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Pathology > Week 4: Neoplasia > Flashcards

Week 4: Neoplasia Flashcards

1
Q

Atrophy

A

Decrease in the size and function of a cell

Causes:

  1. Decreased workload
  2. Decreased blood supply
  3. Loss of innervation
  4. Interruption of trophic signals
  5. Aging

Cells may die.

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2
Q

Hypertrophy

A

Increase cell size (function is altered)

Causes:

  1. Increased functional demand
  2. Hormones
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3
Q

Hyperplasia

A

Increase in cell number in organ or tissue

Causes:

  1. Increased functional demand
  2. Hormones
  3. Persistent cell injury (calluses)
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4
Q

Metaplasia

A

Conversion of one differentiated cell to another

Protective mechanism, but may have loss of function

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5
Q

Dysplasia

A

Alterations in shape, size, and organization of cell components

  1. Enlargement
  2. Irregular
  3. Hyperchromatism of nuclei (dark)

DYSPLASIA IS PREMALIGNANT/PRECANCEROUS - curable if identified.

Cause: persistent injury

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6
Q

Pleomorphism

A

Variation in shape and size (nuclear or cellular). Seen in Dysplasia

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7
Q

Neoplasm

A

Abnormal mass of tissue (tumour). Growth is uncoordinated and massive.

Even if you take away stimuli, it will continue to grow

Named according to the type of tumour cells (indicating the tissue of origin) and the nature of the tumour whether benign or malignant

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8
Q

Cancer

A

Malignant neoplasm

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9
Q

Oncology

A

Study of tumours

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10
Q

Benign Tumours

A

Tissue type + oma

Adenoma: benign tumour that forms a gland or came from glands

Cystadenoma: An adenoma with cystic areas

Papilloma: Benign tumours with finger-like projections.

Polyp: Elevated mucosal lesions (descriptive term).

Exceptions: melanoma/lymphoma are both malignant

All cats poop purple

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11
Q

Malignant Tumours

A

Sarcoma: composed of mesenchymal cells (fat, bone, muscle)

Fibrosarcoma: fibrous tissue

Carcinoma: composed of epithelial cells

Adenocarcinoma: malignant epithelial tumor forming a glandular pattern

Squamous cell carcinoma: squamous cells

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12
Q

Teratoma

A

2 or more germ layers from mesenchymal cells

Benign OR malignant

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13
Q

Choristoma

A

Ectopic rest (when tissues move during development and stay there)

Looks like a tumour but is not

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14
Q

Hamartoma

A

Disorganized normal tissue in normal location

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15
Q

Cyst

A

Fluid filled space

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16
Q

Differentiation

A

How much tumour cells looks like their normal counterparts (morphologically and functionally)

Well –> moderate –> poor

Well = looks like their normal counterpart 
Poor = looks very abnormal (also less functionally active)
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17
Q

Anaplasia

A

Loss of specialized features of a normal cell

Lacks differentiation (looks very abnormal)

used ONLY for INVASIVE NEOPLASM

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18
Q

Features of Anaplastic Cells

A
  1. Variable cell size & shape (cellular pleomorphism).
  2. Variable nuclear size & shape (nuclear pleomorphism).
  3. Increased nuclear cytoplasmic ratio
  4. Hyperchromatic nuclei (Inc. DNA)
  5. Increased mitosis and atypical mitosis.
  6. Loss of polarity
  7. Tumour giant cell
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19
Q

Rate of Growth

A

Benign tumours - slow growing (unless hormonal stimulation)
Malignant tumours - fast growing

FAST rate of growth = INC. blood supply
FAST rate of growth = less differentiation

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20
Q

Invasion

A

Reliable feature of malignancy

Benign tumours DO NOT INVADE - grow by expansion (locally)

Malignant tumours invade and destroy tissue

  • most carcinomas have monoclonal origin
  • if basement membrane is intact, they are carcinoma in situ (severe dysplasia), carcinoma is the final stage
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21
Q

Metastasis

A

Tumour that disconnected from primary tumour.
UNEQUIVOCAL sign of malignancy (NEVER seen in benign tumours) - it will look like the tumour from the origin site.

