Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Disease And Defense > Cancer/Neoplasia Exam 2 > Flashcards

Cancer/Neoplasia Exam 2 Flashcards

1
Q

Morphogenesis

A

normal development which contains active cell growth from single cell and

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Morphogenesis

A

normal development which contains active cell growth from single cell and develops into multicellular organism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what happens in a normal cell’s lifetime?

A

proliferation, migrate, differentiate, change relationship to neighboring cells, apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Three types of adult tissues

A

1) non-dividing (little to no proliferation) 2) quescent tissue (normally no proliferation, but respond to some stimuli - liver) 3) constantly dividing tissue (gut)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypertrophy

A

increase in cell size, in response to stimulus; pathologic and physiologic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hyperplasia

A

increase in cell number, in response to stimulus, physiologic or pathologic, predisposition to neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Metaplasia

A

change from one benign, differentiated cell type to another in response to injury; predispose to neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Neoplasia

A

autonomous, progressive cell growth involving clonal cell population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tumor

A

lating for swelling; however usually synonymous with neoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how doe neoplasias arise?

A

non-lethal genetic damage either acquired or inherited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

targets of genetic mutations that give rise to neoplasia

A

proto-oncogenes, growth suppressive tumor suppressor genes, apoptosis regulators, DNA repair genes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Benign

A

non-invasive, non-metastatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Malignant

A

invasive, metastatic, synonymous with cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cell intrinsic homeostasis

A

differentiation program, age of cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Microenvironment homeostasis

A

ECM and Stroma growth factor and inflammatory signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Macroenvironment homeostasis

A

circulating factors in blood - hormones and cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

External environmental interactions

A

physical environment, infection agents, inhaled/ingested substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Layers of tissue homeostasis

A

external environment interactions, cell extrinsic - macro and microenvironment, cell intrinsic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what happens when homeostatic balance is disturbed?

A

pathology results

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is a physiological hyperplasia?

A

lactation in breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

causes of metaplasia

A

Smoking (columnar to squamous); Barrett Esophaus (acid reflux from squamous to columnar (SI like))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Risks associated with Barrett Esophagus

A

have a higher risk of esophageal cancer with the intestinal epithelium replacing the squamous epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Mucousopathy

A

scraping away the mucosal layer of the esophagus as a measure of preventing cancer development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Clonal Process

A

arrise from a single cell that propagates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cell-Autonomous mechanisms altered in neoplasia

A

Activation of onco-genes or inactivation of tumor suppressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cell-nonautonomous mechanisms altered in neoplasia

A

altered micro: surrounding stroma, vessels, immune cells; altered marco: circulating cells (immune) and factories (hormones, cytokines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Benign Neoplasms

A

Don’t invade or metastasize but cause injury due to compression/interference in function with adjacent structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Malignant neoplasms

A

invade and metastasize; cause injury to both local tissue and distant dissemination.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Gross pathologic features of benign vs. malignant

A

Benign: encapsulated and necrosis is uncommon; malignant: invasive into adjacent tissue and necrosis is common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Microscopic pathologic findings of Benign neoplasia

A

well differentiated; low rate of cell turnover; cytologic uniformity (similar to each other); maintained cell boundaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Microscopic pathologic findings of malignant neoplasia

A

variable differentiation, high rate of cell turnover, cytologic pleomorphism (cells different from each other), generally loss of boundary with adjacent tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

cytologic pleomorphism

A

cells look different from each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Name of benign neoplasia - epithelial

A

Adenoma, less commonly papilloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Name of benign neoplasia - Mesenchymal

A

osteoma, chondroma, fibroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Name of malignant neoplasia - epithelial

A

carcinoma (adenocarcinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Name of malignant neoplasia - mesenchymal

A

sarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Name of malignant neoplasia - hematopoietic

A

lymphoma, leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Adenocarcinoma

A

carcinoma with formation of glandular structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Treatment of benign neoplasm

A

excision along; may reoccur if no excised completely;generally do not progress into malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the exception that benign neoplasms can lead to malignant

A

colonic adenoma - premalignant neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Biological correlates of benign neoplasm

A

not understood very well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

how many people get cancer?

