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Hawk Tuah > CANCER > Flashcards

CANCER Flashcards

1
Q

Define neoplasm.

A

Uncontrolled cell growth
ie tumour

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2
Q

Define cancer.

A

Malignant neoplasm

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3
Q

Carcinomas are defined as…

A

Malignant epithelium neoplasms

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4
Q

Sarcomas are defined as…

A

Malignant mesenchymal neoplasms

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5
Q

What are adenocarcinomas?

A

Malignant epithelium neoplasms of glandular origin

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5
Q

What are adenomas?

A

Benign neoplasms of glandular origin

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6
Q

What are fibroadenomas?

A

Benign neoplasms of fibrous and glandular origin

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7
Q

Most benign neoplasms end with -oma except…

A

Lymphoma
Leukaemia
Hepatoma
Melanoma
Myeloma

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8
Q

What is teratoma?

A

A tumour with tissue or organ components resembling normal derivatives of more than one germ layer

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9
Q

What is a blastoma?

A

A type of cancer caused in malignant precursor cells

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9
Q

Describe 7 microscopic features of malignant tumours.

A

Hyperchromatic nuclei
High mitosis
High nucleo-cytoplasmic ratio
Pleomorphism
Irregular outline
Prominent nucleolus
Enlarged

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9
Q

How do you describe benign tissue?

A

Cells resemble normal tissue
Few mitosis
No invasion
Highly differentiated

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9
Q

What are the histopathological features of squamous cell carcinoma?

A

Keratin pearls
Pavementing
Intercellular bridges

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10
Q

What are the methods of cancer metastasis?

A

Local infiltration
Cavities
Lymphatic spread (Carcinomas)
Hematogenous spread (Sarcomas)

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10
Q

Based on what factors do you stage cancer?

A

T = Tumour size (T1-4)
M = Presence of distant metastasis (M0/1)
N = Presence of regional lymph node metastasis (N0-2)

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10
Q

What are the histopathological features of glandular cancers?

A

Mucin

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11
Q

What does T4 mean?

A

Invasion of other organs by tumours

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11
Q

What is the difference between N1 and N2?

A

N1 = 1-3 lymph nodes involved
N2 = 4 lymph nodes involved

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12
Q

What does Tis mean?

A

No infiltration past the basement membrane

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12
Q

How is stage III cancer diagnosed?

A

N1 required (involvement of 1-3 regional lymph nodes)

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12
Q

What are the different gradings of cancer?

A

Grade 1 = well differentiated (normal cells)
Grade 2 = moderately differentiated (resemble normal cells)
Grade 3 = poorly differentiated

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13
Q

How is stage IV cancer diagnosed?

A

M1 required (presence of distant metastasis)

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13
Q

List the 9 tumour markers and their associated cancers.

A

HCG - Trophoblastic/ Non-seminomatous testicular tumours
Calcitonin - Thyroid medullary carcinoma
Caltechoamines - Pheochromocytoma
AFP - Liver cancer
CEA - Colon cancer
Prostatic acid phosphatase - Prostate cancer
CA-125 - Ovarian cancer
CA-19-9 - Colon/ Pancreatic cancer
CA-15-3 - Breast cancer

13
Q

What are the 10 hallmarks of cancer?

A

Established:
Growth signal autonomy
Evasion of inhibitory growth signals
Evasion of apoptosis
Unlimited replicative potential
Angiogenesis
Invasion & metastasis

Emerging:
Avoiding immune destruction
Reprogramming energy metabolism

Enabling characteristics:
Genome instability
Tumour-promoting inflammation

14
Q

List the broad ways growth autonomy affects the cell.

A

Excessive production of growth factors w/o appropriate stimulus eg PDGF in glioblastomas

Growth factor receptor amplification eg HER2 in breast cancer

Growth factor receptor constitutive activation eg EGFR for lung adenocarcinoma

Signalling molecules activated without receptor eg mutated KRAS => constant MAPK signalling pathway activation => uncontrolled proliferation

Auto transcription by MYC producing proteins/factors that aid replication eg Burkitt lymphoma; starry sky appearance; IgH t(8:14) translocation

14
Q

Name 2 tumour supression genes.

A

p53 and Retinoblastoma

14
Q

How does p53 exert its effect?

A

Safeguards genomic stability
Cell cycle arrest
Cellular senescence
DNA repair
Apoptosis
Inhibit angiogenesis

14
Q

What are the activators of p53?

