Oncology Flashcards
Define cancer (2 points)
Cancer – abnormal cells divide in an uncontrolled way; some cancers may eventually spread into other tissues.
List 7 risk factors for cancer
Risk factors for cancer:
- Smoking
- Excess alcohol intake
- Carcinogenic diet
- Excess sunlight
- Physical inactivity
- Chronic infection
- Genetic predisposition
Recall the cell cycle
The cell cycle:
- How a cell grows and divides – ‘life cycle’
- Interphase:
- Growth of cell, no division (includes G1, S, G2)
- Cells in this phase most of time
- Except cancer cells (division)
- G1: duplicate cell contents (e.g. organelles)
- S: duplicate chromosomes (23 to 46 pairs)
- G2: prepare for mitosis
- G0: no cell division (e.g. neurones)
- Mitosis: active cell division (cytokinesis)
List the two classes of molecule which regulate the cell cycle
Two classes of molecule regulate the cell cycle through various checkpoints:
- Cyclins (Cyc)
- Specific Cyc are made at specific times.
- Cyclin-dependent kinases (CDKs)
- Inactive CDKs always present in cell, activated by Cyc
List the 3 cell cycle checkpoints
Cell cycle checkpoints (3 points):
- M checkpoint
- G1 checkpoint
- G2 checkpoint
Describe positive cell cycle regulation
Positive regulation at internal checkpoints (allows for progression):
- The cell progresses through the cell cycle regulated through various checkpoints:
- Cyclins (Cyc)
- Cyclin-dependant kinases (CDKs)
Describe negative regulation of the cell cycle at G1 checkpoint
Negative regulation of the cell cycle (prevents progression from G1 phase to S phase):
- At G1 checkpoint:
- Tumour suppressor genes control the cell cycle
- Retinoblastoma protein (pRb) normally bound to E2F transcription factors
- When phosphorylated, pRb releases E2F transcription factors which bind to DNA and regulate expression of S phase proteins → progress to S phase
- When unphosphorylated, pRb remains bound to E2F transcription factors → halts progress to S phase
- Therefore, pRb is able to halt cell cycle if conditions are unfavourable (i.e. potential cancer).
Describe the role of tumour suppressor genes (5 points)
Tumour suppressor genes control the cell cycle, p53 (“guardian of the genome”):
- Activated p53 binds to DNA directly, leading to downstream activation of p21
- p21 complexes to CDK2, inhibiting it
- This prevents cell continuing onto cell division
- Mutated p53 → means p21 not available to halt cell division → cancer
- Mutated p53 is in > 50% human cancers.
List 7 types of cancer cell
Types of cancer cells (7 points):
- Carcinoma
- Sarcoma
- Leukaemia
- Lymphoma and myeloma
- Brain and spinal cord (CNS)
- Mixed tumours
- Teratoma
Describe carcinoma and list 4 types
Carcinoma – originates in epithelial tissues (85% of UK cancers):
“Some Apples Taste Bad”
- Squamous cell carcinoma
- Adenocarcenoma
- Transitional cell carcinoma
- Basal cell carinoma
Describe sarcoma and list 2 types
Sarcoma – originates in connective tissues e.g. bones, cartilage, tendons, and muscles (1% of UK cancers):
- Bone sarcoma
- Soft tissue sarcoma
Describe leukaemia
Leukaemia – originates in blood-forming tissues, bone marrow (3% of UK cancers)
Describe lymphoma and myeloma
Lymphoma and myeloma – cancers of the lymphatic system (5% lymphoma and 1% myeloma)
Describe cancer of the central nervous system and name one type
Central nervous system cancers – originate in the cells of the brain or spinal cord (3% of UK cancers):
- Glioma
Describe mixed tumours and list 2 types
Mixed tumours – both epithelial and connective tissue components:
- Carcinosarcoma
- Pleomorphic adenoma
Describe teratoma
Teratoma – originates in the germ cells:
Recall the hallmarks of cancer (10 points)
Hallmarks of cancer are acquired functional capabilities that allow cancer cells to:
- Survive
- Proliferate
- Spread
These functions are acquired in different tumour types in the course of multistep tumourigenesis, via distinct mechanisms at different times (10 mechanisms; *considered in detail):
