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ONC Flashcards

1
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

`

Define Cancer

*LOB; Define the terms “cancer”, “carcinogenesis” and “carcinogen”.

A

A term for diseases in which abnormal cells divide without control and can invade nearby tissues. Cancer cells can also spread to other parts of the body through the blood and lymph systems

NIH

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2
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

`

What are the most common cancers?

*LOB; Define the terms “cancer”, “carcinogenesis” and “carcinogen”.

A

More than half of new cases are
Breast
Prostate
Lung
Bowel

NIH

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3
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

`

Define carcinogenesis and the four steps of cancer formation

*LOB; Define the terms “cancer”, “carcinogenesis” and “carcinogen”.

A

The generation of cancer:

Initiation
Promotion
Progression
Malignant conversion

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4
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Cancer is a genome disease

*LOB; Define the terms “cancer”, “carcinogenesis” and “carcinogen”.

A

Epigenetic, genomic alt
Altered protein
Altered pathways
Altered biology

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5
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

What are the hallmarks of Cancer

Features of cancers

*LOB; Define the terms “cancer”, “carcinogenesis” and “carcinogen”. Demonstrate an understanding of the ‘Hallmarks of Cancer’

A
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6
Q

ONC Mechanisms of Oncogenesis by

Define carcinogen

*LOB; Define the terms “cancer”, “carcinogenesis” and “carcinogen”.

A

Substances and exposures that can lead to cancer
directly- c/s breakage, fusion etc
indirect- ROS, infl,

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7
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Multistage Theory of Carcinogenesis.

*LOB Explain the Multistage Theory of Carcinogenesis.

A

Chromosomal instability pathway (c/s loss and gain)
Mutations in the DNA Repair pathways

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8
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

What are driver mutations?

*LOB Explain the Multistage Theory of Carcinogenesis.

A

2-8 driver mutations are required for carcinogenesis
confer growth/survival advantage

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9
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

What are passenger mutations

*LOB Explain the Multistage Theory of Carcinogenesis.

A

Mutations that are not enough to cause oncogenesis
Conssequence of loss of function of key DNA repair genes

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10
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Targets for cancer therapy

*LOB Explain the Multistage Theory of Carcinogenesis.

A

Hormone responsive tumours= remove oestrogen and androgen

Growth receptor= drugs ‘-mab’ to target EGFR HER2 VEGF

Singalling pathways = BRAF MTCH block

Tumour macroenvironment= checkpoint inhibitor molecules on T Cells can be left on longer. CTLA4 and PD1

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11
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Characteristsics of Primary tumour

*LOB Explain the Multistage Theory of Carcinogenesis.

A

Antigenicity
Growth Rate
Response to hormones
REsponse to cytotoxic drugs
Capacity for invaion on metastasis

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12
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Describe the four main types of carcinogens.

*LOB Describe the four main types of carcinogens.

A

Chemical
Physical
Viral
Hereditary cancer predisposition syndromes

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13
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Describe the four main types of carcinogens.

*LOB Describe the four main types of carcinogens.

A

Chemical
Physical
Viral
Hereditary cancer predisposition syndromes

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14
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Chemical carcinogens

*LOB Describe the four main types of carcinogens.
Give examples of carcinogens and describe their mechanisms of action.

A

Cisplatin and carboplatin,
Irreversibly bind across DNA so unable to be read.

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15
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Physical carcinogens

*LOB Describe the four main types of carcinogens.
Give examples of carcinogens and describe their mechanisms of action.

A

UV
Gamma
X Rays

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16
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Viral carcinogens

*LOB Describe the four main types of carcinogens.
Give examples of carcinogens and describe their mechanisms of action.

A

Adenovirus- DNA
Retroviridae- RNA

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17
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Hereditary cancer predisposition syndromes (genetic risk factors) carcinogens

*LOB Describe the four main types of carcinogens.
Give examples of carcinogens and describe their mechanisms of action.

A

Gene mutations involving oncogenes (activation) or/and tumour suppressors (inactivation) common to other malignancies (TP53- Li-Fraumeni syndrome, NF1-Neurofibromatosis) or specific to the cancer type. Lynch syndrome.

Chromosome aberrations:
Translocations (e.g. BCR-ABL in Leukaemia).
Numerical disorders (e.g. trisomy 21-Down syndrome).

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18
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

What are the mechanisms of DNA damage

*LOB: Give examples of carcinogens and describe their mechanisms of action.

A
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19
Q

`ONC Mechanisms of Oncogenesis by Dr Mark Bodman-Smith

Repair mechanisms of DNA damage

*LOB: Give examples of carcinogens and describe their mechanisms of action.

A

BER
NER
Mismatch
Recombination repair

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20
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

Define progression

*LOB: Understand the molecular mechanisms involved in tumour progression, invasion and metastasis.

A

: Unlimited growth (not self-limited as in benign tumours) - as long as an adequate blood supply is available to prevent hypoxia.

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21
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

Define invasiveness

*LOB: Understand the molecular mechanisms involved in tumour progression, invasion and metastasis.

A

: Migration of tumour cells into the surrounding stroma where they are free to disseminate via vascular or lymphatic channels to distant organs.

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22
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

Define metastasis

*LOB: Understand the molecular mechanisms involved in tumour progression, invasion and metastasis.

A

Spread of tumour cells from the primary site to form secondary tumours at other sites in the body.

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23
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

What is the molecuolar basis for tumour progression?

*LOB: Understand the molecular mechanisms involved in tumour progression, invasion and metastasis.

A

Acquisition of specific mutations – by carcinogens, multiple hits.

Clonal expansion – by tumour promoters.

Genomic instability – by DNA repair defects, aneuploidy (abnormal chromosome number), loss of heterozygosity.

Epigenetic changes – by gene promoter methylation.

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24
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

Tumour progression is associated with…

*LOB: Understand the molecular mechanisms involved in tumour progression, invasion and metastasis.

A

with cellular heterogeneity

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25
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

what is cellular heterogeneity

*LOB: Understand the molecular mechanisms involved in tumour progression, invasion and metastasis.

A

“cellular diversity”
selective pressures determine the cellular composition of tumours:

    • Antigenicity
  • Growth rate
  • Response to hormones
  • Response to cytotoxic drugs
  • Capacity for invasion and metastasis
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26
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

What are the mechanisms of tumour cell invasion?

*LOB: Describe the mechanisms of tumour cell invasion and indicate the key molecules that participate in this process.

A

Increased mechanical pressure caused by rapid cellular proliferation.

Hypoxia and blood supply.

Increased motility of the malignant cells (epithelial to mesenchymal transition- EMT).

Increased production of degradative enzymes by both tumour cells and stromal cells.

Increased cell ECM adhesion

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27
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

What is angiogenesis?

*LOB: Describe the mechanisms of tumour cell invasion and indicate the key molecules that participate in this process.

