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411 Oncology > L1 - Cancer pathophysiology > Flashcards

L1 - Cancer pathophysiology Flashcards

1
Q

What is cancer?

A

Large group of diseases characterised by uncontrolled growth & metastasis of abnormal cells

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2
Q

What does “heterogeneous” mean?

A

Can have multiple cancers in different parts of the body

Can also have subtypes of that cancer which can be quite different from each other

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3
Q

How does cancer arise?

A

Acquired/inherited mutations
–> in genes that affect cell cycle, apoptosis, DNA repair

Accumulation of mutations –> more likely when older

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4
Q

What does “neoplasia” mean?

A

Abnormal growth of tissue

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5
Q

What are “benign tumours”?

A

Tumours that DO NOT SPREAD from site of origin

Generally DO NOT RETURN after being removed

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6
Q

What does “premalignant” mean?

A

Tissue that is not yet malignant but may become cancer

eg. polyps/growths found in colon

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7
Q

What are “malignant tumours”?

A

Tumours that can SPREAD from original site & cause SECONDARY tumours (metastases)

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8
Q

What are the FIVE main types of cancer?

A 
Carcinoma
Sarcoma
Leukaemia
Lymphoma
Central nervous system cancers
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9
Q

Where does carcinoma arise?

A

Epithelial cells that line structures

Carcinoma = not Connective tissue

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10
Q

What are the SIX types of carcinoma & examples?

SAD BIT

A

Squamous cell carcinoma –> skin, oesophageal

Adenocarcinoma –> pancreatic

Ductal carcinoma in situ –> breast cancer of mammary glands (early type, has not invaded tissues surrounding duct)

Basal cell carcinoma –> skin

Invasive ductal carcinoma –> breast cancer that has invaded surrounding ducts

Transitional/urothelial carcinoma –> bladder

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11
Q

Where does sarcoma arise?

A

Mesenchymal tissue
Connective tissue
Non-epithelial tissue

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12
Q

What are examples of sarcoma?

A

Osteosarcoma –> bone

Rhabdosarcoma –> muscle (soft tissue)

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13
Q

Where does leukaemia (blood cancer) arise?

A

Haematopoietic tissue –> begins in bone marrow, causes abnormal/immature WBCs

Myeloid & lymphoid

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14
Q

Acute vs chronic leukaemia

A

Acute: rapid increase in abnormal immature WBCs

Chronic: slower buildup of relatively mature abnormal WBCs (months to years)

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15
Q

Where does lymphoma arise?

A

Haematopoietic tissue –> develop from lymphocytes (type of WBC)

eg. non-Hodgkin’s lymphoma

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16
Q

Where does central nervous system cancer arise?

A

Brain
Spinal cord
Nerves

eg. gliomas

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17
Q

What does “hyperplasia” mean?

A

Increase in number of cells that appear normal (but may develop into cancer)

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18
Q

What does “dysplasia” mean?

A

Cells look abnormal but are not cancer (yet)

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19
Q

What are the THREE types of mutations?

A

Point
Frameshift
Chromosomal

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20
Q

What are point mutations?

A

Change in single nucleotide in a gene

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21
Q

What are the THREE types of point mutations?

A

Silent –> won’t change amino acid in gene

Missense –> will change amino acid, protein structure; alter gene function

Nonsense –> will change amino acid, protein structure; alter gene function

22
Q

What are frameshift mutations?

A

Change in 3-base reading frame

23
Q

What are the TWO types of frameshift mutations?

A

Addition of nucleotide base

Deletion of nucleotide base

24
Q

What are chromosomal mutations?

A

Rearrangement of genes. May include small number or large number

Any change can be quite significant

25
Q

What are the FIVE types of chromosomal mutations?

DID IT

A 
Duplication --> amplification of genes in chromosome
Insertion
Deletion --> less genes in chromosome
Inversion
Translocation
26
Q

What are the THREE ways mutations affect to cause cancer?

A

Protein structure & function

Gene expression & regulation –> promoters & enhancers, gene amplification

Expression & function of non-coding RNAs (gene regulation eg. stop codons, RNA degradation)

27
Q

What are the THREE types of carcinogenesis?

A

Chemical

Physical

Infectious

28
Q

What are “genotoxic chemical carcinogens”?

A

Chemicals capable of causing cancer by DIRECTLY altering DNA

29
Q

What are “direct-acting genotoxic carcinogens”?

A

React directly with DNA

eg. alkylating agents –> nitrogen mustard, cisplatin

30
Q

What are “indirect-acting genotoxic carcinogens”?

A

Pro-carcinogens that require metabolic conversion to become reactive to DNA

eg. hydrocarbons from tobacco smoke

31
Q

What are “non-genotoxic chemical carcinogens”?

