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MM Test 4 > B6.076 Neoplasia Review and Metastatic and Hematopoietic Tumors of Bone > Flashcards

B6.076 Neoplasia Review and Metastatic and Hematopoietic Tumors of Bone Flashcards

1
Q

what is a neoplasm

A

disease caused by uncontrolled proliferation of cells that have undergone genetic alterations (mutations)

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2
Q

characterize benign lesions

A

expansive
slow growth
well differentiated
no metastasis

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3
Q

characterize malignant lesions

A

infiltrative
fast growth
atypical / poor differentiation
metastasis typical

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4
Q

what is invasion

A

extension beyond immediate local environment
-ie in epithelial cells, extension through VM
cells separate from neighboring cells and locomote / migrate

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5
Q

routes of metastasis

A 
direct seeding of body cavities (peritoneum, pleura, pericardium)
lymphatic
hematogenous
-venous (through capillary bed)
-arterial (from or through lung)
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6
Q

common sites of metastasis

A

lymph node
liver (receives large volume of venous drainage)
lung (moves cells into arterial circulation)
bone
brain

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7
Q

most common skeletal malignancy

A 
bone metastases (far more common than primary bone tumors)
**hematopoietic tumors are the second most common malignancy of bone
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8
Q

presentation of bone metastasis

A 
multifocal involvement
axial skeleton > long bones > small bones (corresponds to blood flow / red marrow)
pathologic fracture (due to weakened bones)
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9
Q

pathways of spread of bone metastasis

A

direct extension
lymphatic or hematogenous
intraspinal seeding

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10
Q

most common type of metastatic lesions in bone

A

lytic lesions = increased bone resorption

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11
Q

bone matrix changes that support lytic lesion formation

A

tumor cells secrete PGEs, cytokines, PTHrP

  • upregulate RANKL on osteoblasts and stromal cells
  • stimulate osteoclast activity
  • bone resorption
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12
Q

bone matrix changes that support tumor cell growth

A

stromal cells secrete growth factors

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13
Q

treatment / prognosis of bone metastases

A

poor prognosis (stage 4)
local treatment: surgery / fixation, radiation, bisphosphonates
systemic treatment: chemo, target therapy, immunotherapy, hormonal therapy

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14
Q

most common primary site of bone metastases in adults

A

prostate
breast
kidney
lung

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15
Q

most common primary site of bone metastases in children

A

neuroblastoma
wilms tumor
ewing sarcoma
rhabdomyosarcoma

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16
Q

primary sites that cause lytic bone lesions

A 
RCC
lung cancer
GI carcinoma
thyroid cancer
melanoma
adrenal carcinoma
pheochromocytoma
uterine carcinoma
wilms
ewings
HCC
squamous cell of the skin
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17
Q

primary sites that cause sclerotic bone lesions

A 
prostate (most common)
breast
transitional cell carcinoma
carcinoid
medulloblastoma
neuroblastoma
mucinous adenocarcinoma of the GI tract
small cell lung cancer
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18
Q

system of cancer staging

A

TNM
T: characteristics of primary tumor (size, extent of invasion)
N: involvement of regional lymph nodes
M: distant metastasis

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19
Q

cancer grading

A

histo determination of degree of differentiation

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20
Q

enabling characteristics of cancer

A
  • failure of DNA repair

- tumor promoting inflammation

21
Q

hallmarks of cancer

A
  • activation of growth promoting oncogenes
  • inactivation of tumor suppressor genes
  • alteration in genes that regulate apoptosis
  • angiogenesis
  • escape from immunity
  • additional mutations (enabling replicative immortality, deregulating cellular energetics)
22
Q

translocations associated with cancer

A 
dysregulation of gene expression
-c-MYC (8;14) (Burkitt)
-BCL2 (14;18) (follicular)
-cyclin D1 (11;14) (mantle)
structural alteration of gene
-BCR/ABL (9;22) (CML)
23
Q

deletions associated with cancer

A

RB (retinoblastoma)

24
Q

gene amplifications associated with cancer

A

N-MYC (neuroblastoma)

HER-2/neu (breast cancer)

25
Q

chromothrypsis

A

extensive chromosomal breaks and rearrangements

osteosarcoma, glioma

26
Q

point mutations associated with cancer

A

RAS (many cancers)