A

development of a new blood supply is promoted by hypoxia

This occurs in tumours as they cannot not grow beyond a size of about 2mm without their own blood supply

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28
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

How does tumour vascularisation occur?

*LOB: Describe the mechanisms of tumour cell invasion and indicate the key molecules that participate in this process.

A

1) Hypoxia induces HiF expression which leads to proangiogenic factors such as VEGF

2) Hypoxia encourages protease release to degrade basement membrane

3) Tip cells (expressing VEGFR) migrate along angiogenic gradient

4) Endothelial cells differentiate to produce a stalk

5) VEGF stimulates DLLR binds to Notch-1R which inturn reduces VEGF

6) PDGFβ stimulates pericyte attachment (cross-talk promotes tissue survival)

7) blood supply estabished and promotes further growth of tumour

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29
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

What are the key molecules in angiogenesis?

*LOB: Describe the mechanisms of tumour cell invasion and indicate the key molecules that participate in this process.

A

Vascular Endothelial Growth Factor (VEGF)
Fibroblast Growth Factor-2 (FGF-2)
Transforming Growth Factor-β (TGF- β)
Hepatocyte growth factor/scatter factor (HGF/SF)

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30
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

How does a tumour invade the basement membrane?

*LOB: Describe the mechanisms of tumour cell invasion and indicate the key molecules that participate in this process.

A

remodelling of cell-cell and cell-extracellular matrix (ECM) interactions which leads to the detachment of epithelial cells

Loss of:
Epithelial shape and cell polarity
Cytokeratin intermediate filament expression
Epithelial adherent junction protein (E-cadherin)

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31
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

How does a tumour regulate Proteolytic Activity

*LOB: Describe the mechanisms of tumour cell invasion and indicate the key molecules that participate in this process.

A

Most tissues have large amounts of a family of inhibitors called TIMPs (Tissue Inhibitor of Metalloproteinases).

Some tumours, e.g. pancreatic tumours, have decreased levels of TIMPs

That means that the mechanism to stop MMPs is turned OFF

Matrix metalloproteinases (MMPs) are a family of zinc-dependent extracellular matrix (ECM) remodeling endopeptidases that have the capacity to degrade almost every component of the ECM.

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32
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

What are the steps of metastasis?

*LOB: Summarize the steps involved in the metastatic process.

A

1) Primary tumour formation
2) Localised invasion
3) Intravasation (circulating tumour cells)
4) Transport through circulation
5) Arrest in microvessels
6) Extravasation (leave microvessels)
7) Form micrometastasis
8) Form a macrometastasis

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33
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

What is Seed and Soil hypothesis?

*LOB:Explain the “Seed and Soil Hypothesis”.

A

The concept of tumour success being dependent on the environment

  • “When a plant goes to seed, its seeds are carried in all directions but can only live and grow if they fall on congenial soil”.
  • Specific adhesions between tumour cells and endothelial cells in the target organ, creating a favourable environment in the target organ for colonization.
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34
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

What is MET and EMT

*LOB: Summarize the steps involved in the metastatic process.

A

Epithelial to Mesenchymal Transition
Mesenchymal to Epithelial Transition

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35
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

Compare MET and EMT

*LOB: Summarize the steps involved in the metastatic process.

A
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36
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

What are liquid biopsies and why are they useful?

*LOB: Discuss the application of liquid biopsies in the detection of circulating tumour cells (CTCs).

A

Sampling and analysis of non-solid biological tissue, primarily blood for detection of molecular biomarkers.

Identifies very specific circulating tumour cells in normal blood.

  • Cancer is a heterogeneous disease and mutations (e.g. gain of an oncogene or loss of a tumour suppressor) are highly specific to tumour cells.
  • Type and number of mutations involved in the development of cancer increases as the cancer progresses.
  • Molecular properties within a tumour differ and also between metastatic sites.
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37
Q

ONC Tumour Progression, Invasion, Metastasis by Dr Bodman-Smith

How can liquid biopsies be used?

*LOB: Discuss the application of liquid biopsies in the detection of circulating tumour cells (CTCs).

A

Profile the disease without having to extravate and identify a specific tumour.

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38
Q 

ONC Oncogenes and Tumour Suppressor Genes by  Dr Bodman-Smith

What are the characteristics of proto-oncogenes

*LOB: Describe the main characteristics of the proto/oncogenes and tumour suppressor genes (TSG).

A

normal cellular genes which regulate cell growth and/or division and differentiation

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39
Q 

ONC Oncogenes and Tumour Suppressor Genes by  Dr Bodman-Smith

What are the characteristics of oncogenes

*LOB: Describe the main characteristics of the proto/oncogenes and tumour suppressor genes (TSG).

A

a proto-oncogene that has been activated by mutation or overexpression.

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40
Q 

ONC Oncogenes and Tumour Suppressor Genes by  Dr Bodman-Smith

What are the characteristics of tumour suppressor genes (TSG)

*LOB: Describe the main characteristics of the proto/oncogenes and tumour suppressor genes (TSG).

A

-Tumour suppressor genes (TSG) encode proteins that maintain the checkpoints and control genome stability. Inhibit replication and Repair of DNA damage (e.g. MLH1, BRCA1/2) Apoptosis (TP53)

Oncogenes antagonists
Block proliferation
Repression of transcription factors
Cell cycle inhibitors
Activation of transcription factors
DNA repair
Induce apoptosis

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41
Q 

ONC Oncogenes and Tumour Suppressor Genes by  Dr Bodman-Smith

Explain the mechanisms for the activation of oncogenes

*LOB: Describe the main characteristics of the proto/oncogenes and tumour suppressor genes (TSG).

A
  1. Mutation in the gene results in a different oncoprotein to the normal protein within the cell.
  2. Oncoproteins are the same as the normal protein but expressed at higher levels.

Point Mutation: variant in proto-oncogene (KRAS in lung and pancreatic cancer) or in promoter/regulatory element

Gene Amplification: multiple copies of a gene (HER2 in breast cancer)

Chromosomal Translocation: creation of fusion protein (c-myc in Burkitt’s lymphoma ) or disruption of regulatory elements

One pathogenic mutation on one copy of a proto-oncogene is enough to cause an oncogene
A single copy of an oncogene is sufficient to promote tumorigenesis

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42
Q

`ONC Oncogenes and Tumour Suppressor Genes by Dr Bodman-Smith`

Explain the mechanisms for the inactivation of TSG.

*LOB: Describe the main characteristics of the proto/oncogenes and tumour suppressor genes (TSG).

A

Knudson’s two-hit hypothesis: Most of loss-of-function mutations that occur in tumour suppressor genes are recessive in nature- Generally, one normal allele is sufficient for the cellular control.
A “second hit” affecting the normal allele is needed to disrupt gene’s function.

Heritable cancers develop after additional loss of the normal functional allele (loss of heterozygosity).

