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HistoPathology > [P] Week 4: Neoplasia - Part 1 > Flashcards

[P] Week 4: Neoplasia - Part 1 Flashcards

1
Q

means “new growth,” and the collection of cells and stroma composing new growths

A

Neoplasia

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2
Q

Neoplasia means “new growth,” and the collection of cells and stroma composing new growths are referred to?

A

Neoplasms

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3
Q

Benign or Malignant Neoplasia

  1. Non-cancerous lesions
  2. Cancerous lesions
A
  1. Benign
  2. Malignant
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4
Q

Benign or Malignant Neoplasia

Naming of benign tumors of
mesenchymal cells is relatively simple; in general, the suffix “-oma” is attached to the name of the cell type
from which the tumor arises

A

Benign

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5
Q

Benign or Malignant Neoplasia

Composed of single
parenchymal cell type

A

Malignant

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6
Q

Enumerate the Benign tumors?

A
  • Adenoma
  • Cystadenoma
  • Papilloma
  • Lipoma
  • Leiomyoma
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7
Q

Enumerate the Malignant Tumors

A
  • Carcinoma
  • Squamous Cell Carcinoma
  • Adenocarcinoma
  • Sarcoma
  • Liposarcoma
  • Leiomyosarcoma
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8
Q

Benign Tumors

a gland-forming benign tumor. It is derived from glandular tissues even if the tumor cells fail to form glandular structures

A

Adenoma

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9
Q

Benign Tumors

a gland-forming tumor but with large cystic masses/cavities

A

Cystadenoma

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10
Q

Benign Tumors

a benign epithelial neoplasm producing fingerlike or warty projections from epithelial surfaces.

A

Papilloma

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11
Q

Benign Tumor

Benign fatty tumors

A

Lipoma

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12
Q

Benign Tumor

Composed of smooth muscle cells

A

Leiomyoma

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13
Q

Malignant Tumors

malignant tumor arising in epithelial cells.

A

Carcinoma

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14
Q

Malignant Tumors

a malignant tumor of the skin occurring in the epidermis.

A

Squamous Cell Carcinoma

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15
Q

Malignant Tumors

occurs usually in the colon or large intestine when the neoplastic epithelial cells grow in a glandular pattern. (gland-forming)

A

Adenocarinoma

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16
Q

Malignant Tumor

a malignant tumor arising in solid mesenchymal tissues/cells.

A

Sarcoma

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17
Q

Malignant Tumor

Refers to malignant fatty tumors.

A

Liposarcoma

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18
Q

Malignant Tumor

A malignant tumor found in smooth mucle cells./

A

Leiomyosarcoma

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19
Q

RESEMBLES A MALIGNANT TUMOR BUT NON-NEOPLASTIC

  • Ectopic rests of non-transformed tissue. It is the term applied to a heterotopic (misplaced) rest of cells.
  • EXAMPLE: Pancreatic cells under the small bowel mucosa
A

Choristoma

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20
Q

RESEMBLES A MALIGNANT TUMOR BUT NON-NEOPLASTIC

  • It is known as masses of disorganized tissue indigenous to a particular site or involved tissue.
    ○ The tissue is located in its normal location, only disorganized.
  • EXAMPLES: Cartilage, bronchi, and blood vessels in the lungs
A

Hamartoma

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21
Q

TUMORS COMPOSED OF MORE THAN ONE PARENCHYMAL CELL TYPE

derived from one germ cell layer that
differentiates into more than one parenchymal type.

  • In embryology, there are three germ layers - ectoderm, endoderm, and mesoderm.
  • If the cells that make up the tumor are found in a single germ layer, it is classified as a?
A

Mixed tumors

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22
Q

TUMORS COMPOSED OF MORE THAN ONE PARENCHYMAL CELL TYPE

derived from more than one germ cell layer producing various parenchymal cell types.
- if the cells that make up the tumor are found in two or three germ layers.

A

Teratoma / Teratogenous

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23
Q

CHARACTERISTICS OF BENIGN AND MALIGNANT NEOPLASMS

Refers to the extent to which neoplastic cells resemble the normal cells morphologically and functionally.

A

Differentiation

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24
Q

CHARACTERISTICS OF BENIGN AND MALIGNANT NEOPLASMS

In assessing the differentiation of a tumor, what are the steps?

A
  1. Simillarity of the morphology
  2. Similarity on the function

Example: In assessing the differentiation of a tumor affecting the squamous cells, (1) assess whether they still exhibit the squamoid shape–morphology, and (2) assess whether
they can produce keratin–function

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25
Q

Cancer cells often exhibit other telltale morphologic changes, what are those?

