Oncology- Nursing VI

1. Oncology- Nursing VI Dilum Weliwita B.Sc. Nursing(U.K.)

2. The biology of cancer

3. This session....... Questions to answer • How do cancers Arise? • What is the differences between normal and abnormal cell changes? • What are the biological processes involved? • What are cancer ‘promoters’? • How do cancer advance and disrupt body function

4. Oncology defined • Branch of medicine that deals with the study, detection, treatment and management of cancer and neoplasia

5. What is neoplasia? • Neo- new • Plasia- growth

6. What is cancer?

8. Cancer • Set of diseases. • Abnormal growth of cells. • Regulation of cell growth and maturity is disturbed • Ability to invade adjacent tissue and even distant organs. • Many different types of cancer

9. Cont.... • Same cancers can also behave differently • Eventual death of the affected patient if tumor has progressed beyond the stage when it can be successfully removed

10. Cont..... • Changes in cell and development are governed by genetic control • Genetic alterations: a multistep process

11. Cancer Terminology • Cancer - A group of diseases • Anaplasia - Lack of differentiation • Dysplasia - Abnormal size, shape • Hyperplasia - Increase in number of cells

12. Start from a cell...... • ‘Where a cell arises, there must be a previous cell, just as animals can only arise from animals and plants from plant.......’ • Virchow, 1858

13. Cell structure

14. Nucleus- information • Mitochondria- power • Cytosol- molecule and chemical soup • Golgi apparatus- processing and packing • Lysosomes- digestion • Vesicles- transporters • Cytoskeleton- movement and structure

15. Different cells...... Diffrent jobs • Diverse range of cells • Size and structure depends on its job • Think about the structure of sperm, bacteria, nerve cell, neutrophils

16. But .......... • cells have similarities..... Such as the storage of genetic instructions ( genes) in DNA molecules

17. DNA • DNA is the cell’s blueprint • Chemical building blocks • Carrier of genetic information • Located in chromosomes • Each cell’s nucleus has 23 pairs • Duplicated to pass on genetic information to daughter cells

18. Genes • Segment of DNA • Determines the structure and job of a protein for development, growth, chemical function • Each gene tells a cell to make a different protein

19. Genes--------- ‘ on ‘------ RNA--------information to make new proteins • Protein maybe structural, hormone, growth factors, inhibitors, regulators

20. Process of cell division • Response to a signal • E.g. Hormonal signals in blood loss • growth factor (erythropoetin) produced in the kidney circulates in the bloodstream to tell bone marrow to manufacture more blood cells

21. Cell Division • Mitosis • A type of cell division that result in two daughter cells each with same number as chromosomes as the parent

22. Meiosis • cell division that results in daughter cells with half the chromosome number of the parent e.g. Eggs and sperm

24. Hyperplasia

25. Dysplasia

26. Carcinoma in Situ

27. Tumor Development

28. Cell cycle check points • G1: • is the cell big enough? • is the environment favourable? • is DNA damaged? • G2: • is all DNA replicated? • is the cell big enough?

29. Cellular behaviour • All these events are responses to social controls and signals from chemical or other cells: • Cell division • Cell differentiation (specialisation) • Cell proliferation (rate of division ) • Cell senescence (limits) • Cell survival • Programmed cell death

30. i.e. To regulate cell development only when it is needed

31. Cancer cells • Cancer cells ignore the signals and social controls • Characteristics: • Reproduce in defiance of the normal constraints • Invade and colonize territories normally reserve for other cells

32. Can grow even as far as outstripping their blood supply and destroying the host • Difference between benign and malignant?

33. Benign Tumor • Characteristics typical of tissue of origin • Slow rate of growth • Slowly progressive; Not fatal if untreated • Encapsulated growth • No tissue destruction • Rare recurrence • Poor prognosis only if unable to remove

34. Malignant Tumor • Characteristics atypical of tissue of origin • Slow or rapid rate of growth • Usually progressive; Fatal if untreated • Growth by infiltration or metastasis • Tissue destruction is common • Recurrence is common • Fatal prognosis if uncontrolled

35. Features of cancer cells • Immortality: • - Do not have limits on cell cycle (does not enter senescence) • Possible diminished requirements of growth factor • Loss of ‘point of no return’ in cell cycle • - End of G1 related to the ‘ brake’ protein pRb – activated by cyclin and a cyclin dependant kinase (cdk) • Cancer cells may lack enough pRb

36. Differences in cell structure • Change in cell surface and membrane • Changes in glycoproteins • -changes of cell adhesion, contact inhibition, loss of growth control, and apoptosis • Changes in cell surface antigens • - Tumour antigens • Increased nutrients uptake

37. Differences in differentiation • Cells have same DNA content • But.... Only section of it is expressed for different structure and function • i.e. A distinct ‘personality’ • The more differentiated a cell , the more specialised • Cancer cells are less differentiated from surrounding normal tissue....

38. The transition to Malignancy • They may be..... • -Metaplastic ( mildly less differentiated) • -Dysplastic(deranged cell growth) • -Carcinoma insitu ( cancer in place with no extension or spread) • -Invasive cancer

39. Carcinoma

40. Adenoma

42. Remember some cancers so poorly differentiated- difficult to ascertain the origin

43. The Causes of Cancer: Role of DNA • DNA mutations and cancer • A mutated gene no longer contains the proper code for producing its protein • Oncogene= gene involved in the transformationof a normal cell into acancer cell • Cancer promoters = compounds that accelerate cell growth

44. A genetic disease...... • Two types of genetic mutations

45. Oncogenes • Mutation of the proliferation gene ( proto- oncogene) • This gene encourages cell division • DNA alteration (e.g. Due to exposure to chemical carcinogen) • Result in hyperactive cell multiplication ( accelerated) without regard to the usual cell cycle regulation or apoptosis

46. Tumour suppressor gene mutation • Mutation of a ‘ tumour suppressor gene’ • E.g. An antiproliferation gene ( a TSG ) which controls cell multiplication • Mutation of this may result in no restraints (brakes) on proliferation and cell multiplication is out of control

47. TSG mutations are often called recessive mutations • Each cell has a pair of TSG’s on each chromosome • Both need to be inactivated for a cancer to develop • Important in genetic mapping, inherited cancer • E.g. In a carrier – one gene is mutated already , but the other needs to be lost for a cancer to develop

48. Genetic Regulation • Oncogenes/Proto-Oncogenes • normal exons which when mutated promote oncogenesis • wt = proto-oncogene (no tumor promoting effect) • mutant = oncogene • Tumor Suppressor Genes • Genes which regulate cell proliferation and prevent cell from dividing ‘out of control’ • wt = ‘prevent’ cell from becoming a tumor • mutant = unable to prevent tumor-genesis

49. Gatekeeper Genes(Vogelstein & Kinzler) • Genes that produce proteins to directly regulate tumour growth • Inhibit mitosis • Promote apoptosis • E.g. APC, p53

50. Caretaker Genes • Genes that maintain the integrity of the genome • Inactivation leads to genetic instability and directly promotes tumour growth by causing increased mutation • E.g. BRCA1 with heredity breast and ovarian cancers