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Pathology > Neoplastic > Flashcards

Neoplastic Flashcards

1
Q

Neoplasm

• Not all neoplasms are malignant
• Malignant neoplasms(cancer) characteristics:

A

– Genetic disorder
– These genetic alterations are heritable
– The accumulation of mutations gives rise to a set of properties called the “hallmarks of cancer”

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2
Q

Nomenclature

• All tumors benign and malignant

– Parenchyma:
– Supporting stroma:

A

-transformed neoplastic cells
-connective tissue, blood vessels, and lymphatics

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3
Q

Benign Neoplasms (-oma)

• Classified according to the cell type of origin

A

• Suffix “-oma”
• classified on the basis of macroscopic or microscopic pattern of growth

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4
Q

Malignant Neoplasms

• Classified according to the cell type of origin (4)

A

– Carcinoma: arising from epithelial tissue
– Sarcoma: arising from mesenchymal tissue
– Lymphoma: arising from the lymphoreticular
system
– Leukemia: arising from hematopoietic elements

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5
Q

Exceptions are the Rule

A

• Melanoma • Seminoma • Hamartoma

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6
Q

Neoplasia = New Growth

Neoplasm

A

• Abnormal mass of tissue whose growth exceeds and is uncoordinated with that of the normal tissues
• Persists in an excessive manner after the cessation of the stimuli which evoked the change
• Obvious to normal control mechanisms of replication

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7
Q

Differentiation & Anaplasia

Differentiation:
Anaplasia:

A
  • Differentiation: parenchymal cells of the neoplasm resemble comparable normal cells, both morphologically and functionally
  • Anaplasia: lack of differentiation
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8
Q

Morphology of Anaplasia

A

• a lack of differentiation
• Cellular and nuclear pleomorphism
• Nuclear hyperchromasia
• Increased nuclear to cytoplasmic ratio
• Increased number of mitosis
• Loss of orientation of cells
• Formation of tumor giant cells

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9
Q

Dysplasia

• Disorderly but non-neoplastic growth
• in epithelial lesions

A

– loss of uniformity of cells
– Loss of architectural orientation
– The term dysplasia, without qualifications, does not indicate cancer
– do not necessarily progress to cancer

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10
Q

Differentiation and Anaplasia

  • Benign tumors-
  • Malignant tumors-
A

• Benign tumors- well-differentiated and resemble closely normal cells
• Malignant tumors- well differentiated to undifferentiated

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11
Q

Rate of Growth

  • Benign tumors-
  • Cancers-
A

• Benign neoplasia: grow slowly over a period of years*
• Cancers: grow rapidly or erratically*
• Many exceptions
• *the growth rate of tumors correlates with their level of differentiation

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12
Q

Local Invasion

  • Benign tumors-
  • Malignant tumors-
A

• Benign neoplasms -grow as cohesive expansile masses
– Capsule: derived largely from the stroma of the native tissue as the normal cells atrophy from pressure
• Malignant neoplasms- infiltrative growth with destruction of the surrounding tissue

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13
Q

Local Invasion

A

• Next to the development of metastasis, invasiveness is the most reliable feature of malignancy

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14
Q

Metastasis

A

•

identifies a neoplasm as malignant

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15
Q

Pathways of Spread

A
  • Seeding of body cavities - ovary

* Lymphatic spread - carcinoma, breast
• Hematogenous spread - sarcoma
• Transplantation

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16
Q

Biology of Tumor Growth

A
  • Neoplastic transformation of a cell

* Growth of the transformed cell
• Local invasion
• Distant metastasis

17
Q

Factors Influencing Tumor Growth

A

• Kinetics of tumor cell growth

- how many cells in G1
• Tumor angiogenesis
• Tumor progression & heterogeneity

18
Q

Kinetics of Tumor Growth

A

• Doubling time of tumor cells
– Because of defective controls (Rb, p53), easily triggered into cell cycle
– take longer to complete the cell cycle

  • Fraction of tumor cells in replicative pool
    – Depends on type of tumor
  • Rate of loss of cellsy (dying, differentiation)
19
Q

Tumor Angiogenesis. **

  • cannot enlarge beyond 1-2 mm in diameter or thickness unless they are vascularized
  • Correlates with malignancy
  • How do tumors develop a blood supply?
A

– Factors produced by tumor cells
– Factors produced by inflammatory cells
– The balance between angiogenesis factors and
inhibitors pushed to favor angiogenesis

20
Q

Tumor Angiogenesis

• How do tumors develop a blood supply?