A
  • Pleomorphism
  • Abornmal nuclear morphology
  • Increased N:C ratio from 1:4-1:6 to 1:1
  • Atypical, Bizarre mitotic figures
  • Loss of polarity
  • Tumor giant cells
  • Ischemic Necrosis
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26
Q

CHARACTERISTICS OF BENIGN AND MALIGNANT NEOPLASMS

lack of differentiation, and is considered as the HALLMARK OF MALIGNANCY

A

Anaplasia

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27
Q

CHARACTERISTICS OF BENIGN AND MALIGNANT NEOPLASMS

any disordered growth; the loss of uniformity of individual cells and in architectural orientation.

A

Dysplasia

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28
Q

CHARACTERISTICS OF BENIGN AND MALIGNANT NEOPLASMS

the replacement of one cell type with another, and is considered as a fertile soil for malignancy

A

Metaplasia

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29
Q

Benign or Malignant

Differentiation / Anaplasia

  1. Exhibits anaplasia (lack of differentiation)
  2. Well-differentiated
A
  1. Malignant
  2. Benign
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30
Q

Benign or Malignant

Mitosis
1. Mitotic figures are rare and just follow the normal proliferative rate
2. Mitotic figures may be numerous and abnormal (e.g. sunburst pattern,
tripolar mitotic figures).

A
  1. Benign
  2. Malignant
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31
Q

Benign or Malignant

Local Invasion
1. Usually cohesive and expansile, well demarcated masses that do not invade or infiltrate the surrounding
tissues
2. Invasive, infiltrating the surrounding tissues

A
  1. Benign
  2. Malignant
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32
Q

Benign or Malignant

Metastasis

  1. Frequently metstasize or colonize distant organs
  2. NO metastasis
A
  1. Malignant
  2. Benign
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33
Q

CANCER CELLS OFTEN EXHIBIT OTHER TELLTALE MORPHOLOGIC CHANGES

  • Refers to the variations in size and shape of the cells in the tumor
  • Some tumor giant cells possess only a single huge polymorphic nucleus, while others may have two or more large, hyperchromatic nuclei
A

Pleomorphism

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34
Q

CANCER CELLS OFTEN EXHIBIT OTHER TELLTALE MORPHOLOGIC CHANGES

The nuclear shape is variable and often irregular, and the chromatin is often coarsely clumped and distributed along the nuclear membrane or more darkly stained than normal (hyperchromatic)

A

Abnormal nuclear morphology

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35
Q

CANCER CELLS OFTEN EXHIBIT OTHER TELLTALE MORPHOLOGIC CHANGES

  • Characteristically, cancer cells have nuclei that are disproportionately large, with a nuclear-to-cytoplasm ratio that may approach 1:1 instead of the normal 1:4 to 1:6.
  • Cytoplasm cannot longer be appreciated
A

Increased N:C ratio from 1:4-1:6 to 1:1

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36
Q

CANCER CELLS OFTEN EXHIBIT OTHER TELLTALE MORPHOLOGIC CHANGES

  • Morphologic feature of malignancy
  • Unlike benign tumors and some well-differentiated malignant neoplasms, undifferentiated cancers often contain many cells in mitosis, reflecting their high rate of proliferation
A

Atypical, Bizarre mitotic figures

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37
Q

CANCER CELLS OFTEN EXHIBIT OTHER TELLTALE MORPHOLOGIC CHANGES

  • In addition to cytologic abnormalities, the orientation of anaplastic cells with respect to each other or to supporting structures like basement membranes is markedly disturbed.
  • Sheets or large masses of tumor cells grow in a disorganized fashion
A

Loss of polarity

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38
Q

CANCER CELLS OFTEN EXHIBIT OTHER TELLTALE MORPHOLOGIC CHANGES

While growing tumor cells must have a blood supply, the vascular stroma is often insufficient; as a result, many
rapidly growing cancers develop areas of ischemic necrosis.

