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411 Oncology > L1 - Cancer pathophysiology > Flashcards

L1 - Cancer pathophysiology Flashcards

(51 cards)

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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?

Study These Flashcards
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?

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A

Change in 3-base reading frame

23
Q

What are the TWO types of frameshift mutations?

Study These Flashcards
A

Addition of nucleotide base

Deletion of nucleotide base

24
Q

What are chromosomal mutations?

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A

Rearrangement of genes. May include small number or large number

Any change can be quite significant

25
What are the FIVE types of chromosomal mutations? DID IT
``` Duplication --> amplification of genes in chromosome Insertion Deletion --> less genes in chromosome Inversion Translocation ```
26
What are the THREE ways mutations affect to cause cancer?
Protein structure & function Gene expression & regulation --> promoters & enhancers, gene amplification Expression & function of non-coding RNAs (gene regulation eg. stop codons, RNA degradation)
27
What are the THREE types of carcinogenesis?
Chemical Physical Infectious
28
What are "genotoxic chemical carcinogens"?
Chemicals capable of causing cancer by DIRECTLY altering DNA
29
What are "direct-acting genotoxic carcinogens"?
React directly with DNA eg. alkylating agents --> nitrogen mustard, cisplatin
30
What are "indirect-acting genotoxic carcinogens"?
Pro-carcinogens that require metabolic conversion to become reactive to DNA eg. hydrocarbons from tobacco smoke
31
What are "non-genotoxic chemical carcinogens"?
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
What are THREE examples of "physical carcinogenesis"?
Ionising radiation UV Asbestos
33
What are examples of "infectious carcinogenesis"?
VIRUSES - HPV --> cervical cancer - Epstein-Barr --> lymphoma, nasopharyngeal - Hepatitis B --> liver BACTERIA - H. pylori --> gastric
34
What are oncogenes?
Genes that promote cancer
35
What are proto-oncogenes?
Corresponding normal genes responsible for normal cell growth & division Mutations can convert these into oncogenes
36
How can conversion of proto-oncogenes into oncogenes occur?
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
What are "tumour suppressor genes"?
Genes that help prevent uncontrolled cell growth by: - Repair damaged DNA - Control cell adhesion/contact - Inhibit cell cycle & signalling pathways
38
What is p53?
"Guardian of the genome" tumour suppressor gene Promotes growth arrest, DNA repair, apoptosis
39
People with inherited mutations in BRCA1/BRCA2 genes are more likely to develop what THREE mutations? BOP
Breast Ovarian Prostate
40
What are the SIX original hallmarks of cancer?
``` Sustained proliferative signalling Evading growth suppressors Activating invasion & metastasis Enabling replicative immortality Inducing angiogenesis Resisting cell death ```
41
What are the phases of the cell cycle?
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
What is "sustained proliferative signalling"?
Cancer cells do not need stimulation (eg. growth factors like EGFR & HER2, receptor-complexes) from external signals to replicate --> autocrine stimulation
43
What is the "cancer stem cell hypothesis"?
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
What is "evading growth suppressors"?
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
What is "resisting cell death"?
Loss of p53 tumour suppressor function means that cancer cell apoptosis does not occur --> rate of cell attrition/reduction decreases
46
What is "enabling replicative immortality"?
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
What is "inducing angiogenesis"?
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
What is tumour vasculature like?
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
What is "activating invasion & metastasis"?
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
What are the "emerging hallmarks"?
Deregulating cell energetics --> cell corrupts metabolic processes within cancer cells --> ensures it grows and keeps on proliferating Avoiding immune destruction
51
What are the "enabling characteristics"?
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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