A

1 in 2 americans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how many people die of cancer?

A

1 in 5 americans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Cancer etiology - non-genetic factors

A

Age, lifestyle, occupation/chemical hazards, radiation, infection, inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Dominant Heritable cancer syndromes

A

RB, p53, APC, BRCA1/2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Autosomal recessive Cancer Cydromes

A

Xerderma pigmentoum, fancoli anemia, ataxia-telangiectasia, bloom syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Familial cancer types

A

inherited predispositon, but not clear for each individual. Breast, ovarian, pancreatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Cancer hallmarks

A

1) evading apoptosis 2) self sufficiency for growth signals 3) insensitivity to anti-growth signals 4) tissue invasion/metastasis 5) limitless replicative potential 6) sustained angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what type of cancer is the most common?

A

carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Dysplasia

A

disordered growth; hallmark of early premalignant neoplasia in epithelia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Histology of dysplasia

A

loss of cytologic uniformity, loss of normal histologic maturation, loss of architectural orientation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Low grade dysplasia

A

more normal cells and differentiation and less abnormal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Carcinoma in-situ

A

mose extensive dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How is stage measured?

A

Tumor size/invasion; Region lymph node involvement; metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

trends in tumor stage and clinical outcome

A

As T increases, survival rate drop. Lymph node metastasis drops as well. Malignancy is worst prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

pre-malignant lesion in Carinoma vs. Carcoma vs. Lymphoma/leukemia vs. CNS neoplasms

A

Yes: carcinoma; some L/L (myelodysplasia); NO: sarcoma and CNS neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

In-situ phase in Carinoma vs. Carcoma vs. Lymphoma/leukemia vs. CNS neoplasms

A

Yes: Carcinoma NO: sarcoma, L/L, CNS neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Invasion in Carinoma vs. Carcoma vs. Lymphoma/leukemia vs. CNS neoplasms

A

Yes: carcinoma, sarcoma (faster than carcinoma) and CNS neoplasms; L/L N/A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Metastasis in Carinoma vs. Carcoma vs. Lymphoma/leukemia vs. CNS neoplasms

A

Yes: Carcinoma, sarcoma (faster than carcinoma), rarely in CNS neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Grade predictive of behavior in Carinoma vs. Carcoma vs. Lymphoma/leukemia vs. CNS neoplasms

A

All Carcinomas, sarcomas, L/L and CNS neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Stage predictive of behavior in Carinoma vs. Carcoma vs. Lymphoma/leukemia vs. CNS neoplasms

A

Yes: carcinomas, sarcomas; N?A in L/L and CNS neoplasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Pediatric Neoplasms

A

childhood neoplasms arrise in developing tissue/organs and cause: origin to be in developmental precursors; tend to recapitulate aspects of development of tissue of origin; short latency and early metastasis; fewer mutations (prominent oncogenic fusions and epigenetic dysregulation; chemosensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Price of chemo in pediatric populations?

A

secondary malignancy and developmental problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Carcinoma in situ

A

pre-invasive state of carcinomas; common in skin, breast; without invasion of the basement membrane; precursor step before invasive cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

the term cancer literally means

A

crablike

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Dissemination of cancer (3) pathways

A

1) direct seeding of body cavities or surfaces (tumor cells shed out directly) 2) lymphatic spread 3) hematogenous spread (carried by blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

four main steps in metastatic cascade.

A

1) invasion through BM 2) intravasation - getting to blood or lymph 3) extravasation - getting out of B and L 4) colonization - ability to grow at distant sight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

when is angiogenesis necessary for tumors?

A

bigger than 1 mm^3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

There is a link between the size of the primary tumor and ….

A

whether it has metastasized or not

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Emerging hallmark of malignant cancer..

A

modification of cellular metabolism to support proliferation and avoiding immune destruction; genomic instability and tumor promoting inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

why does cancer start to metastasize?

