Classes 6-7 Neoplasms Flashcards
Normal cell growth requires
- Genetic material (DNA or RNA)
- Signals from one cell to another.
- Growth inhibiting and growth promoting substances.
Neoplasm
New growth. Uncontrolled.
Neoplastic cell proliferation is:
- Autonomous
- Excessive
- Disorganized.
Clinical classification of neoplasms
Benign – limited growth good potential
Malignant – uncontrolled growth. Poor potential.
Benign vs malignant: Macroscopic features
Benign:
- sharply demarcated
- often encapsulated
- expansive growth (may lead to atrophy and fibrosis)
Malignant
- no clear margins
- no encapsulation
- invasive growth.
- hemorrhage and necrosis
Benign vs malignant tumours: microscopic features.
Benign
- resembles original tissue
- show high levels of differentiation
Malignant
- differs from original tissue
- anaplasia (cells take on new tissue)
- undifferentiated.
Benign vs malignant tumours: cellular features
Benign
- homogenous cell population
- well developed cytoplasm
- regular nucleus which occupies small portion of the cell
- even distribution of chromatin
Malignant:
- heterogenous cell populations
- nuclei vary in shape and size. Generally large.
- variable cytoplasm.
- hyper chromatic (more chromatin, uneven distributed in prominent nucleoli)
Aneuploid
Abnormal number of chromosomes
Characteristic of malignant cells.
Metastasis
Process by which malignant cells move from one site in the body to another.
Occurs via:
- Lymphatics
- Blood (hematogenous spread)
- Body cavities.
~Oma
Probably benign tumour of mesenchyme cells.
Fibroma
Benign tumour of fibroblasts
Chondroma
Benign tumour of cartilage
Lipoma
Benign tumour of adipose tissue
Leiomyoma
Benign tumour of smooth muscle cells
Osteoma
Benign tumour of bone
Rhabdomyoma
Benign tumour of striated muscle.
Adenoma
Benign tumour of epithelial cells. Composed of glands or ducts unless otherwise specified.
Villus or tubular adenomas
Adenoma of GI tract
Also known as polyps.
Papilloma
Benign protuberance of skin, bladder, larynx.
Cystadenomas
Benign cystic tumours of hollow spaces lined by neoplastic epithelium
~sarcoma
Malignant tumour of mesenchymal cells
Fibrosarcoma
Malignant tumour from fibroblasts
Chondrosarcoma
Malignant tumour of cartilage
Liposarcoma
Malignant tumour of adipose.
Carcinoma
Malignant tumours of epithelial cells
Adenocarcinoma
Malignant tumour of glands and ducts
3 malignant “~oma”s
Lymphoma (lymphoid cells)
Glioma (glial cells)
Seninomas (testicles)
~blastoma
Malignant tumour composed of embryonic cells from embryonic primordia
Retinoblastoma (eye)
Neuroblastoma (adrenal medulla or immature neural cells)
Hepatoblastoma (liver)
Nephroblastoma (kidney)
Teratoma
Benign tumour derived from germ cells.
Contain tissue derived from ecto, meso and endoderm layers.
Teratocarcinoma
Malignant tumour of germ cells.
Eponymous tumours
Hodgkin’s lymphoma
Ewing’s sarcoma
Kaposi sarcoma
Tumour staging
Based on clinical assessment.
Extent of tumour spread.
Based on size (T), lymph metastases (N), distant metastases (M)
I-IV or A-D.
Better predictive value than grading
Grading of tumours
Grade 1 – well differentiated
Grade 2 – moderately well differentiated
Grade 3 – undifferentiated.
Biochemistry of cancer cells
Simple metabolism. Requires less O2 Fewer mitochondria Fewer enzymes Simpler and less abundant RER Loss of functional capacity Anaplasia
Anaplastic cells
Larger than normal and often with nuclear irregularity.
May regress and assume fetal features.
Ex. Liver cancer cells produce alpha-fetoprotein. Intestinal carcinoma cells produce carinoembryonic antigen.
Where do carcinogens act?
- Site of contact
- Site of digestion
- Site of metabolic activation (liver)
- Site of excretion (urine)
6 steps of chemical carcinogenesis
- Ingestion of procarcinogen
- Initiation – start of genetic changes in cell
- Promotion – initiated cells stimulated to proliferate
- Conversion – to new cell type with ability to proliferate on its own
- Progression – acquisition of new genetic features.
- Clonal expansion
Viral carcinogens
- DNA viruses
- RNA viruses
A. Acute- or slow- transforming
B. Retrovirus
C. Etc.
DNA viruses.
Become directly integrated into cell’s genome.
HPV
Epstein-Barr
Hep B
Epstein Barr Virua
Human herpes DNA virus with predilection for B-cells
May produce infectious mononucleosis
Related to Burkitt’s lymphoma (B cell neoplasia) and nasopharyngeal cancer.
Human T cell lymphoma/leukemia virus 1 (HTLV)
RNA retrovirus
Causes rare form of adult T cell leukemia.
Proto-oncogenes
Normal cellular genes that can be transformed into oncogenes by four factors:
- Point mutation
- Gene amplification
- Chromosomal rearrangement
- Insertion of viral genome. (Typical of slow transforming RNA viruses. Also hep B)
Tumour Supressor Genes
Regulatory mechanism that protect against activated or newly acquired oncogenes.
Cachexia
Wasting. May be a symptom of cancer
Paraneoplastic syndromes
Consequence of Cancer that isn’t a direct effect of cancer. Caused by substances secreted by cancer cells.
Cushing’s syndrome
Paraneoplastic syndrome.
May be caused by small cell carcinoma of the lung which also causes adrenal over activity.
Hypercalcemia
Paraneoplastic syndrome
Squamous cell carcinoma of lung (or breast cancer) may result in weakening of the bones.
Polycythemia
Pathological increase in red blood cells
May be paraneoplastic effect of renal cell carcinoma.
Venous thrombosis can be a paraneoplastic effect of
Pancreatic cancer
Incidence
The number of new cases in a certain population over a specific period.
Prevalence
The number of cases – old and new – in a given population at a certain time.
