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Cancer Flashcards

1
Q

When a proto-oncogene mutates or there are too many copies of it, it can become pathologically turned on at which point it’s now called an oncogene. What is an oncogene? Give examples

A

proto-oncogenes include; growth factors (signalling proteins), receptors (tyrosine kinase receptors), intracellular signalling proteins e.g. kinases, transcription factors, anti-apoptotic proteins

When any of these mutate/ get activated (by mutation, chromosome translocation, gene amplification or retroviral insertion) they get a ‘gain in function’ ( enhanced kinase activity leading to uncontrolled signalling) and become oncogenes. Oncogenes are dominant (activation of one allele sufficient).

Examples: MYCN, MDM2, ALK, ABL1, HRAS, KRAS, NRAS, BRAF

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2
Q

What is a tumour suppressor gene? Give examples

A

A tumour suppressor gene gets mutated and acts by loss of function. The mutation is recessive (inactivation of both alleles necessary).

Tumour suppressor genes are inactivated by mutations, deletions, DNA methylation (epigenetic) and they cause a predisposition to cancer

Examples: RB (Rb protein), WT1, TP53, BRCA1,BRCA2, PTCH1, APC, NF1

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3
Q

Explain the clinical presentation, molecular pathology, predisposition syndromes and treatment of Wilms tumour (aka nephroblastoma) seen in children

A

Wilms tumour (aka Nephroblastoma) is a tumour of the kidney

clinical presentation:
- children under 5 usually
- asymptomatic abdominal mass
- spreads by growth via lymphatics or bloodstream

associated w predisposition syndromes:
- WAGR: Wilms tumour, Aniridia, Genito-urinary abnormalities, mental Retardation
- Beckwith-Wiedeman Syndrome (BWS)

molecular pathology:
somatic gene alterations:
- inactivated / loss of both alleles of WT1, WTX, TP53
- activated CTNNB1 (beta-catenin) gene

treatment:
- surgery, chemotherapy
- use of radiotherapy decreasing
-combination chemotherapy is promising
- counselling is essential if genetic predisposition is suspected

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4
Q

Explain the clinical presentation, cellular origins and molecular pathology of Retinoblastoma seen in children

A

clinical presentation:
Retinoblastoma (tumour of retina)
- usually occurs in children under 5
- 30% heritable; germline mutation of RB1 (tumour suppressor gene)
- tumour grows in vitreous humor of eye
- present with leukocoria

cellular origin:
- originates from cone precursor cells
- signalling pathways promote cell survival after loss of RB1

molecular pathology of retinoblastoma:
In normal cells, phosphorylation of RB1 releases E2F, inducing G1-S; whereas in cancer cells E2F is free to induce G1-S transition
-u need both alleles of RB1 lost= MYCN activation= MDM2 or MDM4 (oncogenes) over-expression= inactivates TP53 (tumour suppressor)

treatment:
-small tumour= cryotherapy
- chemotherapy, surgery or radiation
N.B. patients w germline mutation of RB1 have increased risk of second cancer, esp. if they receive radiation therapy

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5
Q

Explain the clinical presentation, cellular origins and molecular pathology of Neuroblastoma seen in children

A

Neuroblastoma is the most common cancer in first year of life

clinical presentation:
tumour of SNS, usually arises from adrenal gland or sympathetic ganglia, family history (1-2%)

cellular origins:
-derived from sympatho-adrenal lineage of the neural crest during development
-key genes implicated: MYCN, ALK, PHOX2B

molecular pathology:
- MYCN amplification
- germline ALK mutations

treatment:
-surgery, chemotherapy, radiation therapy
- stem cell transplantation
- crizotinib against ALK mutations

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6
Q

Explain the clinical presentation, cellular origins and molecular pathology of Acute lymphoblastic leukaemia seen in children

A

Acute lymphoblastic leukaemia (ALL) is the most common malignancy in children

clinical presentation:
- bruising or bleeding due to thrombocytopaenia
- pallor + fatigue due to anaemia
- infection due to neutropenia

cellular origins
-clonal expansion of immature lymphocytes
-B and T cell leukaemias

treatment:
- induction (vincristine, corticosteroid)
- consolidation; CNS-directed treatment (Methotrexate, Dexamethasone)
- maintenance (methotrexate)
- bone marrow transplantation

