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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

(48 cards)

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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

Study These Flashcards
A
  • failure of DNA repair

- tumor promoting inflammation

21
Q

hallmarks of cancer

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A

RB (retinoblastoma)

24
Q

gene amplifications associated with cancer

Study These Flashcards
A

N-MYC (neuroblastoma)

HER-2/neu (breast cancer)

25
chromothrypsis
extensive chromosomal breaks and rearrangements | osteosarcoma, glioma
26
point mutations associated with cancer
RAS (many cancers)
27
epigenetic changes associated with cancer
``` local hypermethylation (silencing) global changes in methylation changes in histones ```
28
noncoding RNAs associated with cancer
altered expression of microRNAs (miRs) | -interaction with oncogenes and tumor suppressor genes
29
driver mutations
contribute to development of the malignant phenotype
30
passenger mutations
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
tumor mutational burden
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
immune response to tumors
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
anti tumor mechanisms (immune surveillance)
cytotoxic CD8+ T lymphocytes NK cells macrophages
34
how do cancers escape immune surveillance
immune response guides cancer evolution (cancer immunoediting) tumor derived immune suppression and immune tolerance
35
what are examples of tumor antigens
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
what is the result of tumor antigens
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
ways that tumors can escape from immune surveillance
- 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
checkpoints that can be modified by tumor cells
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
hormonal tumor markers
HCG (trophoblastic) calcitonin (medullary carcinoma of the thyroid) catecholamines (pheochromocytoma)
40
oncofetal antigen tumor markers
``` a-fetoprotein (HCC, yolk sac) carcinoembryonic antigen (GI carcinoma, lung, pancreas) ```
41
isoenzyme tumor markers
prostatic acid phosphatase (prostate cancer)
42
specific protein tumor markers
PSA (prostate) | immunoglobulins (MM)
43
mucin and glycoprotein tumor markers
``` CA 19-9 (colon and pancreatic cancer) CA 125 (ovarian) ```
44
hallmarks of cancer
``` 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
what are oncogenes
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
examples of oncogenes
``` 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
what are tumor suppressor genes
products of a tumor suppressor gene has growth inhibiting effect (gatekeeper genes) - insufficient production - abnormal product
48
how do you inactivate a tumor suppressor gene
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

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