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43
Q

` ONC Oncogenes and Tumour Suppressor Genes by Dr Bodman-Smith`

HER-2

*LOB: Give examples of oncogenes and TSG and explain their mechanisms of action.

A

Oncogene
* Growth factor receptor
* c-ERBB2 gene
* encodes for part of the human epidermal growth factor receptor 2
* Receptor dimerization is required for HER2 function.
* has intracellular tyrosine kinase activity.
* HER2 homodimer binds P27 and is degraded and prevented repressing cell division

Amplified in breast cancer

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44
Q

` ONC Oncogenes and Tumour Suppressor Genes by Dr Bodman-Smith`

What is KRAS and its mechanism of action?

*LOB: Give examples of oncogenes and TSG and explain their mechanisms of action.

A
  • KRAS is an oncogene, specifically belonging to the c-RAS and c-SRC gene families.
  • KRAS proteins function as signal transducers within the cell.
  • When activated (turned on), KRAS proteins bind to GTP.
  • This GTP-bound state enables KRAS to** initiate signaling** cascades that control the transcription of genes involved in cellular processes.

Importantly, KRAS mutations often occur at specific hotspots, such as codons 12, 13, 18, 61, 117, and 146.
These mutations render KRAS permanently active, leading to continuous signaling independent of external stimuli.

In colorectal cancer, KRAS mutations are found in approximately 30-40% of cases

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45
Q

` ONC Oncogenes and Tumour Suppressor Genes by Dr Bodman-Smith`

c-MYC

*LOB: Give examples of oncogenes and TSG and explain their mechanisms of action.

A
  • Oncogene (nuclear)
  • Transcription factor activation
  • Myc: family of genes which encode for transcription factors.

Deregulated expression of c-Myc not only promotes proliferation, but also can either induce or sensitize cells to apoptosis

  • Pathogenic alterations in c-myc involve gene retrovirus activation, amplifications and translocations.
  • Translocation between chromosome 8 (c-Myc proto-oncogene) and chromosome 14 (immunoglobulin heavy chain gene) are commonly observed in Burkitt’s lymphoma.
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46
Q

` ONC Oncogenes and Tumour Suppressor Genes by Dr Bodman-Smith`

BRCA1/BRCA2

*LOB: Give examples of oncogenes and TSG and explain their mechanisms of action.

A
  • tumour suppressor gene
  • DNA repair genes
  • Knockout of the DNA repair function of one or more DNA repair genes leads to sequential acquisition of more mutations
  • very high mutational load.
  • No homologous recombination repair.
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47
Q

` ONC Oncogenes and Tumour Suppressor Genes by Dr Bodman-Smith`

RB1

*LOB: Give examples of oncogenes and TSG and explain their mechanisms of action.

A
  • tumour suppressor gene
  • Prevents cell growth by inhibiting cell cycle until cell is ready to divide
  • Phosphorylation=inactivation

Sporadic Retinoblastoma
~60% of Rb cases
No family history
Single tumour
Unilateral

Familial Retinoblastoma
~30% of Rb cases
Family history
Multiple tumours
Bilateral
500x increased risk of subsequent osteosarcoma & other tumours

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48
Q

` ONC Oncogenes and Tumour Suppressor Genes by Dr Bodman-Smith`

TP53

*LOB: Give examples of oncogenes and TSG and explain their mechanisms of action.

A
  • tumour suppressor gene
  • The p53 protein prevents a cell from completing the cell cycle when DNA is damaged
  • High levels actually due to inactive P53 protein
    Normal P53 regulated by negative feedback
    Missense mutations in hotspots (DNA binding domain).
  • In some cancers TP53 mutations correlate pathological stage of cancer.
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49
Q 

ONC Oncogenes and Tumour Suppressor Genes by  Dr Bodman-Smith

Treating HER-2

*LOB: Discuss the molecular basis of current therapeutic approaches for cancer treatment.

A

Trastuzumab and pertuzumab are monoclonal antibodies that target HER2 (targeted therapy). Blocking homodimerization.

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50
Q 

ONC Oncogenes and Tumour Suppressor Genes by  Dr Bodman-Smith

Treating cMYC

*LOB: Discuss the molecular basis of current therapeutic approaches for cancer treatment.

A

There is a lack of strategies to directly target Myc.
Inhibitors of its translation and Myc protein destabilizing drugs show great promise.

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51
Q 

ONC Oncogenes and Tumour Suppressor Genes by  Dr Bodman-Smith

Treating KRAS

*LOB: Discuss the molecular basis of current therapeutic approaches for cancer treatment.

A

Undruggable target
KRAS: point mutations affecting hotspots at codons 12 and 13 and also 18, 61, 117, and 146 at lower frequencies.

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52
Q 

ONC Oncogenes and Tumour Suppressor Genes by  Dr Bodman-Smith

Treating p53

*LOB: Discuss the molecular basis of current therapeutic approaches for cancer treatment.

A

Current advances suggest the use of small molecules (MIRA-1, PRIMA-1) that can restore wild-type p53 functions.

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53
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define Neoplasm

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

new growth

abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of normal tissue and persists in the same excessive manner after cessation of the inciting stimulus

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54
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define Metaplasia

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

change from one differentiated cell type to another differentiated cell type (usually less specialised, reversible process)

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55
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define Dysplasia

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

‘disordered growth’ (encountered in epithelia and refers to cellular pleomorphism and loss of normal architecture)

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56
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define -oma

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

suffix applied to a lump/tumour

Generally, ‘oma’ at the end of a tumour type refers to benign neoplasm (eg. adenoma, papilloma) but there are important exceptions eg. melanoma, seminoma, thymoma

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57
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define Tumour parenchyma

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

proliferating neoplastic cells.

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58
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define Tumour stroma

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

supporting (non-neoplastic) elements

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59
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define -carcinoma

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

suffix applied to malignant epithelial tumours.

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60
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define -sarcoma

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

suffix applied to malignant connective tissue tumours.

