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Patho > Ch 10- Biology of Cancer > Flashcards

Ch 10- Biology of Cancer Flashcards

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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
what is the result of mutations?
- genomically heterogeneous mixture of cells - where subsets accumulate more and more mutations which increases cell's malignant potential
26
how are cells similar to wound healing?
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
27
what happens when there is abnormal wound healing?
- 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
28
what is the effect of abnormal wound healing?
- cancer cells increase proliferation and become more heterogeneous
29
what is the process of abnormal wound healing?
= great deal of cancer cell death - surviving cells are more aggressive - many take on a metastatic phenotype
30
WHICH MECHANISM? Cancer cell: I need the ability of uncontrolled growth
Sustained proliferation signals - Pro-oncogene control this - Oncogene= mutations - Result: blocking of body's mechanism to stop uncontrolled growth
31
how do normal cells normally enter proliferative phases?
in response to growth factors
32
how do growth factors work?
by binding to specific receptors on cell surface and activate intracellular signaling pathways affecting DNA synthesis and cellular growth
33
what are proto-oncogenes?
normal genes that direct protein synthesis and cellular growth
34
what are oncogenes?
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
what do translocations do in terms of signaling?
can cause excessive and inappropriate production of oncogenes
36
WHICH MECHANISM? Cancer cell: I need to stop tumour suppressor genes
Evading growth suppressor - 2 mutations required - Result: inactivation of tumour suppressor genes
37
what needs to occur for cancer proliferation to occur?
tumour suppressor genes must be inactivated
38
what do normal tumour-suppressor genes do?
- inhibit proliferation - stop cell division when cells are damaged - prevent mutations
39
what is P53?
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
WHICH MECHANISM? Cancer cell: there appears to be a limit to how many times i can divide. Must stop that
Telomeres control this - cancer activates telomeres to provide unlimited tickets to divide
41
what are telomeres?
protective caps on each chromosome
42
what happens to telomeres when cells proliferate?
the caps shorten with each divison
43
what happens when telomeres run out?
the cell can no longer divide= cell dies (apoptosis)
44
what is telomerase?
enzyme that maintains telomeres= they dont decrease in number with cell division. usually are only active in ovaries and testes and stem cells
45
how to cancer cells manipulates telomerase?
they activate telomerase which = unlimited telomeres= unlimited proliferation= immortality
46
WHICH MECHANISM? Cancer cell: We need our own blood supply if we are going to move around the body
Angiogenesis - Irregular development of vessels - Increased risk of hemorrhage - Result: cancer has access to systemic blood system
47
what is angiogenesis?
- 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
how does angiogenesis work?
- 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
WHICH MECHANISM? Cancer cell: We need more building blocks to build more cells
Programming energy metabolism - Warburg effect/lactic acid - Increased risk of hemorrhage - Result: rapid cellular growth
50
how do normal cells reprogram energy metabolism?
- with oxygen use aerobic metabolism - with limited oxygen, use gylcolysis (and produce lactic acid)
51
how do cancer cells reprogram energy metabolism?
even in presence of adequate oxygen, use only glycolysis.
52
what is the warburg effect?
aerobic glycolysis
53
how does cancer benefit from the warburg effect?
- 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
WHICH CANCER MECHANISM? Cancer cell: we have the ability to divide unlimitedly, but we want to stop our cells from having to undergo apoptosis
Resisting apoptosis - Intrinsic/Extrinsic pathway - Activate BAK - Result: apoptosis blocked
55
how is apoptosis controlled?
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
what happens if both intrinsic and extrinsic pathways are activated?
T cells and natural killer cells induce apoptosis
56
what are apoptotic pathways in cancers?
dysregulated
57
WHICH MECHANISM? Cancer cell: Now I am ready to travel throughout the body. I need to overcome this final hurdle
EMT - Result: ability to metastasize
58
what does metastasis mean?
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
how to cancer cells develop ability to metastasize?
model for transition to metastatic cancer cells is called epithelial-mesenchymal transition (EMT)
60
where do carcinomas originate?
Form highly differentiated epithelial cells that form structure sheets stabilized by multiple adhesions to neighbouring cells.
61
what needs to happen for cells to metastasize?
they must dissociate from ECM
62
what is the intravasation entry?
entry of tumor cells into circulation - often via "leaky" angiogenesis vessels cancer has created - spread through both vascular and lymphatic pathways
63
what is the extravasation exit?
exit of tumor cells from circulation to host tissue
64
what is survival in circulation?
platelets coat tumor= provide protection (cancer clot)
65
how do cells survive in new locations once metastasize?
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
what does dormancy mean?
A stable non-proliferating state that is reversible
67
how do cancer cells avoid immune detection?
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
what does the release of immunosuppressive factors into tumour microenvironment?
it increases resistance of tumour to chemotherapy and radiotherapy
69
what do classic macrophages respond to?
to the inflammatory stage to perform phagocytosis
70
what do TAMs do?
they block T cells and NK cells and produce cytokines advantageous to tumour growth and spread
71
what are the stages of cancer?
Stage I: No metstasis Stage II: Local invasion Stage III: Spread to regional structures Stage IV: Distant metastasis
72
what are some cancer treatment?
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
what are clinical manifestations of cancer?
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
what is asthenia?
weakness, lack of energy and strength

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