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HYMS Block 9 > Cancer Biology > Flashcards

Cancer Biology Flashcards

1
Q
  1. what is a neoplasm?
  2. what does the term cancer usually describe?
  3. name the 6 hallmarks of cancer
A
  1. an abnormal mass of cells resulting from poorly regulated cell proliferation and growth in the absence of an initiating event
  2. malignant tumour or neoplasm

3, - sustained proliferation

  • evading apoptosis and growth suppression
  • genomic instability
  • resistance to cell death
  • ability to induce angiogenesis and metastasise
  • ability to evade host immunity
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2
Q
  1. what type of DNA damage to UVA radiation induce?

2. What type of DNA damage does UVB radiation induce?

A
  1. ds DNA breaks

2. pyramidine dimers

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3
Q

Define the following:

  1. metaplasia
  2. dysplasia
  3. neoplasia
  4. Anaplasia
A
  1. reversible, non cancerous transformation of one type of fully differentiated cell into a different differentiated cell type. Result of an adaptive process in response to a change in environment
  2. disordered growth (morphological transformation, increased cell division and loss of differentiation/architectural relationships. Not neoplastic but may progress to malignant change
  3. abnormal and unco-ordinated cell gorwth. Heterogeneity.
  4. neoplasm composed of undifferentiated cells
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4
Q

define the following:

  1. papiloima
  2. adenoma
  3. carcinoma

What are tumours of the following connective tissue origins called?

  1. fibrous
  2. bone
  3. cartilage
  4. adipose
  5. skeletal muscle
  6. smooth muscle
A
  1. tumour of surface epithelia
  2. tumour of glandular epithelia
  3. malignant neoplasm of epithelila origin
  4. fibroma (B) or fibrosarcoma (M)
  5. osteoma or osteosarcoma
  6. chondroma or chondrosarcoma
  7. lipoma or liposarcoma
  8. rhabdomyoma or rhabdomyosarcoma
  9. leiomyoma or leiomyosarcoma
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5
Q
  1. what are teratomas?
  2. what are lymphomas?
  3. what are leukeamias?
  4. what are hamartomas?
  5. what is a choristoma?
A
  1. tumours containing elements of all three embryological germ cell layers
  2. malignancy of lymphoid cells with a tumour mass
  3. malignancy of lymphoid cells that only have circulating cells
  4. disorganised mass of mature specualised cells indiginous to the particular site
  5. normal tissue growth in an abnormal location
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6
Q

Describe the following routes of metastasis

  1. haematogenous
  2. lymphatic
  3. transcoelomic
A
  1. spread via the bloodstream (usually veins because their thinner walls makes them easily penetrable). Venous tumour emboli follow normal drainage
  2. travel via lymphatic vessels that drain the primary site
  3. spread across coelomic spaces and surfaces - pleural or peritoneal cavities.
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7
Q
  1. what does tumour grade relate to?
  2. what is examined to determine tumour grade?
  3. what does tumour stage relate to?
  4. what is examined to determine tumour stage?
A
  1. the degree of differentiatiation
  2. tubule/acinar/glandular formation
    nuclear pleomorphism
    frequency of mitoses
  3. extent of tumour spread
  4. Size of primary tumour (T), lymph node status (N), metastasis (M)
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8
Q
  1. what is paraneoplastic syndrome?

2. what is cachexia?

A
  1. symptom complexes that are not due to mass effect of the tumour, but due to humoural factors secreted by the tumour or as an immune response to the tumour.
  2. wasting syndrome caused by factors secreted by the neoplasm, and host response
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9
Q

what occurs at the following cell cycle checkpoints?

