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ESA 2 > MoD session 11: incidence, prognosis and treatment of malignant neoplasms > Flashcards

MoD session 11: incidence, prognosis and treatment of malignant neoplasms Flashcards

1
Q

The 4 most common types of cancer make up 54% of all cancers in the UK. What are they (in order from most common)?

A

Breast
Lung
Prostate
Bowel

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2
Q

What are the most common cancers in children younger than 13?

A

Leukaemia, CNS tumours and lymphomas

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3
Q

Describe the variation in 5 year survival rates

A

Testicular (98%), melanoma (90% if early stage) and breast (87%) are much better than pancreatic (3%), lung (10%) and oesophageal (15%). Lung is biggest cause of cancer-related deaths in UK

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4
Q

What factors are considered when predicting outcome of cancer?

A 
Age
General health status
Tumour type
Grade (differentiation)
Stage
Availability of effective treatments
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5
Q

What is tumour stage and how is it usually measured?

A

A measure of the malignant neoplasm’s overall burden, which gives a strong indication of survival. E.g. melanoma survival is very high at stage I but by stage IV is very low

Usually measured using the TNM staging system:

  • T refers to size of tumour, typically T1 to T4 (small to large)
  • N: extent of regional node metastasis, e.g. N0 to N3
  • M: extent of distant metastatic spread, e.g. M0 or M1
  • each cancer has its own specific TMN criteria

T, N and M status then converted into a stage from I to IV. Details vary but in general stage I=early local disease, stage II=advanced local disease (i.e. N0, M0), stage III=regional metastasis (i.e. any T, N1 or more, M0) and stage IV is advanced disease with distant metastasis (i.e. any T, any N and M1)

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6
Q

Describe the staging system for lymphoma

A

Ann Arbor
Stage I: lymphoma in a single node region
Stage II: two separate regions on one side of the diaphragm
Stage III: spread on both sides of diaphragm
Stage IV: diffuse/disseminated involvement of one or more extra-lymphatic organs such as bone marrow or lungs

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7
Q

Describe Dukes staging for colonic carcinoma with the % 5 year survival

A

Dukes’ A: invasion into but not through the bowel. 93%
Dukes’ B: invasion through the bowel wall. 77%
Dukes’ C: involvement of lymph nodes. 48%
Dukes’ D: distant metastases. 6%

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8
Q

What is tumour grade?

A

Describes the degree of differentiation of a neoplasm. Not as standardised as staging, but usually G1 is well-differentiated, G2 is moderately differentiated, G3 is poorly differentiated and G4 is anaplastic. This system is used for squamous cell carcinoma and colorectal carcinoma.
Grading is more important for planning treatment /prognosis in certain types of cancer such as soft tissue sarcoma, primary brain tumours, lymphomas, breast and prostate cancer

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9
Q

Describe the modified Bloom Richardson grading for breast cancer

A

G1: tubules
G2: mitoses (number of mitotic figures)
G3: nuclear pleomorphism
Each given a score then total score to decide grade

Not really used any more! Used Nottingham prognostic index scoring for the past 20 years but have to know Bloom-Richardson for exam

Big survival drop between G2 and G3.

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10
Q

What is the difference between adjuvant and neoadjuvant treatment of cancer?

A

Adjuvant: given after surgical removal of a primary tumour to eliminate subclinical disease
Neoadjuvant: given to reduce the size of a primary tumour prior to surgical excision

Surgical excision can be thought of as curative treatment

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11
Q

How is radiation therapy used to treat cancer?

A

Radiotherapy: focused on the tumour with shielding of surrounding healthy tissue. Given in fractionated doses to minimise normal tissue damage. X-rays/other types of ionising radiation used to kill rapidly dividing cells, especially in G2 of the cell cycle.

Mechanism:

  • causes direct or free radical induced DNA damage that is detected by the cell cycle checkpoints, triggering APOPTOSIS
  • double stranded DNA breakages cause damaged chromosomes that prevent M phase from completing
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12
Q

Why is radiotherapy given in multiple small doses?

A

X-ray energy is absorbed by some tissues and some of the energy passes straight through. Multiple doses culminating in the same dose overall gives more differential effects on cancer cells so more get destroyed

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13
Q

How does chemotherapy affect proliferating cells?

A

AFFECT ALL PROLIFERATING CELLS AS NON-SPECIFIC

ANTIMETABOLITES: mimic normal substrates involved in DNA replication, e.g. fluorouracil which mimics uracil

ALKYLATING and PLATINUM-based drugs e.g. cyclophosphamide and cisplatin: cross-link the two DNA strands in the helix

ANTIBIOTICS: act in several ways. E.g. doxorubicin inhibits DNA topoisomerase needed for DNA synthesis, while bleomycin causes ds DNA breaks

PLANT-DERIVED drugs: e.g. vincristine, which blocks microtubule assembly and interferes with mitotic spindle formation

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14
Q

How might hormones be used to target malignant tumours?

