Principles of neoplasia Flashcards
Define neoplasia and briefly explain how they start. Talk about the suffixes used to class neoplasias as benign or malignant
- It is the presence or formation of new, abnormal growth of tissue (aka tumour)
- Neoplasms may be benign (not cancer), or malignant (cancer)
- Neoplasms occur due to genetic damages. These can be either inherited or acquired mutations
- Neoplasia’s that are benign usually end in the suffix of “oma”
- Malignant neoplasms usually end with “carcinoma” or “sarcoma”
List the nomenclature used to classify neoplasms
Neoplasms are classed by three things:
- Malignancy (or benign)
- Architectural growth pattern
- Texture
Define sarcoma and carcinoma
Carcinoma
• Malignant neoplasm of epithelial linings
• Affects organs or glands capable of secretion, such as the breasts, which produce milk, or the lungs, which secrete mucus, or colon or prostate or bladder.
Sarcoma
• Originates in supportive and connective tissues such as bones, tendons, cartilage, muscle, and fat.
Describe nomenclature in terms of its prefix of architectural growth pattern
○ Follicular (forming follicles)
○ Cyst (forming cystic spaces)
○ Papillary (form projections)
○ Cribriform (pierced by small holes)
Describe nomenclature in terms of its prefix of texture
○ Medullary (soft like marrow)
○ Colloid (gelatinous, mucinous)
○ Scirrhous (hard)
Differentiate the benign and malignant neoplasms in terms of:
○ rate and mode of growth
Benign:
• Grows slower
• Compresses surrounding tissue into a capsule that separates the tumour from normal tissue
Malignant
• Grows quickly
• Not confined
• Have the ability to produce enzymes that dissolve the native tissue = invasiveness
Describe malignant neoplasms in terms of invasion and metastasis
Malignant tumours are:
· Invasive: invade surrounding tissues and organs by dissolving them with enzymes
· Metastatic: spread to distant organs (though not always)
List the methods of metastasis for malignant neoplasms, particularly
· Carcinoma
· Sarcoma
And define traumatic seeding
· Haematogenous dissemination (through blood): Sarcomas
· Lymphatic dissemination (through lymph nodes): Carcinoma
Traumatic seeding:
· Dislodgement of neoplastic cells from a tumour during biopsy or surgical interventioninto surrounding tissues. This happens since tumour cells lack cell to cell cohesiveness
List the histological features of benign tumours in terms of:
· Degree of cell differentiation
· Overall cell appearance
· Amount of mitotic figures
· Nuclei chromatism (amount of nuclei staining)
· Amount of cell nuclei
· Border/ outline
· Effect on tissue
· Stroma (spongy, colorless matrix of a cell that functionally supports the cell)
Degree of cell differentiation:
• Well differentiated
Overall cell appearance:
• Uniform appearance
Amount of mitotic figures:
• Few mitotic figures
Nuclei chromatism:
• Normal nuclear chromatism
Amount of cell nuclei
• Uni- nuclear
Border/ outline
• Well defined and encapsulated
Effect on tissue
• Displacement of adjacent tissue
Stroma:
• Stroma well formed
List the histological features of malignant tumours in terms of:
· Degree of cell differentiation
· Overall cell appearance
· Amount of mitotic figures
· Nuclei chromatism (amount of nuclei staining)
· Amount of cell nuclei
· Border/ outline
· Effect on tissue
· Stroma (spongy, colorless matrix of a cell that functionally supports the cell)
Degree of cell differentiation:
• Poorly differentiated
Overall cell appearance:
• Cells are pleomorphic (each cell differs in size, shape and nuclei)
Amount of mitotic figures:
• Frequent mitotic figures (due to high cell division)
Nuclei chromatism:
• Hyperchromatic nuclei
Amount of cell nuclei
• Mutli- nuclear
Border/ outline
• Ill- define
Effect on tissue
• Replacement of adjacent tissue
Stroma:
• Stroma inadequate
List the clinical features of benign tumours in terms of: • Extent of growth • Effect on tissue • Rate of growth • Degree of movement • Consistency (hardness) • Necrosis • Haemorrhagic • Paraneoplastic syndromes (rare disorders that are triggered by an altered immune system response to a neoplasm)) • Neural involvement • Pain
Extent of growth
• Localised
Effect on tissue
• Displacement
Rate of growth
• Slow
Degree of movement
• Immobile
Consistency (hardness)
• Soft
Necrosis
• No
Haemorrhagic
• No
Paraneoplastic syndromes (rare disorders that are triggered by an altered immune system response to a neoplasm)) • No
Neural involvement
• No
Pain
• No
List the clinical features of malignant tumours in terms of: • Extent of growth • Effect on tissue • Rate of growth • Degree of movement • Consistency (hardness) • Necrosis • Haemorrhagic • Paraneoplastic syndromes (rare disorders that are triggered by an altered immune system response to a neoplasm)) • Neural involvement • Pain
Extent of growth
• Generalised due to metastasis
Effect on tissue
• Replacement
Rate of growth
• Fast
Degree of movement
• Mobile
Consistency (hardness)
• Very hard/ indurated
Necrosis
• Yes, and ulcerated
Haemorrhagic
• Yes
Paraneoplastic syndromes (rare disorders that are triggered by an altered immune system response to a neoplasm)) • Yes
Neural involvement
• Yes, leads to paraesthesia or anaesthesia
Pain
• Yes, as a late event
Discuss the molecular pathogenesis of cancer and understand the role of tumour suppressor gene using p53 as an example
- Tumour suppressor gene P53 is agene that codes for a protein that regulates the cell cycle and hence functions as a tumour suppression
- In normal cells, the p53 protein level is low. DNA damage and other stress signals may trigger the increase of p53 proteins
- The p53 protein has three major functions:growth arrest,DNA repairandapoptosis
- In growth arrest, the progression of cell cycle is stopped, thus preventing replication of damaged DNA
- During the growth arrest, p53 may activate the transcription of proteins involved in DNA repair
- Apoptosis is the “last resort” to avoid proliferation of cells containing abnormal DNA
- The cellular concentration of p53 must be tightly regulated. While it can suppress tumours, high level of p53 may accelerate the aging process by excessive apoptosis
- Inactivation of p53 leads to proliferation and a predisposition to neoplasia
List risk factors for developing neoplasia/ cancer
- Radiation - UV light induces skin cancers
- Chemicals/carcinogens
- Polycyclic hydrocarbons
- Aromatic amines
- Asbestos
- DNA viruses: human papilloma virus – genital warts, cervical carcinoma, oropharyngeal cancer; hepatitis B and C viruses – hepatocellular carcinoma
- RNA viruses: human T-cell leukaemia virus; HIV
- Hormones. For examples, low oestrogen = breast cancer, endometrial cancer
- Chronic inflammation
List the health effects neoplasms can have
• Growth of a mass can impinge upon critical organ and tissue
• Ulcerations
• Cachexia/wasting syndrome –Anorexia and a progressive loss of adipose tissue and skeletal muscle mass (seen late stages of almost all major chronic diseases like COPD, CKD)
• Paraneoplastic endocrine syndromes: Tumour production of hormones or peptides that lead to metabolic derangements
• Invasion of a nerve can lead to neurologic deficits or pain.
○ Brain = seizures
○ Colon = constipation, bleeding
○ Bone destruction = fracture
