Neoplasia 1 Flashcards
Tumour define
any clinically detectable lump or swelling
Neoplasm define
Abnormal new growth of cells that persists after stimulus is removed
(Type of tumour)
Oncology define
Study of tumours and neoplasms
Benign neoplasm define
Gross and microscopic appearances are considered to be innocent
Implying that it will Remain localised will not spread to other sites
Cancer define
Layman
Malignant neoplasm
Malignant neoplasm define
Abnormal growth of cells that persists after stimulus is removed
Invades surrounding tissues and potential to spread distally
Metastasis define
malignant neoplasm that has spread from original site to a new non-contiguous site
What is dysplasia?
Pre-neoplastic alteration in which
cells show disorganised tissue organisation (confined to epithelia layer)
Reversible
Appearance dysplasia
Pleomorphism
Large hyperchromatic nuclei
High nuclei to cytoplasm ratio
(similar to poor differentiation malignant)
2 sites of malignant neoplasm
Primary site (original location) Secondary site (spread to)
Benign vs Malignant
Benign: Remain confined and DO NOT metastasise
Malignant: Invade and DO metastasise
3 features of benign tumours
Confined local area growth Psuedocapsule (pushing outer margin) Rarely dangerous (depending on location though)
3 features of malignant tumours
Irregular outer margin and shape
Ulcerations and central necrosis
Infiltrative (breach basement membrane)
Differentiation benign vs malignant
Benign: well differentiated (resemble parent tissue)
Malignant well-poor differentiated (don’t resemble origin tissue)
Cells with no resemblance to any tissue are called…
Anaplastic tissue
What happens as differentiation worsens (poor differentiation)?
Increase: size of nucleus nuclear to cytoplasmic ratio nuclear staining (hyperchromasia) Numbers of mitotic figures
Abnormal mitotic figures (Benz)
Variation in cell and nuclei shape/size (pleomorphism)
How do clinicians define differentiation?
Grades
Higher grade = more poorly differentiated
(eg grade 3 cancer = very poorly differentiated)
Grading breast tissue
Grade 1: glandular structure preserved mostly, uniform cells
Grade 2: loss of some glands, cells larger and variable in shape
Grade 3: minimal glands, lots of mitosis, variable cell shape
Gleasons pattern
Prostate grading
1-5 with worsening gland formation
Why is grading important?
If later grade, lower chance of survival and determines treatment
eg higher grades need more aggressive treatment
Steps of cell becoming neoplastic
Normal
Dysplasia
Carcinoma in situ (no breach of BM)
Invasive carcinoma
Cervical dysplasia grading
Normal CIN 1 (lower grade, lower 3rd affected) CIN 2 (moderate, lower 2/3rds affected) CIN 3 (carcinoma in situ, entire thickness affected)
Why do we get neoplasia?
Lots of new cells dividing every day Introduction of mutations - from INITIATORS Accumulate PROMOTORS cause proliferation = tumour from clonal expansion
What sort of damage causes neoplasia?
Non-lethal genetic damage
Initiators of mutations include…
Chemicals (eg smoking, alcohol, diet, obesity)
Infectious agents (HPV)
Radiation
Inherited mutations
Steps of neoplasm
Initiator = mutation
Promotor (proliferation of cells with mutation)
Progression (accumulate more mutations to enhance survival)
What genes are often affected by cancer causing mutations? (4)
Proto-oncogenes
Tumour suppressor genes
Genes that regulated apoptosis
DNA repair genes
What are proto-oncogenes?
Drive proliferation
Proto-oncogene mutation do?
Excessive increase in normal functions or give a new function (GAIN OF FUNCTION mutation)
Proto-oncogene mutation explained
Proto-oncogene (mutates) –> oncogene –> oncoprotein
oncoproteins promote growth without signals now
Oncogene importance
Dominate over counterparts (only one allele needs to be affected)
Example of PO mutation
BRAF (v600e) mutation
Tumour suppressor gene function mutation
Usually stop cell proliferation
Mutation = loss of function (fail to inhibit growth)
(p53)
Mutations needed TSG
Both alleles must be damaged to occur (recessive)
Apoptosis regulating genes mutation
Abnormalities = less programmed cell death and enhanced survival of cells
DNA repair gene mutations
Loss of function
Impair ability for cell to recognise and repair non-lethal genetic damage
Cells acquire mutations quicker
DNA repair gene mutation known as
Mutator phenotype (marked by genetic instability)
How are neoplasms named?
Benign end in -oma
Malignant end -carcinoma (if epithelial 90%) or sarcoma (if stromal)
benign epithelial neoplasms
Squamous papilloma (skin) Transitional cell papilloma (bladder mucosa)
Adenoma (glands)
Cystadenoma (ovary gland)
How are polyps of epithelial neoplasms named?
Villous (finger like)
Sessile (box)
Tubular
(polyp of colon)
Malignant epithelial neoplasms
Squamous cell carcinoma (skin, lung)
Transitional cell carcinoma (bladder)
Adenocarcinoma (glandular)
Basal cell carcinoma
Connective tissue benign neoplasms
Leiomyoma (smooth muscle) Fibroma Osteoma Chondroma (cartilage) Lipoma Neuroma Neurofibroma (nerve sheath) Glioma (glial cells)
Connective tissue malignant neoplasms
Leiomyosarcoma (smooth muscle) Osteosarcoma Fibrosarcoma Chondrosarcoma Liposarcoma Malignant glioma
Germ cell neoplasms malignant vs benign
Malignant teratoma and Seminoma (testes, exception to -oma benign rule, ITS MALIGNANT)
Benign teratoma in ovaries = dermoid cyst (benign, follows rule)