A

– Early in their growth—no angiogenesis
– months to years
– Then- “angiogenic switch”
–the change of some cells within the tumor to an angiogenic phenotype

21
Q

Tumor Angiogenesis

  • is controlled by a balance between pro- and anti- angiogenesis factors
  • These controlling factors may be produced…
A

directly by the tumor cells themselves, or by inflammatory or stromal cells adjacent to the tumor

22
Q

Tumor Angiogenesis

• Angiogenesis inducers:

A

– VEGF (vascular endothelial growth factor)
• (Early) tumors do not induce angiogenesis
• They remain small until the angiogenic switch terminates this phase
• Angiogenesis inhibitor: TSP-1(thrombospondin-1)
– P53 (a tumor suppressor gene) induces the synthesis of TSP-1

23
Q

Tumor Angiogenesis

• The molecular basis of the angiogenic switch involves…

A

increased production of angiogenic factors and/or the loss of angiogenesis inhibitors

• Proteases elaborated by the tumor cells, or by stromal cells in response to the tumor affect the balance

24
Q

Tumor Angiogenesis

• Proteases can
– Release

A

the angiogenic factor basic FGF (fibroblast growth factor)
– also release potent angiogenesis inhibitors
• Angiostatin
• Endostatin
• Vasculostatin

• Stromal fibroblasts can produce TSP-1

25
Q

Tumor Angiogenesis: Angiogenic Switch

  • Controlled by
  • Stimulates
A
  • Controlled by physiologic stimuli such as hypoxia
  • Stimulates the production of a variety of pro-angiogenic cytokines (VEGF) through the action of HIF-1α (hypoxia-inducible factor-1α)
26
Q

Tumor Angiogenesis

• Morphology:

A

• Morphology:
– Tumor vasculature is abnormal – Vessels are leaky and dilated
– Tend to have a haphazard pattern of connections

27
Q

Tumor Progression and Heterogeneity

A
  • Despite the fact that most malignant tumors are monoclonal in origin, by the time they become clinically evident, the cells are extremely heterogeneous
  • Subpopulations arise which have greater metastatic potential, resistance to chemotherapy, greater invasive potential
28
Q

Tumor Heterogeneity

• Why does this happen?

A

– Tumor cells are genetically unstable

– High rate of random mutations
– Sub clones are subjected to selection pressure from immune and non-immune sources

29
Q

Mechanisms of Invasion and Metastasis

A

Invasion
Metastasis
Vascular Dissemination and Homing

30
Q

Invasion

A

• Detachment of tumor cells from each other
• Attachment to matrix components
• Degradation of ECM and basement membrane
• Migration of tumor cells

31
Q

Vascular Dissemination **

A

• Similar to invasion,except that vessels are breached
• Formation of tumor emboli
• Adhesion to vascular wall
• Extravasation
• Metastatic deposit
• Angiogenesis
• Growth

32
Q

Homing of Tumor Cells

• Site where tumor cells lodge and form secondary growths is influenced by:

A

– Vascular and lymphatic drainage from the primary site
– Interaction of tumor cells with organ-specific receptors-adhesion molecules
– Chemokines and their receptors
– Microenvironment: favorable or unfavorable

33
Q

Grading and Staging of Malignant Neoplasms

Grading. ****

A

• Based on the degree of differentiation of malignant cells
• The number of mitosis is presumed to correlate with the aggressiveness of the tumor
• Criteria vary with each form of neoplastic tumor
• Inexact and subject to observer bias

34
Q

Staging ***

• Attempts to assess biologic potential through observation of:

A

– Size of the primary tumor
– Extent of local growth, extent of spread to regional lymph nodes
– Presence or absence of metastasis

35
Q

Staging. **

A

• Reasonably accurate and objective
• Provides a basis of comparison for therapy
• Facilitates communication between medical establishments
• Expression of the extent and quantity of tumor in a specific patient

36
Q

Staging. ***

• Two major systems

A
  1. Union Internationale Contre Cancer (UICC)
    • TMN
    – T: size of the primary tumor
    – M: metastases ( distant)
    – N: regional lymph node involvement
  2. American Joint Committee (AJC)
    • Stages 0 to IV

Pathology (15 decks)

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