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7
Q

define monogenic

A

monogenic= controlled by a single gene

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8
Q

define aniridia

A

Aniridia= congenital condition where part or all of the iris missing

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9
Q

What is Beckwith-Wiedeman Syndrome (BWS)

A

Beckwith-Wiedemann Syndrome (BWS) is a congenital overgrowth disorder characterized by a spectrum of clinical features and an increased predisposition to tumor development.
Clinical Features:
BWS presents with a wide range of clinical manifestations, which can vary significantly among individuals. Some of the hallmark features include:
- Macrosomia: Increased birth weight and length, often above the 97th percentile.
- Macroglossia: Enlarged tongue, which may interfere with breathing, swallowing, and speaking.
- Abdominal Wall Defects: Conditions such as omphalocele (protrusion of abdominal organs through the umbilical cord) or umbilical hernia.
- Hemihyperplasia: Asymmetric overgrowth of one side of the body or specific body parts.
- Visceromegaly: Enlargement of internal organs, including the liver, spleen, kidneys, adrenal glands, and pancreas.
- Neonatal Hypoglycemia: Low blood glucose levels in infancy, which can be persistent and may require medical intervention.
- Ear Anomalies: Creases or pits in the skin near the ears.

N.B. BWS IS A SPECTRUM: individuals may exhibit many of these features or only one or two.

Genetic and Epigenetic Basis:
BWS is associated with abnormalities in the imprinted gene regions on chromosome 11p15.5. These abnormalities can include:
- Loss of Methylation at IC2: Accounts for approximately 50% of BWS cases.
- Paternal Uniparental Disomy (UPD): Presence of two paternal copies of chromosome 11p15.5, leading to overexpression of paternally expressed genes.
- Gain of Methylation at IC1: Found in about 5% of individuals with BWS.
- Mutations in the CDKN1C Gene: Occur in a subset of cases and can be inherited in an autosomal dominant manner with variable expressivity.
These genetic and epigenetic alterations disrupt the normal regulation of growth-controlling genes, leading to the overgrowth and tumor predisposition seen in BWS.

Tumor Risk and Surveillance:
Children with BWS have an increased risk of developing embryonal tumors, particularly Wilms tumor (a type of kidney cancer) and hepatoblastoma (a liver cancer). Tumors develop in about 10% of individuals with BWS, usually appearing in childhood.

Regular surveillance, including abdominal ultrasound every three months until at least eight years of age and measurement of serum alpha-fetoprotein (AFP) every six weeks until at least four years of age, is recommended to facilitate early tumor detection and treatment

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10
Q

Which Wilm’s tumour suppressor gene has been show to be an essential regulator of ureteric development?

A

The Wilms’ tumor suppressor gene WT1 has been shown to be one of these essential regulators of kidney/ ureteric development and mutations in this gene result in the formation of tumors and developmental abnormalities such as the Denys-Drash and Frasier syndromes.

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11
Q

what do we mean by stage and grade in cancer

A

Stage = describes the extent or spread of cancer in the body at the time of diagnosis. It helps determine how advanced the disease is.

Grade= refers to the behavior of cancer cells/ aggressiveness of tumour

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12
Q

what is leukocoria and what is it indicative of?

A

leukocoria is an abnormal white reflection from the retina when you shine a torch; it is indicative of retinoblastoma (tumour of retina)

the tumour grows in the vitreous humor of the eye

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13
Q

Genetic predisposition syndromes for childhood cancer. Name the syndrome and the mutation it causes

A

WAGR= 11p13 deletion= Wilms tumour

Beckwith-Wiedeman= 11p15 abnormal imprinting= Hepatoblastoma, Wilms tumour

Familial Retinoblastoma= RB1 (tumour suppressor gene inactivated)= Retinoblastoma, sarcoma, melanoma, glioma, carcinoma

Familial Neuroblastoma= ALK (anaplastic lymphoma kinase) = neuroblastoma

Basal-cell nevus= PTCH1= medulloblastoma, basal-cell carcinoma, ovarian fibromas

Li-Fraumeni= TP53= brain tumour, bone or soft tissue sarcoma

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14
Q

define hypertelorism

A

Hypertelorism is a term used to describe an abnormally large distance between the eyes.