27
Q

epigenetic changes associated with cancer

A 
local hypermethylation (silencing)
global changes in methylation
changes in histones
28
Q

noncoding RNAs associated with cancer

A

altered expression of microRNAs (miRs)

-interaction with oncogenes and tumor suppressor genes

29
Q

driver mutations

A

contribute to development of the malignant phenotype

30
Q

passenger mutations

A

no effect on proliferation; but may lead to neo-antigens and affect immune surveillance
reflect loss of ability to maintain genomic integrity
more common than driver mutations

31
Q

tumor mutational burden

A

as # of mutations increases, there is a decrease in successful DNA repair
as # of mutations increases, there is an increased expression of abnormal antigens (cant be targeted by immune response if immune response is turned on)

32
Q

immune response to tumors

A

lymphoid response to tumors and in draining lymph nodes
increased incidence of tumors in immunodeficiency
tumor specific T cells and Abs
tumor suppression by stimulating host T cell surveillance

33
Q

anti tumor mechanisms (immune surveillance)

A

cytotoxic CD8+ T lymphocytes
NK cells
macrophages

34
Q

how do cancers escape immune surveillance

A

immune response guides cancer evolution (cancer immunoediting)
tumor derived immune suppression and immune tolerance

35
Q

what are examples of tumor antigens

A

products of mutated genes
aberrantly expressed proteins
antigens from oncogenic viruses
oncofetal antigens
altered cell surface glycoproteins and glycolipids
cell type specific differentiation antigens

36
Q

what is the result of tumor antigens

A

affect immune response to tumor
-T and B cell response
-inhibition / silencing of immune response
serve as markers for tumors
-diagnosis
-screening
cell specific differentiation antigens can be targets for immunotherapy

37
Q

ways that tumors can escape from immune surveillance

A
  • immunodeficiency / immunosuppression
  • outgrowth of antigen-negative variants (cancer immunoediting)
  • loss of MHC molecules
  • activation of immunoregulatory pathways (checkpoints)
  • secretion of immunosuppressive factors
  • induction of Treg cells
38
Q

checkpoints that can be modified by tumor cells

A

downregulation of costimulatory factors on APCs
-APC fails to sensitize T cell
-inhibits T cell by activating CTLA-4
upregulation of PD-L1/PD-L2 on tumor cells
-activate PD-1 on T cell with consequent T cell inhibition

39
Q

hormonal tumor markers

A

HCG (trophoblastic)
calcitonin (medullary carcinoma of the thyroid)
catecholamines (pheochromocytoma)

40
Q

oncofetal antigen tumor markers

A 
a-fetoprotein (HCC, yolk sac)
carcinoembryonic antigen (GI carcinoma, lung, pancreas)
41
Q

isoenzyme tumor markers

A

prostatic acid phosphatase (prostate cancer)

42
Q

specific protein tumor markers

A

PSA (prostate)

immunoglobulins (MM)

43
Q

mucin and glycoprotein tumor markers

A 
CA 19-9 (colon and pancreatic cancer)
CA 125 (ovarian)
44
Q

hallmarks of cancer

A 
avoid immune destruction
evading growth suppressors
enabling replicative immortality
tumor promoting inflammation
activating invasion and metastasis
genomic instability
inducing resisting cell death
deregulating cellular energetics
sustaining proliferative signaling
45
Q

what are oncogenes

A

products of an oncogene has growth promoting effects
-excessive production
-abnormal product unresponsive to normal inhibitory influences
mutations (gain of function) yield an oncogene

46
Q

examples of oncogenes

A 
growth factors
growth factor receptors 
-RET (MEN)
-her-2-neu (breast cancer)
signal transducing protein
-RAS
non-receptor tyrosine kinase
-ABL (CML)
transcription factors
-MYC (Burkitt, neuroblastoma)
cyclins/CDKs
-cyclin D1 (mantle)
47
Q

what are tumor suppressor genes

A

products of a tumor suppressor gene has growth inhibiting effect (gatekeeper genes)

  • insufficient production
  • abnormal product
48
Q

how do you inactivate a tumor suppressor gene

A

requires inactivation of both alleles or inactivation of a protein product

  • inactivation of one allele only with one normal allele is sufficient to prevent neoplasia
  • loss of heterozygosity predisposes to neoplasia
  • many oncogenic DNA viruses (HPV) act by inactivating tumor suppressor genes

MM Test 4 (20 decks)

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