Session 12: Neoplasia IV Flashcards

1
Q

TNM staging system

A

T (how big the primary Tumour is)

-TIS carcinoma in situ, T1 <2cm, T2 2-5cm, T3 >5cm, T4 through the chest wall/skin

N (extent of regional lymph node metastasis)

  • N0 no nodal, N1 Axillary, N2 mammary, N3 supraclavicular
  • >this refers specifically to breast cancer

M (extent of distal metastatic spread)

M0 no metastasis, M1 presence of metastasis

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2
Q

General staging of maligant tumour, and definition of staging

A

Staging: the extent of spread of tumour

I: early local disease, T1/2, N and M0

II: advanced local disease, T3/4, N and M0

III: regional metastasis, T-, N1/2/3, M0

IV: advanced disease w/ distant metastasis, T-, N-, M1

While it is general, it is also exactly how melanoma is measured

also used to describe prostate, bladder and breast cancer

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3
Q

Dukes’ staging

A

for colorectal carcinomas

A: confined to bowel wall, not extending through muscularis propria, >90% 5 year survival

B: through bowel wall (muscularis propria/externa), 70% 5 year survival

C1/2: lymph nodes involved, 30% year survival

  • C1: regional lymph nodes involved
  • C2: apical node (furthest away node) involved

D: distant metastases

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4
Q

which stage is this?

A

Dukes’ stage 1: innermost lining of the bowel, slightly growing into the muscle layer

>90% 5 year survival

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5
Q

which stage is this?

A

Dukes’ stage B: grown thorugh muscle layer

70% 5 year survival

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6
Q

which stage is this?

A

Dukes’ stage C1/2 (probably C1 as it looks like the regional lymph nodes)

30% 5 year survival

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7
Q

which stage is this?

A

Dukes’ stage D: distant metastases

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8
Q

Ann Arbor classification

A

staging used in Hodgkin’s disease

I: 1 lymph node/nodal group involved

II: 2 lymph nodes/nodal groups on side of the diaphragm

III: more than 2 lymph nodes/nodal groups on both sides of the diaphragm

IV: multiple foci (bloody everywhere) - diffuse/disseminated involvement of 1/more extra-lymphatic organs eg bone marrow, lungs

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9
Q

Define grading and give classes

A

Based on the degree of differentiation of tumour cells. Attempts to judge the extent to which tumour cells resemble/fail to resemble their normal counterparts

not international classifications, somewhat subjective

Gx: grade of differentiation cannot be assessed

G1: well differentiated

G2: moderately differentiated

G3: poorly differentiated

G4: undifferentiated

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10
Q

Scarff-Bloom-Richardson grading

A

international objective grading for breast cancer

Depends on: degree of tubule formation, extent of nuclear variation and number of mitoses:

  • Grade 1: 85% 10 year survival - tubules present
  • Grade 2: 60% 10 year survival - no tubules, mitoses
  • Grade 3: 15% 10 year survival - no tubules, mitoses, nuclear pleomorphisms
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11
Q

Grading of colon cancer

A

same classification is used for all intestinal cancers

Grade 1: grows slowly, low chance of spreading beyond bowel

Grade 2: grows moderately, medium chance

Grade 3: grows rapidly, high chance

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12
Q

how are prostate carcinomas graded?

A

Gleason grading system

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13
Q

Discuss the biological basis for the use of different cancer treatments

A

adjuvant: remove microtubules (a subclinical disease)

neo adjuvant: reduce size of primary tumour before surgical excision

Surgery: use knife to cut out tumour, can only cure the cancer when the primary tumour has not metastasised, palliative elesewhere to relieve symptoms and remove the bulk of the tumour

Radiotherapy: external radiation to tumour in small doses w/ shielding of adjacent normal tissues, causes damage to DNA of rapidly dividing cells in G2 cycle, if DNA damage (single/double strand breaks) is extensive -> apoptosis

-Sensitivity: High - lymphoma, leukaemia, seminoma - Fairly high - squamous carcinoma - Moderate - GI, breast - Low - Sarcoma

Chemotherapy: Antimetabolites mimic normal substrates involved in DNA replication eg fluorouracil

  • Alkylating and platinum based drugs eg cyclophosphamide and cisplatin X-link the two strands of the DNA helix
  • Antibiotics act in several different ways eg doxorubicin inhibits DNA topoisomerase needed for DNA synth., bleomycin causes double-stranded DNA breaks
  • plant derived drugs include vincristine, which blocks m.tubule assembly and interferes w/ mitotic spindle formation

Hormone Therapy: Tamoxifen: competes for binding to oestrogen receptor - selective oestrogen receptor modulators (SERMs), 50-80% of breast cancers express oestrogen receptors

  • Herceptin: a humanised monoconal AB that binds to HER-2 (human epidermal GF receptor)-2 which is overexpressed in 20-30% of breast carcinomas
  • > this is an example of oncogene therapy, it is non toxic and only targets molecules in cancer cells
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14
Q

surgical treatment of cancers

A

use knife to cut out tumour, can only cure the cancer when the primary tumour has not metastasised, palliative elesewhere to relieve symptoms and remove the bulk of the tumour