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15
Q

what are the 8 hallmarks of cancer?

A
  1. self-sufficiency in growth signals (autocrine signalling)
  2. insensitivity to anti-growth signals
  3. evading apoptosis
  4. limitless reproductive potential
  5. sustained angiogenesis
  6. tissue invasion + metastasis
  7. deregulating cellular energetics
  8. avoiding immune detection
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16
Q

which growth factor is closely associated with angiogenesis of cancer cells

A

Vascular Endothelial Growth Factor (VEGF) causes angiogenesis (blood vessel formation) to be sustained and increased around tumours

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17
Q

If a HER2 receptor (member of a tyrosine kinase receptor) is mutated and activated, what happens?

A

Human epidermal growth factor receptor 2 (HER2) is a member of the epidermal growth factor receptor family having tyrosine kinase activity. When its mutated it is a oncogene (previously a proto-oncogene)

The activation as a result of mutation of HER2 will activate initiation of growth pathway: autophosphorylation of tyrosine= the receptor changes shape= activated= enhanced kinase (PI3K, MAPK) activity= uncontrolled signalling= tumour

N.B. HER2 IS HIGHLY ONCOGENIC AS IT DOES NOT NEED A GROWTH FACTOR TO BE ACTIVATED hence why we screen for HER2 mutations in families!

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18
Q

Which 2 pathways activate gene expression

A

PI3K (Phosphatidylinositol 3-kinase) pathway + MAPK (Mitogen-activated protein kinase) pathway activate gene expression

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19
Q

What is immunohistochemistry (IHC)?

A

This technique employs antibodies that specifically bind to antigens (proteins) of interest, when diagnosing cancer.

The antibody is conjugated to a detectable label, such as:

Enzymes (e.g., horseradish peroxidase or alkaline phosphatase): These enzymes catalyze colorimetric reactions, producing a visible signal (e.g., a brown or red stain).

Fluorescent dyes: These allow visualization under a fluorescence microscope.

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20
Q

Fecal occult blood tests (FOBTs) and Immunochemical Fecal Occult Blood Test (iFOBT or FIT) both take a stool sample to detect either colorectal cancer or GI bleeding. Which test is preferred due to its higher sensitivity + specificity?

A
  1. Guaiac-Based Fecal Occult Blood Test (gFOBT)= Detects both human and animal hemoglobin (non-specific). Therefore
    requires dietary restrictions (e.g., avoiding red meat, certain vegetables, and vitamin C before the test).
  2. Immunochemical Fecal Occult Blood Test (iFOBT or FIT); Detects heme, a component of hemoglobin, by reacting with a chemical substrate to produce a colour change.
    FIT/iFOBT is preferred due to its higher sensitivity and specificity

N.B. bleeding in stool can be due to ulcers, polyps or malignancies

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21
Q

what is the antibody to HER2 used to detect the tumour? (immunohistochemistry technique)

A

antibody used to detect HER2 is HERCEPTIN (antibody that binds to HER2 and is used to detect it with a dye)

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22
Q

CDK4/6 and cyclin D together form active complexes, which phosphorylates Rb protein. Phosphorylated Rb1 releases transcription factor E2F. Explain how E2F effects cell cycle

A

CDK4/6 and cyclin D together form active complexes, which phosphorylates Rb protein. Phosphorylated Rb1 releases transcription factor E2F…. Release from Rb1 allows for E2F-driven transcription of genes triggering the cell cycle progression

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23
Q

How does p53 transcription factor (aka TP53) tumour suppressor gene work?

