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Flashcards in Neoplasia Deck (71):
1

Neoplasia

New Growth

2

Tumor

abnormal growth of tissue

3

Oncology

Study of Cancer

4

Dysplasia

Reversible,abnormalgrowthordevelopmentoftissue,organsor cells

5

Anaplasia

Irreversible, reversion of cells to an immature or a less differentiated form

6

PARENCHYMA

Anaplastic Cell

7

Stroma

Connective tissue of a tumor. Very well supplied with blood vessels. Has angiogenic properties.

8

Mesenchymal Cells vs Epithelial Cells (Nomenclature)

Mesenchymal cells
a. Benign – “oma” suffix
b. Malignant – “ sarcoma” suffix
Epithelial cells
a. Benign – “oma” suffix
b. Malignant – “carcinoma” suffix

9

Exemptions to nomenclature rule (7)

Lymphomas – lymphoid cells
• Gliomas – glial cells
• Seminomas – testicular seminferous epithelium
• Blastomas – embryonic cells
Retinoblastomas – retina Hepatoblastomas – liver Nephroblastomas – kidney
• Teratomas–germcells

10

Benign vs Malignant Tumors

Benign:
Small
Demarcated
Localized
Slow Growth
Non Invasive
Non Metastic
Well Differentiated
No loss of Function
Doesn't move

Malignant:
Large
Poorly demarcated
Rapidly growing with hemorrhage and necrosis
Fast Growth
Locally Invasive
Metastic
Poorly Differentiated
Loss of Function
Moves (to brain)

11

Metastasis

transmission of pathogenic microorganism or cancerous cell from an original
site to one or more sites in the body

12

Mechanism of metastasis (3)

a. Seeding of body cavity
b. Lymph system
c. Hematogenous spread

13

Most used system for metastasis

Hematogenous spread

14

Ways to describe Cancer

Tumor staging & Tumor grading

15

Tumor Staging Stage 0

Carcinoma in situ

16

Tumor Staging Stage 1

tumor is localized, small (less than 2 cm) and has
not spread to the lymph nodes

17

Tumor Staging Stage 2

tumor has invaded the tissue, may have spread into the lymph nodes, larger in size (2-5 cm)

18

Tumor Staging Stage 3

tumor has spread into the lymph nodes and locally more advanced

19

Tumor Staging Stage 4

tumor has metastasized to other organs

20

Tumor Staging

Based on tumor size and lymph node involvement

21

Tumor Grading

Based on cell differentiation

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Grade I

(Low grade) Cancer cells are well differentiated and slow growing

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Grade II

(intermediate grade) cancer cells look only moderately differentiated and grow faster than cell at grade I

24

Grade III

(high grade) cancer cells are poorly differentiated and aggressively spread

25

Grade IV

( high grade) cancer cells undifferentiated

26

Steps of Carcinogenesis

Procarcinogen carcinogen
• Initiation – carcinogen acts on DNA to
induce irreversible genetic change
• Promotion – cells are stimulated to proliferate
• Conversion – genetically altered cells have ability to proliferate on their own and are giving rise to a new cell type
• Progression – expression of new genetic features & proliferation of new genetic cell
• Clonal expansion – cells grow and give rise to daughter cells (clones)
• Selection – expansion of most vital clones

27

What happens during Initiation?

carcinogen acts on DNA to
induce irreversible genetic change

28

What happens during promotion?

cells are stimulated to proliferate

29

What happens during conversion?

genetically altered cells have ability to proliferate on their own and are giving rise to a new cell type

30

What happens during progression?

expression of new genetic features & proliferation of new genetic cell

31

What happens during clonal expansion?

cells grow and give rise to daughter cells (clones)

32

What happens during selection?

expansion of most vital clones

33

protooncogenes

gene product promotes normal growth and cells

34

oncogenes

mutated protooncogene that causes cancer

35

Classes of oncogenes

a) Growth factors
b) Growth factor receptors
c) Signal transduction proteins
d) Nuclear regulatory proteins
e) Cell cycle regulators

36

Mutations of these 4 cause carcinogenesis

Growth promoting oncogenes
growth inhibiting tumor suppressor genes
genes regulating apoptosis
genes involved in DNA repair

37

Carcinogenesis results from accumulation of....

mutations (tumor progression)

38

How are oncogenes activated?

Oncogenes are activated by mutation in the protooncogene or mutation in the regulatory element of a gene

39

Overexpressed

increase in gene product (protein)

40

Amplification

overexpression causes an increased # of gene (example: Erb-B2)

41

Growth-inhibiting tumor suppressor genes

Genes that block cell proliferation
Known as recessive cancer genes

42

Known as recessive cancer genes

Growth-inhibiting tumor suppressor genes

43

Retinoblastoma gene (Rb)

normal function is as a protein that blocks the transition between the G1 and S phases of the cell cycle (osteosarcoma and retinoblastoma)

44

Tumor protein p53 (TP53)-

normal function is as a protein that causes cell cycle arrest and apoptosis (most common mutation in all cancers)