A

Chemicals that do NOT DIRECTLY damage DNA

eg. mitogens –> stimulation of proliferation may lead to replication errors & promote growth of pre-neoplastic cells (eg. oestrogen)

32
Q

What are THREE examples of “physical carcinogenesis”?

A

Ionising radiation
UV
Asbestos

33
Q

What are examples of “infectious carcinogenesis”?

A

VIRUSES

  • HPV –> cervical cancer
  • Epstein-Barr –> lymphoma, nasopharyngeal
  • Hepatitis B –> liver

BACTERIA
- H. pylori –> gastric

34
Q

What are oncogenes?

A

Genes that promote cancer

35
Q

What are proto-oncogenes?

A

Corresponding normal genes responsible for normal cell growth & division

Mutations can convert these into oncogenes

36
Q

How can conversion of proto-oncogenes into oncogenes occur?

A

Translocation of DNA within genome (eg. transcription may increase if gene is placed close to promoter)

Amplification of chromosomal region containing proto-oncogenes

Point mutations in: proto-oncogenes which alter function; promoters & enhancers –> both lead to increased gene expression

37
Q

What are “tumour suppressor genes”?

A

Genes that help prevent uncontrolled cell growth by:

  • Repair damaged DNA
  • Control cell adhesion/contact
  • Inhibit cell cycle & signalling pathways
38
Q

What is p53?

A

“Guardian of the genome” tumour suppressor gene

Promotes growth arrest, DNA repair, apoptosis

39
Q

People with inherited mutations in BRCA1/BRCA2 genes are more likely to develop what THREE mutations?

BOP

A

Breast
Ovarian
Prostate

40
Q

What are the SIX original hallmarks of cancer?

A 
Sustained proliferative signalling
Evading growth suppressors
Activating invasion & metastasis
Enabling replicative immortality
Inducing angiogenesis
Resisting cell death
41
Q

What are the phases of the cell cycle?

A

G1: mRNA & protein synthesis
S-phase: DNA replication
G2: Cell growth & protein synthesis
M: Mitosis & cell division

G0: quiescence-reversible (cells can enter back into cell cycle) or senescence-irreversible (no longer replicates)

42
Q

What is “sustained proliferative signalling”?

A

Cancer cells do not need stimulation (eg. growth factors like EGFR & HER2, receptor-complexes) from external signals to replicate –> autocrine stimulation

43
Q

What is the “cancer stem cell hypothesis”?

A

Tumour growth is fuelled by a small number of tumour cells hidden in cancers

  1. Normal stem cell or progenitor cell is mutated
  2. Differentiated cell is mutated & driven back along differentiation path, becoming more stem-cell-like
44
Q

What is “evading growth suppressors”?

A

Cancer cells are resistant to growth suppressing signals & evade “contact inhibition” –> normal cells that come into contact stop growing, but cancer cells do not

45
Q

What is “resisting cell death”?

A

Loss of p53 tumour suppressor function means that cancer cell apoptosis does not occur –> rate of cell attrition/reduction decreases

46
Q

What is “enabling replicative immortality”?

A

Cancer cells have limitless replicating potential

Normal cells undergo discrete number of cell divisions before it enters senescence –> associated with telomere length (which decreases with each division until exposure & cell death)

Cancer cells may also producer telomerase which maintains telomere length

47
Q

What is “inducing angiogenesis”?

A

Tumour induce blood vessels by secreting growth factors eg. VEGF –> protects existing vessels & promotes growth of new vessels

Regions of tumour hypoxia can upregulate angiogenesis –> when they get far from blood supply

48
Q

What is tumour vasculature like?

A

Disorganised, constant state of change

  • Individual cells may be far from blood vessel –> drug diffusion rate decreases
  • Poor blood supply –> “sanctuaries” with reduced drug access
  • Hypoxia –> drug action & radiotherapy affected
49
Q

What is “activating invasion & metastasis”?

A

Cancer cells must acquire ability to migrate & invade distant cells –> epithelial-mesenchymal transition

Cells become more motile, do not need to be attached to basement membrane, can secrete factors to degrade matrix

50
Q

What are the “emerging hallmarks”?

A

Deregulating cell energetics –> cell corrupts metabolic processes within cancer cells –> ensures it grows and keeps on proliferating

Avoiding immune destruction

51
Q

What are the “enabling characteristics”?

A

Genome instability & mutation –> more unstable = more chromosome abnormalities that can contribute to mutations

Tumour-promoting inflammation –> may support hallmarks of cancer and promotes progression into cancer

411 Oncology (9 decks)

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