A

n.b. in human cancers, TP53 is the most commonly mutated gene

p53 transcription factor increases expression of p21 (cyclin dependent kinase inhibitors)

-inhibits cyclin B/CDK1 complex causing G2/M arrest

-inhibits cyclin E/CDK2 complex stopping G1/S phase progression so DNA repair can occur

if however p53 gains a ‘loss in function’ then these processes will go unchecked = cancer/tumour

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24
Q

Breast cancer susceptibility gene BRCA1 + BRCA2 are tumour suppressor genes responsible for DNA repair (‘caretakers’) at the G2M checkpoint.

BRCA2 specifically appears to involve regulating the function of RAD51 (ATPase) in the repair by homologous recombination. Promoting efficient and precise repair of double strand breaks.

What happens when BRCA1/2 are mutated?

A

Mutated BRCA1 + BRCA2= repair of double strand DNA breaks by a homologous recombination is severely impaired

  • increase use of error prone pathways e.g. non homologous end joining (NHEJ) or single stranded annealing (SSA) result in insertions, deletions or chromosomal rearrangements.
  • genomic instability mutations lead to accumulation of unrepaired or misrepaired DNA damage
  • elevated cancer risk mutations and BRCA1/2 strongly associated with hereditary breast, ovarian, prostate and pancreatic cancer
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25
Anti-apoptotic proteins are _____. Pro-apoptotic proteins are ______.
Anti-apoptotic proteins (e.g. BCL-2) are ONCOGENES. Pro-apoptotic proteins are TUMOUR SUPPRESSOR GENES. n.b. think anti-death vs pro-death
26
What is quality-adjusted life year (QALY)
A Quality-Adjusted Life Year (QALY) measures both the quality and quantity of life gained from a treatment. Calculated as: Quality of Life Score (0–1) × Number of Years. Used to compare treatments and allocate healthcare resources efficiently.
27
What is 5-Fluorouricil? Name its drug class, indication, and mechanism of action.
5-Fluorouricil is an antimetabolite used for solid tumours. Its mechanism of action is dTMP (thymidylate synthase) synthesis inhibitor.
28
What is 6-Mercaptopurine? Name its drug class, indication, and mechanism of action.
6-Mercaptopurine is an antimetabolite used for leukaemias. Its mechanism of action is purine synthesis inhibitor
29
What is Methotrexate? Name its drug class, indication, and mechanism of action
Methotrexate is an antimetabolite used for leukaemias and lymphomas. Its mechanism of action is dihydrofolate reductase inhibitor.
30
What is 6-Thioguanvis? Name its drug class, indication, and mechanism of action.
6-Thioguanvis is an antimetabolite used for acute myeloid leukaemia. Its mechanism of action is purine synthesis inhibitor.
31
What is Bleomycin? Name its drug class, indication, and mechanism of action.
Bleomycin is an antibiotic used for squamous cell carcinoma. Its mechanism of action is DNA strand breaker.
32
What is Dactinomycin? Name its drug class, indication, and mechanism of action.
Dactinomycin is an antibiotic used for Wilms tumour and placental tumour. Its mechanism of action is DNA synthesis inhibitor.
33
What is Carmustine (nitrosurea)? Name its drug class, indication, and mechanism of action.
Carmustine is an alkylating agent used for glioma, Hodgkin’s, and non-Hodgkin’s. Its mechanism of action is inhibition of DNA replication.
34
What is Cyclophosamide (mustard)? Name its drug class, indication, and mechanism of action.
Cyclophosamide is an alkylating agent used for lymphoma, leukaemias, and neuroblastoma. Its mechanism of action is cross-linking of DNA strands.
35
What is Vincristine? Name its drug class, indication, and mechanism of action.
Vincristine is a microtubule inhibitor used for lymphoma, leukaemias, and neuroblastoma. Its mechanism of action is inhibition of microtubule formation.
36
What is Paclitaxol? Name its drug class, indication, and mechanism of action.
Paclitaxol is a microtubule inhibitor used for non-small cell lung, ovarian, and breast cancers. Its mechanism of action is hyperstabilisation of microtubules.
37
What is Anastrozole? Name its drug class, indication, and mechanism of action