List the two main types of cancer characteristics
Characteristics of cancer are grouped into two main types:
- Emerging characteristics
- Enabling characteristics
List 2 emerging characteristics of cancer
Emerging characteristics of cancer:
- Avoiding immune destruction
- Deregulating cellular energetics
List 2 enabling characteristics of cancer
Enabling characteristics of cancer:
- Genome instability and mutation
- Tumour-promoting inflammation
Emerging characteristic of cancer
Describe how cancer cells avoid immune distruction
Avoiding immune destruction – active evasion by cancers cells from attack and elimination by immune cells (e.g. NK cells):
- Cancer immunoediting – tumour cells with downregulation or loss of MHC class I escape surveillance by cytotoxic T cells
Emerging characteristic of cancer
Describe how cancer cells derugulate cellular energetics
Deregulation of cellular energetics
Cancer cells favour aerobic glycolysis pathway over normal respiration – inefficient but fast:
- Produces a lot less ATP per glucose but they make it much faster
- Increases glucose transporters to take in more glucose
- Produces intermediate precursors for building proteins and DNA needed by rapidly dividing cells
This phenomenom is referred to as the Warburg effect
Describe the Warbug effect
The Warburg effect
Refers to the fact that cancer cells, somewhat counter intuitively, prefer fermentation as a source of energy rather than the more efficient mitochondrial pathway of oxidative phosphorylation.
Enabling characteristic of cancer
Describe genetic instability and mutation for enabling cancer
Genetic instability and mutation:
- Certain genetic mutations confer selective advantage on a subset of cells, enabling outgrowth and dominance in local tissue environment.
Compare inherited vs acquired genetic mutations found in cancers
The appearance of abnormal characteristics reflects altered patterns of gene expression in cancer cells, resulting from inherited or acquired mutations:
Enabling characteristic of cancer
Describe how inflammation can enable tumour progression (4 key points)
Tumour-promoting inflammation:
- Historically thought that immune response was only to allow body to eradicate tumour (partly true)
“Inflammation Promotes Growth & Survival”
Inflammation enables tumours by supplying bioactive molecules to environment:
- Inductive signals activate epithelial mesenchymal transition
- Proangiogenic factors and ECM modifying enzymes facilitate angiogenesis, invasion and metastasis
- Growth factors sustain proliferative signalling
- Survival factors limit cell death
Recall the targeted therapies for the 10 different hallmarks of cancer
Compare benign tumour (4 points) vs malignant tumour (4 points)
Benign – non-cancerous tumour (4 points):
- Enclosed in connective tissue
- Confined to site of origin
- May grow but does not spread to other parts of body (i.e. does not metastasize)
- May turn malignant – best to resect when noticed
Malignant – cancerous tumour (4 points):
- Not enclosed in any tissue
- Not confined to site of origin
- Grows rapidly and spreads to other body parts via blood (metastases)
- Earlier intervention tends to have better prognosis
Describe DNA point mutations and list 3 key types
DNA point mutations:
- Common types of mutations to DNA sequence include:
- Substitution (a different nucleotide is substituted)
- Insertion (the addition of a new nucleotide)
- Deletion (the loss of a nucleotide)
Point mutations because only one nucleotide is substituted, added, or deleted
-
Insertions and deletions are usually more harmful than a substitution
- Results in a frame-shift that changes the reading of subsequent codons
- Alters the entire amino acid sequence following the mutation, producing abnormal protein
List and describe 3 types of germline mutation
Germline ⇒ germline is the population of a multicellular organism’s cells that pass on their genetic material.