How well did you know this?
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61
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define Hamartoma

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

benign, tumour-like mass comprising mature, differentiated tissues arranged in a haphazard fashion but normally found at that site

Remember HAMartoma HAPHAZARD AND MATURE

62
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define Choristoma

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

normal, but ectopically/heterotopically located tissue eg. adrenal rest in the kidney

khōristós, “separate”

63
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define Differentiation

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

degree to which a malignant tumour resembles the cell or tissue of origin (well/moderate/poor/undifferentiated) which also links to tumour grade

64
Q

ONC Classification of Tumours by Dr Lida Alarcon

Define Choristoma

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

normal, but ectopically/heterotopically located tissue eg. adrenal rest in the kidney

65
Q

ONC Classification of Tumours by Dr Lida Alarcon

3 Points about epidemiology

The triangle

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

A basic model to study health: a disease is produced when a suitable host is exposed to an agent in the context of environmental factors than aid or hinder disease development

Host
Environment
Agent

66
Q

ONC Classification of Tumours by Dr Lida Alarcon

Factors contributing to cancer

*LOB: Demonstrate an awareness of the epidemiology of common cancers and precipitating factors

A

Genetic
Environmental
Infectious agents
Smoking
Alcohol consumption
Diet
Obesity
Reproductive history
Enviromental carcinogens

67
Q

ONC Classification of Tumours by Dr Lida Alarcon

Benign neoplasms macroscopic features

*LOB: Recognise the macro- and microscopic characteristics of benign and malignant neoplasms

A
  • Well circumscribed
    (+/- capsule)
  • Pushing margin
  • Homogenous cut surface
    with little or no
    haemorrhage/necrosis
  • Organ confined
68
Q

ONC Classification of Tumours by Dr Lida Alarcon

Benign neoplasms micrsocopic features

*LOB: Recognise the macro- and microscopic characteristics of benign and malignant neoplasms

A
  • Resemble tissue of origin
  • Low cellularity
  • Low nuclear:cytoplasmic ratio (1:4)
  • Regular round or oval nuclei
  • Dispersed chromatin
  • Rare mitotic figures (N)
  • No necrosis
  • No lymphovascular
    invasion
69
Q

ONC Classification of Tumours by Dr Lida Alarcon

Malignant neoplasms macroscopic features

*LOB: Recognise the macro- and microscopic characteristics of benign and malignant neoplasms

A
  • Ill-defined or
    irregular/infiltrative
    margin
  • Extension beyond capsule
  • Heterogenous cut surface
    (necrosis & haemorrhage)
  • Infiltration of adjacent
    organs
  • Spread to lymph nodes
70
Q

ONC Classification of Tumours by Dr Lida Alarcon

Malignant neoplasms microscopic features

*LOB: Recognise the macro- and microscopic characteristics of benign and malignant neoplasms

A
  • Little resemblance to cell of origin
  • High cellularity
  • High NCR (1-2:1)
  • Irregular, pleomorphic
    nuclei, macronucleoli
  • Coarse chromatin
  • Frequent mitotic figures
  • Necrosis
  • Lymphovascular invasion
71
Q

ONC Classification of Tumours by Dr Lida Alarcon

Teratoma

*LOB: Show familiarity with tumour classification by histological subtype and nomenclature

A
  • Teratoma: Tumor containing multiple tissue types
  • Can occur in ovaries, testes, and other germ cell sites
  • Classified as mature (benign) or immature (potentially malignant)
  • Arises from germ cells, giving rise to eggs or sperm
  • Contains tissues from ectoderm, mesoderm, and endoderm
  • Diagnosed through imaging and biopsy
  • Treatment involves surgical removal
  • Additional therapies for malignant or recurrent cases
72
Q

ONC Classification of Tumours by Dr Lida Alarcon

Embryonal tumours

*LOB: Show familiarity with tumour classification by histological subtype and nomenclature

A
  • Neuroblastoma
  • Nephroblastoma
  • Pleuropulmonary blastoma
  • Medulloblastoma
  • Gonadoblastoma

Embryonal tumours are brain tumours. They develop from cells that are left over from the early stages of our development.

Previously known as primitive neuro ectodermal tumours (PNETs)

73
Q

ONC Classification of Tumours by Dr Lida Alarcon

Glial tumours

*LOB: Show familiarity with tumour classification by histological subtype and nomenclature

A
  • Astrocytoma
  • Glioblastoma
  • Oligodendroglioma etc etc
74
Q

ONC Classification of Tumours by Dr Lida Alarcon

Haematolymphoid

*LOB: Show familiarity with tumour classification by histological subtype and nomenclature

A
  • Hodgkin lymphoma
  • Non-Hodgkin lymphoma
  • Multiple myeloma
  • Leukaemia
75
Q

ONC Classification of Tumours by Dr Lida Alarcon

Placental tumours
(epithelial/trophoblastic)

*LOB: Show familiarity with tumour classification by histological subtype and nomenclature

A
  • Choriocarcinoma
  • Hydatidiform mole (a cluster of fluid-filled sacs formed in the uterus by the degeneration of chorionic tissue around an aborting embryo.)
76
Q

ONC Classification of Tumours by Dr Lida Alarcon

Tumour arising from vessels and surface coverings

*LOB: Show familiarity with tumour classification by histological subtype and nomenclature

A

Benign
Haemangioma
Lymphangioma
Benign fibrous tumour
Meningioma

Malignant
Angiosarcoma
Lymphangiosarcoma
Mesothelioma
Invasive meningioma

77
Q

ONC Classification of Tumours by Dr Lida Alarcon

Non-epithelial (mesenchymal neoplasms)

*LOB: Show familiarity with tumour classification by histological subtype and nomenclature

A

Benign
Lipoma
Fibroma
Leiomyoma
Rhabdomyoma
Osteoma
Chondroma
Schwannoma

Malignant
Liposarcoma
Fibrosarcoma
Leiomyosarcoma
Rhabdomyosarcoma
Osteosarcoma
Chondrosarcoma
MPNST

78
Q

ONC Classification of Tumours by Dr Lida Alarcon

Tumour arising from vessels and surface coverings

*LOB: Show familiarity with tumour classification by histological subtype and nomenclature

A

Benign
Haemangioma
Lymphangioma
Benign fibrous tumour
Meningioma

Malignant
Angiosarcoma
Lymphangiosarcoma
Mesothelioma
Invasive meningioma

79
Q

ONC Classification of Tumours by Dr Lida Alarcon

What are the characteristics of glandular epithelium?

*LOB: Show familiarity with tumour classification by histological subtype and nomenclature

A
  • Found in various organ systems, including the gastrointestinal tract, respiratory tract, and female genital tract
  • Lines ducts and acini of glands, such as those in the breast, prostate, pancreas, biliary tract, salivary glands, and endocrine organs
  • Adenocarcinoma can develop from metaplastic glandular epithelium, as seen in conditions like Barrett’s esophagus, progressing through dysplastic stages
80
Q

ONC Classification of Tumours by Dr Lida Alarcon

Epithelial neoplasm

*LOB: Show familiarity with tumour classification by histological subtype and nomenclature

A

BENIGN
Squamous papilloma
Adenoma
Urothelial papilloma
Hepatic adenoma

MALIGNANT
Squamous cell carcinoma
Adenocarcinoma
Papillary urothelial carcinoma
Hepatocellular carcinoma

81
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

Whats the difference between grade and stage?

*LOB: Explain the difference between tumour grade and stage

A

Tumor grade is a measure of how abnormal cancer cells look under a microscope compared to normal cells

Tumor stage, on the other hand, describes the extent of cancer’s growth and spread within the body.

82
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

The rationale for staging and grading

*LOB: Explain the rationale for the staging and grading of cancers

A

Staging helps oncologists determine the appropriate treatment strategy and predict the patient’s prognosis.

Grading provides information about the aggressiveness of the cancer. It helps in making treatment decisions.