A

Relatively non-toxic
E.g. selective oestrogen receptor modulators (SERMs) e.g. TAMOXIFEN bind to oestrogen receptors, preventing oestrogen from binding. Used to treat hormone receptor positive breast cancer

E.g. androgen blockage used in prostate cancer

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15
Q

Give 2 examples of oncogenes that are targeted by cancer therapy

A

Trastuzumab (HERCEPTIN): as 25% of breast cancers have gross over-expression of the HER-2 gene and Herceptin can block Her-2 signalling

Imatinib (GLEEVEC): CML shows a chronic chromosomal rearrangement (t9:22) creating an abnormal Philadelphia chromosome in which an oncogenic fusion protein (BCR-ABL) is encoded. Imatinib inhibits the fusion protein

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16
Q

What are tumour markers? Give some examples

A

Substances released by cancer cells into the circulation, which are most useful for monitoring tumour burden during treatment and follow up (with some role in diagnosis).

Examples:

  • Hormones e.g. human chorionic gonadotrophin released by testicular tumours
  • Oncofetal antigens e.g. alpha fetoprotein released by hepatocellular carcinoma
  • Specific proteins e.g. prostate-specific antigen released by prostate carcinoma
  • Mucins/glycoproteins e.g. CA-125 released by ovarian cancer
  • Carcinoemrbyonic antigen (CEA), CA 19-9 and K-RAS mutations for colon cancers
  • Oestrogen e.g. endometrial carcinoma
17
Q

What are the problems associated with cancer screening?

A

Lead time bias
Length bias
Over diagnosis (especially in prostate cancer in elderly men, will most likely die of something else first as is very slow growing)

18
Q

Describe the national cancer screening programmes for the UK

A

Cervical: women aged 25 to 49 receive invitations every 3 years and aged 50 to 64 every 5 years. Sample of cells from cervix assessed microscopically, aiming to identify when in CIN I or II (confined to lower or lower and middle thirds of epithelium respectively)

Breast: all women aged 50-70 who are registered with a GP are invited for a mammogram every 3 years

Bowel: all men and women aged 60-74 who are registered with a GP, every 2 years. 60-74 foecal occult blood test (send foecal sample). New one off test for over 55s where can insert thin instrument to remove polyps at GP if high risk

19
Q

Which sorts of tumours occur commonly in the testis? Which is most common in teenagers?

A

Germ cell:

  • Seminomas
  • Non seminomas: teratoma, embryonal carcinoma, choriocarcinoma, yolk sac tumours

Very rarely in men >60 lymphoma can start here

20
Q

What markers are commonly raised in non-seminoma testicular cancer?

A

Alpha feta protein
HCG
Lactate dehydrogenase

21
Q

What are the characteristic cells in Hodgkin’s lymphoma? They are necessary for diagnosis of HL, but not unique to it

A

Reed-Sternberg cells: malignant lymphocytes (usually a B cell). Histologically appear very large with a pale cytoplasm and two or more oval lobulated nuclei

22
Q

What are B symptoms in Hodgkin’s lymphoma and what is their significance?

A

Systematic systems: fever, weight loss and night sweats

Indicates poorer prognosis

23
Q

Describe the T1 to T4 stages from the TMN classification for breast cancer

A

Diameter of primary tumour:

  • T1: 2cm or less
  • T2: 2-5cm
  • T3: bigger than 5cm
  • T4: invades the chest wall
24
Q

Describe the diagnosis of prostate cancer

A

Hard craggy prostate and PSA in double digits indicates prostate cancer. Biopsy shows fibrous tissue.

Graded using GLEASON system: grades 1-5. Grade 1 most similar to normal prostate tissue; however, only grades 3-5 are cancer. Grade 4 glands start to fuse, grade 5 is sheets.
In real life don’t report grades 1 and 2

25
Q

Where is the common site of metastasis for prostate cancer?

A

Bone

Especially the lumbar spine

26
Q

Risk factors for cervical carcinoma

A 
HPV 16 and HPV 18
Ages 25-34
Multiple sexual partners
Smoking
Immunosuppression
27
Q

Describe the sequence events which occur in the cervical epithelium to produce cervical carcinoma

A

CIN: cervical intraepithelial neoplasia:

  • CIN I in lower 1/3 of epithelium
  • CIN II in lower and middle 1/3s
  • CIN III full thickness

Micro-invasion of basement membrane

Invasive: if deeper than 5mm or wider than 7mm; formal staging required

28
Q

Abnormalities in which gene may be identified in some breast cancers?

A

Retinoblastoma gene

29
Q

Why might castration be indicated in prostate cancer?

A

Reduces testosterone supply to the tumour and patient

30
Q

What is the commonest cause of cancer death in the UK?

A

Lung

31
Q

What is Ewing’s sarcoma?

A

A rare bone cancer of children and adolescents

32
Q

What is a Wilm’s tumour?

A

Aka nephroblastoma

Kidney cancer affecting children

33
Q

What type of tumour produces vanillyl mandelic acid?

A

Pheochromocytoma (adrenal tumour of chromaffin cells)

34
Q

What type of tumour is associated with Aspergillus flavus?

A

Hepatocellular carcinoma

35
Q

What type of tumour commonly produces ectopic ADH production?

A

Small cell carcinoma of lungs

36
Q

What is choriocarcinoma?

A

Tumour of uterus where placental cells would usually be

Often produces HCG

37
Q

What type of thyroid tumour can produce calcitonin?

A

Medullary carcinoma

ESA 2 (58 decks)

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