Germline mutations can have large or small negative effects:
-
Neutral mutations:
- Non-coding sequence of DNA (intron)
- Changes in DNA sequence but no noticeable effect on the phenotype of an organism
-
Selected mutations:
- Coding sequence of DNA (exon)
- Defective gene, abnormal protein produced
-
Mutations to control genes:
- Control genes regulate expression of other genes
- Mutation causes big change occurs in phenotype
- HOX genes germ line mutations:
- Fly – legs instead of antennae – mutation in HOM-C
- Human – microtia → mutation in HOXA2
List 7 chromosome mutations
Chromosome mutations:
- Chromosomal aneuploidy (abnormal number of chromosomes in a cell)
- Point mutations
- Deletions
- Duplications
- Amplifications
- Translocations
- Inversions
Describe epigenetics in cancer (4 points)
Epigenetics – study of heritable changes in gene expression that do not involve changes in underlying DNA sequence:
- A change in phenotype without a change in genotype, which in turn affects how cells read the genes
- Inherited or environmental exposures during development and lifetime chemically modify DNA and the proteins bound to it
Describe chromosomes and the 4 primary functions of chromatin
In a cell nucleus, DNA is packaged into chromosomes.
Chromatin forms chromosomes:
- Complex of DNA and proteins
- DNA tightly coiled around proteins called histones – support DNA structure
__The primary functions of chromatin (4 points):
- To package DNA into a more compact, denser shape
- To reinforce the DNA macromolecule to allow mitosis
- To control gene expression and DNA replication
- To prevent DNA damage
Describe DNA methylation (4 points)
DNA methylation:
- Methylation of DNA and histones causes nucleosomes to pack tightly together
- Transcription factors cannot bind the DNA → genes are not expressed
- DNA methylation is almost exclusively found in CpG islands
- In cancer typically, there is hypermethylation of tumour suppressor genes and hypomethylation of oncogenes
Describe histone acetylation and deacetylatoin (5 points)
Histone acetylation:
- Lysine residues of N-terminal tail protruding from the histone core of the nucleosome can be acetylated and deacetylate
- Histone acetylation results in loose packing of nucleosomes, transcription factors can bind the DNA and genes are expressed
- Histone acetylation induced by histone acetyl transferases (HATs) and is associated with gene transcription
- Histone hypoacetylation induced by histone deacetylase (HDAC) activity is associated with gene silencing
- In cancer typically, decrease in histone acetylation (hypoacetylation) is involved in tumourigenesis, tumour invasion and metastasis
Outline the TNM classifcation system
T – size or direct extent of the primary tumour:
- Tx: tumour cannot be assessed
- Tis: carcinoma in situ
- T0: no evidence of tumour
- T1, T2, T3, T4: size and/or extension of the primary tumour.
N – degree of spread to regional lymph nodes:
- Nx: lymph nodes cannot be assessed
- N0: no regional lymph nodes metastasis
- N1: regional lymph node metastasis present; at some sites, tumour spread to closest or small number of regional lymph nodes
- N2: tumour spread to an extent between N1 and N3 (N2 is not used at all sites)
- N3: tumour spread to more distant or numerous regional lymph nodes (N3 is not used at all sites).
M – presence of distant metastasis:
- M0: no distant metastasis
- M1: metastasis to distant organs (beyond regional lymph nodes).