83
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

Cellular and architectural features

*LOB: Describe cellular and architectural features which influence the grade of a tumour

A

size and shape of the cell nuclei
the mitotic rate
the presence of abnormal cellular structures

arrangement of cells in the tumor,
the presence of necrosis (dead tissue)
the presence of tissue differentiation

84
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

How is Lung cancer staged with TMN and Dukes

*LOB: Demonstrate an understanding of how common cancers (lung, breast, colorectal, prostate) are staged with reference to the TNM and Dukes staging systems

A

T (Tumor): T1-T4, where T1 indicates a small tumor in the lung, and T4 indicates a large tumor with invasion of nearby structures.
N (Nodes): N0-N3, where N0 means no regional lymph node involvement, and N3 indicates extensive lymph node involvement.
M (Metastasis): M0 or M1, where M0 means no distant metastasis, and M1 indicates the presence of distant metastasis.

85
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

How is breast cancer staged with TMN and Dukes

*LOB: Demonstrate an understanding of how common cancers (lung, breast, colorectal, prostate) are staged with reference to the TNM and Dukes staging systems

A

T (Tumor): T0-T4, where T0 indicates no evidence of a primary tumor, and T4 indicates a large primary tumor.
N (Nodes): N0-N3, where N0 means no regional lymph node involvement, and N3 indicates extensive lymph node involvement.
M (Metastasis): M0 or M1, where M0 means no distant metastasis, and M1 indicates the presence of distant metastasis.

86
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

How is colorectal cancer staged with TMN and Dukes

*LOB: Demonstrate an understanding of how common cancers (lung, breast, colorectal, prostate) are staged with reference to the TNM and Dukes staging systems

A

T (Tumor): T1-T4, where T1 indicates the tumor has invaded the submucosa, and T4 indicates invasion through the visceral peritoneum.
N (Nodes): N0-N2, where N0 means no regional lymph node involvement, and N2 indicates more extensive lymph node involvement.
M (Metastasis): M0 or M1, where M0 means no distant metastasis, and M1 indicates the presence of distant metastasis.

Duke’s A: Cancer is confined to the mucosa.
Duke’s B: Cancer has invaded the muscle layer but is still localized to the bowel.
Duke’s C: Cancer has spread to regional lymph nodes.
Duke’s D: Cancer has metastasized to distant organs or lymph nodes.

87
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

How is prostate cancer staged with TMN and Dukes

*LOB: Demonstrate an understanding of how common cancers (lung, breast, colorectal, prostate) are staged with reference to the TNM and Dukes staging systems

A

T (Tumor): T1-T4, where T1 indicates a small tumor confined to the prostate, and T4 indicates a tumor that has spread to nearby structures.
N (Nodes): N0 or N1, where N0 means no regional lymph node involvement, and N1 indicates regional lymph node involvement.
M (Metastasis): M0 or M1, where M0 means no distant metastasis, and M1 indicates the presence of distant metastasis.

88
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

What investigations are used to stage cancers?

*LOB:Outline the investigations necessary to support the grading and staging of common cancers

A

Imaging studies (CT scans, MRI, PET scans) help determine tumor size and spread.
Biopsy and histopathological examination assess the tumor’s cellular and architectural features, contributing to grading.
Lymph node sampling and analysis help determine lymph node involvement.

89
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

Alterantive staging and why they are used

*LOB: Recognise why alternative staging classifications are needed for malignant lymphomas

A

These systems focus on the involvement of lymph nodes and extralymphatic organs.

Ann Arbor staging system (I-IV) for Hodgkin lymphoma

Lugano classification for non-Hodgkin lymphoma.

90
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

Ann arbour

*LOB: Recognise why alternative staging classifications are needed for malignant lymphomas

A

Hodgkin Lymphoma

Stage I: Involvement of a single lymph node region or a single extralymphatic organ.
Stage II: Involvement of two or more lymph node regions on the same side of the diaphragm or a localized involvement of an extralymphatic organ and its regional lymph nodes.
Stage III: Involvement of lymph node regions on both sides of the diaphragm, which may include the spleen.
Stage IV: Widespread involvement, including one or more extralymphatic organs, and distant (extranodal) organ involvement.

91
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

Lugano

*LOB: Recognise why alternative staging classifications are needed for malignant lymphomas

A

Stage I: Involvement of a single lymph node region (I) or a single extranodal site (IE).
Stage II: Involvement of two or more lymph node regions on the same side of the diaphragm (II) or localized involvement of an extranodal site and its regional lymph nodes (IIE).
Stage III: Involvement of lymph node regions on both sides of the diaphragm (III) or localized involvement of extranodal sites on both sides of the diaphragm with or without associated lymph node involvement (IIIE).
Stage IV: Widespread involvement of one or more extranodal sites with or without associated lymph node involvement or any involvement of the liver, bone marrow, or nodal regions outside the lymphatic system.

92
Q

ONC Grading and Staging of Cancer by Dr Paul Johns

Other Factors Guiding Cancer Treatment

*LOB: Outline other factors which guide the treatment of cancer

A

Patient’s overall health and comorbidities.
Molecular and genetic characteristics of the tumor, which can guide targeted therapies.
Patient preferences and values.
Response to previous treatments (if applicable).
Availability of treatment options and clinical trials.

93
Q 

ONC Melanoma by Dr Emily Morrison

What are the sings and symptoms for malignant melanoma?

*LOB: Identify the red flag signs and symptoms for suspected malignant melanoma

A

A is for asymmetrical shape.
B is for irregular border.
C is for changes in color.
D is for diameter.
E is for evolving.

Ugly Duckling Sign

94
Q 

ONC Melanoma by Dr Emily Morrison

Differential Diagnoses

*LOB: Identify the red flag signs and symptoms for suspected malignant melanoma

A
  1. Melanocytic naevi( moles)
  2. Seborrhoeic keratoses
  3. Dermatofibromas
  4. Lentigos
  5. Pigmented Basal Cell Carcinomas
95
Q 

ONC Melanoma by Dr Emily Morrison

Melanoma subtypes

*LOB: Identify the red flag signs and symptoms for suspected malignant melanoma

A

Superficial Spreading Melanoma (SSM): Slow-growing skin cancer.

Lentigo Maligna Melanoma: Sun-exposed, invasive skin cancer.

Nodular Melanoma: Aggressive, raised skin tumor.

Acral Melanoma: Develops on palms/soles/nailbeds.

Amelanocytic Melanoma: Lacks typical melanin pigment.

Desmoplastic Melanoma: Fibrous tissue-invading skin cancer.

Nevoid Melanoma: Resembles a benign nevus.

96
Q

ONC Melanoma by Dr Emily Morrison

Melanoma Patient Phenotype

*LOB: Outline the pathogenesis of malignant melanoma with specific reference to the role of sun exposure

A
  • Skin type 1
  • Multiple (>50) melanocytic naevi
  • Atypical melanocytic naevi
  • Large diameter
  • Irregularborders
  • Multiple colours
97
Q

ONC Melanoma by Dr Emily Morrison

What are the risk factors for melanoma?