Pathway:

  1. Seeding via body cavities (peritoneal)
  2. Lymphatic spread: most common; follows natural drainage
  3. Hematogenous spread (blood vessels): favoured by sarcoma but also used by carcinoma. Lung and liver, other tissues. Follows routes of venous drainage
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22
Q

Transformation

A

Most tumours are derived from a single transformed cell. Not subject to normal growth/differentiation control.

  • Self sufficiency in growth signal (autonomous)
  • Insensitivity to growth-inhibitory signal
  • Resistant to apoptosis
  • Defective DNA repair
  • Unrestricted proliferation
  • Angiogenesis, invasion and metastasis
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23
Q

Tumour Growth

A

Excess cell production = rapid growth

Growth fraction = #cycling cells / # total cells

Doubling time is similar/more than normal cells.

Minimum size for clinical detection: 1cm3 (1gm) = 108-109 cells

If more proliferative = chemotherapy

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24
Q

Tumour Angiogenesis (munchy time)

A

Blood supply is a major factor for growth.

Angiogenic (food):

  1. produced by tumour cells
  2. produced by inflammatory cells infiltrating tumours

Induces production of proteolytic enzymes (VEGF)

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25
Q

Tumour Progression and Heterogeneity

A

Over time, tumours develop subpopulations that vary in invasiveness, metastatic potential, growth factor requirement, antigenicity

Subpopulation “beat the odds and survive

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26
Q

Warburg Metabolism

A

Cancer cell metabolism

Prefer glycolysis over oxphos

Some oncoproteins causes formation of abnormal metabolite causing epigenetic changes

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27
Q

Autophagy of Cancer Cells

A

Normal cells can cannibalize their own organelles during nutrient deficiency

Cancerous cells avoid this, can sustain growth on marginal conditions

28
Q

Tumour dormancy

A

Metastasis may be dormant for years and become apparent randomly

They do not appear at the time they leave the primary tumours

29
Q

Stroma

A

Tumour stroma interactions = play a role in carcinogenesis

30
Q

Mechanism of Tumour Invasion and Metastasis

A
  1. Proteolytic enzymes released from tumour cells, ECM is degraded
  2. Tumour can bind to altered components of ECM
  3. Adhesion molecules mediate this
  4. Cancer penetrates blood vessels and lymphatics
  5. Tumour enters circulation + attach to new site + grow
31
Q

Invasion of ECM

A

Cancer cells are less adherent to each other due to a lack of cell adhesion molecules (Cadherins)

They degrade the basement membrane by secretion of proteolytic enzymes that dissolve matrix proteins, e.g., collagenase, cathepsin B.

Benign tumours secrete little or no such enzymes.
They attach to the basement membrane through laminin receptors and integrins.

Tumour cells trigger the production of cytokines, such as autocrine motility factors and cleavage products of matrix components.

Enters blood/lymphatic vessels, attaches to new site = new tumour

32
Q

Vascular Dissemination and Homing

A

Single or many tumour cells form emboli by aggregating with platelets & WBC.

They form adhesion with endothelium and finally exit through the basement membrane

Site of metastasis may be predicted by vascular or lymphatic drainage.

Metastatic site (homing) may be related to:

  1. Presence or absence of endothelial adhesion molecules in some sites.
  2. Chemoattractant.
  3. Unfavourable environment (e.g.: skeletal muscle).
33
Q

Local Effects of Tumours

A

Seen in both malignant and benign

  1. Benign submucosal leiomyoma - bleeding.
  2. Neoplasms (benign or malignant in gut) → obstruction.
  3. Pituitary adenoma → expansive growths destruction of the remaining gland.
  4. Gastrointestinal tumours/urogenital tumours → bleeding
  5. Ovarian tumours → torsion.

Tumour may undergo infarction, rupture, ulceration and secondary infection.

