1. Mylene Freires Advanced Nurse Practitioner, Haematology
Overview of Cancer
Mylene Freires
Advanced Nurse Practitioner, Haematology

2. Aim of the Presentation
Review basic concepts of cancer
Gain some understanding of the socio-economic impact of cancer

3. Order of Presentation:
A. Global Cancer Statistics and in the UK
B. Cancer Basic Concepts
C. Grading, Risk Factors and Genetics
D. Diagnosis and Staging
E. Prognosis and Treatment

4. Why is Cancer everyone’s business?
Personal reasons
Professional reasons
Socio-economic impact

5. A. Worldwide Cancer Statistics:
In 2012,
14.1 million of new cases worldwide
8.2 million deaths worldwide
33% are linked with smoking; 6% alcohol drinking prevalent in Europe and America
Higher in males then females

6. UK statistics:
< X X
Survivors in 10 years

7. UK statistics,2015 New cases 359,960 More males than females
Deaths 163,444
Only 50% survive cancer for 10 years or more
42% of Cancers are preventable
More males than females
Incidence rates are highest in people aged 85 to 89

8. Most common cancers: Lung -1/5 of all cancer deaths Bowel Prostate
Breast

10. Financial Impact to Economy:
Loss of people from the labour force
50,000 deaths = £585 million loss and across their lifetime = £6.8 billion

11. Financial Impact to: Families and communities: Loss Caregivers
Loss or Reduced Income =£570- £860/month
Increased costs related to inpatient and outpatient attendances
Loss of Vital volunteers
£236 million/year

12. Cancer Survivors:

13. Cancer Survivors’ estimated contribution:
1.8 million survivors = £6.9 million contribution through paid employment
Informal care = 258 million hours
Volunteering = 52 million hours
Domestic work = 1.5 billion hours

14. Financial Cost £16.7 billion
Cancer Survivors’ social contribution is estimated at:
£16.7 billion

15. B. Cancer Basics:
What is Cancer?

16. Cell Cycle

17. Phases of cell cycle G1, S & G2 Known as the interphase
Cells spend more time in interphase than mitosis
At each phase there are check points, if conditions are right proteins determine whether enter into the next phase
If conditions not right will stay in GO Phase ( resting phase)

18. G0 Known as the resting phase . The cell is not currently in it’s cycle.
G1 Cell increases in size checkpoints occur prior to Synthesis
Synthesis The cell replicates
G2- The gap between synthesis and mitosis another checkpoint prior to mitosis

19. Mitosis ( Also known as cell division)
Cell growth stops and cells divide into 2 daughter cells.
Goes through 4 phases during this phase
Prophase
Metaphase
Anaphase
Telophase
Cytokinesis

20. What is Cancer? Is a collection of related disease.
A complex disease with variable presentation, development and outcome from one patient to another.
It is a multi-step process- involving cellular metabolic and behavioural changes leading to untimely and excessive proliferation.
Cumulative modifications in the genetic programmes that control cell proliferation, lifespans and the ability to escape the immune system.

21. Why cells become malignant?

22. Three Conditions In Cancer Transformation:
cells should proceed to divide only when they receive appropriate signals
when confronted by stressful or improper conditions for DNA replication, cells activate self-destruction programmes rather than allow DNA replication to proceed in conditions where genes may become damaged
normal cells divide only a limited number of times

23. Genetic Drivers in Cancer:
Proto-oncogenes- (KRAS)
Proto-oncogenes are genes that normally helps cells grow. They help regulate cell growth. However, proto-genes can mutate or if there is a change in their dna sequence, they change they can become oncogenes. When this happens, this leads to unregulated cell division, a slower rate of cell differentiation and increased inhibition of cell death. Together, these features define cells that have become cancerous.
Tumour suppressor genes act as braking signals during phase G1 of the cell cycle, to stop or slow the cell cycle before S phase. If tumor-suppressor genes are mutated, the normal brake mechanism will be disabled, resulting in uncontrolled growth, i.e. cancer.
DNA repair genes code for proteins whose normal function is to correct errors that arise when cells duplicate their DNA prior to cell division.
DNA repair genes are active throughout the cell cycle, particularly during G2 after DNA replication and before the chromosomes divide.
Mutations in DNA repair genes can lead to a failure in repair, which in turn allows subsequent mutations to accumulate.