A

Ischemic necrosis

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39
Q

defined as the spread of a tumor to sites that are physicallydiscontinuous with the primary tumor, an event that unequivocally marks a tumor as malignant

A

Metastasis

q

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40
Q

What are the pathways of spread/metastasis? enumerate

A
  1. Seeding within body cavities and surfaces
  2. Lymphatic spread
  3. Hematogenous spread
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41
Q

Pathways of spread/metastasis

occurs when a malignant neoplasm penetrates into a natural “open field” lacking physical barriers

A

Seeding within Body Cavities and Surfaces

For example: Masses such as gastric tumor or colonic mass had already invaded down to the serosa surface of the colon or the stomach

42
Q

Pathways of spread/metastasis

  • A characteristic of ovarian cancer
  • Sometimes, mucus-secreting appendiceal carcinomas or ovarian carcinomas fill the peritoneal cavity with a gelatinous neoplastic mass referred to as pseudomyxoma peritonei.
A

Seeding within Body Cavities and Surfaces

43
Q

Pathways of spread/metastasis

Transport through lymphatic vessels is the most common pathway for the initial dissemination of carcinomas.

A

Lymphatic spread

44
Q

Pathways of spread/metastasis

  • typical of sarcomas but is also seen with carcinomas.
  • Sarcomas are the malignant tumors arising in solid mesenchymal (mesenchymal lesions) which initially spread by hematogenous route or through the bloodstream
A

Hematogenous spread

45
Q

MOLECULAR BASIS OF CANCER

Cancer starts with a?

A

Nonlethal genetic damage

This means that the cell has to survive, otherwise, there will be no cancer

46
Q

Molecular basis of cancer

enumerate the steps of genetic and epigenetic alteration

A
  1. Cancer starts with a nonlethal genetic damage
  2. Clonal expansion
  3. Tumor progression
47
Q

MOLECULAR BASIS OF CANCER

Cancer starts with a nonlethal genetic damage, this can involve?

A
  • Growth-promoting proto-oncogenes
  • Growth-inhibiting tumor suppressor genes
  • Genes that regulate apoptosis
  • Genes involved in DNA repair
48
Q

MOLECULAR BASIS OF CANCER

Once the cell survives the genetic damage, it will undergo?

A

Clonal expansion

  • They multiply in number
49
Q

MOLECULAR BASIS OF CANCER

this means that whatever is the genetic aberrations in that signeld cell (first cell) in carcinogenesis, all of the succeeding cells will also have the same genetic aberration?

A

Clonal (under clonal expansion)

50
Q

MOLECULAR BASIS OF CANCER

  • Accumulation of multiple mutations generating subclones
  • Example: There are 1 million cells after clonal expansion. In tumor progression, 100 thousand out of
    1 million cells will have (aside from the original mutation) the mutation A, and then another 100,000 thousand will have on top of the original mutation, mutation B, and so on.
A

Tumor progression

51
Q

Four classes of genes are the principal targets of cancercausing mutations, what are those?

As the cells proliferate and become clinically apparent in solid tumors that can be palpated, these lesions/tumors, when examined, will harbor many genetic mutations due to continuous tumor progression

A
  • Growth promoting proto-oncogenes (GOF)
  • Tumor suppressor genes (LOF)
  • Genes that regulate apoptosis (GOF/LOF)
  • Genes that involve DNA repair (LOF)
52
Q

4 CLASSES OF NORMAL REGULATORY GENES

They promote entry into the cell cycle. For these genes to participate in oncogenesis/carcinogenesis, they must suffer from ‘gain of function’ mutation.

A

Growth promoting proto-oncogenes (GOF)

53
Q

4 CLASSES OF NORMAL REGULATORY GENES

These genes produce products and encode for proteins that serve to apply brakes in the cell cycle. For them to participate in carcinogenesis, they must suffer from ‘loss of function’

A

Tumor suppressor genes (LOF)

54
Q

4 CLASSES OF NORMAL REGULATORY GENES

These genes may suffer from ‘gain of function’ or ‘loss of function’ mutations, depending on the specific role of the gene product in the regulation of apoptosis.

Q

A

Genes that regulate apoptosis (GOF/LOF)

55
Q

4 CLASSES OF NORMAL REGULATORY GENES

For them to participate in carcinogenesis, they must suffer from ‘loss of function’ mutation. And if the proteins of these genes are already absent, there will be no repair

A

Genes that involve DNA repair (LOF)

56
Q

4 CLASSES OF NORMAL REGULATORY GENES

Here, the mutation leads to the acquisition of mutations at an accelerated rate. The cell enters a MUTATOR PHENOTYPE STATE, leading to genomic instability.

A

Genes that involve DNA repair (LOF)

57
Q

are mutated genes that cause excessive cell growth, even in the absence of growth factors and other
growth-promoting external cues.