  1. start
  2. G2>M checkpoint
  3. anaphase to metaphase transition
  4. what complexes regulate cell cycle progression?
A
  1. checks environment is favourable for proliferation. cell commits to cell cycle entry and chromosome duplication
  2. ensures DNA has been replicated and environment is still facourable
    triggers mitotic events that lead to chromosomal alignment on spindle
  3. ensures all chromosomes are attached to spindle with proper alignment
    triggers sister chromatid separation
  4. CDK-cyclin complexes. Levels of cyclinss change cyclically at different stages, leafing to changes in phosphorylation of proteins that control chromosome condensation and spindle assembly
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10
Q
  1. what does ATM/ATR detect?
  2. Name 2 targets of ATM
  3. name 3 consequences of ATM signalling
A
  1. ds DNA breaks
  2. p53, BRCA1 (and various other tumour suppressors)
  3. cell cycle arrest, DNA repair or apoptosis
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11
Q
  1. name 5 ways in which oncogenes can arise

2. name 3 examples of oncogenes

A 
1. point mutations
gene amplifations (HER2)
chromosomal translocation (BCR-ABL)
local DNA rearrangeements (e.g. insertion, deletion)
insertional mutagenesis - e.g. viral DNA
  1. HER2, ras, BCR-ABL
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12
Q
  1. what are gatekeeper genes?

2. what are caretaker genes?

A
  1. control proliferation. Loss directly opens the gates to cell proloferation
  2. maintain genetic stability
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13
Q
  1. what is the role of p53?
  2. how does ATM signalling activate p53?
  3. what is the role of Rb?
  4. which oncogenic proteins are produced by the HPV virus?
  5. How do they affect p53 and Rb?
A
  1. respond to DNA damage and inhibit G1/S CDK. Halts cell cycle so DNA can be repaired or apoptosis is triggered
  2. under conditions favouring proloferation, p53 is sequestered by mdm2 and is therefore degraded
    ATM phosphorylates p53 when DNA damage is detected; activates DNA repair genes and promotes transcription of CDK inhibitors or inhibitors of apoptosis
  3. controls the start checkpoint. Phosphorylated by G1-CDK which causes it to release a transcription factor
  4. E6 (inactivates p53) and E7 (inactivates Rb)
  5. E6 stimulates ubiquitination of p53
    E7 competitively inhibits its sequestration of the transcription factor
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14
Q

describe the DNA damage response pathway

A
  1. ATM/ATR survey DNA for damage. They activate checkpoint kinases in response to damage
  2. checkpoint kinases phosphorylate p53; as a result, p35 is not degraded and thus accumulates
  3. p53 induces cell cycle arrest via p21 (CDK inhibitor)
  4. DNA is repaired or apoptosis is induced
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15
Q
  1. what type of DNA lesions does UV radiation cause?
  2. what can these lesions lead to if uncorrected?
  3. what do alkylating agents do to DNA?
  4. What is the consequence of 3?
A
  1. pyramidine dimers (thymine dimers, CC dimers). These are bulky lesions which distort DNA
  2. cause misreading during transcription or replication, or lead to an arrest of replication
  3. add an alkyl group to different sites on the DNA bases
  4. can lead to misparing (e.g. alkylated guanine can mispair with thymine)
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16
Q
  1. what is biotransformation?
  2. which enzymes carry out first phase biotransformation reactions?
  3. what is aflatoxin?
  4. how is aflatoxin biotransformed?
  5. describe the effects of aflatoxin metabolities
A
  1. enzymatic process that transforms chemicals into entities that can be readily excreted from the body
  2. cytochrome p450
  3. a carcinogen produced by certain moulds, which can be found in improperly stored foods
  4. Cytochrome P450 adds a highly reactive epioxide group
  5. aflatoxin metabolites can alkylate bases
17
Q
  1. How can alkylation damaged be repaired?
  2. what are suicide enzymes? Give an example
  3. describe base excision repair
  4. what forms of DNA damage are corrected by base excision repair?
A
  1. direct reversal via covalent transfer of the alkyl group from the modified base to a cysteine residue on the DNA repair enzyme
  2. repair enzymes that accept the cysteine residue. e.g. O6-methylguanine
  3. DNA glycosylases remove the base - this produces a abasic AP site (gap)
    AP endonuclease realise the AP site
  4. single base damage (alkylation, oxidised, deaminated)
18
Q
  1. describe nuceotide excision repair

2. What type of damage is corrected by nucelotide excision repair?

A
  1. multienzyme complex scans DNA for bulky lesions. Phosphodiesterase backbone is cleaved either side of lesion. DNA helicase pulls away ss oligonucleotide containing the lesion. Large gap is repaired by DNA polymerase and ligase
19
Q
  1. why is repair of double stranded breaks difficult?