Define carcinogenesis (3 points)
Carcinogenesis: the process by which normal cells are transformed into cancer cells
- A complex multistage process usually involving more than one genetic change
- Mutations in oncogenes and tumour suppressor genes induce malignant change
Compare the function of oncogenes in health and in cancer
Oncogenes:
- Normal function: Proto-oncogenes normally control cell division, apoptosis and differentiation
- In cancer: Activation of proto-oncogenes to oncogenes e.g. c-Myc gene
- Mutant oncogene alleles are typically dominant
Compare the function of tumour supressor genes in health and in cancer
Tumour suppressor genes in health and in cancer
- Normal function: slow down cell division, repair DNA mistakes, initiate apoptosis
- In cancer: inactivation of tumour suppressor genes e.g. TP53 gene (> 50% human tumours)
Mutant tumour suppressors alleles are usually recessive
Describe how tissues minimize progressive accumulation of mutations
Mutations happen all the time, but cells have repair mechanisms:
- Stem cell compartment – progenitor cells are shielded from toxic agents
- Transit-amplyifying cells – frequent mitosis increases risk of mutation
- Post-mitotic, highly differentiated cells (e.g. hepatocytes) are exposed to toxic agents as part of their role
- If irreparable damage, these terminal cells undergo apoptosis
Describe the two-hit hypothesis of cancer
Knudson’s two hit-hypothesis – first proposed by A. G. Knudson (1971) for cases of retinoblastoma caused by mutated tumour suppressor gene, Rb:
- Unlike oncogenes, tumour suppressor genes generally follow the “two-hit hypothesis”
- Implies that both alleles that code for a particular protein (e.g. Rb) must be affected to promote malignancy (hence “two-hit” ⇒ both alleles are mutated)
- If only one allele for the gene is damaged, the second can still produce the correct protein
- Mutant tumour suppressors alleles are usually recessive whereas mutant oncogene alleles are typically dominant
Recall the difference betwen sporadic and hereditary retinoblastoma
Sporadic retinoblastoma ⇒ (Rb+/Rb+)
- Requires two mutations of (Rb+/Rb+) → (Rb/Rb)
- Less likely to happen, and if it does, single tumour in one eye with late onset
Hereditary retinoblastoma ⇒ (Rb/Rb+)
- Only requires on mutation of (Rb/Rb+) → (Rb/Rb)
- More likely to happen, and if it does, multiple tumours in both eyes with early onset
Describe the multistage model of carcinogenesis and list the 5 key stages
Multistage model of carcinogenesis (Armitage-Doll model)
Multistep process which involves a series of cellular and molecular changes, as a result of the progressive accumulation of mutations and alterations in proto-oncogenes and tumour suppressor genes.
5 Key stages:
- Normal
- Dysplastic
- Benign
- Pre-malignant
- Malignant
Stages 1→3: proliferation and survival
Stages 4→5: angiogenesis and invasiveness
Recall the multiage model of bowel cancer
Describe HPV pathogenisis and carcinogenesis
Pathogenesis of infection:
- HPV infects the epithelium. The viral DNA either integrates into the DNA of the crypt-lining epithelial cells or remains in their cytoplasm.
- Viral proteins E6 and E7 bind to and inactivate the tumour suppressor proteins p53 and retinoblastoma protein respectively
- Inhibiting apoptosis
- Increasing cell proliferation
- Generating genomic instability
- After a prolonged latent period of 20–30 years, carcinoma may result.
- Human papillomavirus–associated carcinomas almost always arise in the oropharynx, specifically in the tonsil and minor tonsils of Waldeyer’s ring, around the base of tongue, soft palate and pharynx.
- Tonsil crypts are lined by non-keratinised and permeable epithelium designed to allow antigens to penetrate into the lymphoid tissue below (i.e. MALT).
- The mechanisms are slightly different from the way HPV causes cancer of the uterine cervix, but the differences are not yet understood.
List the proteins involved in HPV-induced carcinogenesis (2 points)
Oncogenic HPV E6 and E7 genes induce carcinogensis:
- E6 binds to p53 and induces its degradation
- E7 binds the pRb and causes E2F transcription factor to become unbound and free
- Results in cell cycle activation and unregulated proliferation of epithelial cells
Recall the role of HPV strains in multistage cervical cancer
HPV strains and multistage cervical cancer:
- Low risk strains:
- HPV6
- HPV10
- HPV11
- High risk strains:
- HPV16 – also responsible for oral cancer (via loss of cell cycle control)
- HPV18
- HPV31
- HPV33
- HPV45
Describe the multistage model of oral cancer (2 points)
Multistage model of oral cancer:
- Genetic alterations that are observed at the different stages of oral carcinogenesis
- Mutations in p53 and pRb implicated in oral carcinogenesis
Describe the clonal expansion theory
The theory of clonal expansion follows on from the multistage model:
- Also assumes that the accumulation of mutations causes cancer
- But it does not assume that all the mutations happen in the same cell
- A subset of mutations will confer a selective growth advantage/survival advantage and the cells carrying those mutations will outgrow their neighbouring cells.