Anastrozole is an aromatase inhibitor used for steroid positive breast cancer. Its mechanism of action is blocks steroid production
38
What is Tamoxifen? Name its drug class, indication, and mechanism of action.
Tamoxifen is a SERM used for steroid positive breast cancer. Its mechanism of action is oestrogen receptor antagonist.
39
What skin cancer is known as a malignancy of immunosuppression
Kaposi sarcoma is a cancer that develops from connective tissue and is associated with immunosuppression, often seen in individuals with HIV/AIDS or organ transplant recipients
40
Mesothelioma most common cause?
Mesothelioma is a malignancy arising in the mesothelium, and its most common cause is asbestos exposure.
41
5-Fluorouracil MoA
5-Fluorouracil MoA= inhibition of thymidylate synthase, and incorporation into DNA and RNA 5-Fluorouracil (5-FU) acts during the S-phase of the cell cycle as a thymidylate synthase inhibitor inhibiting DNA synthesis. 5-FU inhibits the enzyme, thymidylate synthase and inhibits the formation of thymidine monophosphate (a major building block of DNA) and thus inhibits DNA synthesis. This arrests the tumour cells in the S-phase of the cell cycle which reduces tumour cell proliferation and survival.
42
Methotrexate MoA
Methotrexate MoA= Inhibition of tetrahydrofolate synthesis
43
Cisplatin MoA
Cisplatin MoA= Cross linkage with purines in DNA
44
Docetaxel MoA
Docetaxel MoA= Inhibition of microtubular depolymerization
45
Doxorubicin MoA + RISK
Doxorubicin MoA= Inhibition of enzyme topoisomerase II, and DNA intercalation Doxorubicin is a cytotoxic anthracycline antibiotic and is used as a chemotherapeutic agent for a number of cancers such as metastatic breast cancer. Chemotherapy related cardiotoxicity induced by doxorubicin is a serious adverse effect and leads to cardiomyopathy WHICH LEADS TO HEART FAILURE!
46
Ovarian cancer is associated with elevation in what tumour biomarker
elevated CA 125 → Ovarian Cancer
47
Hepatocellular Cancer is associated with elevation in what tumour biomarker
elevated AFP → Hepatocellular Cancer
48
Testicular Cancer is associated with elevation in what tumour biomarker
AFP, HCG → Testicular Cancer
49
Breast Cancer is associated with elevation in what tumour biomarker
CA 15-3 → Breast Cancer
50
Pancreatic Cancer is associated with elevation in what tumour biomarker
CA 19-9 → Pancreatic Cancer
51
Colorectal Cancer is associated with elevation in what tumour biomarker
CEA → Colorectal Cancer
52
Prostate Cancer is associated with elevation in what tumour biomarker
PSA → Prostate Cancer
53
HPV is primarily associated with cancers of the cervix, anus, and some cancers of the head and neck, as well as penile cancer. What are low risk vs high risk strains of Human Papilloma Virus and what they cause?
Low-risk strains, e.g. HPV-6 and HPV-11, tend to cause genital warts and milder skin changes while high-risk, e.g. HPV-16 and HPV-18, are more likely to induce cancerous changes.
54
Risk Factors for colorectal cancer/ CRC (3rd most common cancer in west)
Age 60-79 years (Greatest RF for sporadic CRC) Family History Genetics: - Familial Adenomatous Polyposis (FAP) → autosomal dominant disease caused by a mutation in APC gene (Chr 5q). - Lynch Syndrome (Heriditary Non-polyposis Colorectal Cancer - HNPCC) → autosomal dominant disease caused by a mutation in mismatch repair genes. - MYH-associated Polyposis (MAP) → recessive disease of polyposis caused by a mutation in both alleles of MUTYH gene. Inflammatory Bowel Disease Obesity Men > Women
55
causes of Horner's syndrome
Central: Stroke, Multiple sclerosis, Brain tumour Pre-ganglionic: Pancoast tumour, Thyroidectomy, Thyroid carcinoma Post-ganglionic: Carotid artery dissection Carotid artery aneurysm Cavernous sinus thrombosis
56
What is a Sister Mary Joseph nodule?
Sister Mary Joseph nodule, which is a malignant metastatic umbilical nodule. Sister Mary Joseph's node is a palpable nodule protruding from the umbilicus – it is a sign of an advanced-stage gastrointestinal or genitourinary tract malignancy.
57
Syndrome of inappropriate ADH secretion (SIADH) is associated with what cancer?