24. Tumour suppressor genes (TP53 and RB1)

25. DNA Repair Genes

26. Cells become cancerous due to the accumulation of defects, or mutations, in their DNA
Certain inherited genetic defects (for example, BRCA1 and BRCA2 mutations) and infections can increase the risk of cancer.
Environmental factors (for example, air , pollution , poor life style choices eg smoking alcohol can increase cancer

27. Sources of DNA Damage:

28. Cancer occurs when when certain cells in the body keep dividing without the ability to stop
Feeds off the body ( contributes to weight loss)
Carcinogenesis- or oncogenesis or tumorigenesis is the actual formation of a cancer, whereby normal cells are transformed into cancer cells. The process is characterized by a progression of changes at the cellular, genetic, and epigenetic level that ultimately reprogram a cell to undergo uncontrolled cell division, thereby forming a malignant mass.

30. Types of Cancers: Haematological Malignancies Solid tumours Carcinoma
adenocarcinoma
basal cell carcinoma
squamous cell carcinoma
transitional cell carcinoma
Sarcoma
Melanoma
Brain and Spinal Cord Tumours
Other Tumours: germ cell tumours
Leukaemias
Lymphomas
Multiple Myelomas
Carcinoma from epithelial cells; adenocarcinoma from those producing fluids or mucus; basal cell; lower layer of the epidermis; squamous cell those that lie beneath the outer surface of the skin; transitional cell those that can get bigger and smaller i.e bladder, ureters, kidneys
Sarcomas form from bone and soft tissues, including fat, muscles blood vessels
Melanoma from melanocytes or melanin

31. C. Grading Tumours: Well-differentiated tumours
Poorly differentiated or “undifferentiated”
Assigned with numerical grade and is not the same as cancer staging Or
Grade 1
Grade II
Grade III

32. D. Cancer Staging:
Refers to the location and extent of the tumour spread
4 Factors:
Location of Primary tumour
tumour size and extent
Lymph node involvement
Presence or absence of metastasis

33. TNM staging system N : number of nearby lymph nodes with cancer
T : size and extent the main tumour
N : number of nearby lymph nodes with cancer
M : metastasized
Numbers after each letter provides more details
e.g: Primary tumour (T)
TX: main tumour cannot be measured
T0: main tumour cannot be found
T1, T2 etc: refers to the size and/ or extent of main tumour

34. Regional Lymph Nodes:
NX: cancer in lymph nodes cannot be measured
N0: No cancer in nearby lymph nodes
N1, N2, N3: Number and location of lymph nodes with cancer;
Distant Metastasis: (M)
MX: metastasis cannot be measured
M0: cancer has not spread
M1: Cancer has spread

35. Stage Meaning Stage 0 Stage I, II and III Stage IV
Abnormal cells are present but not spread nearby tissue i.e CIS
Cancer is present. The higher the number, the larger the cancer tumour and spread
Cancer has spread to other parts

36. Other staging categories:
In situ
Localised
Regional
Distant
Unknown
Abnormal cells but have not spread Limited to the place where it started with no sign of spread Has spread to nearby lymph node, tissues or organs Has spread to distant parts of the body Not enough information

37. E. Prognosis in Cancer: “prediction about a patient’s future”
Refers to the likelihood of response to treatment and survival

38. Factors affecting Prognosis of Cancer:
The type of cancer and where it is in
The stage of the cancer, which refers to the size and if it has spread
The cancer’s grade, which refers to how abnormal the cancer cells look under a microscope. Grade provides clues about how quickly the cancer is likely to grow and spread.
Certain traits of the cancer cells
Age and fitness before cancer
Response to treatment

39. F. Treatments for Cancer:
Chemotherapy
Surgery
Radiation Therapy.
Immunotherapy.
Targeted Therapy.
Hormone Therapy.
Stem Cell Transplant.
Precision Medicine

40. Thank you.

41. Resources: National Cancer Institute Cancer Research UK
UK Statistics office
Macmillan