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cancer Flashcards

1
Q

What is cancer?

A

a group of diseases characterised by uncontrolled cell division leading to growth of abnormal tissue

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2
Q

What does cancer result from?

A
  • the accumulation of many genetic alterations

- that disrupt function of many different genes

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3
Q

What does the complexity of cancer come from?

A

the diversity of genetic defects

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4
Q

What type of event must cell division be and how many divisions should occur under what control?

A
  • a controlled sequence of events with a delicate balance between cell division and death
  • a finite number of divisions controlled by activation of ‘suicide genes’
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5
Q

How many cells die per day due to apoptosis in the average human adult?

(Hint - two odd number billions - a range)

A

50-70 billion cells/day

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6
Q

State the events in the evolution of a tumour.

like a box of smarties

A
  • a normal cell triggered by a carcinogen (tar, HPV) → uncontrolled cell proliferation
  • some cells undergo mutations along the way leading to a diverse collection of cells with different genetic mutations
  • as they mutate → become more resilient + survive (require fewer GFs)
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7
Q

Give a quick background on cancer

A
  • > 200 types of cancer
  • different causes, symptoms, treatments and prognoses
  • every 2 mins someone is diagnosed with cancer in the UK
  • > 1 in 2 people will develop some form of cancer during their lifetime
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8
Q

Why say that cancer is a group of diseases?

A

there are many groups of diseases characterised by uncontrolled cell growth

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9
Q

Is lung cancer the same as colon cancer or breast cancer?

A

no, different organ and different gene mutations involved

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10
Q

Is one lung cancer the same as another lung tumour?

A
  • no, different stages and grades etc…
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11
Q

Is one cancer cell the same as the neighbouring cancer cell?

A

not always → they may be slightly different as you go along (better/worse)

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12
Q

What is the pathogenesis of cancer, when can it develop and where does non-melanoma skin cancer most often develop?

A
  • the mechanism that causes the disease
  • can develop at any age but most common in older people
  • on areas of skin regularly exposed to the sun, i.e. face, ears, hands, shoulders, upper chest and back
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13
Q

State some stats of cancer.

A
  • breast, lung, bowel and prostate cancers → over 1/2 of all new cancers each year
  • have been 18.1 million new cases of cancer worldwide (2018), where cancer incidence rates projected to increase by 62% by 2030
  • approx. 3/4 of cases in people aged 60+
  • around 1% of cancers occur in children, teenagers and young adults (up to age 24)
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14
Q

State 3 initiatives we have come up with to combat cancer incidence in the UK.

A
  • cervical smears
  • HPV Vaccination
  • Cancer Strategy 2015-2020 (CRUK, 2015)
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15
Q

Why have cancer death rates in the UK have fallen by?
• 1/5 over last 30 years
• by 9% over last 10 years

A
  • due to strategic initiatives

- e.g.: introduction of: PSA tests, anti-smoking campaigns, diet-specific initiatives

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16
Q

What is the median age of all cancers and where do around ¾ of cancer deaths occur in?

A
  • all median age 13

- people aged 65 and over

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17
Q

What are the top 3 cancer killers in men?

Hint - LPC

A
  • lung cancer
  • prostate cancer
  • colon cancer
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18
Q

What are the top 3 cancer killers in women?

Hint - BLC

A
  • lung cancer
  • breast cancer
  • colon cancer
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19
Q

State some of the root causes and co-factors of cancer.

A
  • chronic inflammation
  • oxidative stress
  • pharmaceutical stress
  • toxicity/acidity
  • environmental toxins
  • smoking/alcohol
  • genetics
  • nutritional deficiencies
  • sedentary lifestyle
  • weakened immunity
  • stress/insomnia
  • poor diet
  • type 2 diabetes
  • obesity
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20
Q

For each type of risk factor for cancer, state if it is modifiable and give examples of it:

a) intrinsic risk factors
b) non-intrinsic endogenous risk factors
c) non-intrinsic exogenous risk factors

A

a) unmodifiable i.e. random errors in DNA replication
b) partially-modifiable i.e. biological aging, genetic susceptibility, DNA repair machinery, hormones, GFs, inflammation etc…
c) modifiable i.e. radiation, chemical carcinogens, tumour-causing viruses, bad lifestyles

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21
Q

What are the three main risk factors of pancreatic cancer?

Hint - SOD

A
  • smoking
  • obesity
  • diabetes
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22
Q

Name the one main risk factor for skin cancer.

A
  • excessive exposure to UV radiation (from the sun/sunbeds)
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23
Q

What are carcinogens?

