Neoplasm Flashcards

1
Q
Characteristic of Benign
Differentiation:
(similarity to source tissue)
Rate of growth:
Local invasion:
Metastasis:
A

Well differentiated (similar to tissue structure, well organised)
Slow growth
No invasion
Absent

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2
Q
Characteristic of Malignant 
Differentiation:
(similarity to source tissue)
Rate of growth:
Local invasion:
Metastasis:
A

Undifferentiated (disorganised + not similar to usual tissue structure)
Rapid
Invasive with poorly defined margin
Common

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3
Q

Neoplasia definition and the 2 classifications

A

New abnormal growth that exceeds normal tissues.

Benign + malignant

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4
Q

What do neoplasms (tumours) arise from

A

accumulation of genetic alterations (mutations, deletions, translocations + epigenetic changes)

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5
Q

What do the genetic alteration changes result in to form a neoplasm

A

neoplastic (abnormal) cell growth

forming a mass of tumour cells

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6
Q

What direction of growth is malignant and is cell death is common

A

endophytic

necrosis - common

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7
Q

Clinical problems of malignant tumours

A

pressure/destruction of adjacent tissues
formation of secondary tumours (metastases)
obstruction of BF flow
production of hormone

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8
Q

What type of growth is benign tumour and is cell death common?

A

Exophytic - tumour grows away from surface

Necrosis is rare

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9
Q

Clinical problems that can arise in benign tumours

A

can lead to malignant tumour
Pressure of adjacent tissues
Obstruction of BF
Production of hormone

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10
Q

What is the tumour “stroma”

A

Greek = mattress
supported connective tissue which neoplastic cells are embedded in.
provides mechanical support, intracellular signalling + nutrition to neoplastic cells

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11
Q

What is an Oncogene

A

Genes driving neoplastic behaviour cells

Activation of this gene leads to hallmarks of cancer

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12
Q

What is a Tumour suppressor gene

A

Slows down cell division, repairs DNA or plans a role in ‘apoptosis’ (programmed cell death)
Inactivation of this gene leads to hallmarks of cancer

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13
Q

Name the 2 Tumour suppressor genes and their role

A

Caretaker - repair DNA damage

Gatekeeper - promote death of cells with damaged DNA (apoptosis)

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14
Q

Hallmarks of cancer list 8

A
Self-sufficiency in growth signals
Insensitivity to growth-inhibitory signals
Altered cellular metabolism
Evasion of apoptosis
Limitless replicative potential (immortality)
Sustained angiogenesis 
Invasion + metastasis 
Evasion of immune survelliance
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15
Q

What is the ‘Knudson Two-hit Hypotheses’?

A

Hypothesis that most suppressor genes require both alleles to be inactivated.
Normal cells have 2 undamaged chromosomes 1 inherited from the mother and other from the father.
People with hereditary susceptibility to cancer inherit a damaged gene on one chromosome that is the first ‘hit’. If cell receives damage to the same gene on 2nd chromosome that is the second ‘hit’ and that cell can produce cancer

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16
Q

What is the process ‘carcinogenesis’

A

Formation of normal cells into neoplastic cells (cancer cells)
Capable of autonomous growth + in malignant neoplasms invasion + metastasis

17
Q

What are the two processes in carcinogenesis

A

Initiation - where a carcinogen induces genetic alteration which gives transformed cell neoplastic potential
Propagation -
Promotion = stimulation of clonal proliferation of transformed cell
Progression = process into malignant behaviour by invasion

18
Q

What is ‘targeted therapy’ in cancer treatment

A

Type of treatment that targets proteins to control how cancer cells grow, divide + spread

19
Q

What is cancer immunotherapy?

A

Helps immune system fight cancer, boosting the natural defences of your immune system to attack neoplastic cells