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MP421 > CANCER DEVELOPMENT AND THERAPEUTIC DIFFERENTIALS > Flashcards

CANCER DEVELOPMENT AND THERAPEUTIC DIFFERENTIALS Flashcards

1
Q

appearance of malignant cells under the microscope

A
  • large number of irregularly shaped dividing cells
  • large, variably shaped nuclei
  • small cytoplasmic volume relative to nuclei
  • variation in cell type and shape
  • loss of normal specialised cell features
  • disorganised arrangement of cells
  • poorly defined tumour boundary
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2
Q

cell characteristics in benign tumours

A

similar to cell of origin (well differentiated)

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3
Q

cell characteristics in malignant tumours

A

dissimilar from cell of origin (poorly differentiated)

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4
Q

growth characteristics of benign tumours

A

tumour edges move outward in a smooth manner (encapsulated), grows by expansion and compresses and displaces surrounding tissues

tumour cells stay attached to the clone or mass of cells and do not break away and start new growths elsewhere in the body

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5
Q

growth characteristics in malignant tumours

A

the tumour edges move outward in an irregular fashion (usually no capsule) and can infiltrate, invade, and destroy surrounding tissues

tumour cells can break away from the cloned mass, live independently, move to other area of the body and start new clones or growths

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6
Q

rate of growth in benign tumours

A

slow growth rate

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7
Q

rate of growth in malignant tissues

A

rapid growth rate

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8
Q

degree of vascularity in benign tumours

A

slight vascularity

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9
Q

degree of vascularity in malignant tissues

A

moderate-marked vascularity

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10
Q

recurrence after surgical removal in benign tumours

A

seldom recurs after removal

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11
Q

recurrence in surgical removal in malignant tumours

A

frequently recurs after removal

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12
Q

degree of necrosis and ulceration in benign tumours

A

necrosis and ulceration unusual

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13
Q

degree of necrosis and ulceration in malignant tumours

A

necrosis and ulceration common

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14
Q

likelihood of benign tumours causing systemic effects

A

systemic effects are unusual unless the tumour is a secreting endocrine neoplasm

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15
Q

likelihood of malignant tumours causing systemic effects

A

systemic effects are common and usually life-threatening

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16
Q

what is tumour grade based on

A
  • degree of differentiation
  • spread
  • size
  • organisation of tumour
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17
Q

a feature of both benign and malignant cells

A

LOCAL INVASION

however all benign tumours grow as cohesive, expansive masses

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18
Q

invasion features in benign tumours

A
  • benign remain localised to their site of origin
  • as they grow, usually develop a rim of compressed connective tissue, a fibrous capsule that separates them from the host tissue
19
Q

invasion features in malignant tumours

A
  • growth accompanied by invasion and destruction of the surrounding tissue
  • poorly demarcated from the surrounding normal tissue and a well defined ‘cleavage plane’ is lacking
  • most malignant tumours are obviously invasive
20
Q

metastasis

A

tumours that develop secondary to and discontinuous with the primary tumour

marks a tumour as malignant as benign neoplasms do not metastasise

21
Q

exceptions of tumours that metastasise

A

exceptions are neoplasms of the glial cells in the CNS, called gliomas, and basal cell carcinomas of the skin. both are highly invasive forms of neoplasia but they rarely metastasise

22
Q

angiogenesis

A

formation of new blood vessels

23
Q

stages in formation of metastases

A
  1. malignant cell breaks down intercellular matrix
  2. malignant cell enters capillary
  3. malignant cells circulate round body in blood
  4. malignant cell adheres to blood vessel wall
  5. malignant cell travel into tissue at new site
  6. malignant cell divides to form metastasis at new site
24
Q

3 cancer types

A

leukaemias
sarcomas
carcinomas

25
Q

leukaemia

A

cancers of the blood or bone marrow

26
Q

sarcomas

A

cancers of the connective or supportive tissue (bone, cartilage, fat, muscle, blood vessels) and soft tissues

sarcomas are rarer

27
Q

carcinomas

A

cancers that arises from epithelial cells, these include breast, liver, lung, stomach etc.

28
Q

cancer treatment strategies

A

surgery
radiotherapy
chemotherapy

29
Q

differential sensitivity in treatment

A

want to kill cancer cells - not normal cells

benefit/harm = relief of cancer symptoms/treatment-related toxicity

therapeutic index

30
Q

What’s different about cancer

A

metastasis
angiogenesis
antigens expressed
cancer cells grow and divide faster than normal cells

31
Q

the main goal of antineoplastic agents

A

is to eliminate the cancer cells without affecting normal tissues (is the concept of differential sensitivity). In reality, all cytotoxic drugs affect normal tissues as well as malignancies - aim for a favourable therapeutic index (therapeutic ratio)

32
Q

therapeutic index

A

the lethal dose of a drug for 50% of the population (LD50) divided by the minimum effective dose for 50% of the population (ED50)

therapeutic index = LD50/ED50

33
Q

what do most conventional chemotherapy drugs and radiotherapy target and why

A

cell division

the main feature of cancer cells that they are growing fast or “proliferating”

34
Q

factors that regulate the cell cycle and ensure a cell divides correctly

A
  1. before a cell divides, the DNA is checked to sure it has replicated correctly (if DNA does not copy itself correctly, a gene mutation occurs)
  2. this is done during the normal cell cycle
    - the cell cycle regulates cell growth and division
    - 4 stages: G1, S, G2, M
    - M, mitosis is the point in the cycle where the cell divides into two
    - cells can also go into G0, which is known as quiescence, cells no longer divide, quiescence is reversible
35
Q

cell cycle - GAP 1

A

cell increases in size, produces RNA and synthesises proteins

36
Q

cell cycle - GAP 0

A

cell will leave the cycle and stop dividing

37
Q

cell cycle - GAP 2

A

cell will continue to grow and produce new proteins required for cell division

38
Q

cell cycle - synthesis phase

A

DNA replication takes place

39
Q

what controls the cell cycle

A
  • cyclins are the proteins which control the progression through the cell cycle
  • each gets turned on when required to allow progression through next phase
40
Q

cyclin-dependent kinases

A
  • CDKs signal to the cell that is ready to pass into the next stage of the cell cycle
  • cyclins bind to CDKs, activating the CDKs to phosphorylate other molecules
41
Q

regulation of CDKs

A
  • CDKs controlled by inhibitors of the cell cycle
  • many of these are tumour suppressor genes such as P21
  • which are in turn controlled by oncogenes and tumour suppressor genes such as P53, which is a protein that regulates the cell cycle and hence functions as a tumour suppressor
42
Q

cell cycle checkpoints that can lead to cell cycle arrest (to ensure damaged cells don’t go on to divide)

A
  • checks on DNA damage and chromosome alignment
  • cell either repair or die (apoptosis)
  • in cancer cells often repaired but repair is faulty then cells progress and divide > genomic instability and mutation
  • arrest is controlled by tumour suppressors p53 and pRB
43
Q

treating cancers

A
  • includes drugs that can stop cancer cells from dividing and induce apoptosis
  • different drugs act at different phases of the cell cycle

MP421 (12 decks)

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