A

when cells build up in layers in a tumor, you get hypoxia and the cells are forced to alter metabolism, selection of the fittest, gene mutations occur and they start to invade through the basement membrane to reach more nutrients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

In Metastatic Cascade carcinoma cells must

A

1) invade basement membrane 2) traverse CT 3) gain access to circulation by vascular basement membrane (intravasation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Intravasion

A

gain access to circulation by penetrating basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Invasion

A

active process; loss of E-cadherin to cause loosening up: degradation of ECM; attachment to ECM compounds, migration of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Step 1 of Invasion

A

Dissociation of cells from one another - alterations in adhesion molecules; down regulation of E-caderin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

E-Cahderin

A

transmembrane glycoprotein that holds epithelial cells together.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what does E-cadherin attach to

A

B-catenin (underlies plasma membrane) and actin cytoskeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Step 2 of Invasion

A

local degradation of basement membrane and interstitial connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

MMP

A

Matrix Metallo-proteases are involved in invasion; released by tumor cells or induced by stormal cells to cause remodeling of basement membrane and release ECM sequestered growth factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Cleavage products of basement membrane/ECM by MMPs

A

collagen, proteoglycans, chemotatic angiogenic, and growth promoting restuls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

2nd method of invasion

A

ameboid migration - cell squeezes through spaces in matrix instead of using proteases; quicker. Tumor cells switch between these two forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Step 3 of invasion

A

Changes in attachment of tumor cells to ECM proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Integrins

A

epithelial cells normally have these receptors that maintain them on the basement membrane, can send out signals that they are no longer attached and cause apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

how does matrix modification aide in invasion?

A

cleavage generates novel sites that bind to receptors on tumor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Step 4 of invasion

A

Locomotion - propelling tumor cells through basement membrane through leading edge and detachment from matrix at trailing edge through action cytoskeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Types of tumor cell motility

A

collective (retain epithelial connections); mesenchymal; ameboid (squeezing of cell body)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

how is movement directed in tumor cells?

A

tumor cell derived cytokines act as autocrine motility factors; cleavage products of matrix and GFs are chemotactic; stomal cells produce paracrine effectors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

loss of e-Cadherin

A

associated in invasive phenotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

how does loss of e-cadherin happen?

A

LOH, mutation (rare), silence of gene exp by hypermethylation, transcriptional repressors (snail slug, twist, ZEB1/2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Where are transcriptional repressors usually held?

A

in fibroblasts, but are activated in tumor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Epithelial to Mesenchymal Tranision

A

TFs (snail, tiwst, ZEB1/2) repress E-cadherin to make more like fibroblast so they are better able to change shape, be mobile and are able to survive in the fluid (normally epithelial free cells would be apoptosed); normal embryonic development but co-opted by cancer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

EMT where does it occur in normal deelopment?

A

palatogenesis, neural crest formation, cardic valve, myogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

how is repression of E-cadherin used in normal development?

A

want to repress it, so cells are more motile to move to their proper locations during embryogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

MET

A

Mesenchymal to Epithelial transition occurs after extravasation where the cancer cells acquire characteristics of epithelial cells again at distant site.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Downregulation in EMT

A

e-cadherins, cytokeratin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Upregulation in EMT

A

Vimentin, fibronectin, N-Cadherin, Motility and invasiveness, increased protease secretion, fibroblast-like morphology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Is EMT all or none?

A

no, they retain some epithelial cells markers, but have mesenchymal qualities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

how do you find Circulating tumor cells?

A

use epithelial and mesenchymal marker antibody cocktail to see both qualities in the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Which cancers metastasize the fastest?

A

those that loose the most epithelial characteristics and gain the most mesenchymal; this makes it easy for the tumors to resist chemotherapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

how does tumors resist chemotherapy?

A

develop mesenchymal characteristics though EMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Tumor microenvironment

A

mesoderm derived cells, ECM, soluble matrix-associated GFs, cytokines and proteases; environment where signaling can affect tumor supressor, promotion or progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

mesoderm derived cells in tumor microenvironment

A

firbroblasts, adipocytes, immune cells, endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Free cancer cells in bloodstream are..