A

Oncogenese

58
Q

These are genes that encode for proteins (oncoproteins) that when expressed, promote and can participate in autonomous cell
growth in cancer cells

A

Oncogenes

59
Q

A major discovery in cancer was that oncogenes are?

A

mutated or overexpressed versions of normal cellular genes, which are called proto-oncogenes

60
Q

STEPS IN CELL PROLIFERATION

Physiologic growth factor–induced signaling can be resolved into the what steps?

A
  1. Binding of a growth factor to its specific receptor
  2. transient and limited activation of growth factor receptor
  3. induction and activation of nuclear regulatory factors
  4. Expression of genes and encoded factors that promote entry and progression of the cell into the cell cycle,
61
Q

are products of oncogenes, and they dont depend on growth factos or external signal of them to act

A

Oncoproteins

62
Q

The growth factor will act on the growth factor receptor through what receptor?

A

Paracrine Action

63
Q

The growth factor will act on the growth factor receptor through PARACRINE ACTION, meaning the growth factors originate from?

A

Different cells in the surrounding tissue

64
Q

Many cancer cells acquire the ability to synthesize the same growth factor to which they are responsive, creating an?

A

Autocrine loop

65
Q

Growth Receptors

A large number of oncogenes encode growth factor receptors, of which receptor ____ ____ are arguably the most important in cancer.

A

tyrosine kinases

66
Q

Growth Factor Receptors

Even if the growth factor will not act on the growth factor receptor, the growth factor of the cell can be constitutively activated due to?

A
  • Mutation
  • Gene rearrangement
  • overexpression

It will continuously deliver signals inside the cell for the cell to proliferate.

This is the problem in certain lung and breast cancer

67
Q

Growth Factor Receptors

FILL THE BLANKS
Genetic Aberration: Point Mutation

Gene: ERBB1

Protein:

Disease:

A

Protein: EGFR
Disease: Lung Cancer

68
Q

Growth Factor Receptors

FILL THE BLANKS
Genetic Aberration: Gene Amplification

Gene: ERBB2

Protein:

Disease:

A

Protein: HER2
Disease: Breast Cancer

69
Q

Growth Factor Receptors

FILL THE BLANKS
Genetic Aberration: Gene Rearrangement

Gene: EML4-ALK

Protein:

Disease:

A

Protein: EML4-ALK
Disease: Lung Cancer

70
Q

If growth factors are activated you will have ____ ____ carried out by signal transducing proteins

A

Signal transduction

71
Q

Signal Transducing Proteins

what signal transducing proteins is the Single most common abnormality of proto-oncogene

A

RAS oncogene

72
Q

Signal Transducing Proteins

Mutated RAS is trapped in its activated ____ form and if it is activated it will continuously flood the nucleus with signals for proliferation causing continuous entry of cell into the cell cycle

A

GTP-bound

73
Q

Transcription factors that can be included in carcinogenesis:

A

TF Oncogenes: MYC, MYB, JUN, FOS, REL

MYC is most commonly affected in
cancer,

74
Q

This orchestrates the orderly progression of cell through cell cycl by bindin to cyclins

A

Cyclin-Dependent Kinase (CDK)

75
Q

Give the 2 examples of CDK

A

Cyclin D, CDK4

76
Q

Tumor Suppressor Genes

  • GOVERNOR OF PROLIFERATION
  • A gene that is located on long arm of chromosome 13 region 1 band 4 (13q14)
A

RB

77
Q

Tumor Suppressor Genes

This can be mutated in several tumors but it is highly associated with Retinoblastoma in the eye

A

RB

78
Q

Tumor Suppressor Genes

  • GUARDIAN OF THE GENOME
  • Most common target for genetic alteration in human tumors
A

p53

79
Q

Tumor Suppressor Genes

  • Gene located on the short arm of chromosome 17 region 1 band 3 sub band 1 (17p13.1)
  • If this is active and not mutated, links cell damage with repair, promotes cell cycle arrest to be allowed for repair and if beyond repair, it will promote apoptosis to prevent neoplastic transformation
A

p53

80
Q

Tumor Suppressor Genes

  • GATEKEEPER OF COLONIC NEOPLASIA
  • This gene is located on long arm of chromosome 5 region 2 band 1 (5q21)
A

APC (Adenomatous polyposis coli)

Associated with Adenomatous polyposis coli (many polyps in the colon) and colon cancer

81
Q

EVASION OF CELL DEATH/APOPTOSIS

You will recall there are two pathways that lead to apoptosis, what are those?