34
Q

Hormonal Effects of Tumours

A
  1. β cell adenoma in pancreas → too much insulin production → hypoglycemia, may be lethal.
  2. Adrenal cortex adenoma → too much steroid production → secondary effects.
  3. Carcinoid tumour - hormones → carcinoid syndrome
35
Q

Cancer Cachexia

A

Loss of fat/lean body mass with weakness, anorexia, anemia

Factors:

  1. Reduced food intake
  2. Reduced synthesis/storage of fat
  3. TNF a

causes fever:

  • correlates with tumour growth
  • disappears following treatment
  • due to TNF/IL1
36
Q

Paraneoplastic Syndrome

A

Symptom complex in cancer patients that cannot be readily explained

  • May be the earliest manifestation of an occult neoplasm.
  • May cause significant even lethal clinical problems.
  • May mimic metastatic disease.
Lung cancer can cause:
Cushing's Syndrome
Syndrome of inappropriate antidiuretic hormone secretion.
Hypercalcemia
Myesthesia
Acanthosis Nigricans
Hypertrophic osteoarthropathy
Venous thrombosis
37
Q

Grading of Cancer

A

ONLY IN MALIGNANT

Estimate of the AGGRESSIVENESS of the neoplasm based on level of differentiation

well, poor, moderate

38
Q

Staging of Cancer

A

ONLY IN MALIGNANT
GREATER CLINICAL IMPORTANT THAN GRADING

Estimate of the EXTENT of the spread based on tumour size, lymph node spread, and metastasis to other organs.

Clinical staging: evidence prior to treatment
Pathological staging: examine tissue microscopically

Based on:
1. Size (T) - primary lesion
2. Nodes (N) - spread to lymph nodes
3. Metastasis (M) - presence or absence
(developed by UICC, AJC)
39
Q

Laboratory Diagnosis of Cancer

A

Tissues used: formalin fixed usually

Sampling method: biopsy, excision, fine needle aspiration biopsy, smear, body fluid

Tissue processing: formalin, dehydration in alcohol, xylene, paraffin, cut and stained with H&E

40
Q

Fine Needle Aspiration Biopsy (FNAB)

A

Useful for palpable lesions

  • office procedure: thyroid, breast, salivary glands
  • deeper tissues (liver)
  • smear, cell blocks
41
Q

Cytologic smear

A

Cervical cancer

42
Q

Cytology of Body Fluids

A
  • pleural/peritoneal fluid
  • CSF
  • sputum
  • urine
43
Q

Immunocytochemistry

A

Identify proteins

44
Q

Flow Cytometric Analysis

A

Maturation markers in lymphoma/leukemia

  • DNA
  • biochemical markers
  • molecular diagnosis
  • cytogenetics
45
Q

Biochemical tumour markers

A

NOT DIAGNOSTIC because they may be elevated in inflammatory conditions, good for screening studies

PSA (prostate specific antigen): prostatic adenoCA
CEA (carcino embryonic antigen): colonic adenoCA

46
Q

Carcinogenesis

A

Non-lethal genetic damage is a KEY EVENT in carcinogenesis caused by chemicals, radiation, viruses

normal cell + carcinogen mutation –> precursor –> cancer –> heterogenous cancer

Development of cancer = using stepwise accumulation of complementary driver mutations (random order)

47
Q

Driver Mutations

A

Direct contributors to development/progression of cancer (tightly clustered in cancer genes)

48
Q

Passenger Mutations

A

Acquired mutations that DO NOT AFFECT cellular behaviours (occurs randomly throughout the genome)

MAY BECOME DRIVER MUTATIONS if selective pressure on tumour changes

49
Q

Genetic Change in Tumours

A
  1. Karyotypic Change
    a. balanced translocation
    b. deletion
    c. gene amplification
  2. Point mutations
    a. RAS in colon carcinoma
    b. carcinogenesis affects oncogenes, tumour suppressor, apoptosis regulating, mutator (caretaker) genes
50
Q

Oncogenes

A

Deregulated/altered proto-oncogenes that lead to cancer

Activation: Secondary to change in gene structure or due to a change in regulation of gene expressions.
The changes are secondary to the following mechanisms.
1. Point Mutation: RAS mutation is the most common mutation in human cancer.
2. Translocation: e.g. t(9,22) in chronic myeloid leukemia.
3. Gene Amplification: NMYC in neuroblastoma

Protein Products: Oncogenes encode for protein products called oncoproteins.

  • No regulatory elements
  • Oncogenes may lead to the development of tumour by acting at different levels of signal transduction.
51
Q

Proto-oncogenes

A

Normal genes that control cell proliferation and differentiation.

52
Q

Tumour Suppressor Genes

A

These genes act as an inhibitor of cell proliferation.