A

vulnerable to destruction by mechanical stress, apoptosis simulated by loss of adhesion, immune defense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

anoikis

A

apoptosis stimulated loss of adhesion in epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Adhesion in circulation

A

cancer cells aggregate in clumps and with blood cells and platelets to enhance survival and implant ability - form emboli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Extravasion

A

tumor emboli arrest at different site, ahdesion to endothelium, and egress through basement membrane using adhesion molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

where does extraversion occur?

A

Combination of Seed and Soil theory and Mechanical Arrest theory - work in concert to produce successful metastasis + the use of chemical signals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Seed and Soil theory

A

seed and soil - organ specific pattern are explained by needs of cancer cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Mechanical Arrest theory

A

tumor cells get trapped in first capillary bed they encounter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Organ Tropism

A

1) adhesion to endothelium via expression of adhesion molecules that interact with ligands on tissue (tissue ligands are specific) 2) Chemokines - tumor cells have chemokine receptors and tissue expresses chemokine (IGF1 and 2) 3) some tissues are non-permissive environment - ie. skeletal muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

CXCR4

A

chemokines in breast cancer cells that react with CXCL12/SDF1 that are expressed from lungs, liver and bone. (these are the favored sites for breast cancer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Colonization

A

tumor cells growing and developing at distant sites - inefficient! Tumors secrete cytokines, GF, and ECM molecules that act on stromal cells to make metastatic site habitable.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Dormancy

A

prolonged survival of micrometaises without progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Direct effect of metastases

A

invasive masses which interfere with normal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Indirect effect of metastases

A

paracrine/endocrine effects (7-15% of patients)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Paraneoplastic syndrome

A

indirect paracrine/endocrine effects due to hormones or cytokines excreted by cancer cells OR immune response triggered.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Examples of Paraneoplastic syndrome

A

Ectopic hormone production, arthropathies, joint pain, muscle pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Causes of death in cancer pt.

A

most often is Infection (41.6%); organ failure (19.2%); Thromboembolism (12.2%); Hemorrhage (8.8%); emaciation (7.7%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

what percentage of cancer is caused by environmental factors?

A

> 80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

why is cancer most due to environmental factors?

A

1) variation within country 2) variation among countries 3) migrants adopt new cancer risk when they move.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What # cause of death is malignant neoplasms?

A

2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

how many cases of cancer are predicted to be in colorado?

A

24,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

leading cancers in colorado?

A

Breast, colon/rectum, lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

leading causes of cancer deaths in CO?

A

Lung and bronchus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

How many cancer deaths in CO?

A

7,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

trend of lung, trachea, bronchus, and pleura in white males

A

mostlly in south - most due to lung cancer, but aslo petroleum, paper, ship building, chemical insdustries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Rate of Cancer in denver compared to national average

A

similar/high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

why does boulder have higher breast cancer risk?

A

women delay having children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

what cancer is most and least prevalent in Africa?

A

Liver Cancer; esophageal is uncommon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Where is esophageal cancer prevalent?

A

Iran - Solinium in soil, certain tea they drink

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What are the post prevalent cancers in US?

A

Breast, prostate, lung, colon/rectum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

what % of cancer does smoking contribute to?

A

30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

what cancers are attributed to smoking?

A

Lung, esophagus, oropharynx, larynx (slight increased for stomach and pancreatic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Other health problems due to smoking?

A

chronic bronchitis emphysema, MI, atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

how many deaths are attributed to smoking?

A

443,000 a year

136
Q

Leading new cases of cancer in 2016 men

A

prostate, lung and bronchus, colon and rectum

137
Q

Leading new cases of cancer in 2016 women

A

breast, lung and bronchus, colon and rectum

138
Q

Leading causes of death in males in 2016

A

Lung/Bronchus, prostate, C and R

139
Q

leading causes of death in females fin 2016

A

Lung/bronchus, breast, C and R

140
Q

why has stomach cancer decreased so dramatically?

A

refrigeration - prevents fungi from growing on food that releasing carcinogens. We eat less smoked fish.