*LOB: Identify the red flag signs and symptoms for suspected malignant melanoma

A
  • Skin type 1 and 2
  • Personal or family history of melanoma
  • or other skin cancers
  • History of sun burn/sun exposure & or tanning beds
  • Severe sunburn during childhood & teenage years
  • Cancer-prone syndrome (e.g. familial atypical mole/dysplastic naevi or xeroderma pigmentosum)
  • Immunosuppressed- HIV, medications
  • Prolonged phototherapy - PUVA
98
Q

ONC Melanoma by Dr Emily Morrison

Pathogenesis of Malignant Melanoma

*LOB: Outline the pathogenesis of malignant melanoma with specific reference to the role of sun exposure

A
99
Q

ONC Melanoma by Dr Emily Morrison

Breslow thickness and staging

*LOB: Outline what is meant by the Breslow thickness and how it can be used in staging

A

The Breslow thickness describes how thick the melanoma is. It measures in millimetres (mm) how far the melanoma cells have grown down into the layers of skin.

There are 5 levels of tumour (T) thickness:

Tis – the melanoma cells are only in the very top layer of the skin (epidermis)
T1 – the melanoma is 1mm thick or less
T2 – the melanoma is between 1mm and 2mm thick
T3 – the melanoma is between 2mm and 4mm thick
T4 – the melanoma is more than 4mm thick.

100
Q

ONC Melanoma by Dr Emily Morrison

TMN

*LOB: Outline what is meant by the Breslow thickness and how it can be used in staging

A

TNM staging system
* Tumour–Breslow thickness,Ulceration
* Nodes–how many lymphnodes the melanoma has spread to
* Metastases–whether the melanoma has spread to other parts of the body

101
Q

ONC Melanoma by Dr Emily Morrison

Breslow thickness and margins

*LOB: Outline what is meant by the Breslow thickness and how it can be used in staging

A

Margins recommended:
* In situ: 5mm
* Breslow <1mm: 10 mm
* Breslow 1–2mm: 10–20 mm
* Breslow >2mm: 20 mm

102
Q 

ONC Tissue Growth Disorders and Dysplasia

Hyperplasia

*LOB: Define the following disorders or growth, giving physiological and pathological examples: hyperplasia, hypertrophy, atrophy, aplasia, hypoplasia, metaplasia.

A

**Hyperplasia is the increase in the number of cells in an organ or tissue. **

Physiological: during pregnancy mammary glands undergo hyperplasia to prepare for lactation

Pathological : Benign prostatic hyperplasia (BPH), the prostate gland undergoes excessive cell proliferation, leading obstructive symptoms.

103
Q

```ONC Tissue Growth Disorders and Dysplasia

Hypertrophy

*LOB: Define the following disorders or growth, giving physiological and pathological examples: hyperplasia, hypertrophy, atrophy, aplasia, hypoplasia, metaplasia.

A

**Hypertrophy refers to the enlargement of cells. **

Physiological:hypertrophy of the heart muscle (myocardium) in response to regular exercise (athlete’s heart).

Pathological : Pathological cardiac hypertrophy

104
Q

```ONC Tissue Growth Disorders and Dysplasia

Atrophy

*LOB: Define the following disorders or growth, giving physiological and pathological examples: hyperplasia, hypertrophy, atrophy, aplasia, hypoplasia, metaplasia.

A

Atrophy defined as a decrease in the size of a tissue or organ due to cellular shrinkage

Physiological:Muscles undergo atrophy when they are not used regularly

Pathological : conditions like Alzheimer’s disease, resulting in cognitive decline

105
Q

```ONC Tissue Growth Disorders and Dysplasia

Aplasia

*LOB: Define the following disorders or growth, giving physiological and pathological examples: hyperplasia, hypertrophy, atrophy, aplasia, hypoplasia, metaplasia.

A

Aplasia refers to the absence or underdevelopment of an organ or tissue due to the failure of cell development.

For example, aplastic anemia is a condition where the bone marrow fails to produce enough blood cells.

106
Q

```ONC Tissue Growth Disorders and Dysplasia

Hypoplasia

*LOB: Define the following disorders or growth, giving physiological and pathological examples: hyperplasia, hypertrophy, atrophy, aplasia, hypoplasia, metaplasia.

A

underdevelopment or incomplete development of an organ or tissue.
for instance, renal hypoplasia refers to the incomplete development of the kidneys.

107
Q

```ONC Tissue Growth Disorders and Dysplasia

Metaplasia

*LOB: Define the following disorders or growth, giving physiological and pathological examples: hyperplasia, hypertrophy, atrophy, aplasia, hypoplasia, metaplasia.

A

Metaplasia involves the conversion of one type of mature cell into another type in response to a chronic irritation or stress

In the respiratory tract, ciliated columnar cells may change into stratified squamous cells due to smoking, a condition known as squamous metaplasia.

108
Q

```ONC Tissue Growth Disorders and Dysplasia

Hamartoma

*LOB: Define hamartoma, ectopia, heterotopia.

A

A hamartoma is a benign tumor-like growth composed of mixed normal mature cells that are usually found in the affected tissue or organ.

For example, a lung hamartoma may contain lung tissue components like bronchial and alveolar cells.

109
Q

```ONC Tissue Growth Disorders and Dysplasia

Ectopia

*LOB: Define hamartoma, ectopia, heterotopia.

A

Ectopia refers to the abnormal location of an organ or tissue.

An example is ectopic pregnancy, where a fertilized egg implants outside the uterus, usually in a fallopian tube.

110
Q

```ONC Tissue Growth Disorders and Dysplasia

Heterotopia

*LOB: Define hamartoma, ectopia, heterotopia.

A

Heterotopia is the presence of **normal tissue in an abnormal location within the body. **

For instance, ectopic thyroid tissue can be found in the neck or other areas not typical for the thyroid gland

111
Q

```ONC Tissue Growth Disorders and Dysplasia

Dysplasia

*LOB: Define dysplasia, giving examples, and explain the link between dysplasia and invasive malignancy.

A

Dysplasia refers to the abnormal development of cells or tissues, which may look different from normal cells but are not yet cancerou

112
Q

```ONC Tissue Growth Disorders and Dysplasia

Examples of Dysplasia

*LOB: Define dysplasia, giving examples, and explain the link between dysplasia and invasive malignancy.

A

Cervical dysplasia, for example, can be a precursor to cervical cancer. The link between dysplasia and invasive malignancy is that if dysplastic cells continue to progress without treatment, they can become cancerous and invade nearby tissues.

