Cellular basis of cancer

Question 1

1. neoplasia
2. benign tumor
3. malignant
4. sarcoma

Answer 1

neoplasia= new growth

benign tumors= localised growth, do not spread to other sites. usually have suffix ‘oma’. they compress surrounding structures but do not destroy them

malignant= destroy surrounding structures and spread to distant sites.

sarcoma (soft tissue) lymphoma (lymph) melanoma (melanocyte) carcinoma (any epithelium- oesophagus, skin, intestine)

Question 2

anaplasia

dysplastic

Answer 2

complete lack of differentiation
(no keratinisation, no gland formation)

within the epithelium= dysplastic (transformed and potentially malignant)
then attach to lymph etc and form an embolus

Question 3

tumour spread

Answer 3

lymphatic channel

first lymph node in the area- sentinel nodes

Question 4

sentinel node

Answer 4

the first node in the regional lymphatic basin that received lymph flow from the primary tumour

Question 5

microbial carcinogenesis

Answer 5

oncogenic RNA virus (human T cell leukaemia virus type 1)

oncogenic DNA (HPV)

EBV implicated in the pathogenesis of Burkitt lymphoma

Question 6

cellular and molecular hallmarks of cancer

Answer 6

sustained proliferative signalling
evading growth suppressors
activate invasion and metastasis
enable replicative immortality
induce angiogenesis
resisting cell death

Question 7

proto-oncogene

accelerator

Answer 7

part of a normal cell cycle to identify abnormal cells
once an abnormal cell is identified it undergoes cell death

once it’s a cancer cell it can avoid this pathway

proto-oncogenes= mutated to oncogenes which promotes autonomous…

Question 8

insensitivity to the growth inhibitor
tumour suppressor cell
(break)

Answer 8

RB gene- retinoblastoma gene
p53

tumour suppressor genes apply breaks to cell proliferation and abnormalities in these genes lead to failure of growth inhibition

2 hit hypothesis RB gene
p53 central monitor of stress in the cell

if DNA damage within a cell can not be repaired then p53 would induce apoptosis.

Question 9

two hit hypothesis

Answer 9

when both alleles of a tumor supressor gene (RB gene) are acquired then children can develop retinoblastoma.

familial- inherit one abnormal allele (first hit)

sporadic- both normal RB alleles undergo somatic mutation

Question 10

Li- Fraumeni syndrome

Answer 10

one abnormal allele of p53

x25 fold greater chance of developing a malignant tumour by the age of 50

Question 11

BCL2

Answer 11

prevents the abnormal cells from being destroyed

Question 12

genomic instability

Answer 12

ability to repair DNA to help maintain the integrity of the genome (defect) so at an increased risk of developing a cancer.

Question 13

Lynch syndrome

Answer 13

example of mismatch repair defects leading to microsatellite instability.

tandem repeats of one to six nucleotides

in tumors they are unsable an dincrease or decrease inlength

link to colorectal and endometrial cancer

Question 14

staging and grading of tumours

Answer 14

based on tumour size, extend to regional lymph nodes, presence or absence of blood-borne metastasis

if there is a localised cancer mass= resection
if there are a tumour and lymph nodes has spread= metastatic