A

any substance, radionuclide, or radiation that promotes carcinogenesis

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24
Q

What is carcinogenesis?

A

formation of cancer

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25
Q

Why may a carcinogen be able to cause cancer? Give examples of carcinogens.

A
  • due to ability to damage genome/disrupt cellular metabolic processes, i.e.:
    • radiation-UV light, X-rays, ß,γ
    • chemicals
    • cigarette smoke
    • viral infections e.g. HPV causes cervical cancer
    • genetic pre-disposition
    • diet
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26
Q

How many infectious agents (certain viruses) play a key role in causing certain types of cancer?

A
  • a small number
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27
Q

What percentage of all cancers do inherited factors cause?

A

up to 10% of all cancers

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28
Q

Which factors massively affects the risk of most common female cancers?

A

age at which a women has first child & number of children

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29
Q

How do obesity and diet link to cancer and what has this brought about?

A
  • current levels of obesity could lead to approx. 19,000 cases cancer/year in U.K.
  • each of the following increase risk of certain cancers:
    • alcohol consumption
    • low fibre diet
    • low consumption of fruit and vegetables
    • high consumption of red and processed meats
    • higher intake of salt/saturated fats
    → brought about several government initiatives
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30
Q

For which activity have many significant links with cancer recently been found?

(Hint - one is newer with nice-smelling vapours)

A

smoking (and hookah)

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31
Q

What has been found to suggest a link between exposure to radiation and cancer?

(Hint - Mr Lee physics)

A
  • risk projections suggest Chernobyl may have caused many cases of the thyroid and other cancers in Europe
  • models predict that by 2065 many more cases of cancers may be expected due to radiation from accident
  • Marie Curie ‘mother of modern physics’, died from aplastic anaemia (condition linked to high levels radioactive element exposure)
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32
Q

What has been found to suggest genes have a link to cancer and what does the strength of these links depend on?

A
  • specific types of cancer have a strong familial link
    • genetic counselling and testing
    • prognosis
  • strength of your family history depends on:
    • who in your family has had cancer
    • how old they were at diagnosis
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33
Q

What is meant by sporadic vs hereditary cancer?

A

all cancer is genetic, not all cancer is inherited

34
Q

What is genetic predisposition/susceptibility?

A

an increased likelihood of developing particular disease based on person’s genetic makeup

35
Q

What does genetic predisposition/susceptibility result from and what has contributed to it?

A
  • specific genetic variations often inherited from a parent

- development of disease but do not directly cause it

36
Q

What is the spectrum of genetic predisposition to cancer?

A
  • genetic variations can have large/small effects on likelihood of developing particular disease
  • i.e. mutations inBRCA1/BRCA2genes → greatly increase risk of developingbreast and ovarian cancer
37
Q

For each cancerous syndrome, state the associated gene:

a) familial retinoblastoma
b) Li-Fraumeni
c) familial adenomatous polyposis
d) hereditary nonpolyposis colorectal cancer
e) wilm’s tumour
f) breast and ovarian cancer
g) von Hippel-Lindau
h) Cowden

A

a) RB1
b) TP53 (p53 protein)
c) APC
d) MLH1, MSH2, MSH6, PMS1, PMS2
e) WT1
f) BRCA1, BRCA2
g) VHL
h) PTEN

38
Q

How is cancer pathologically organised?

A
  • cancer pathologists identify tumours at different stages of development
  • by close examination of pathological appearance different stages have been ordered
  • for certain tumour types → pathological progression from normal tissue to malignant tumour has been defined + mapped
  • i.e. colorectal cancer, uterine cancer, cervical cancer
39
Q

What is hyperplasia?

A

an increase in the number of cells orproliferation of cells

40
Q

What is adenoma?

A

a benigntumourofepithelialtissue withglandularorigin and/or glandular characteristics

41
Q

What is carcinoma?

Hint - any type of cancer which develops from a certain tissue

A

a type ofcancerthat develops fromepithelial cells

42
Q

Where does the evolution of a colorectal tumour specifically begin and what is its progression?

(Hint - n → h → ea → ia → la → c/m)

A
  • begins in a tissue that lines inner/outer surfaces of the body
  • normal epithelium → hyperproliferative epithelium (hyperplasia) → early adenoma (benign tumour) → intermediate adenoma → late adenoma → carcinoma (malignant tumour)
43
Q

What are the characteristics of benign cancer (i.e. adenomatous polyposis colon cancer)?

(Hint - area first attacked and the a → c formed, p growth in wall, how progression is driven)

A
  • mucosa (innermost wall) is attacked first resulting in the formation of adenomas and eventually carcinomas.
  • polyposis (polyps)- growths in wall of colon
  • progression commonly-driven by loss of cell cycle inhibition and genomic stability
44
Q

what is the evolution of a uterine tumour driven by and how does it occur?

