapid cell growth
54
Q

WHICH CANCER MECHANISM?
Cancer cell: we have the ability to divide unlimitedly, but we want to stop our cells from having to undergo apoptosis

A

Resisting apoptosis
- Intrinsic/Extrinsic pathway
- Activate BAK
- Result: apoptosis blocked

55
Q

how is apoptosis controlled?

A

by 2 pathways
- Intrinsic pathway: monitors cellular stress. If cell can recover= activation of BAX, if cell must be destroyed= activation of BAK. Both BAX and BAK groups regulate mitochondrial release of pro-apoptotic molecules (Cytochrome c)
- Extrinsic pathway: dormant until death receptor is activated (BAK)

56
Q

what happens if both intrinsic and extrinsic pathways are activated?

A

T cells and natural killer cells induce apoptosis

56
Q

what are apoptotic pathways in cancers?

A

dysregulated

57
Q

WHICH MECHANISM?
Cancer cell: Now I am ready to travel throughout the body. I need to overcome this final hurdle

A

EMT
- Result: ability to metastasize

58
Q

what does metastasis mean?

A

Spread of cancer cells from site of original tumour to distant tissues and organs through body
- Defining characteristic of cancer
- Major caus of death from cancer

59
Q

how to cancer cells develop ability to metastasize?

A

model for transition to metastatic cancer cells is called epithelial-mesenchymal transition (EMT)

60
Q

where do carcinomas originate?

A

Form highly differentiated epithelial cells that form structure sheets stabilized by multiple adhesions to neighbouring cells.

61
Q

what needs to happen for cells to metastasize?

A

they must dissociate from ECM

62
Q

what is the intravasation entry?

A

entry of tumor cells into circulation
- often via “leaky” angiogenesis vessels cancer has created
- spread through both vascular and lymphatic pathways

63
Q

what is the extravasation exit?

A

exit of tumor cells from circulation to host tissue

64
Q

what is survival in circulation?

A

platelets coat tumor= provide protection (cancer clot)

65
Q

how do cells survive in new locations once metastasize?

A

only a few cancer cells required to establish a tumour in new location. They are called tumour-initiating cells
(TICs) or cancer stem cells
- metastasis doesnt guarantee proliferation

66
Q

what does dormancy mean?

A

A stable non-proliferating state that is reversible

67
Q

how do cancer cells avoid immune detection?

A
  1. Failure to produce tumour antigen
  2. Mutation in MHC genes needed for antigen-presenting
  3. Production of immunosuppressive proteins or expression of inhibitory cell surface proteins
68
Q

what does the release of immunosuppressive factors into tumour microenvironment?

A

it increases resistance of tumour to chemotherapy and radiotherapy

69
Q

what do classic macrophages respond to?

A

to the inflammatory stage to perform phagocytosis

70
Q

what do TAMs do?

A

they block T cells and NK cells and produce cytokines advantageous to tumour growth and spread

71
Q

what are the stages of cancer?

A

Stage I: No metstasis
Stage II: Local invasion
Stage III: Spread to regional structures
Stage IV: Distant metastasis

72
Q

what are some cancer treatment?

A

Surgery:
- to prevent cancer
- biopsy for diagnosis and staging
- lymph node sampling
- palliative surgery
Radiation:
- ionizing radiation damages cancer cell’s DNA
- goals: eradicate cancer without excessive toxicity and avoid damage to normal structures
Chemotherapy:
- Takes advantage of specific vulnerabilities in target cancer cells
- Usually given in combinations designed to attack cancer from many different weaknesses at same time

73
Q

what are clinical manifestations of cancer?

A

Paraneoplastic syndromes:
- a group of rare disorders that are triggered by an abnormal immune system response to a cancerous tumour
- caused by biological substances released by tumour
- may be the earliest symptom of unknown cancer
Pain:
- Little or no pain is associated with early stages of malignancy
- influenced by fear, anxiety, sleep loss, fatigue, and overall physical deterioration
Cachexia syndrome:
- weakness and wasting of body due to severe chronic illness
- most severe form of malnutrition
Direct tumour invasion of bone marrow causes leukopenia and thrombocytopenia
Infection:
- Risk increases when absolute neutrophil and lymphocyte count falls

74
Q

what is asthenia?

A

weakness, lack of energy and strength

Patho (7 decks)

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