141
Q

why has colon cancer decreased?

A

Screening, but BC pills may be protective

142
Q

risk of cancer in CO for males

A

1 in 2

143
Q

Risk of cancer in CO for females

A

2 in 5

144
Q

why is cancer a disease of 70-80 year olds?

A

accumulation of mutations - in proto-oncogenes, loss of tumor supressor, DNA repair mechanism; changes in immunity (immunosuppression with age)

145
Q

Hodgkin’s Disease - age peak

A

peaks are 32-33;

146
Q

ALL - age peak

A

children

147
Q

exception for cancers in younger generation

A

Hodgkins, ALL, brain cancers

148
Q

Classes of chemical carcinogens

A

1) polycyclic aromatic hydrocarbons (burning fossil fuels and cigarettes smoke) 2) Aromatic amines (dye industry and insecticide) 3) Nitrosamines and Nitrosamides (preservatives in food - ham, bologna) 4) aflatoxins (contaminants in ground nuts and grains)

149
Q

how are polycyclic aromatic hydrocarbons developed?

A

burning fossil fuels and cigarette smoke

150
Q

aromatic amine origin

A

dye industry and insecticides

151
Q

Nirtosamine and nitrosamides origin

A

food preservatives

152
Q

Alfatoxins origin

A

contaminants in ground nuts and grain

153
Q

why makes all of these chemical carcinogens related?

A

all need to activated by the cytochrome P450 system

154
Q

Cyto P450

A

microsomal enzyme, induced or constitutively expressed, oxidize H groups and make products that are mutagenic.

155
Q

Miller’s Theory

A

1) chem carcinogens are metabolized by microsomal enzymes into active form 2) active metabolite is strong electrophile 3) electrophilic can modify proteins, RNA, DNA

156
Q

DNA modification by chemical carcinogen is due to…

A

attach of the four bases, modified bases are not fixed in MMR and frameshift

157
Q

Asbestos Can cause which types of cancer?

A

Lung cancer, Larynx, Mesothelioma (only thing that causes this!)

158
Q

how many cancer patients are caused by known carcinogens?

A

less than 1%- most are unknown!

159
Q

AIMS test

A

measures ability of chemical in presence of CytoP450 to mutagenize strain of salmonella that is histidine - (can’t grow on histamine lacking agar). if enzyme is capable of making a mutagenic form, reverence emerges which are capable of growing in absence of histidine supplement (mutating genome)

160
Q

Why is there a clear zone right around the disc in the AIMs test?

A

many of the chemicals are toxic at too high of a dose.

161
Q

results of AIMS test?

A

1) substances that cause cancer mutate DNA 2) potency of mutagen parallels its carcinogenicity 3) mutagens are very prevalent in our environment!

162
Q

what we learned from experimentation with animals?

A

1) cancer is dose dependent to chemical 2) specific carcinogens cause specific cancer types 3) carcinogens require time 4) carcinogens require cell proliferation 5) cellular changes trigger carcinogens are stably transmitted to daughter cells 6) stem cells become malignant 7) malignant stem cells fail to differentiate normally

163
Q

Two stage cancer theory

A

stage 1: initiation stage mutagen that is irreversible 2: promotion stage - not mutagenic, reversible (often irritants)

164
Q

what are tumor promotors

A

phorbol, esters, bile acids, pheobarbital, phenols, etc.

165
Q

what types of inflammation promote carcinogenesis?

A

ulcerative colitis, cholecystistis, chronic osteomyelitis, chronic hepatitis, chronic pancratitis, schisotsomiasis of urinary bladder

166
Q

Driver mutations

A

125 mutations, promote growth advantage and passenger mutations that regulate signaling pathway that impact cell fate, survival and genome maintenance.

167
Q

Carcinoma

A

malignant neoplasms of epithelium - arise form malignant stem cells with oncogenes, loses tumor suppressor, develops genome instability and/or loses ability to apoptosis

168
Q

carcinomas can….