(Hint - to do with the unopposed signalling of a particular hormone: n → i → h → ah → c → m/spreading)

A
  • progression commonly-driven by unopposed oestrogen signalling due to genetic alterations
  • stages histologically monitored
  • one of the molecular mechanisms involves unopposed oestrogen signalling gene iteration:
    normal endometrial cell → increased cell growth → hyperplasia → atypical hyperplasia → carcinoma (now cancerous) → metastasis
45
Q

How does the evolution of a cervical tumour occur?

Hint - the virus which causes it

A

viral infection can trigger sequence of events leading to alteration in genes leading to cervical cancer

46
Q

What is a koilocyte?

Hint - main virus affecting flat epithelial cells

A

asquamous epithelialcell that has undergone number of structural changes due to infection byHPV

47
Q

How does the pathological progression for certain cancers differ?

A
  • a clearly defined pathological progression for colorectal, uterine and cervical cancers.
  • various stages in the progression of other tumour types less clear
  • e.g. ovarian cancers:
    • often detected only at late stages.
    • early pre-cancer stages not clear
    • several different ovarian cancer types exist
48
Q

Do ovarian cancers show a pathological progression from normal to abnormal to benign tumour to malignant tumour to metastasis?

A
  • it is possible that they evolve directly to a malignant but localised tumour
  • but it is also possible that we have just not yet identified the pathological precursors
  • likely to be clarified by genetic/molecular analysis
49
Q

Cancer is caused by accumulation of multiple gene mutations. Which genes in which combinations mutated in which order?

A
  • list is endless, thus the reason why it is so difficult to treat and cure
  • multifactorial
50
Q

How can we study the genetic evolution of cancer?

Hint - X, Y, Z

A
  • take sample of abnormal cells from patient at defined point in pathological progression
  • analyse and catalogue genetic changes present
  • repeat many times with samples from all known pathological stages of development.
  • if gene X is frequently mutated:
    • = an important gene for that cancer.
    • = an early event for that cancer.
  • if when gene Y is mutated, gene X is nearly always mutated too:
    • = gene X mutation is an earlier event than gene Y.
    • = disruption of gene X and Y likely co-operate.
  • If gene Z is frequently mutated at late stage, but rare at early stage of cancer development = gene Z mutation is likely late occurring
51
Q

What are the stages in the evolution of a colorectal tumour?

(Hint - n → mucosa at → a → c)

A

normal colon → mucousa at risk → adenomas → carcinoma (accumulation of genes leads to end stage of histological change)

52
Q

What is a vogelgram?

A
  • Bert Vogelstein
  • developed this correlation of pathological stages and genetic alterations for colorectal cancer → similar correlations deduced for other tumours (e.g. uterine)
  • molecular pathology is crucial to our understanding of cancer development and avenues for potential treatment
53
Q

What does the genetic heterogeneity of tumours have implications for?

A

diagnosis and prognosis → treatment options

54
Q

How do we define tumours?

Hint - t, b/m, t.g, t.s, t.h

A
  • pathologists are central to clinical management of cancer
  • tumours are defined by a number of histological characteristics (predictive info. too):
    • tissue of origin
    • benign or malignant
    • tumour grade
    • tumour stage
    • tumour histology
55
Q

What are benign tumours?

A
  • localised, well-differentiated (low grade) and slow-growing, proliferating masses
  • lack the ability to invade surrounding tissues + usually easily-resectable by surgery and curable
56
Q

What are malignant tumours?

A
  • abnormal (anaplastic) cells with rapid growth rate that can be invasive and can cause significant harm → much harder to resect as they are invasive
57
Q

How do we name tumours?

A
  • benign tumours end in ‘-adenoma’
  • malignant tumours usually end in ‘-carcinoma’
  • the prefix is usually the name of the tissue affected i.e. type of epithelia/muscle etc…
58
Q

What is a tumour grade and how is it determined?

A
  • a measure of how abnormal the cancer cells look compared to normal tissue →
    • analyses of cancer cell appearance
    • mitotic behaviour
    • growth rate (measures how tumour disseminates)
    • lymph node involvement (very important in prognosis)
59
Q

Describe tumour histology.

A
  • for some cancers, different tumours can arise from same cell type, but adopt highly-different histological appearances
  • ovarian epithelial cancer can be serous, endometrioid, mucinous or clear cell type
  • different histologies → different gene mutations, clinical behaviours, prognoses, and drug sensitivities
  • histological findings → crucial in developing + prescribing treatments
60
Q

Which genes are switched on and off in cancer?