Syndrome of inappropriate ADH secretion (SIADH) is associated with small-cell lung cancer. It causes the excessive release of ADH, which reduces blood sodium levels. The resulting hyponatraemia can cause confusion and seizures to develop.
58
Paraneoplastic syndromes of Small cell carcinoma
- Syndrome of inappropriate ADH secretion (SIADH) - Increased ACTH release - Carcinoid Lambert-Eaton syndrome - Superior vena cava syndrome
59
Paraneoplastic syndromes of Squamous cell carcinoma
- Parathyroid hormone-related protein (PTHrP) - Horner syndrome - Pancoast tumour
60
Most Pancoast tumors are what type of lung cancer?
Most Pancoast tumors are non-small cell lung cancers (NSCLC)
61
Paraneoplastic syndromes of Adenocarcinoma
- Pulmonary osteoarthropathy - Marantic endocarditis
62
Paraneoplastic syndromes of Large cell carcinoma
- Superior vena cava syndrome - Gynaecomastia
63
An enlarged node in the left supraclavicular fossa (Virchow's node) is most commonly a sign of what metastatic malignancy
gastric carcinoma Virchow's node is typically enlarged in metastatic gastrointestinal carcinoma. It is seen clinically as an enlarged, firm and, palpable node in the left supraclavicular region. This finding is also referred to as Trosier's sign.
64
Ann Arbor cancer staging system
Stage I - 1x node involved Stage II - 2+ nodes involved, all found on ONE side of the diaphragm Stage III - 2+ nodes involved, found on BOTH sides of the diaphragm Stage IV - Widespread, multifocal, extra-nodal involvement The above stages are further combined with letters A OR B. 'A' indicates the absence of B symptoms, whereas 'B' indicates the presence of B symptoms. 'B symptoms' = Fever, night sweats, weight loss e.g. if a man has fever, weight loss and 2 lymph nodes involved above the diaphragm= his Ann Arbor score is IIB
65
What is the first-line targeted therapy for non-squamous non-small cell lung cancer (NSCLC)
Bevacizumab is used as a first-line targeted therapy for non-squamous non-small cell lung cancer (NSCLC).
66
Iron deficiency anaemia in individuals aged 60 years is first assumed as what?
Iron deficiency anaemia in individuals aged 60 years and above is due to an underlying GI malignancy until proven otherwise. The next most appropriate step in management is to make an urgent 2-week wait referral for an upper and lower GI endoscopy.
67
individuals with carcinoid syndrome typically present with what symptoms?
Individuals with carcinoid syndrome typically present with a flushed face, abdominal pain, diarrhoea, dyspnoea, a systolic murmur over tricuspid area
68
Patients with Xeroderma Pigmentosum present with freckling of the sun-exposed areas of skin. What is this caused by?
This is caused by the inability to repair ultraviolet-induced DNA damage due to defects in the nucleotide excision DNA repair (NER) pathway. XP is an autosomal recessive inherited condition, that presents with skin disorders caused by defects in the nucleotide excision repair (NER) pathway. Patients characteristically have symptoms of freckling of the skin, burning of skin upon sun exposure, dry skin, and pigmentation.
69
What is Bowen's disease?
Bowen's disease, also known as 'squamous cell carcinoma in situ', is a reddish scaly precancerous skin lesion that typically arises due to chronic sun exposure, and is associated with the risk of progression to squamous cell carcinoma.
70
The formation of the philadelphia chromosome, the 9;22 translocation is associated with which cancer?
The 9;22 translocation, i.e. formation of the Philadelphia chromosome, is associated with chronic myeloid leukaemia. This translocation fuses ABL gene of chromosome 9 with the BCR gene of chromosome 22 forming, BCR-ABL1. This BCR encodes for a tyrosine kinase enzyme, and its fusion with ABL1 transforms the enzyme so it become constitutively active. This means that it constantly produces signals for cell growth without requiring a stimulus to activate it. This causes cells to divide immeasurably leading to the development of a malignancy. The Philadelphia chromosome is most commonly found in chronic myeloid leukaemia but it may also be present in acute lymphoid leukaemia.