2. how are double stranded breaks corrected?

A
  1. because there is no template strand for accurate repair

2. non homologous end joining or homologous recombination

20
Q

Familial Adenomatous Polyposis

  1. what is the inheritance pattern?
  2. which gene is implicated?
  3. What is the role of this gene?
  4. what happens if this gene is mutated
A
  1. autosomal dominant
  2. APC
  3. involved in Wnt signalling - normally sequesters beta catenin, a transcription factor in the absence of the wnt ligand (gatekeeper gene)
  4. tumour initiation
21
Q

Hereditary non-polyposis colon cancer

  1. what is the inheritance pattern?
  2. which genes are implicated?
  3. what are the roles of these genes?
  4. what happens if this gene is mutated?
A
  1. autosomal dominant
  2. HPNCC - mismatch repair genes
  3. implicated in the repair of single base mismatch and replication errors at short repeats (caretaker genes)
  4. mutator phenotype - promote mutation of gatekeeper and accumulation of further mutation)
22
Q
  1. How does Radiotherapy treat cancer?
  2. Direct action of radiotherapy?
  3. Indirect action of radiotherapy?
A
  1. induces DNA damage which drives the cell to death
  2. photon strikes an atom which then emits an electron. This electron directly damages DNA
  3. photon strikes an atom which emits an electron. The electron interacts with water to produce a superoxide free radical which damages DNA
23
Q
  1. What is external beam radiotherapy?
  2. what to linacs generate?
  3. What are superficial voltage and orthovoltage x-rays used to treat?
  4. what is a gray?
A
  1. generation of radiation from an external source which is directed at the tumour from outside the body
  2. megavoltage x rays (treat deep tumours)
  3. superficial tumours
  4. unit of absorbed radiation, equal to the dose of one joule of energy per kg matter/100 rads
24
Q
  1. what is 3D conformal radiotherapy?
  2. what is a multileaf collimator?
  3. what is SABR?
A
  1. radiation beam is shaped to match the tumour. It is more sparing for healthy tissue and enables higher doses to be administered.
  2. a device made up of individual leaves that can move independently in and out of bath of a beam, to enable the beam to conform to the shape of the tumour.
  3. intense regime of radiotherapy where very few fractions are delivered.
    many, small beams are directed from different angles and meet at the tumour; sparing of healthy tissue
25
Q
  1. what is brachytherapy?
  2. name 2 examples of brachytherapy treatments
  3. name 2 advantages of brachytherapy
  4. name 2 disadvantages of brachytherapy
A
  1. internal radiotherapy - a radioactive source is placed in direct contact with a tumour
  2. mould treatment - sources are placed directly over a superficial tumour fixed in plastic moulding
    intracavity treatment - sources placed within a body cavity
  3. greater deliverable dose via continuous low dose rate
    shorter treatment times
  4. tumour must be accessable
    can’t be only treatment used for tumours with high risk of regional lymph node involvement
26
Q
  1. name 2 acute tissue reactions to radiotherapy
  2. when do epithelial surfaces generally heal?
  3. what is considered an intensity limiting side effect?
  4. name 6 late tissue reactions
A
  1. mucosal reactions - week 2
    skin reactions - week 5
  2. 20-40 days from treatment cessation
  3. mucositis
4. xerostomia - dry mouth
    fibrosis - woody skin texture
    soft tissue necrosis
    nerve damage (dementing process)
    ocular damage
    otologic damage
27
Q
  1. what is one of the major difficulties in treating cancer?
  2. why does continuous exponential growth not usually occur in tumours?
  3. what is the log-kill hypothesis?
  4. which cells do cytotoxic drugs target?
  5. based on 4, which tumour cells present a problem?
A
  1. tumour growth is usually far advanced before the cancer is diagnosed (only a small number of doublings is required to go from a tumour that would easily be unnoticable to a tumour that is lethal)
  2. not all cells are proliferating continuously; the tumour outgrows its blood supply
  3. a given dose of chemotherapy kills the same fraction of tumour size, regardless of the size of the tumour at the time of treatment
  4. dividing cells
  5. resting cells, that are not dividing but have the potential to do so. This is because they are not killed so remain after treatment and have the potential to establish a second tumour.
28
Q