A
  • tumour suppressor genes OFF

- oncogenes switched ON

61
Q

Name some inhibitors and drivers of the cell cycle.

Hint → (-) t,d and (+) c,g,o,t

A

inhibitors:

  • tumour suppressors
  • drivers of apoptotic pathways

drivers:

  • cell cycle activators
  • growth factors
  • oncogenes
  • transcription factors

(imbalance = carcinogenesis)

62
Q

Which three biological properties does a tumour acquire during its evolution?

(Hint - can’t fix broken genes, new blood vessels, escapes LNs)

A
  • failure to repair DNA damage
  • angiogenesis
  • escape from immunity
63
Q

Which random mutations provide a selective advantage to developing tumour?

(Hint - tumour-producers on, tumour-producers off, alteration in genes of normal cell death)

A
  • growth-promoting oncogene activation
  • tumour-suppressor gene inactivation
  • alterations in apoptotic genes
64
Q

Name 6 biological hallmarks of cancer.

Hint - ESISLT

A
  1. evading apoptosis
  2. self-sufficiency in growth signals
  3. insensitivity to antigrowth signals
  4. sustained angiogenesis
  5. limitless replicative potential
  6. tissue invasion and metastasis
65
Q

How do tumours acquire their hallmarks by cell cycle control and growth factor signalling?

(Hint - cell cycle control is about cells dividing GFs and growth factors causing processes to go into overdrive = uncontrolled cell proliferation)

A

• cell cycle control:
- (majority) non-dividing body cells pushed into cell cycle via growth stimulus
- cancer cells independent of normal GF signalling → acquire mutations to `short-circuit’ pathways → unregulated growth (proto)
• GF signalling:
- genetic mutations up-regulate processes → steps affected by gene mutations → activation of uncontrolled cell proliferation

66
Q

What is an oncogene?

A

normal gene that becomes an oncogene (cancer-producing) due to mutations or increased expression

67
Q

For which four reasons may a cell acquire a growth advantage?

(Hint - secretion, mutation of STP, continuous TFA, over-p of CC)

A
  1. secretion of a growth factor for which cell already expresses receptor (autocrine loop)
  2. mutation of components of signal transduction pathway → become constitutively-activated
  3. continuous activation of transcription factors controlling cyclin expression (due to mutation)
  4. over-expression of Cyclin and CDK protein-complexes which drive cell cycle
68
Q

Describe, using examples, two events where the inhibition of anti-growth signals allow cells to acquire a growth advantage.
(analogy – “brakes don’t work”)

(Hint - (1) cell cycle inhibitors disrupted (2) apoptosis disrupted)

A
  1. expression of cell cycle inhibitors disrupted →
    - mutation/loss of retinoblastoma, p53, CDK inhibitors
    - p53 is tumour suppressor → a TF which can activate p21 gene → inhibits cyclin/CDK function
    - loss of p53 function removes inhibition of cell growth (mutated in 70% of cancers)
  2. expression of genes promoting cell apoptosis is disrupted → mutation/loss of p53 or dysregulated components of extrinsic and intrinsic apoptosis pathway
69
Q

Describe the apoptosis pathway.

(Hint - is it inside/outside, cap-controlled, how does it not damage tissues, a named receptor forms bridge between F and P → death complex)

A
  • apoptosis has an intrinsic and extrinsic pathway
  • caspase-mediated
  • recognised by phagocytes → removed w/o inflammation (controlled)
  • adrenoceptor FAAD forms bridge between FAS (first apoptosis signal) and procaspase 8 → formation of a death-inducing signalling complex
70
Q

Why do normal cells have a limited life span and which genes induce this process?

A
  • erosion of telomeres (allow chromosome rearrangements in replication) → p53 and Rb recognise these breaks and induce apoptosis
71
Q

How can tumours avoid senescence (ageing) and in how many cancer cells can this be seen?

A
  • many cancers have lost p53 and Rb function → ageing cells with shortened telomeres undergo chromosome rearrangements (e.g. dicentric chromosomes)
  • during cell division, dicentrics fragment → broken chromosomes should induce apoptosis but don’t
  • activation of telomerase gene allows restoration of telomeres → crucial event for cell survival during tumorigenesis
  • up-regulation of telomerase occurs in 85-95% of all tumours
72
Q

What is sustained angiogenesis and when does it occur?