Recall how a cross-section of a tumour would appear following clonal expansion
Eventually if you take a cross section of a tumour following clonal expansion
- Not all cells in the tumour will have the same mutations
- Subset of tumour cells will have the ability to metastasise
- Other subset of tumour cells will not
Define cancer stem cells
Cancer stem cells (CSCs) – those cells within a tumour that can self-renew and drive tumourigenesis
Describe the hallmark responsible for replicative immortality associated with oral cancer
Hallmark for oral cancer – immortalization:
- hTERT – human telomerase
Describe the role of telomeres in a healthy cell (5 points)
Role of telomeres in health cells:
- Telomeres are located at the ends of chromosomes
- Protect genetic material and allow cell division
- Get shorter as cell divides → causing senescence
Describe the role of human telomerase and hTERT (5 points)
Hallmark for oral cancer – immortalization:
- hTERT – human telomerase reverse transcriptase (catalytic subunit of the enzyme telemorase)
Telomerase expression:
- Human telomerase reverse transcriptase is up-regulated in practically all human cancers
- Telomerase enzyme repairs telomeres – increased expression in cancer cells and prolongs survival (resisting cell death)
Describe the role of epidermal growth factor in healthy cells (2 points) and cancer cells (3 points)
Healthy cells require growth signals before they can progress through the cell cycle:
- Signalling transduction pathways initiated by growth factor acting at their receptors
- Epidermal growth factor (EGF) stimulates cell growth and differentiation by binding to its receptor, EGFR
Cancer cells have:
- Increased production of EGF
- Mutation in EGFR results in constitutively active receptor
- Abnormal cell signalling and growth
Describe the drugs (monoclonal antibodies) used to treat aberrant cell signalling associated with increased epidermal growth factors
Monoclonal antibodies and protein kinase inhibitors:
- Many tumours overexpress growth factors, stimulating cell proliferation and tumour growth:
This can be inhibited by:
- Monoclonal antibodies → bind to growth factor receptors (Trastuzumab, Cetuximab) or neutralise growth factors (Bevacizumab)
- Protein kinase inhibitors → prevent downstream signalling triggered by growth factors by inhibiting specific oncogenic kinases (Imatinib).
Describe angiogenesis in cancer with reference to hypoxia and tumour vessel abnormalities (5 points)
Vascular endothelial growth factor (VEGF) – released to promote growth of new blood vessels.
The transcription factor, hypoxia-inducible factor 1 (HIF-1), is a major regulator of tumour cell adaptation to hypoxic stress:
- Hypoxia → the angiogenic switch
Tumour vessels are abnormal (3 × larger diameter):
-
Leaky and vasculature architecture is haphazard, but they do the job
- Supply oxygen and nutrients to the tumour
- Remove waste products from the tumour
Identify 2 key proteins which activate invasion of cancers into surrounding tissues
PDPN – podoplanin:
- Small membrane glycoprotein → increased cancer cell invasion into lymphatic and blood vessels
MMP1 – matrix metalloproteinase 1
- Enzyme which breakdowns of extracellular matrix
Describe how a cancer becomes metastatic with reference to epithelial-mesenchymal transition (8 points)
In order to become metastatic cancers undergo epithelial–mesenchymal transition (EMT):
- Epithelial cells lose their cell polarity and cell-cell adhesion
- Gain migratory and invasive properties to become mesenchymal stem cells
- E-cadherin (epithelial) – cell adhesion molecule found in epithelial tissue
- ZO-1 – tight junction protein binds actin cytoskeleton
- N-cadherin (neural) – cell adhesion molecule found in migrating neurons and mesenchymal cells during organogenesis
- Β-catenin – binding to N-cadherin and in turn interacts with the actin cytoskeleton
List the 5 sites by which head and neck cancers are classified
Head and neck cancer refer to cancers of the UADT (upper aero digestive tract)
This region is divided into six sites by which cancers are classified (5 points):
- Oral cavity
- Pharynx
- Larynx
- Nasal cavity and the paranasal sinuses
- Major and minor salivary glands
- Skin
List the anatomical components of the oral cavity where cancers can develop (8 points)
Oral cavity:
- Lips
- Buccal mucosa
- Anterior tongue
- Floor of the mouth
- Hard palate
- Upper gingiva
- Lower gingiva
- Retromolar trigone (anatomical triangle)
List and describe the 3 anatomical divisions of the pharynx where cancers can develop
Pharynx – divided into the nasopharynx, the oropharynx, and the hypopharynx.