71
the t(8;14) translocation is associated with which cancer?
t(8;14) ~ B-cell malignancies e.g. Burkitt's lymphoma, acute lymphocytic leukaemia (ALL)
72
the t(14;18) translocation is associated with which cancer?
t(14;18) ~ Follicular lymphoma
73
the t(8;21) translocation is associated with which cancer?
t(8;21) ~ Acute myeloid leukaemia (AML)
74
the t(15;17) translocation is associated with which cancer?
t(15;17) ~ Acute promyelocytic leukaemia (APML)
75
Which tumour suppressor genes are gatekeepers and which are caretakers
p53 and pRb are examples of the 'gatekeeper' class of tumour suppressor genes, which are important in regulating cell cycle progression, cellular lifespan, and cell death. BRCA and MMR belong to the 'caretaker' class of tumour suppressor genes, which are important in maintaining genomic stability by regulating DNA repair and preventing mutations.
76
what are the steps in development of colorectal carcinoma
1) mutation in APC = loss of APC= dysplastic epithelium 2) KRAS activation= adenoma 3)Loss of p53= carcinoma 4) metastatic colorectal cancer
77
Trastuzumab targets what receptor?
Trastuzumab is a monoclonal antibody that targets the HER2 receptor and is used in the treatment of HER2-positive breast can Trastuzumab provides targeted therapy by attaching to and neutralising the HER2 receptor. As a result, cancer cells do not receive extracellular signals via this receptor, thus inhibiting cancer cell growth, replication and survival.
78
which lymph nodes do breast cancer cells most commonly metastasise to first
breast cancer cells most commonly metastasise to the axillary lymph nodes first
79
what is the most common site for colorectal cancer metastasis
The liver is the most common site for colorectal cancer metastasis
80
The Glasgow 7-point checklist is a clinical tool used by GPs when assessing patients in primary care with a suspected melanoma. What are the major and minor features of the Glasgow 7-point checklist
Major features: Change in size Irregular shape Irregular colour Minor features: Crusting/bleeding Inflammation Itch/altered sensation Diameter ≥ 7mm Major features score 2 points each, whereas minor features score 1 point each. If a patient scores ≥ 3 (total score), they are referred under the urgent 2-week wait referral service to dermatology, for further specialist investigation, in order to rule out a potential melanoma
81
for women under 40 what is the preferred modality for breast cancer screen?
An ultrasound is more commonly the first-line imaging test that is done in women under 40 In women aged under 40 years, mammograms are not typically recommended as younger women have more dense breast tissue which can make the images less clear and harder to interpret abnormal areas.
82
for women over 40 what is the preferred modality for breast cancer screen?
X-ray (mammogram) Mammograms are most commonly taken in 2 planes/views: - Craniocaudal (CC) view - Medial Lateral Oblique (MLO) view n.b. pectoralis muscle should be in view in this plane.
83
What is curative chemotherapy + give examples
Curative chemotherapy aims to cure cancer and is typically limited to haematologic malignancies and germ cell tumours (eg. R-CHOP treatment for non-Hodgkin lymphoma) Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, Prednisone (prednisolone is the active form of prednisone)
84
Neoadjuvant chemotherapy, also known as induction chemotherapy, is a chemotherapy regimen administered prior to surgery in order to shrink a tumour and increase its operability. What is an example of neoadjuvant chemo?
neoadjuvant chemo= Shrink tumors before surgery to enhance operability 1) EC-T therapy for breast cancer (combo of 3 cytotoxic drugs for primary breast cancer): Epirubicin Cyclophosphamide Docetaxel (Taxotere) 2) Durvalumab with platinum-based chemotherapy for resectable non-small-cell lung cancer (NSCLC) - Durvalumab – PD-L1 inhibitor - Platinum-based agents – e.g., Cisplatin or Carboplatin
85
Palliative chemotherapy aims to reduce symptoms and alleviate suffering from a terminal cancer. What is an example of palliative chemo?
