Neoplasia Flashcards

(46 cards)

1
Q

Neoplasia

A

New growth of tissues and cells (transformed)

  • have high degree of autonomy
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2
Q

Benign neoplasm

A

Tumors that are considered innocent and will remain localized

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3
Q

malignant neoplasm

A

Tumor that will invade nearby tissues and can metastize into blood stream

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4
Q

Two basic opponents of all neoplasms

A

Parenchyma is transformed

Has own stroma

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5
Q

Parenchyma

A

Determines biological behavior of the neoplasm, also gives name

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6
Q

Stroma

A

Provides support/nutrients to the parenchyma of the neoplasm

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7
Q

Benign tumor nomenclature

A

Prefix is what tissue neoplasm arose from

Suffix is always “oma”

Ex: fibroma (fibrous tissue)

Ex: conformant (cartilage tissue)

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8
Q

Papillomas

A

Benign epithelial neoplasms

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9
Q

Adenoma

A

Neoplasms arising from glands generally.

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10
Q

Sarcoma

A

Malignant neoplasm in solid mesenchymal tissues

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11
Q

Leukemia vs lymphoma

A

Malignant tumor in blood vs malignant tumor in lymph respectively.

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12
Q

3 fundamental features that determine benign vs malignant

A

Differentiation/anaplasia

Local invasion

Metastasis

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13
Q

Pleomorphism

A

Variation in size and shape of same cells

Often possessed by anaplasic cells

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14
Q

Anaplasia

A

Very poorly differentiated tumor

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15
Q

Tumor capsule

A

Large ECM and fibroblast aggregation

Allows for non-fixed tumors and easily able to be remove. Common in benign tumors

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16
Q

3 pathways of metastasis

A

Seeding in local body cavities

Lymphatic spread

Blood circulatory spread

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17
Q

Paraneoplastic syndromes

A

Symptom complexes in cancer patients that cannot be explained general tumor characteristics

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18
Q

Paraneoplastic syndrome groupings

A

Endocrine

Hematologists

Osteoarticular

Cutaneous

Neurological

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19
Q

Most common paraneoplastic syndrome symptoms

A

Hypercalcemia

Cushing syndrome

Nonbacterial thrombotic endocarditis

20
Q

Most important Environmental factors for cancer

A

Smoking

Alcohol consumption

Reproductive history

Diet

Infectious agents

21
Q

Most important acquired factors to cancer

A

Chronic inflammation

Chronic immunodeficiency

Precursor lesions

22
Q

Precursor lesions

A

Changes (metaplasia, hyperplasia or dysphasia) in Epithelial cells that occur not by cancer.

23
Q

4 major function classes of cancer genes

A

Oncogenes

Tumor suppressor genes

Apoptosis regulation genes

Host/tumor communication genes

24
Q

Oncogenes

A

Mutated genes that induce cancer-like phenotypes in healthy cells

Produces oncoproteins that are self-induced and self-regulated

This includes increased unregulated cellular growth

25
Proto-oncogenes
Normal unmutated versions of oncogenes. Produce Normal oncoproteins that are regulated by signals Participate in signal pathways that drive controlled proliferation
26
Possible functions/classes of oncoproteins
Growth factors Growth factor receptors Signal transducers Transcription factors Cell cycle components
27
PDGF and TGF (alpha)
Examples of growth factors produced by oncogenes Many produce autocrine loops that causes unregulated cell growth
28
ERBB1 & HER2
Growth factor receptors that act as oncoproteins in epithelial and breast cancers respectively
29
RAS
Most commonly mutated oncogene in tumors - remains fixed in proliferating state when point mutations occur
30
ABL
Proto-oncogene that has tyrosine kinase activity. Oncogenes form is caused by a translocation of chromosome 9 -> 22. t(9;22) - Oncogene forms BCR-ABL hybrid protein
31
Oncoproteins that function as pseudo-transcription factors for growth-promoting genes in DNA transcription
MYC, JUN & FOS
32
MYC
Activates transcription of genes. - targets genes with CDKs and that produce common macromolecule building blocks - dysregulation causes unregulated of the above.
33
Burkett lymphoma
Type of B-cell tumor that causes t(8;14) of MYC gene, causing over production of MYC protein
34
cyclic dependent kinases (CDKs)
Bind to cyclin and phosphorylate protiens that push G0 cells into the cycle cycle to proliferate Usually are around inhibitors that tightly regulate them
35
Main cell cycle checkpoints where CDKs playa role
G1/S (most targeted) G2/M
36
Cell cycle oncogenes two main effects
Gain o function of CDK4 Loss o function of CDKis
37
RB tumor suppressor gene
Key negative regulator of cell cycle. Inactivation usually causes cancer (Retinoblastoma primarily)
38
Two-hit hypothesis
Two mutations in tumor suppressor genes are needed to produce a cancer. Has familial and sporadic cases
39
Familial cases of RB
Children inherit 1 defective copy of RB gene. The other is normal, but undergoes somatic mutation in cases where retinoblastoma is seen.
40
Sporadic cases of retinoblastoma
Possess 2 normal RB alleles that are both lost via somatic mutation in retinoblastoma production.
41
TP53
Most commonly mutated gene in human cancer
42
TP53 protein
Activates quiescence Induces senescence when needed Triggers apoptosis when needed -production is triggered via anoxia (DNA damage)
43
Quiescence
Temporary cell cycle arrest
44
Senescence
Permanent cell cycle arrest
45
Li-framumeni syndrome
Inherited mutant TP53 allele - increases likelihood of cancer due to one “hit”already being present - roughly 25x likelier
46
BCL2 overexpression
anti-apoptosis proteins Over-expression allows cancers to form and not induce apoptosis