A

invade and metastasize

169
Q

Grade (cancer diagnosis)

A

extent of differentiation - low grade is well differentiated; oftentimes associated with how agressive the cancer is

170
Q

Stage (cancer diagnosis)

A

extent of tumor spread at diagnosis - best predictor of prognosis.

171
Q

TNM classification

A

T= size of tumor (1-4) N = lymph node involvement (none or #) M = metastasis (yes or no)

172
Q

Which cancers have the lowest prognosis at 5 years (5 year survival)?

A

Lung 16%; Pancreas

173
Q

colorectal survival rate at 5yrs?

A

65%

174
Q

Prostate survival rate at 5 years?

A

99%

175
Q

Lung Cancer cure

A

surgical excision: lobectomy or pneumonectomy; Chest- C-irradiation, chemo

176
Q

Peak incidence in lung cancer

A

70 for men and women

177
Q

% of smokers that develop lung cancer?

A

10%

178
Q

Other factors of lung cancer besides smoking?

A

family Hx, industrial metal vapors uranium mining, asbestos, radon gas

179
Q

Lung carcinoma symptoms

A

Persistent cough/change in cough, difficulty breathing, chest pain, obstructive pneumonia, horsiness, facial swelling, weight loss

180
Q

why does lung cancer present with horseness?

A

involvement of recurrent laryngeal N.

181
Q

Horner Syndrome in Lung Cancer

A

swelling of the face, dropping, small pupils, ptosis, little to no sweating due to sympathetic ganglia invasion

182
Q

Diagnosis of Lung Cancer

A

CT, MRI, PET scan, x ray, Tissue diagnosis is essential, Mediatinoscopy to assess for lymph node involvement.

183
Q

what lines the respiratory track?

A

pseudo stratified columnar epithelium

184
Q

in lung carcinoma it arrises from..

A

the bronchus (vs a metastases where it arrises from somewhere else MET)

185
Q

Hamartoma

A

disorganized collection of tissue types that resembles a neoplasia but are not cancerous. Must do testing to conform that the mass is cancerous.

186
Q

Stage Ia lung carcinoma

A

T1 N0 M0

187
Q

Stave 4 lung carcinoma

A

Any T, Any N, M1

188
Q

what cancer of lung is not treated by surgery?

A

small cell carcinoma

189
Q

4 types of lung cancer

A

1) squamous, adenocarcinoma, small cell, large cell

190
Q

Squamous Carcinoma

A

20-40% of lung cancer cases; strongly linked to smoking, arrises centrally in bronchi;

191
Q

Squamous carcinoma lab finding

A

resembles squamous epithelial from skin, forms Keratin Pearls; visible central necrosis

192
Q

Adenocarcinoma subtypes

A

acinar predominant; papillary predominant; micropapillary predominant; solid predominant; invasive mucinous

193
Q

Adenocarcinoma prevalence

A

25-40% of lung cancer cases; many linked to smoking, central in lung

194
Q

how do never smokers get adenocarcinoma?

A

mutation in EGFR - most common in Asian Women

195
Q

Targeted therapy of Adenocarcinoma

A

drugs target AIK fusion protein, ROS1 fusion protein which increase tyrosine kinase activity in cells

196
Q

crizotinib

A

effective for tumors with fusions involving ALK or ROS1 in adenocarcinomas.

197
Q

drugs that target mutation in EGFR

A

gefitnib, erlotinib, afatinib

198
Q

Adenocarcinoma Lab findings

A

occur most often in periphery and appears like scarring; white ; microscopically cancer cells attempt to form glands with cells of large nuclei and not differentiated.

199
Q

Bronchioalveolar carcinoma

A

variant of adenocarcinoma - not associated with smoking, tumor along alveolar septa that occurs anywhere in lung. Prognosis is better than other lung carcinomas.

200
Q

large cell

A

10-15% of lung cancer cases; cells do not produce keratin or mucin or form glands; highly undifferentiated; tend to be centrally located

201
Q

Large cell carcinoma of lung lab findings

A

unorganized big and little cells with no cohesive patterns or keratin pearls; bizarre mitotic figures

202
Q

Small cell carcinoma of lung

A

20-25% of lung cancer; strongly associated with smoking, terrible prognosis, Mets to brain are common; tend to be centrally located; no surgery for removal

203
Q

Small cell carcinoma of lung lab findings

A

cells with dar, angulated nuclei that crowd.