A

Hypoxia
Damaged DNA
Inappropriate oncogene signalling

15
Q

How does Retinoblastoma exert its effect?

A

Inhibits cell division (no apoptosis capabilities)
Acts on G1/S transition phase of cell cycle

15
Q

How is Retinoblastoma inactivated by cancer cells?

A

Inactivated via hyperphosphorylation
Cancer gene amplification of cyclin D and CDK4 gene / mutate both Rb alleles

16
Q

What is the intrinsic pathway of apoptosis?

A

DNA damage triggers p53
Upregulation of apoptotic factors BAX/BAK
Egression of cytochrome C & capase production
Apoptosis

16
Q

How do tumour cells overcome intrinsic apoptosis pathways?

A

Upregulation of BCL2
Lose p53

16
Q

What does TP53 mutation cause?

A

Li-Fraumeni syndrome

16
Q

What gene is activated and what translocation occurs in follicular lymphoma?

A

BCL2 gene due to t(14,18) translocation in B cells

16
Q

What allows for unlimited replicative potential in tumour cells?

A

Telomerase reactivation causing evasion of hayflick limit and divide infinitely

16
Q

What are the anti-angiogenic factors?

A

p53 producing TSP-1

16
Q

What are the pro-angiogenic factors?

A

PDGF
EGF
VEGF (from hypoxia producing HIF-a / oncogenes ras, myc)

16
Q

How does invasion and metastasis occur?

A

Detachment of tumour cells by inactivating E-cadherin function
Mobilised by epithelial-mesenchymal transition
Breach basement membrane via secretion of proteolytic enzymes
Circulate as emboli => extravasate => angiogenesis

16
Q

How do tumour cells evade immune destruction?

A

Downregulate MHC
Secrete inhibitory cytokines TGF-B
Engage inhibitory receptors PD1
Lose expression of tumour antigens
Promote Tregs

16
Q

How do tumour cells reprogram energy metabolism?

A

Aerobic glycolysis
Lactic acid fermentation causes diversion of glycolytic intermediates, which enable synthesis of macromolecules and organelles for cell growth

16
Q

How does genomic instability affect tumour cell?

A

Loss of MMR protein (eg MLH1) leads to high levels of macrosatellite instability causing the cell to be more prone to mutations

16
Q

How does loss of MMR protein occur?

A

Gene deletion
LOF mutation

16
Q

How does inflammation enhance tumours?

A

Inflammation provides growth factors, pro-angiogenic factors, ECM modifying enzymes

16
Q

Name 2 classes of anti-cancer drugs.

A

Cell cycle specific and cell cycle non-specific

16
Q

What are the 3 cell cycle specific drugs?

A

Anti-metabolites
Microtubule inhibitors
Topoisomerase I/II inhibitors

16
Q

What are the 3 cell cycle non-specific drugs?

A

Alkylating agents
Platinating agents
Cytotoxic antibiotics

16
Q

Name 2 anti-metabolite anti-cancer drugs and what they inhibit.

A

Methotrexate inhibits dihydrofolate reductase
5-flourouracil inhibits thymidylate synthase

16
Q

Name 2 microtubule inhibitors and state their functions.

A

Vinblastine (binds polymerising ends preventing elongation)
Paclitaxel (stabilise microtubules prevents depolymerisation)

16
Q

Name an alkylating agent and state its function.

A

Cyclophosphamide (Crosslink DNA and prevent transcription and translation)

16
Q

Name 2 platinizing agents and state their functions.

A

Cisplatin and Carboplatin (Crosslink DNA and prevent transcription and translation)

16
Q

Name 2 cytotoxic antibiotic anti-cancer drugs and state their functions.

A

Anthracyclie and Doxorucibin (crosslink and damage DNA)

16
Q

What are the adverse effects of alkylating agents?

A

Haemorrhagic cystitis

16
Q

What are the adverse effects of Platinating agents?

A

Nephro/Ototoxicity

16
Q

What are the adverse effects of cytotoxic antibiotics?

A

Cardiotoxicity

16
Q

What are the general adverse effects of anti-cancer drugs?

A

Alopecia
GI toxicity
Myelosupression

17
Q

What is associated with Hodgkin’s lymphoma?

A

Reed-sternberg cells

18
Q

What is an effective treatment for MMR deficient tumour cells with micro satellite instability?

A

Anti-PD1 therapy

Hawk Tuah (12 decks)

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