- The nasopharynx – the narrow tubular passage behind the nasal cavity, is the upper part of the pharynx.
- The oropharynx – the middle part of the pharynx, includes the tonsillar area, the tongue base, the soft palate, and the posterior pharyngeal wall.
- The hypopharynx – which is the lower part of the pharynx, includes the pyriform sinuses, the posterior surface of the larynx (postcricoid area) and the inferoposterior, and inferolateral pharyngeal walls.
List and describe the 3 anatomic divisions of the larynx where cancers can develop
Larynx is divided into three anatomic regions:
- Supraglottic larynx,
- Glottic larynx (true vocal cords and the anterior and posterior commissures)
- Subglottic larynx.
List the nasal cavity and paranasal sinuses where cancers can develop (4 points)
Nasal cavity
Paranasal sinuses:
- Maxillary sinus
- Ethmoid sinus
- Sphenoid sinus
- Frontal sinus
List the major and minor salivary glands where cancers can develop (5 points)
Major salivary glands:
- parotid gland
- submandibular gland
- sublingual gland
Minor salivary glands (multiple glands located throughout):
- Submucosa of the mouth
- Upper aerodigestive tract
List 5 key benign salivary neoplasms
Key benign salivary neoplasms (5 points):
“PWOHL”
- Pleomorphic adenoma*
- Warthin’s tumour*
- Oncocytoma*
- Haemangioma
- Lymphangioma
*Considered in detail
Describe pleomorphic adenoma (4 points) and its signs (5 points)
Pleomorphic adenoma – mixed tumour:
- Mixed tumour: contains both epithelial and mesenchymal elements
- Most common benign tumour of salivary glands
- Can arise from parotid, submandibular
- Parotid – usually arises from its tail, deep lobe
- Encapsulated
- Slow growing tumour
Signs of pleomorphic adenoma:
- Swelling in front, below and behind ear
- Raises ear lobule
- Retromandibular groove is obliterated
- Any swelling which raises ear lobule is due to parotid gland neoplasm unless proved otherwise
- It sends ‘pseudopods’ into surrounding gland → surgical excision of the tumour should include normal tissue around it: superficial parotidectomy
Describe Warthin’s tumour (11 points)
Warthin’s tumour (adenolymphoma) – rule of 7’s:
- Encapsulated
- Exclusively in parotid gland
- Parotid tail
- Commonly seen between 5th – 7th decade
- Male: female (7:1)
- ~7% of salivary gland tumours
- Usually fluctuant, slow growing
- 10% of cases are bilateral
- Histologically: epithelial and lymphoid elements
- Never malignant
- Treatment → wide local excision (resection to remove)
(Warthin’s ⇒ Wide local excision)
Describe oncocytoma (6 points)
Oncocytoma (oxyphil adenoma):
- Rare – 2.3% of benign salivary tumours
- Occurrence – 6th decade
- Usually benign – malignant oncocytoma less common but can occur
- Major salivary glands: parotid, submandibular gland
- Minor salivary glands: palate, buccal mucosa, tongue
- Treatment → superficial parotidectomy
List 6 key malignant salivary neoplasms
Malignant salivary neoplasms (6 points):
“MACSAN”
- Mucoepidermoid carcinoma
- Adenoid cystic carcinoma
- Carcinoma ex-pleomorphic adenoma
- Squamous cell carcinoma
- Adenocarcinoma
- Non-Hodgkin’s lymphoma
Describe mucoepidermal carcinoma (9 points)
Mucoepidermoid carcinoma:
- Most common salivary gland malignancy
- Not encapsulated