When mutated the inhibition is lost → uncontrolled proliferation

eg. P53 → lung, colon, breast, ovary & other cancers.
BRCA1, BRCA2 → Breast carcinoma
RB → retinoblastoma

53
Q

Apoptosis Regulating Genes

A

Genes that prevent or induce apoptosis may also be important in carcinogenesis. eg. BCL2 in lymphoma.

54
Q

Mutator (Caretaker) Genes

A

These are DNA repair genes.

They are not oncogenic by themselves.

However, when mutated, they allow mutation in other genes in normal cell division.

eg. MSH2, MLH2 in hereditary non-polyposis colon cancer.

55
Q

Telomeres

A

Cancer cells make the enzyme telomerase which maintain their ability to replicate.

56
Q

Epigenetic

A

DNA methylation, histone acetylation and deacetylation microRNA alteration play important roles in carcinogenesis.

57
Q

Multi-step Carcinogenesis

A

Carcinogenesis is a multistep process.

Multiple oncogene as well as one or multiple tumour suppressor genes works together to produce cancer

58
Q

Geographic Factors

A

-age adjusted death rate for breast cancer: US - 27, England - 36, & Japan - 7.
-stomach cancer - 7 times higher in Japan than US
hepatocellular carcinoma
-infrequent in US/Canada, some African populations #1 lethal cancer.

59
Q

Environmental Factors

A 
Smoking - lung cancer
Sunlight - UV light = skin cancer
Virus - EB Virus = lymphoma 
Food - colorectal cancer 
Higher incidence in Canada/US (one factor is high fat content of diet)
Radiation
60
Q

Age Factors

A

-in general increases with age. Peak 55-75 yrs.
Exceptions:
-Sarcomas younger age group (osteosarcoma)

Childhood cancers: occurs exclusively in children.

  • neuroblastomas
  • Wilms tumour
  • Retinoblastoma
61
Q

Hereditary Factors

A
  1. Inherited Cancer Syndromes (autosomal dominant)
    a. Patients show multiple neoplasms (MEN, Familial polyposis)
  2. Familial Cancers: Shows clustering but hereditary predisposition in individual cases is not clear.
    e. g. breast/colon/ovary
  3. Hereditary Preneoplastic Conditions
    a. DNA repair defect (autosomal recessive).
    b. Makes you susceptible for cancer
    c. e.g. xeroderma pigmentosa → squamous cell carcinoma from DNA repair enzyme dysfunction
62
Q

Acquired Preneoplastic Conditions

A

Barrett’s esophagus (intestinal metaplasia)
Adenocarcinoma
Cirrhosis of liver → hepato cellular carcinoma
Ulcerative colitis → colonic adenocarcinoma

63
Q

Carcinogenic Agents

A

Cancer is a genetic disease. Agents are:

chemicals.
physical agents such as radiation.
oncogenic virus.
bacteria.

64
Q

Chemical Carcinogens

A

Diverse natural & synthetic products are of importance.

They may be direct acting or indirect acting (following conversion in the body) from pre carcinogens to carcinogens in the body.

They are highly reactive molecules which react with RNA or DNA or proteins.

Several chemical carcinogens may act together or along with other viruses or radiation.

EX Polycyclic aromatic hydrocarbons → tobacco (lung cancer)
Asbestos → mesothelioma (lung cancer)

65
Q

Radiation Carcinogenesis

A

Radiant energy, whether in the form of ultraviolet (UV) rays of sunlight or as ionizing electromagnetic and particulate radiation can transform virtually all cell types.

EX
UV rays – squamous cell carcinoma
Ionizing radiation – leukemia
radiation directly ionizes and through free radical generation and damages critical molecules.

66
Q

Viral Oncogenesis

A

A large number of viruses have proved to be oncogenic in animals. Only few have been linked with human cancer.

Oncogenic viruses fall into two classes:

  1. DNA oncogenic viruses
    a. HPV (Human papillomavirus) - Cervical cancer
    b. EBV (Epstein-Barr virus) - Nasopharyngeal Ca o Burkitt’s lymphoma
    c. HBV (hepatitis B virus) - hepatocellular Ca
  2. RNA oncogenic viruses
    a. Human T-cell leukemia virus(HTLV-1) - human T cell leukemia/lymphoma.
67
Q

Bacterial Infection

A

H. pylori is associated with B cell lymphoma in the Mucosa Associated Lymphatic Tissues (MALToma).

Pathology (7 decks)

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