The document discusses several key aspects of cancer at the cellular level and genetics. It notes that normal cells have controlled growth, while cancer cells have uncontrolled growth and do not respect tissue boundaries. The document also outlines several theories of carcinogenesis, such as cellular transformation and genetic mutations. Genetics play a role through oncogenes, tumor suppressor genes, and DNA damage. Carcinogens like viruses, chemicals, radiation, and genetics can also influence cancer development.

1. Cellular
Aberrations

2. NORMAL CELL CANCER CELL
Have limited cell division Cell division is rapid
Undergo apoptosis
Partial or complete
differentiated function of
parent cell is lost
Show specific morphology
Have a small nuclear-
cytoplasmic ratio
There is a large nucleus-
cytoplasm ratio
Are no migratory/
nonmigratory Cells can migrate

3. Adhere tightly together Cells are loosely adherent
Grow in an orderly and well-
regulated manner
Growth rate is not well
regulated
Cells recognize or respect
tissue borders
Cells do not recognize or
respect tissue borders
Cells are contact inhibited Cells are not contact inhibited
NORMAL CELL CANCER CELL

8. 5 THEORIES OF CARCINOGENESIS
1. Cellular Transformation and Derangement
Theory
2. Failure of the Immune Response Theory
3. Genetic Code
4. The Somatic Mutation Theory (SMT)
5. The Tissue Organization Field Theory (TOFT)

9. GENETICS and Cancer
1. Carcinogen
- any substance, situation, or exposure that can
damage genetic material (DNA)
2. Oncogene
- genetic material that carries the ability to
induce cancer.
3. Proto-Oncogene
- a normal gene that has the potential to
transform itself into an oncogene.

10. GENETICS and Cancer
4. Tumor Suppressor Gene
- are a family of normal genes that instruct cells
to produce proteins that restrain cell growth and
division.
5. P53 Gene
- are a family of tumor suppressor gene that
trigger apoptosis.
6. DNA Repair Gene
- are a code for proteins whose normal function is
to correct errors that arise when cells duplicate
their DNA prior to cell division.

11. Differentiation

12. Related Terminologies
Carcinogen
Genotoxic
Promoter substance
Carcinogenesis
Oncogene
Tumor
Benign/Malignant
Secondary Tumor
Neoplasia
Neoplasm
Mutation
Oncology
Oncologist
Remission
Genetic testing

13. Dysplasia
the presence of cells of an abnormal type within a
tissue, which may signify a stage preceding the
development of cancer.

14. the enlargement of an organ or tissue caused by an
increase in the reproduction rate of its cells, often as
an initial stage in the development of cancer.
Hyperplasia

15. abnormal change in the nature of a tissue.
Metaplasia

16. is a condition of cells with poor cellular differentiation,
losing the morphological characteristics of mature cells
and their orientation with respect to each other and to
endothelial cells.
Anaplasia

17. Carcinogenesis
a process by which normal cells are transformed into
cancer cells

18. The Carcinogenesis Process
1. Initiation - irreversible mutation of a gene,
that leads to a malignant transformation
2. Promotion - cell becomes malignant; the
promoting agent stimulates the growth and
division of cell
3. Progression - refers to a series of changes
that lead to the characteristics of an
undifferentiated cell.

23. Metastasis
Types:
1. Transcoelomic
2. Lymphatic spread
3. Hematogenous
spread
4. Canalicular spread

24. Hematogenous
spread of tumor
cells involves
many steps.

27. Carcinogens

28. A. Viruses or Oncogenic
Prolonged and recurrent viral infections may lead to
the breakdown of the immune system. The
overwhelmed immune system may fail to destroy the
cancer cells present in the body. The human
papillomavirus
1. Human Papilloma Virus (HPV) are particularly
common cancer-causing virus which is well-known for
causing genital warts and all cases of cervical cancer.

29. 2. Epstein-Barr Virus
3. Cytomegalovirus
4. Hepatitis Virus
5. HIV
6. Helicobacter Pylori
7. Human T-cell
Lymphotropic Virus

30. B. Chemical Carcinogens
These chemicals cause cell mutation or alter the cell
enzymes and proteins.
1. Industrial Compounds
• Vinyl chloride – plastic manufacture, asbestos
factories, construction works
• Polycyclic aromatic hydrocarbons
• Fertilizers

31. • Weed killers
• Dyes – analine dyes (most commonly found in
beauty shops and used at homes), hair bleach
• Drugs – cytotoxic drugs, tar nicotine in
tobacco, alcohol

32. Estrogen
Diethystilbesterol (DES)
Foods, preservatives
Nitrites in bacon or smoked
meat
2. Hormones

33. Talc (polished rice, salami and chewing gum)
Food sweeteners
Nitrosomines (rubber baby nipples)
Aflatoxins (mold in nuts, grains, milk, cheese and peanut
butter)
Polycyclic hydrocarbons

34. C. Physical Agent
1. Radiation
• From x-rays or radioactive isotopes
• From sunlight or UV rays

35. 2. Physical Irritation or Trauma
• Pipe smoking
• Multiple deliveries

36. D. Genetics
Risk Factors:
Older individuals
Women are more prone to breast, uterine and
cervical cancer
Men are more prone prostate and lung cancer
Urban dwellers
Chemical factory workers
Farmers
Personnel of radiology department
Obesity
Stress

37. Family History
Hallmark of families with hereditary cancer
syndrome:
a. cancer in two or more relatives.
b. cancer in family members younger than 50
years old.
c. same type of CA in several family
members/family member with more than one
type of CA.
d. a rare cancer in one or more family members.

39. E.Immune Function

41. T-lymphocytes or T-cells
Roles and functions
1. Killer T cells
2. Helper T cells
3. Regulatory T cells or Tregs
4. Memory T cells
5. Natural killer T cells

43. B lymphocytes or B cells
Roles and functions
Memory B cell
Regulatory B cells

49. Gene Mutations

50. Tumor
Suppressor
Gene
gene that protects a
cell from one step on
the path to cancer.
When this gene
mutates to cause a
loss or reduction in its
function, the cell can
progress to cancer,
usually in combination
with other genetic
changes

54. Proto-oncogenes
A proto-oncogene is a normal gene
that could become an oncogene due to
mutations or increased expression.
Proto-oncogenes code for proteins that
help to regulate the cell growth and
differentiation.

56. Predisposing Factors
1. Age
2. Gender
3. Geographic Locations
4. Occupation
5. Heredity
6. Stress
7. Precancerous Lesions
8. Health Practices

57. • Benign Tumor
• Potentially-Malignant Neoplasms
• Malignant Neoplasms
• Secondary Neoplasm
• Cancer of unknown primary origin
TYPES OF NEOPLASM

58. BENIGN MALIGNANT
1. Differentiation Well-
differentiated
Undifferentiated
2. Encapsulation capsulated uncapsulated
3. Metastasis (-) (+)
4. Prognosis good
5. Therapeutic Surgery
BENIGN VS MALIGNANT

60. 1. Carcinoma
2. Sarcoma
3. Lymphoma
4. Leukemia
5. Myeloma
Categories Of Neoplasm