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Pathological Processes > Neoplasia 2 > Flashcards

Neoplasia 2 Flashcards

1
Q

What is 2-napthylamine

A

Industrial carcinogen used in the dye industry which causes malignant neoplasm

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2
Q

What did 2-naphthylamine show

A
  • there is a long delay sometimes decades between carcinogen exposure and malignant neoplasm onset
  • the risk of cancer depends on total carcinogen dosage
  • there is sometimes organ specificity for particular carcinogens- bladder carcinoma
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3
Q

How does HPV affect DNA

A

It is a direct carcinogen because it expresses the E6 and E7 proteins that inhibit p53 and pRB protein function respectively which re both important in cell proliferation

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4
Q

How do hepatitis B and C affect the body

A

They are indirect carcinogens that cause chronic liver cell injury and regeneration

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5
Q

What does helicobacter pylori do

A

It causes chronic gastric inflammation

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6
Q

What do parasitic flukes do

A

They cause inflammation in bile ducts and bladdder mucosa increasing the risk for gastric inflammation in bile ducts an bladder mucosa increasing the risk or gastric, cholangio- and bladder carcinomas

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7
Q

How can HIV increase susceptibility to cancer

A

Acts indirectly by lowering immunity and allowing other potentially carcinogenic infections to occur

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8
Q

Wha are tumour suppressor genes

A

Genes that inhibit neoplastic growth

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9
Q

What are oncogenes

A

Genes that enhance neoplastic growth- mutations of proto-oncogenes

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10
Q

What does the RAS gene do

A

The RAS encodes a protein that is always active ultimately producing a constant signal to pas through the cell cycles restriction point

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11
Q

What does the RB gene

A

retinoblastoma- It restrains cell proliferation by inhibiting passage through the restriction point

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12
Q

What are the hall marks of cancer

A

1- self sufficiency in growth signals
2-resistance to growth stop signals
3-no limit on the number of times a cell can divide - cell immortalisation
4- sustained ability to induce new blood vessels- angiogenesis
5- resistance to apoptosis
6-the ability to invade and produce metastasis

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13
Q

What are promotors

A

That cause sustained proliferation

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14
Q

Wha are initiators

A

Cause mutation in DNA

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15
Q

what is the adenoma-carcinoma sequence

A

ordered sequence of mutations that need to occur in specific genes in a specific order

the accumulation of mutations that normal epithelium undergoes to become the carcinoma

early adenoma, late adenoma carcinoma in situ, invasive carcinoma

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16
Q

What is T IN TNM

A

Size of the primary tumour and is typically expressed as T1 through fo T4

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17
Q

N in TNM

A

Extend of regional node metastasis

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18
Q

M in TNM

A

denotes the extent of distant metastatic spread

19
Q

Stage 1

A

Early Local disease

20
Q

Stage 2

A

Advanced local disease N0 M0

21
Q

Stage 3

A

Regional metastasis

Any T, N1 or more, M0

22
Q

Stage 4

A

Advanced disease with distant metastasis

Any T, Any N and M1

23
Q

How is lymphoma staged

A

Ann Arbor staging.

24
Q

G1 stage

A

Well differentiated

25
Q

G2

A

Moderately differentiated

26
Q

G3

A

Poorly differentiated

27
Q

G4

A

Undifferentiated or anaplastic

28
Q

When is the grading systems used

A

Squamous cell carcinoma and colorectal carcinoma

29
Q

How is cancer treated

A

Surgery
Radiotherapy
Chemotherapy
Hormone therapy

30
Q

Adjuvant therapy

A

After surgical removal of a primary tumour to eliminate subclinical disease

31
Q

Neoadjuvant treatment

A

Given to reduce the size of primary tumour prior to surgical excision

32
Q

What is radiotherapy

A

Focused on the tumour with shielding of surrounding healthy tissue

Given in fractionated doses to minimise damage to normal tissue

33
Q

Hormone therapy

A

Selective oestrogen receptor modulators (SERMs), such as tamoxifen, bind to oestrogen receptors, preventing oestrogen from binding. They are used to treat hormone receptor- positive breast cancer. Androgen blockade is used for prostate cancer.

34
Q

What do trastuzamab and Imatinib work

A

Identify cancer specific alterations such as oncogene mutations which provide an opportunity to target drugs specifically at cancer cells

35
Q

how is the dye industry involved in cancer

A

2-napthylamine was a chemical used in the dye manufacturing industry. However, it was later found to be a carcinogen which causes bladder cancer, so is now no longer used.

36
Q

what is an oncogene

A

A mutated proto-oncogene

37
Q

normal function of p53

A

Normally encodes for a transcription factor involved in repairing DNA.
Repairs damage in the S phase of the cell cycle or causes apoptotic cell death if the damage is too extensive.

38
Q

what is the 2 hit hypothesis

A

a person with a germline mutation of a tumour suppressor gene on one chromosome is more likely to develop a neoplasm. If one tumour suppressor gene is inherited as mutated – the “first hit” - then the second gene can still protect the cell to supress tumour growth. However, if the second gene becomes mutated and the cell is no longer protected – the “second hit” – then the chance of tumour growth is very high.

39
Q

what is RAS

A

a proto-oncogene
Codes for a G protein which signals for a cell to get past the restriction point in the cell cycle.
A mutation causes this protein to always be active, and therefore the cell constantly moves through the cell cycle and divides.

40
Q

what is HER-2

A
  • Codes for growth factor receptors.
  • Overexpression of this gene leads to many growth factor receptors being expressed on the tumour cell surface, increasing the sensitivity of the cell to growth factors.
  • This accelerates growth of the neoplasm, and is particularly associated with breast cancer.
41
Q

what is xeroderma pigmentosa

A

reduced ability to repair UV damage, and therefore they are more likely to develop skin cancer at a young age.

42
Q

familial breast carcinoma

A

associated with mutations to the BRCA1 or BRCA2 genes, which are normally involved in repairing double strand DNA breaks.

43
Q

Hereditary non-polyposis colon cancer (HNPCC)

A

condition affecting DNA mismatch repair genes, which increases the risk of developing colon cancer.

44
Q

what are the 6 hallmarks of cancer

A

Self-sufficiency in growth signals

Resistance to growth stop signals

Cell immortalisation through the action of telomerase

Angiogenesis; the ability to produce new blood vessels

Resistance to apoptosis

Ability to invade and produce metastases

Pathological Processes (10 decks)

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