45

2 Types of tumor suppressing genes

RB (Retinoblastoma)
TP53 Tumor protein p53

46

what do Bcl-2 - mutations cause?

block normal apoptosis

47

What is nucleotide excision repair?

mechanism that removes DNA damage induced by ultraviolet light

48

XERODERMA PIGMENTOSUM (XP)

Extreme sensitivity to UV rays
• Develop freckling of the skin in sun exposed areas
• Develop dry skin (xeroderma) and changes in skin coloring (pigmentation)
• Half of all individuals develop skin cancer if proper sun protection protocols are not followed
• Caused by a mutation in genes involved in nucleotide excision repair

49

XERODERMA PIGMENTOSUM (XP) Causes

• Caused by a mutation in genes involved in nucleotide excision repair

50

Carcinogen

anything that produces cancer

51

Types of Carcinogens

1. chemical
2. radiation
3. microorganism

52

5 Oncogenic Viruses
Which are derived from RNA, DNA, Bacteria?

Human T-cell lymphoma/leukemia virus 1 (HTLV-1) RNA
Epstein-Barr Virus (EBV) DNA
Hepatitis B (HBV) and Hepatitis C (HCV) virus DNA
Helicobacter pylori (H. pylori) Bacteria
Human Papillomavirus (HPV) DNA

53

Human T-cell lymphoma/leukemia virus 1 (HTLV-1)

RNA virus
HTLV-1 encodes TAX protein
TAX protein activates expression of genes that encode cytokines and cytokine receptors
secondary mutations lead to leukemia

54

Epstein-Barr Virus (EBV)

a. DNA virus
b. Implicated in pathogenesis of nasopharyngeal carcinoma
c. EBV gene products stimulate B-cell proliferation
d. EBV causes chromosomal breaks

55

Hepatitis B (HBV) and Hepatitis C (HCV) virus

a. DNA virus
b. Do not encode oncogenes
c. Immune mediated chronic inflammation leading to hepatocyte death which triggers regeneration and genomic damage

56

Helicobacter pylori (H. pylori)

a. Bacteria
b. Immune-mediated chronic inflammation leading to gastric cell proliferation, production of ROS and damage of DNA
c. Gastric adenocarcinoma contains H. pylori cytotoxin associated A (CagA) gene

57

Human Papillomavirus (HPV)

a. DNA virus
b. Activates expression of oncoproteins
c. Infections with low-risk HPV usually give rise to benign tumors
d. Infections with high risk HPV stimulates mutations to regulatory genes involved in
tumor progression

58

Tumor Immunity

Tumor antigens will induce antibody production and cell mediated immune response

59

What mediates host response in tumor immunity?

Host response is mediated by lymphocytes, macrophages and neutrophils

60

Tumor growth most frequent in

Immunosuppresed host (AIDS, elderly)

61

Immunotherapy

Use your own immune system to get rid of cancerous growth

62

Immunotherapy best used in what kind of cancers?

Melanomas

63

What is the treatment of bladder cancer

injection of attenuated tuberculosis bacillus into the bladder..triggers cellular responses of immune system.

64

Seven warning signs of cancer

C - changes in bowel or bladder habits
A - a sore that doesn’t heal
U - unusual bleeding or discharge
T - thickening of lump in breast or elsewhere on the body
I - indigestion or difficulty in swallowing
O - obvious change in wart or mole
N - nagging cough or hoarseness

65

Clinical Aspects of Neoplasia (4)

1.Malignant tumor growth causes dysfunction of adjacent normal tissues and causes destruction of normal organs

Invasion of blood vessels often results in hemorrhage

Causes cachexia

Causes paraneoplastic syndromes that lead to changes in the endocrine, neuromuscular and
hematologic system

66

Whats cachexia?

wasting of the body, atrophy of muscle

67

How does Exercise in cancer patients help?

1. Enhances immune function
2. Minimizes muscle wasting
3. Enhances quality of life
4. Must consider the stage of disease along with type and medical intervention

68

Red flags during exercise with cancer patients

a. Exercise is contraindicated in patients with platelet counts 20,000 or less
b. Exercise with caution in patients with platelet counts (20,000 – 50,000)
c. * Normal platelet count 150,000 – 450,000 cells/mm3

69

Red Flags Physical agents

a) Do not use physical agents directly over a tumor
b) Do not use physical agents over tissue exposed to radiation therapy
c) Do not use physical agents in patients with decreased sensation to temperature or
pain

70

Guidelines for referral

A. Early warning signs of cancer (CAUTION)
B. All soft-tissue lumps that persist or grow
C. Any woman presenting with chest, breast, axillary or shoulder pain of unknown etiology
D. Bone pain that persists more than 1 week
E. Proximal muscle weakness
F. Changes in deep tendon reflexes

71

Review of Systems

A. Constant intense pain
B. Loss of appetite
C. Excessive fatigue
D. Unusual lumps or change in lumps
E. Unusual or prolonged bleeding
F. Proximal muscle weakness
G. Unexplained weight loss
H. Unusual skin lesion or rash
I. Chronic cough
J. Changes in bowel or bladder habits