name 4 uses of chemotherapy

A
  1. curable chemotherapy for solid tumours (usually following a reduction of tumour burden by surgery/radiotherapy)
  2. curable chemotherapy for disseminated cancers
  3. palliative chemotherapy - aims to shrink tumour to improve QOL and reduce cancer related symptoms
  4. Adjuvant chemotherapy - “mopping up” of residual microscopic cancer cells following surgery or radiotherapy
29
Q
  1. what is the MOA of alkylating agents
  2. name 3 examples of alkylating agents
  3. what is the MOA of folate antagonists.
  4. name an example of folate antagonist
  5. what is the MOA of pyramidine analogues?
  6. name an example of pyramidine analogues
A
  1. alkylate replicating DNA within cancer cells thus inducing DNA damage
  2. cyclophosphamide, lomustine, cisplatin
  3. inhibit dihydrofolate reductase, preventing the production of THF, thus interfering with thymidine synthesis
  4. methotextrate
  5. converted to a fraudulent nucleotide, thus interfering with DNA replication
  6. flurouracil
30
Q
  1. what is the MOA of cytotoxic antibiotics?
  2. name an example of a cytotoxic antibiotic
  3. what is the MOA of plant derivatives?
  4. name 3 examples of plant derivatives
A
  1. interferes with DNA and RNA synthesis
  2. doxorubicin
  3. affecting microtubule function and hence the formation of the mitotic spindle
  4. vinca alkaloids, campothecins, taxanes
31
Q

name 6 mechanisms of chemotherapy resistance

A
  1. change in sensitivity/decreased binding affinity of target proteins
  2. decreased drug accumulation via decreased permeability/increased expression of glycoprotein transporters
  3. formation of drug inactivating enzymes
  4. production of reactive chemicals that trap the cancer drug
  5. increased nucleic acid repair mechanisms
  6. reduced activation of prodrugs
32
Q
  1. why is conventional cytotoxic therapy limited? (4)
  2. what is a driver mutation?
  3. name 3 what in which targeted therapies are different from conventional cytotoxic therapies
A
  1. lack of specificity
    toxicity
    lack of effectiveness
    lack of individualisation
  2. a mutation that pushes a cell towards cancer (often target of targeted therapy)
  3. act on specific molecular targets associated with the cancer
    deliberately chosen/designed to interract with their target
    often cytostatic rather than cytotoxic
33
Q
  1. name 5 general approaches to targeted therapies

2. name 6 side effects associated with targeted therapies

A 
1. hormone therapies
   signal transduction inhibitors
   angiogenesis inhibitors
   immunotherapies
   monoclonal antibodies that deliver toxic 
   molecules
2. diarrhoea
    liver problems
    skin problems - rash, dry skin etc
    problems with blood clotting and wound healing
    GI perforation
34
Q
  1. what type of receptor is EGFR?
  2. which drug specifically targets EGFR+ cancers?
  3. how can resistance develop to this drug?
  4. which drug is used to combat this resistance?
  5. Which drug targets the bcr-abl product?
A
  1. RTK
  2. gefitinib
  3. T790M mutation impairs gefitinib affinity for EGFR
  4. Rociletinib
  5. imatinib
35
Q
  1. what is the role of CTLA-4?
  2. how do CTLA-4 inhibitors act as targeted cancer therapies?
  3. Name a CTLA-4 inhibitor
  4. What is the role of the programmed death receptor?
  5. How do PD-1 inhibitors act as targeted cancer therapies?
A
  1. it binds to a APC protein that provides a co-stimulatory signal to the T cell. By doing so, it inhibits T cell activation
  2. they prevent CTLA from providing their inhibitory signal, therefore promoting an immune response to tumour cells
  3. Ipilimumab
  4. promotes apoptosis of antigen specific T cells
  5. Tumours can upregulate PD ligands thus downregulating the immune response towards them
    these inhibitors prent the tumour mediated T cell death, therefore promoting an immune response towards tumour cells

HYMS Block 9 (9 decks)

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