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15
Q

radiotherapy treatment of cancers

A

external radiation to tumour in small doses w/ shielding of adjacent normal tissues, causes damage to DNA of rapidly dividing cells in G2 cycle, if DNA damage (single/double strand breaks) is extensive -> apoptosis

-Sensitivity: High - lymphoma, leukaemia, seminoma - Fairly high - squamous carcinoma - Moderate - GI, breast - Low - Sarcoma

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16
Q

Chemotherapy treatment of cancers

A

Chemotherapy: Antimetabolites mimic normal substrates involved in DNA replication eg fluorouracil

  • Alkylating and platinum based drugs eg cyclophosphamide and cisplatin X-link the two strands of the DNA helix
  • Antibiotics act in several different ways eg doxorubicin inhibits DNA topoisomerase needed for DNA synth., bleomycin causes double-stranded DNA breaks
  • plant derived drugs include vincristine, which blocks m.tubule assembly and interferes w/ mitotic spindle formation
17
Q

Hormone therapy of cancers

A

Tamoxifen: competes for binding to oestrogen receptor - selective oestrogen receptor modulators (SERMs), 50-80% of breast cancers express oestrogen receptors

  • Herceptin: a humanised monoconal AB that binds to HER-2 (human epidermal GF receptor)-2 which is overexpressed in 20-30% of breast carcinomas
  • > this is an example of oncogene therapy, it is non toxic and only targets molecules in cancer cells
18
Q

use of tumour markers in diagnosis and monitoring of disease

A

some are not universally sensitive and are found in normal cells

  • Carcinoembryonic antigen: normally only in embryonic tiss., but cancer expresses it as well, clinically useful to see if any residual disease is left after the removal of tumours
  • hCG (human Chorionic Gonadotrophin) used: in evaluation of testicular masses
  • >to indicate residual diseases after orchidectomy
  • >in monitoring response to therapy and prediction of reccurence
  • >raised in nonseminomatous testicular tumours, esp. when choriocarcinomatous elements present (high levels)
  • >in seminomas w/ syncitiotrophoblastic giant cells
  • Alpha-Fetoprotein (AFP): normally synth. early in foetal life by yolk sac, foetal liver and foetal GI tract
  • >raised plasma levels assoc. w/ cancer of liver and yolk sac tumour of testes (ie nonseminomatous testicular tumours)
19
Q

carcinoembryonic antigen

A

tumour marker

normally only in embryonic tiss., but cancer expresses it as well, clinically useful to see if any residual disease is left after the removal of tumours

20
Q

hCG

A

tumour marker

used: in evaluation of testicular masses
- >to indicate residual diseases after orchidectomy
- >in monitoring response to therapy and prediction of reccurence
- >raised in nonseminomatous testicular tumours, esp. when choriocarcinomatous elements present (high levels)
- >in seminomas w/ syncitiotrophoblastic giant cells

21
Q

Alpha-Fetoprotein (AFP)

A

tumour marker

normally synth. early in foetal life by yolk sac, foetal liver and foetal GI tract

->raised plasma levels assoc. w/ cancer of liver and yolk sac tumour of testes (ie nonseminomatous testicular tumours)

22
Q

Value of screening

A

aims to detect pre-malignant, non invasive and early invasive cancers to improve prognosis

Cervix: cytological smears to detect ‘early’ precancerous changes eg cervical intraepithelial neoplasia (CIN), treatment can then be given before invasion occurs and is curative

-first at 25 yrs, 25-49 every 3 yrs, 50-64 every 5 yrs, 64< those who have not been screened since the age of 50/who have had recent abnormalities

Breast: identify invasive tumours before they can be felt - 10-15mm in size, relies on mammography (x-ray of breast) by identifying densities and calcifications, one in 500 women screened will have their life saved, 50-69 yrs every 3 yrs

Problems w/ calculations: Lead time bias (survival appears to inc. if detected early), length bias (screening may only pick up slow growing tumours, as faster ones will be presented to doctors by patient

23
Q

cervix screening

A

cytological smears to detect ‘early’ precancerous changes eg cervical intraepithelial neoplasia (CIN), treatment can then be given before invasion occurs and is curative

-first at 25 yrs, 25-49 every 3 yrs, 50-64 every 5 yrs, 64< those who have not been screened since the age of 50/who have had recent abnormalities

24
Q

breast screening

A

identify invasive tumours before they can be felt - 10-15mm in size, relies on mammography (x-ray of breast) by identifying densities and calcifications, one in 500 women screened will have their life saved, 50-69 yrs every 3 yrs

25
Q

problems w/ calculation of statistics of screenings

A

Lead time bias (survival appears to inc. if detected early), length bias (screening may only pick up slow growing tumours, as faster ones will be presented to doctors by patient