1. Introduction to Cancer
Definitions
Naming
Benign vs. Malignant
Hallmarks of cancer

2. Define Neoplasm
Abnormal growth of cells which persists after initial stimulus has been removed Or
Cell growth which has escaped from normal regulatory mechanisms
Is it benign or malignant?
- Can be either!

3. Define Benign Neoplasm
Cells which grow as a compact mass and remain at the site of origin

4. Define Malignant Neoplasm
Growth of cells is uncontrolled
Cells can spread to surrounding tissue and to distant sites

5. Define Dysplasia Pre-Malignant Condition Describes:
Increased Cell Growth
Altered Differentiation
Cellular Atypia
Common Sites = Cervix, Bladder, Stomach and Oesophagus
Cervical Dysplasia can be caused by Human Papilloma Virus (HPV)
Bladder Dysplasia – Urothelial Dysplasia which can lead to Transitional Cell Carcinoma

6. Define Differentiation
The degree of similarity of tumour cells to the structure of the organ from which the tumour arose
Well differentiated cancer cells look more like normal cells and tend to grow and spread more slowly (low grade)

7. How to Name a Neoplasm Originating Tissue Benign Malignant Bone
Osteoma
Osteosarcoma
Smooth Muscle
Leiomyoma
Leiomyosarcoma
Cartilage
Chondroma
Chondrosarcoma
Fat
Lipoma
Liposarcoma
Nerve
Nurofibroma
Neurofibrosarcoma
Nerve Sheath
Neurilemmoma
Neurilemmosarcoma
Fibrous Tissue
Fibroma
Fibrosarcoma
Squamous Epithelium
Papilloma
Squamous cell carcinoma
Transitional Epithelium
Transitional cell carcinoma
Glandular Epithelium
Adenoma
Adenocarcinoma
Skin Melanocyte
Naevus
Malignant melanoma

8. Match each benign neoplasm with its connective tissue origin
Bone
Neurofibroma
Smooth Muscle
Lipoma
Fat
Osteoma
Benign Connective Tissue Neoplasm always has the suffix = oma
Exception to the rule = Glioma – as they are malignant
Malignant Connective Tissue Suffix = Sarcoma
Fibrous Tissue
Leiomyoma
Nerve
Fibroma

9. Describe the Behaviour of Neoplasms
Benign
Malignant
No invasion
No metastasis
Retains function
Variable growth rate, often low
Invades
Metastasises
Lose function
Variable growth rate, may be high

10. Can you describe the Macroscopic differences of neoplasms
Benign
Malignant
Capsule
Well defined edge
Ill-defined margin
Haemorrhage
Necrotic Centre

11. Can you describe the Microscopic differences of neoplasms
Benign
Malignant
Low mitotic count, normal mitoses
Retention of specialisation
Organised
Structural differentiation retained
Low to high mitotic count, abnormal mitoses
Loss of specialisation
Unorganised
Structural differentiation has wide range of changes

12. What are the 10 Hallmarks of Cancer?
Oncology at a Glance, First Edition. Graham G. Dark. © 2013 John Wiley & Sons, Ltd. Published 2013 by John Wiley & Sons, Ltd.

13. 10 Hallmarks of Cancer Mnemonic
Immune System Evasion
Invasion and Metastasis
Inducing Angiogenesis
Genomic Instability
Tumour-promoting Inflammation
Metabolism Reprogramming
Sustaining Proliferative Signalling
Replicative Immortality
Resisting Apoptosis
Growth Suppressor Evasion

14. What Happens First?
Genomic Instability
Metabolism Reprogramming
Multistep genetic mutations occur, each enabling further clonal expansion of pre-malignant cells
In cancer cells, the accumulation of mutations goes unchecked and therefore, these cells are more sensitive to mutagenic actions
To sustain proliferation, cancer cells make adjustments to their energy production by:
Reprogramming their glucose metabolism
Upregulating glucose transporters such as glucose transporter 1 (GLUT1)
Depending on alternate metabolic pathways

15. How Does It Survive?
Sustaining Proliferative Signalling
Growth Suppressor Evasion
Healthy tissues regulate growth-promoting signaling pathways, which are responsible for driving progression of cells through the cell cycle.
These signaling mechanisms are deregulated in cancerous cells.
Tumour suppressors (Rb and TP53) halt cell cycle progression if excessive genome damage occurs
Cancer cells are able to proliferate independantly of these signals

16. How Does It Survive?
Replicative Immortality
Tumour Promoting Inflammation
Normal cells are able to divide a finite no. of times and then cell division is blocked
Cancer cells overcome this by over-expressing telomerase, an enzyme that maintains telomere length, which protects the ends of chromosomes and allows the cell to continue proliferating.
Tumour-associated inflammation may aid in tumour growth by supplying the tumour microenvironment with:
Growth Factors
Pro-Angiogenic Factors
Survival Factors

17. How Does It Survive?
Resisting Apoptosis
Immune System Evasion
All cancer cells dysregulate 2 signalling pathways by:
Overexpressing anti-apoptotic proteins
Silencing pro-apoptotic proteins
Also resist cell death by altering normal cellular autophagy and necrosis
Immune surveillance is an essential cellular process that proactively prevents tumor formation in the human body. Preclinical studies have suggested that an active immune system continuously recognizes and eliminates the vast majority of cancer cells before they establish themselves and form a tumor mass.
However, cancer immunoediting, an emerging hallmark, includes 3 key phases — elimination, equilibrium, and escape.
The immune system successfully recognizes and eliminates cancer cells, a process often described as the elimination phase. Tumor cells not eliminated by the immune system proceed to the equilibrium phase, in which the immune system controls cancer cell growth but does not completely eliminate the transformed cells. Tumor cells not susceptible to immune destruction progress into the escape phase. In this phase, the “escaped” tumor clones—not effectively detected and destroyed by the immune system—continue to divide and grow

18. How Does It Thrive? Infiltration of nearby blood and lymphatic vessels
Invasion and Metastasis
Inducing Angiogenesis
Infiltration of nearby blood and lymphatic vessels
Cancer cells are transported to non-contiguous tissues (forming metastatic lesions)
Development of new blood vessels
All cancers require a vascular network to supply nutrients and remove waste
VEGF and PDGF are key players