A
  1. the extrinsic (death receptor) pathway - triggered by death receptors of the tumor necrosis factor (TNF) receptor family, such as FAS, and their ligands
  2. the intrinsic (mitochondrial) pathway - initiated by various stresses, such as the absence of growth factors and DNA damage.
82
Q

EVASION OF CELL DEATH/APOPTOSIS

the most frequently disabled in the carcinogenesis

A

INTRINSIC PATHWAY

83
Q

EVASION OF CELL DEATH/APOPTOSIS

In cancer formation, the goal of cancer cell is to avoid?

A

Apoptosis

84
Q

EVASION OF CELL DEATH/APOPTOSIS

enumerate the 2 major mechanism by which apoptosis is avoided by cancer cells

A
  • Loss of TP53
  • Overexpression of BCL2
85
Q

EVASION OF CELL DEATH/APOPTOSIS

Loss of p53 function prevents the upregulation of?

A

PUMA - a pro-apoptotic BH3-only protein, in response to DNA damage and other stresses, allowing cells to survive that otherwise would be killed

86
Q

EVASION OF CELL DEATH/APOPTOSIS

If there is loss of p53, there will be no upregulation of?

A

BAX and PUMA

87
Q

EVASION OF CELL DEATH/APOPTOSIS

Overexpression of ____ is a common event leading to the protection of tumor cells from apoptosis

A

BCL2 - anti-apoptotic gene

88
Q

THE STEM CELL–LIKE PROPERTIES OF CANCER CELLS

Cells do not die and are able to continuously proliferate because they are capable of the following, enumerate

A
  1. Evasion of senescence
  2. Evasion of Mitotic Crisis
  3. Self-renewal
89
Q

THE STEM CELL–LIKE PROPERTIES OF CANCER CELLS

Cells do not age—forever young, due to RB-dependent G1/S cell cycle checkpoint is disrupted

A

Evasion of Senescence

90
Q

THE STEM CELL–LIKE PROPERTIES OF CANCER CELLS

  • If the cells continuously proliferate, the telomerase shortens. Eventually the cell will age and die, this is called the mitotic crisis which can be evaded by cancer cells. They can do that by upregulation of telomerase (85-95% of cases) — an enzyme that
    is almost absent in our somatic cells.
  • Alternative lengthening of telomeres
A

Evasion of mitotic crisis

91
Q

THE STEM CELL–LIKE PROPERTIES OF CANCER CELLS

Long lived cancer stem cells possess another critical property, the capacity for?

A

Self-renewal

92
Q

Even if a solid tumor possesses all the genetic aberrations that are required for malignant transformation, it cannot enlarge beyond 1 to 2 mm in diameter unless it has the capacity to induce?

A

Angiogenesis

93
Q

Sustained Angiogenesis

Tumors that are more than 1-2 mm need blood supply, otherwise, there will be?

A

Ischemic Necrosis

94
Q

Sustained Angiogenesis

occurs when there is change in
phenotype that induces angiogenesis mostly controlled by hypoxia.

A

Angiogenic Switch

95
Q

Sustained Angiogenesis

The molecular basis of the angiogenic switch involves what increased local production of angiogenic factors

A
  • VEGf and bFGF
  • Loss of angiogenic inhibitors (thrombospondin-1)
96
Q

ABILITY TO INVADE AND METASTASIZE

Steps in invasion

  1. ____ or ____ of cancer cells from one another
A

Dissociation or detachment

Detachment is due to the downregulation of Ecadherin

97
Q

ABILITY TO INVADE AND METASTASIZE

Steps in invasion

(2) Degradation of the?

A

basement membrane and ECM/ interstitial connective tissue

98
Q

ABILITY TO INVADE AND METASTASIZE

(From step 2) Tumor cells are able to move after detachment because they secrete?

`

A

proteolytic enzymes or induce stromal cells to secrete enzymes

99
Q

ABILITY TO INVADE AND METASTASIZE

(3) Changes in attachment of tumor cells to?

A

ECM Protein

Tumor demonstrate complex changes in the expression of integrins

100
Q

ABILITY TO INVADE AND METASTASIZE

what is the final step of evasion

A

Locomotion

101
Q

ABILITY TO INVADE AND METASTASIZE

Such movement for locotiom is stimulated and directed by what factors?

A

▪ Cytokines from tumor cells themselves
▪ Stromal cell motility factors
▪ Cleavage products of matrix components (e.g., collagen, laminin)

HistoPathology (10 decks)

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