204
Q

Pancreatic Carcinoma Symptoms

A

back pain, unexplained jaundice (block of common bile duct), migratory thromophlebitis, cachexia

205
Q

cachexia

A

weakness or wasting away of the muscles

206
Q

Pancreatic Carcinoma

A

terrible 5 year survival; misdiagnosed as chronic pancreatitis, arose in major ducts of pancreas - not acini

207
Q

pancreatic cancer mutations possess

A

Ki-ras mutation, loss of p16, SMAD4, p53

208
Q

where does pancreatic carcinoma arise?

A

major ducts not acini

209
Q

Best case of pancreatic cancer

A

small tumor found at head of pancreas —> painless jaundice that is easily detected

210
Q

where doe mets form in pancreatic carcinoma?

A

liver, abdominal lymph nodes, celiac plexus of nerves

211
Q

Risk factors for pancreatic cander

A

Most unknown, less commonly: Smoking, Family hx, alcoholism, chronic pancreatitis, DM, Peutz-jeghers/BRCA2

212
Q

What stage in tumor development - PanIN 1 (A or B)

A

telomere shortening, mutation in K-Ras (step 1)

213
Q

PanIN-2

A

inactivation of p16 (stage 2)

214
Q

PanIN-3

A

inactiation of p53, SMAD4, BRCA2 (stage 3)

215
Q

Pancreatic cancer diagnosis

A

CT, MRI, tissue diagnosis, US guided endoscopy

216
Q

pancreatic cancer lab findings

A

white, rock hard growth with lots of scar tissue; growth often blocks common bile duct

217
Q

treatment for blockage of common bile duct in pancreatic cancer

A

canula to prevent infection - prolongs life to give as much time as possible.

218
Q

what ares of the colon most commonly develop colon carcinoma?

A

Ascending or sigmoid; but can really develop anywhere

219
Q

how many carcinomas of colon are adenocarcinoms?

A

98%

220
Q

Sporadic or genetic colon cancers?

A

most are sporadic,

221
Q

adenomatous polyp

A

premalignant growth; flat, with mulberry shape that sometimes extend by a stalk. Can be irritated by stool. More often than not beigne.

222
Q

Adenomatous polyp lab findings

A

don’t invade, looks like glandular tissue

223
Q

Polyps in rectum

A

colliflower look called villous adenoma; longer fingerlike projection into the lumen. Benign.

224
Q

Why are polyps important to find

A

they are precursors for malignancy - removing polyps prevents colo-rectal cancer during.

225
Q

Two types of polyps in colon

A

Predunculated Tubular Polyp (with stalk) Sessile Villous (lacking stalk)

226
Q

Cells within the polyps - mutations and differentiation

A

are less differentiated than the cells that line the colon mucosa; most have mutations in APC gene in Ch5 that participates in WNT that regulates level of Beta-katenin.

227
Q

Beta-Katenin

A

activation of signaling cascade that allows for cell growth and proliferation - mutated in polyps.

228
Q

Growing circumferentially around the colon

A

to produce obstruction/constipation.

229
Q

Circumferential pattern of growth in colon

A

dilate proximally, narrowing around the tumor and normal following.

230
Q

staging and colon cancer prognosis

A

limited to mucosa - very good; but if invade through the walls - not good prognosis.

231
Q

FAP

A

Familial adenomatous polyposis coli: lost gene for FAP protein involved in regulating proteolytic processing of Beta-Catenin; structural tethering of nucleus.

232
Q

mutation in most sporadic colon cancers

A

loss of APC (as in familial)

233
Q

Lynch Syndrome

A

defect in proteins required for MMR -to make them a high risk for cancer - most often occur in the right side of the colon.

234
Q

MutY

A

protein involved in BER; MUTy glycolsylase. Loss increase risk of colo-rectal cancer.