Colorectal Polyps

113
Q

```ONC Tissue Growth Disorders and Dysplasia

Dysplasia as screening tool

*LOB: Define dysplasia, giving examples, and explain the link between dysplasia and invasive malignancy.

A

allows for early intervention and treatment, potentially preventing the development of invasive malignancies.

Pap smears

Colonoscopy for Colorectal Polyps

114
Q

```ONC Tissue Growth Disorders and Dysplasia

Premalignant

*LOB: Understand the difference between the term ‘premalignant’ condition and a condition which ‘predisposes to’ the development of malignancy

A

A ‘premalignant’ condition is one in which cellular changes have occurred that make it highly likely to progress to cancer if left untreated.

For example, cervical dysplasia is considered premalignant because it can evolve into cervical cancer.

115
Q

```ONC Tissue Growth Disorders and Dysplasia

Pre-disposes

*LOB: Understand the difference between the term ‘premalignant’ condition and a condition which ‘predisposes to’ the development of malignancy

A

A condition that ‘predisposes to’ the **development of malignancy increases the risk of cancer but doesn’t necessarily guarantee cancer. **

For instance, having a family history of breast cancer predisposes an individual to a higher risk of developing breast cancer, but it doesn’t mean they will definitely get it.

116
Q

Grade vs Staging

A

Grade applies to single cell
Staging compares tumour to body

117
Q

First event in tumour

A

Disregulation of cell cycle.

118
Q

Myeloma Workshop (missing)

What is Myeloma?

*LOB: Define myeloma and recognise its typical symptoms and clinical presentation

A

Malignant Tumour of
Bone Marrow
Of Plasma cells

119
Q

Myeloma Worksgop

Myeloma Presentation

*LOB: Define myeloma and recognise its typical symptoms and clinical presentation

A
  • Fractures
  • Spine fractures with associated nerve symptoms (tingling) (TUNAFISH back pain flags)
  • Anaemia (microcytic)
  • Infections
  • Elevated Calcium (hypercalaemic symptoms incl thirst)
  • Bleeding or Clotting
  • Kidney associations- weight loss, oedema
120
Q

Myeloma Workshop

Laboratory Findings

*LOB: Describe the common laboratory abnormalities detected in myeloma and clinical significance of these abnormalities

A
  • M Protein (Clonal plasma cells produce Monoclonal protein)
  • Elevated Se Calcium
  • Reduced eGFR
  • Elevated Creatinine
  • Anaemia- RBC, MCV, Fe
  • Thrombocytopenia- Reduced Plt.
  • Hypogammaglobulinemia- reduced IgG and IgA
  • Elevated Lactate Dehydrogenase (aggressive disease)
  • Elevated B2 Microglobulin (tumour burden)
121
Q

Myeloma Workshop

How is Myeloma Diagnosed?

*LOB: Demonstrate an understanding the tests required to make a diagnosis of myeloma

A
  • Pt Hx and associated symptoms
  • FBC
  • M Protein (serum protein electrophoresis)
  • IgG, IgA (Serum immunofixation)
  • Serum free light chain assay (FLC) for κ λ chains
  • Bone marrow aspiration
  • 24 Hour protein
  • X Ray, CT, Bone density, MrI
  • Calcium, Renal, Serum markers
122
Q

Myeloma Workshop

Myeloma Pathology

*LOB: Briefly explain the pathology of myeloma associated bone disease

A
  • Osteoclast activation by IL6, RANKL
  • Osteoblast suppression
  • Bone distruction factors: MMPs, TNFα, degrade extracellular matrix
  • No bone remodelling- lytic lesions, weakened bones.
123
Q

Myeloma Workshop

Renal failure in myeloma

*LOB: Outline the possible causes of renal failure in myeloma

A

Cath Nephropathy monoclonal light chains produced by malignant plasma cells produce casts that precipitate in tubules -> Inflammation

Light chain deposit disease deposits in glomeruli- direct chains not casts

Amyloidosis abnormal proteins (amyloid fibrils) derived from monoclonal immunoglobulins deposit in various organs

Direct tumour infiltration

Hypercalcaemia

Dehydration

Infections

Drug side effect including NSAID for pain use.

124
Q

Myeloma workshop

Amyloidosis in Myeloma

*LOB: Demonstrate an understanding of the pathological link between myeloma and amyloidosis

A
  • Multiple myeloma and amyloidosis are both plasma cell dyscrasias, meaning they involve abnormalities in plasma cells
  • Monoclonal gammopathy
  • Abnormal proteins- M protein, IgG IgA or chains κ, λ
  • And amyloidosis abdnormal plasma cells produce precursor proteins that misfold and insoluble fibrils
    *

There can be clinical overlap between multiple myeloma and amyloidosis, as both diseases may present with similar symptoms such as fatigue, weakness, renal dysfunction, and proteinuria. Additionally, some patients may have concurrent multiple myeloma and amyloidosis.

125
Q

Myeloma Workshop

Bacterial Lobar Pneumonia

*LOB: Describe the microbiological investigation of a case of bacterial lobar pneumonia

A
  • Clinical Assessment incl Hx
  • Sputum culture and Gram stain
  • Blood culture for bacteraemia
  • BAL- Brochoalveolar lavage fluid analysis- lower resp tract fluid
  • Serological tests for specific pathogens
  • Molecular incl PCR
  • Pleural fluid if pleural effusion present
126
Q

Myeloma Workshop

Herpes Zoster

*LOB: Describe the microbiological investigation of a case of herpes zoster

A
  • Clinical assessment incl Hx
  • Viral culture from lesions
  • PCR (VZV vs HSV)
  • Tzanck smear- staining for multinucleated cells
  • Serological
127
Q

Myeloma workshop

Concurrent infection

*LOB: Explain how immunological defects in myeloma may result in susceptibility to infections

A
  • Hypogammaglobulinemia- reduction in IgA, IgM, IgG so humoural response weaker
  • Impaired Ab function
  • Supression of normal plasma cells
  • Disrupted cell mediated immunity incl T Cells and NK
  • Bone marrow supression- nuetropenia (bacterial and fungal risk)
128
Q

What is the link between dysplasia and invasive malignancy?

*LOB: Define dysplasia, giving examples, and explain the link between dysplasia and invasive malignancy

A

Dysplasia is considered a precursor to invasive malignancy because it represents an abnormal proliferation of cells that have acquired genetic and epigenetic alterations.

The progression from dysplasia to invasive malignancy involves a series of steps known as the dysplasia-carcinoma sequence. Initiation, Promotion, Progression.

129
Q

Dysplasia as screening

*LOB: Understand the importance of recognising dysplasia as a screening tool and give 2 examples of this

A

