tumour nomenclature

Question 1

hyperplasia

Answer 1

increase in the number of normal cells

Question 2

hormonal hyperplasia causes

Answer 2

1) increased hormonal stimulation, endometrial gland hyperplasia due to increased oestrogen, cancer risk increases.
2) benign prostatic hyperplasia (BPH), which is caused by an increase in sensitivity to dihydrotestosterone (DHT), no effect on Ca risk.

Question 3

chronic irritation hyperplasia causes

Answer 3

1) constant scratching of itchy skin, which may produce thickening (hyperplasia) of the epidermis
2) bronchial mucous gland hyperplasia, which commonly occurs in smokers and asthmatics

Question 4

chemical imbalance causing hyperplasia

Answer 4

iodine deficiency, which produces thyroid enlargement (goitre) as the gland works hard to increase thyroid hormone synthesis (mix of hyperplasia and hypertrophy)

Question 5

stimulating antibody causing hyperplasia

Answer 5

hyperthyroidism in Gaves disease is due to thyroid-stimulating antibodies (IgG) directed against thyroid hormone receptors, which cause the gland to synthesise excess thyroid hormone

Question 6

viral infections causing hyperplasia

Answer 6

skin infection by the human papillomavirus (HPV) produces epidermal hyperplasia or the common wart. viral genes produce growth factors causing epidermal hyperplasia

Question 7

neoplasia

Answer 7

new overgrowth of abnormal tissue not under normal physiological control.
this describes both benign and malignant tumours.

Question 8

benign vs malignant tumour

Answer 8

• benign tumours are usually well differentiated, even through they are a neoplasm they resemble their parent tissue and have no metastatic potential.
• cancer refers to a malignant process involving a neoplasm, which can be a blood cancer.

Question 9

malignant cancer grading

Answer 9

does the tissue resemble parent tissue?

• well differentiated or low grade cancer- resembles parent tissue
• poorly differentiated, high grade or anaplastic don’t resemble parent tissue

Question 10

anaplasia

Answer 10

the loss of the mature or specialised features of a cell or tissue, as in malignant tumours.

Question 11

benign tumours- epithelial

Answer 11

benign tumours are of epithelial or connective tissue origin, originating from ectoderm (squamous) or endoderm (like glandular epithelium).

• tumours of glandular epithelium- adenomas
• tumours of squamous and transitional epithelium- papillomas

Question 12

mixed tumours

Answer 12

neoplastic cells with two morphological patterns but deriving from the same germ layer e.g. pleomorphic adenoma of parotid gland

Question 13

teratoma

Answer 13

derived from all germ layers. often found at ovaries, mediastinum and pineal gland, can have metastatic potential.

Question 14

carcinoma- a malignant neoplasm

Answer 14

derive from epithelial tissue (squamous, glandular and transitional)

1) squamous cell carcinoma
2) adenocarcinoma (glandular epithelium- columnar, cuboidal)
3) transitional cell carcinoma (TCC)

Question 15

sarcoma- a malignant neoplasm

Answer 15

derive from connective tissue, therefore they are all of mesodermal origin. approx. 40% are located in the lower extremities

Question 16

growth rate in benign and malignant tumours

Answer 16

• benign- slow growth rate (low-grade)
• malignant- variable growth.
• growth rate correlates with degree of anaplasia in tumour.

Question 17

monoclonality in benign and malignant tumours

Answer 17

• nonneoplastic proliferations derive from a single precursor cell hence display monoclonality.

Question 18

upregulation of decal accelerating factor (DAF) by malignant cells

Answer 18

• DAF normally degrades C3 convertase and C5 convertase in the classical and alternative complement pathways
• upregulation of DAF ensures that degradation of the convertases just mentioned prevents formation of the membrane attack complex (MAC; C5b-9); therefore cancer cells cannot be killed by the MAC

Question 19

local invasion and metastasis

Answer 19

benign tumours do not invade.
benign tumours usually enclosed by fibrous capsule.
malignant tumours invade tissues. all malignant tumours require oxygen and nutrients to survive and do so by stimulating angiogenesis within the tumour and its metastatic sites.

Question 20

telomere complexes

Answer 20

repetitive sequences nontranscribed DNA at the end of chromosomes. prevent end-to-end fusion of chromosomes chromosomes during mitosis; important for cell longevity. shorten with each round of replication.

Question 21

telomerase activity in benign and malignant tumours

Answer 21

when only a few nucleotide bases remain, the genome becomes unstable, which produces a signal for apoptosis. benign tumours have normal telomerase activity.
malignant cells have upregulation of telomerase activity, which prevents the naturally programmed shortening of telomere complexes with cell replication; hence the cell no longer undergoes apoptosis.