FOLFIRI for metastatic colorectal cancer: - Folinic acid (Leucovorin) – Enhances 5-FU efficacy - Fluorouracil (5-FU) – Antimetabolite - Irinotecan – Topoisomerase I inhibitor FOLFIRINOX for advanced pancreatic cancer: - Includes all FOLFIRI components plus Oxaliplatin (Platinum-based agent)
86
What is adjuvant chemotherapy + give examples
Adjuvant chemotherapy is used following surgery to eradicate micro-metastasis and reduce the chance of relapse e.g. radiotherapy after surgery e.g. Pembrolizumab (PD-1 inhibitor) following surgery for NSCLC
87
what is intraoperative chemotherapy and what is the procedure largely limited to?
Intraoperative chemotherapy is a novel regimen in which chemotherapy is administered during surgery. It is largely limited to advanced abdominal cancers. i.e. HIPEC (Hyperthermic Intraperitoneal Chemotherapy) for advanced abdominal cancers.​ - Mitomycin C – Antitumor antibiotic - Cisplatin – Platinum-based agent​
88
Cancers Associated with Keratin Pearls
Squamous cell carcinoma of the skin Squamous cell carcinoma of the lung Squamous cell carcinoma of the oesophagus Squamous cell carcinoma of the vagina and cervix Squamous cell carcinoma of the bladder
89
Which chromosomal abnormality is required to be present to treat the haematological malignancy that Imatinib is indicated for?
Chronic myeloid leukaemia (CML) is a haematological malignancy well known for its underlying chromosomal translocation (9;22). First-line treatment in CML involves the administration of Imatinib, a BCR-ABL tyrosine kinase inhibitor.
90
Gleason Grading System for prostate cancer
the first number applies to the most predominant cell pattern and the second number applies to the second most predominant cell pattern in the sample. A Gleason score is typically presented with both numbers - such as 3+4 (7). The features which govern each score are shown below: 1 → Small, uniform, well-defined glandular architecture (Most well-differentiated) 2 → Increased stroma formation between glands; looser gland arrangement 3 → Distinct infiltration of neoplasm; glands are alternating in shape and size 4 → Irregular masses of neoplastic glands which have fused together; glands no longer distinct 5 → Very few uniform glands (Most poorly-differentiated)
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Bevacizumab is a novel targeted agent used as first-line therapy for the management of non-squamous non-small cell lung cancer (NSCLC). What growth factor does it target?
Bevacizumab is a monoclonal antibody which selectively binds to the vascular endothelial growth factor (VEGF) receptor, inhibiting its activation. The VEGF signalling pathway plays a key role in tumorigenesis and survival. VEGF is a potent growth factor for vascular endothelial cells and promoting angiogenesis (growth of new blood vessels) supports tumour growth and metastasis. Bevacizumab inhibits angiogenesis, prevents the formation of new vessels, restricting the growth of the tumour.
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Rituximab targets which blood cell?
Rituximab selectively targets B lymphocytes via CD20 binding.
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What is a common benign breast tumour found in young women?
Fibroadenoma (well-defined, mobile, encapsulated nature)
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Triple-negative breast cancer (TNBC) (BRCA 1 type) refers to a subtype of breast cancer that lacks three key receptors typically targeted in breast cancer treatment
Triple-negative breast cancer (TNBC) refers to a subtype of breast cancer that lacks three key receptors typically targeted in breast cancer treatment: Estrogen receptor (ER): Negative (no estrogen receptor expression) Progesterone receptor (PR): Negative (no progesterone receptor expression) HER2 receptor: Negative (no HER2 overexpression) In the context of BRCA1 mutations, triple-negative breast cancer is a common feature. This means the cancer cells lack all three of these receptors and do not respond to hormonal therapies (like tamoxifen) or HER2-targeted therapies (like trastuzumab).

Y2 (38 decks)

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