Recognizing dysplasia as a screening tool is crucial for the early detection and prevention of cancer

Pap Smear
Colonoscopy

130
Q

What is
‘premalignant’ condition
and a condition which ‘predisposes to’

*LOB: Understand the difference between the term ‘premalignant’ condition and a condition which ‘predisposes to’ the development of malignancy

A

A premalignant condition is a state in which cellular changes have occurred that are associated with an increased risk of developing cancer but have not yet progressed to invasive malignancy.

cervical dysplasia, Barrett’s esophagus, and colorectal adenomatous polyps.

A condition predisposing to the development of malignancy refers to any factor or circumstance that increases the likelihood of developing cancer, including genetic, environmental, or behavioral factors.

BRCA1/2 mutations predisposing to breast and ovarian cancer

131
Q

Classification of tumours M5

Common Cancers

*LOB: Demonstrate an awareness of the epidemiology of common cancers and their preciptating factors

A
132
Q

Classification of tumours

Benign vs Malignant Neoplasms

Outline the macro- and microscopic characteristics of benign and malignant neoplasms

A
133
Q

Key Nomenclature

Demonstrate a familiarity with tumour classification nomenclature

A
134
Q

Acute Lymphoblastic Leukaemia

A
  • Common in children
  • immature lymphocytes (pre-B, pre-T)

Pc:
* Lethargy and Pallor (Anaemia)
* Frequent, Severe infections (neutropaenia)
* Easy bruising, petechia (thrombocytopaenia)
* Bone Pain
* Splenomegaly
* Hepatomegaly
* Fever

135
Q

Acute Myeloid Leukaemia

A

Meloidblast (pre monocyte, pre granulocyte)
PC
* pallor, lethargy, weakness (anaemia)
* High white cell
* Low Neutrophil
* Bleeding (thrombocytopaenia)
* Splenomegaly
* Bone Pain

t(15:17)

136
Q

Burkitts Lymphoma

A

High grade B Cell neoplasm
Cause: CMyc t(8:14)
Starry sky lymphocytes with macrophages containing tumour

137
Q

Breast Cancer

A

BRCA1/2
Increased Ovarian risk

The invasive component is usually comprised of ductal cells (unless it is an invasive lobular cancer). In situ lesions may co-exist (such as DCIS).

**Changes with invasive: **
1. Nuclear pleomorphism
2. Coarse chromatin
3. Angiogenesis
4. Invasion of the basement membrane
5. Dystrophic calcification (may be seen on mammography)
6. Abnormal mitoses
7. Vascular invasion
8. Lymph node metastasis

138
Q

Cervical Cancer

A
  • HPV 16, 18 and 33 are carcinogenic
  • (6 and 11 not cancer, just warts)
  • endocervical cells may develop koilocytes
  • enlarged nucleus
  • irregular nuclear membrane contour
  • the nucleus stains darker than normal (hyperchromasia)
  • a perinuclear halo may be seen

PC
heavier periods than you normally have. vaginal bleeding between periods, after sex, or after the menopause.

139
Q

Chronic Lymphocytic Leukaemia

A
  • common in adults
  • monoclonal proliferation of well-differentiated lymphocytes which are almost always B-cells

PC Incidental, anorexia, weightl loss, bleeding, infections, lymphadenopathy

Find lymphocytosis, anaemia, thrombocytopaenia, smudge cells

complications anaemia, hypogammaglobulinaemia, warm autoimmune haemolytic anaemmia, transformation to high-grade lymphoma (Richters)

140
Q

Chronic Myeloid Leukaemia

A
  • t(9:22)(q34; q11)
    PC”:
  • lethargy (anaemia)
  • Weight loss, sweating, splenomegaly
  • Decreased leukocyte alkaline phosphatase
  • granulocytes, monocytes

Treat
Imatinib

141
Q

Hodgkins Lymphoma

A
  • Cause: HIV, EBV
  • Lymphocytes

PC:
* lymphadenopathy
* weight loss
* pruritus
* night sweats
* fever
* LDH raised, Reed Sternberg cells

Ann Arbour Staging

142
Q

Lymphadenopathy

A

enlarged lymph nodes

Causes
Infective
infectious mononucleosis
HIV, including seroconversion illness
eczema with secondary infection
rubella
toxoplasmosis
CMV
tuberculosis
roseola infantum

Neoplastic
leukaemia
lymphoma

Others
autoimmune conditions: SLE, rheumatoid arthritis
graft versus host disease
sarcoidosis
drugs: phenytoin and to a lesser extent allopurinol, isoniazid

143
Q

Mantle Cell

A

B Cell lymphoma
t 11:14
widespread lymphadenopathy
poor prognosis

144
Q

Multiple myeloma (MM)

A

haematological malignancy
B-lymphocytes diffx to plasma cells

CRABBI
Calcium (hyper)
Renal (monoclonal immunoglobulins and amyloidosis)
Anaemia
Bleeding (thrombocytopenia)
Bones (lytic lesions- Osteoclasts)
Infection (susceptible)

145
Q

Para-aortic lymphadenopathy

A

Organ sites that may metastasise (early) to the para-aortic lymph nodes:
Testis
Ovary
Uterine fundus

146
Q

Superior vena cava obstruction

A
  • oncological emergency caused by compression of the SVC
  • common malignancies: small cell lung cancer, lymphoma
  • other malignancies: metastatic seminoma, Kaposi’s sarcoma, breast cancer
147
Q

Richter’s transformation

A

leukaemia cells enter the lymph node and change into a high-grade, fast-growing non-Hodgkin’s lymphoma.

148
Q

Non-Hodgkins

A
  • Epstein–Barr virus: Burkitt’s lymphoma, follicular dendritic cell sarcoma, extranodal NK-T-cell lymphoma, diffuse large B-cell lymphoma.
  • Human T-cell leukemia virus: Adult T-cell lymphoma.
  • Helicobacter pylori: Gastric lymphoma.
  • HHV-8: Primary effusion lymphoma, multicentric Castleman disease.
  • Hepatitis C virus: Splenic marginal zone lymphoma, lymphoplasmacytic lymphoma, diffuse large B-cell lymphoma.
  • HIV infection.
  • Polychlorinated biphenyls (PCBs)
  • Diphenylhydantoin
  • Dioxin
  • Phenoxy herbicides
  • Medical treatments:
  • Radiation therapy
  • Chemotherapy
  • Genetic diseases:
  • Klinefelter syndrome
  • Chédiak–Higashi syndrome
  • Ataxia–telangiectasia syndrome
  • Autoimmune diseases:
  • Sjögren syndrome
  • Celiac disease
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
149
Q

Lymphoma vs Leukaemia

A

Cells: Lymphoma is lymphocytes (b and t), leukaemia is all blood cells such as lymmphocytes and myeloid

  • Location: Lymphoma in lymphatic tissues; leukemia in bone marrow and blood.
  • Cell Type: Both can involve lymphocytes, but leukemia can also affect other blood cell types
    .
  • Symptoms: Lymphoma often presents with swollen lymph nodes, while leukemia typically causes symptoms related to abnormal blood cell counts (e.g., anemia, infections, bleeding).
150
Q

Oncogenes and their cancer

A
151
Q

TSG and their cancer

A

Med 2 Life Protection (4 decks)

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