- Commonly found in parotid gland
- Slow growing
- May cause facial nerve palsy
- Presentation:
- High-grade: rapidly enlarging, +/- pain
- Low-grade: slow growing, painless mass
- Treatment → total conservative parotidectomy
Describe adenoid cystic carcinoma (9 points)
Adenoid cystic carcinoma (cylindroma):
- Second most common salivary gland malignancy
- Slow growing
- Infiltrates widely into the tissue planes and muscles
- Perineural spread
- Commonly in submandibular gland, sublingual or minor salivary glands
- Less commonly in parotid gland
- Occasionally lymph node metastasis
- Local recurrence after surgical excision (perineural and lymphatic spread)
- Treatment:
- Radical parotidectomy
- Post-operative radiotherapy
- Wide local excision of palate – for tumours of palate
Describe carcinoma ex-pleomorphic adenoma (2 points)
Carcinoma ex-pleomorphic adenoma:
- Usually from pre-existing pleomorphic adenoma (only 1% arise ab-initio)
- Malignancy takes about 10 years to develop in an adenoma
Describe squamous cell carcinoma and adenocarcinoma
Adenocarcinoma and squamous cell carcinoma:
- Rare
- Highly aggressive
- Rapidly growing tumours
- Local and distant metastases
- Prognosis → very poor
Squamous cell carcinoma (SCC) – rule out metastasis in the parotid gland from neighbouring skin cancer or other head and neck tumor.
Pathology of SCC:
- Squamous cell carcinomas account for 90 to 95 percent of the lesions in the head and neck
- They can be categorized as well differentiated (greater than 75 percent keratinization), moderately differentiated (25 to 75 percent keratinization), and poorly differentiated (less than 25 percent keratinization) tumours
- Less common histologies include verrucous carcinoma (a variant of squamous cell carcinoma), adenocarcinoma, adenoid cystic carcinoma, and mucoepidermoid carcinomas.
Recall the head and neck lymph nodes levels (7 points)
Lymph node levels:
- Level I: submental and submandibular
- Level II: superior internal jugular (deep cervical) chain
- Level III: middle internal jugular (deep cervical) chain
- Level IV: inferior internal jugular (deep cervical) chain
- Level V: posterior triangle
- Level VI: central (anterior) compartment
- Level VII: mediastinum and infraclavicular
Recall 4 common oral cancer presentations
Describe oral cancer in white lesions (6 points)
Oral cancer in white lesions (leukoplasia/leukoplakia):
- Lesion which are white → keratinized
- Incidence 0.2-4%
- Wide variation in different populations
- Malignant change
- Most under 4%
- Period prevalence
- 2.5% in 10 years
- 4% at 20 years
- Most oral cancer originates in normal oral mucosa
- Most cancers in high incidence areas (India) from potentially malignant lesions
- Worldwide leukoplakia is 50–100 times more likely to become malignant than normal mucosa
- Hence increased risk of cancer secondary to oral hairy leukoplakia
List 7 clinical features of oral hairy leukoplakia
Describe oral cancer in red lesions
Oral cancer in red lesions (erythroplasia/erythroplakia):
- Erythroplakia is less frequent than leukoplakia
- Higher risk of cancer
- Greater dysplasia risk – ~50% are already malignant
- Very few informative follow up studies
Recall the 4 diagnositic stages of cancers in reference to TNM staging
