tumour nomenclature Flashcards
hyperplasia
increase in the number of normal cells
hormonal hyperplasia causes
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.
chronic irritation hyperplasia causes
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
chemical imbalance causing hyperplasia
iodine deficiency, which produces thyroid enlargement (goitre) as the gland works hard to increase thyroid hormone synthesis (mix of hyperplasia and hypertrophy)
stimulating antibody causing hyperplasia
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
viral infections causing hyperplasia
skin infection by the human papillomavirus (HPV) produces epidermal hyperplasia or the common wart. viral genes produce growth factors causing epidermal hyperplasia
neoplasia
new overgrowth of abnormal tissue not under normal physiological control.
this describes both benign and malignant tumours.
benign vs malignant tumour
- 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.
malignant cancer grading
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
anaplasia
the loss of the mature or specialised features of a cell or tissue, as in malignant tumours.
benign tumours- epithelial
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
mixed tumours
neoplastic cells with two morphological patterns but deriving from the same germ layer e.g. pleomorphic adenoma of parotid gland
teratoma
derived from all germ layers. often found at ovaries, mediastinum and pineal gland, can have metastatic potential.
carcinoma- a malignant neoplasm
derive from epithelial tissue (squamous, glandular and transitional)
1) squamous cell carcinoma
2) adenocarcinoma (glandular epithelium- columnar, cuboidal)
3) transitional cell carcinoma (TCC)
sarcoma- a malignant neoplasm
derive from connective tissue, therefore they are all of mesodermal origin. approx. 40% are located in the lower extremities
growth rate in benign and malignant tumours
- benign- slow growth rate (low-grade)
- malignant- variable growth.
- growth rate correlates with degree of anaplasia in tumour.
monoclonality in benign and malignant tumours
- nonneoplastic proliferations derive from a single precursor cell hence display monoclonality.
upregulation of decal accelerating factor (DAF) by malignant cells
- 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
local invasion and metastasis
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.
telomere complexes
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.
telomerase activity in benign and malignant tumours
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.