Hint - VEGF, Ras and Myc, adaptive

A
  • tumours need vascularisation to grow big enough → cancers must acquire mechanisms to promote neo-angiogenesis
  • in hypoxic conditions, cells secrete VEGF (stimulates vasculogenesis and angiogenesis) further up-regulated by Ras and Myc oncogenes
  • several acquired changes in tumours can enhance adaptive mechanism for angiogenesis
73
Q

For each of the three properties, of tumour blood vessels state why they are required:

a) leaky and dilated with haphazard connection pattern
b) new endothelial cells secrete GFs
c) leaky vasculature

(Hint - supply, drive and route)

A

a) good delivery of oxygen/nutrients to a tumour
b) drive tumour growth
c) route for tumour growth (dissemination)

74
Q

Which three things does tumour dissemination require?

Hint - detachment, degradation, migration

A
  • detachment of tumour cells from neighbouring cells
  • degradation of ECM + attachment to novel ECM components
  • migration of tumour cells
75
Q

For the four different types of tumour dissemination stated, which molecules are they caused by:

a) cell detachment? (Hint - inactivation of attachment molecules)
b) degradation of ECM? (Hint - matrix mellos proteins)
c) attachment? (Hint - degraded matrix)
d) migration and vascular dissemination? (Hint - cyt, chem and GFs)

A

a) inactivation of adhesion molecules e.g. E-cadherin
b) expression of matrix metalloproteinases
c) degraded matrix components create novel sites for cell-attachment promoting migration of cells
d) cytokines, chemokines and GFs from a tumour, stroma and inflammatory cells

76
Q

What happens to a tumour cell following dissemination?

Hint - spread, prolif. + remodel + new vessels, produce new one

A
  • tumour cells escape blood vessel at another site around body → migrate through surrounding tissue
  • proliferate + remodel surrounding matrix → stimulate new blood vessel growth
  • produce new (secondary) tumour in different anatomical site to original (primary) tumour
77
Q

What are the causes of and treatments for chronic myelogenous leukaemia?

(Hint - disordered myeloid growth, movements of two chr. s, philly chr. bcr-alby, abel-1 w/o DNA reps + deregs, ABL K stopper)

A
  • unregulated growth of myeloid cells in BM
  • chromosomal translocation of chr. 9 (ABL1 gene) + 22 (BCR gene)
  • philadelphia chromosome → fused protein BCR-ABL1
  • ABL1- tyrosine kinase (on switch) fusion with BCR results → deregulation of gene expression by increasing cell division + preventing DNA repair
  • treatments → ABL kinase inhibitor (Imatinib)
78
Q

What are the causes of and treatments for cervical cancer?

Hint - E6 E7 E2F

A
  • Human papilloma virus (HPV) → 70% of cervical cancers
  • virus carries 2 oncogenes → E6 (inactivates p53) + E7 (competitive pRb binding → so E2F freed to transactivate targets + drive cell division)
  • treatment → vaccination (gardasil, cervarix)
79
Q

What are the causes, risk factors and treatments for breast cancer?

(HInt - two types of carcinomas L and D, GF egfr and her aswell, treated with the usual and a her-susceptible mnc antibody against the receptor)

A
  • lobular (produce milk) or ductal (carry milk) carcinomas
  • risk factors → gender, age, (lack of) childbearing/breastfeeding, smoking, obesity, alcohol, diet, carcinogens, BRCA1/2
  • epidermal growth factor receptor (EGFR, HER2) over-expressed
  • treatments → surgery, radio/chemotherapy, herceptin–monoclonal antibody against HER2 receptor
80
Q

What are causes and treatments for a melanoma?

(Hint - genes affected are Raf, p16, p53 → different axes if growth and VGP cells for metastasis, treatments → s,c/r, those which interfere and interlook)

A
  • causes → mutations in Raf (oncogene), p16 (tumour suppressor), a negative regulator of p53(tumour suppressor)
  • initial radial growth phase (non-invasive) followed by vertical growth phase (invasive) → VGP cells target for metastases (growth)
  • treatments → surgery, chemo/radiotherapy, immunotherapy (IFN-α, IL-2)
81
Q

What the causes of and treatments for retinoblastoma?

Hint - single change in younger people, your form PRB, all forms of therapy and e and LP

A
  • heritable and non-heritable retinal cancer caused by single gene mutation, usually in juveniles
  • i.e. pRb1 (tumour suppressor) gene mutations
  • treatments → chemo/radio/cryo/thermo/brachytherapy, enucleation, laser photocoagulation
82
Q

What is Knudson’s Two-Hit Hypothesis and in which cancer is it used?

A
  • hypothesisthat mostgenesrequire two mutationsto cause phenotypicchange
  • retinoblastoma

IMS (11 decks)

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