235
Q

where does prostate cancer occur in the prostate?

A

periphery over central part

236
Q

BPH

A

benign prostatic hyperplasia targets central area of prostate; overgrowth of glandular tissue. benign; Not cancerous.

237
Q

Prostate components

A

glandular tissue imbedded in smooth muscle storma - glands are lined by two cells layers (basal and apical - secretory).

238
Q

prostate cancer epidemiology

A

common in US among African americans and then whites; common in europe; not common in asia.

239
Q

Risk factors for prostate cancer

A

Age, Race, Genetics

240
Q

incidence of prostate cancer in white vs Arfican american men around country

A

high latitudes high risk (vitamin D?); but with african americans more associated with southeast.

241
Q

Transition zone

A

peripheral area of prostate that is cancer is most common in.

242
Q

Diagnosis of prostate cancer

A

Screening: PSA, digital rectal exam; random biopsies event hough they are only 50% senstivie.

243
Q

PSA

A

prostate specific antigen, produced by cell in prostate gland. measures level of PSA in man’s blood.

244
Q

Prostatic intraepithelial neoplasm

A

some of the prostate’s epithelial cells look abnormal under microscope. These cells occur at the lining of the acini sacs and the ejaculatory duct (contrasted to cancer where it penetrates into the tissue itself)

245
Q

relationship between PIN and PCa

A

PIN is non-invasive precursor to some prostate cancer; peak prevalnce 5-10 years before PCa; 30-50% of PIN harbor prostate cancer

246
Q

Gleason Grading

A

rating of morphological resemblance to normal prostate; based on appearance of cancer glands - uniform round are Grade 1; less uniform is 5; Score = most prominent + second most prominent cell type; lowest score is pretty well with treatment.

247
Q

Prostate cancer diagnositics

A

uniform round gland, infiltrative pattern, single cell layer (loss of basal cells); nuclear enlargement; perineural invasion

248
Q

where does prostate cancer metastesize?

A

bone and spine

249
Q

What is the most detrimental risk of prostate cancer progression?

A

pelvic lymph nodes; seminal vesicles

250
Q

how many men in autopsy have prostate cancer?

A

30% above 50 years old; but commonly not the cause of death!

251
Q

Alkylating Agents - Anti-Cancer Method

A

Add covalent adducts and cross link to prevent DNA replication

252
Q

Alkylating agents - used in what cancers?

A

Lymphoma, Childhood tumor, solid tumor

253
Q

Alkylating Agents - Resistance Mechanisms

A

Drug inactivation and Adaptive Response

254
Q

Drug inactivation of Alkylating agents mechanism

A

Inactivates glutathione tripeptide

255
Q

Adaptive response of alkylating agents resistance mechanism

A

Upregulation of DNA repair mechanism; remove alkyl groups from guanine, high NER to remove cross link

256
Q

Toxicity of Alkylating Agents

A

Hematopoetic Stems cell death; Nausea vomit, gonadal toxic, alopecia, carcingogenesis - leukemia

257
Q

Examples of Alkylating Agent drugs

A

Cyclophosphamade which is activated by metabolism

258
Q

Cyclophosphamde resistance

A

activated metabolite is substrate of ALDH, so at high levels of ALDH is it sequestered out of solution and excreted, so it is less effective

259
Q

Cisplatin - anti-cancer method

A

Platinum compounds that creates CpG crosslinks and promotes apoptosis

260
Q

What cancers is cisplatin used for?

A

Testicular, ovarian, H/N, lung, bladder

261
Q

Resistance mechanisms of cisplantin

A

Decreased uptake, increase efflux, drug inactivation, adaptive response, dysfunctional apoptosis

262
Q

How do tumor cells inactivate cisplatin?

A

react it with glutathione

263
Q

how do tumor cells generage an adaptive response against cisplantin?

A

Increased NER

264
Q

How is dysfunctional apoptosis generated in cisplatin resistance?

A

decreased MMR cannot trigger apoptosis

265
Q

Cisplatin toxicity

A

High nephrotoxicity, N/V, ototoxicity, neurotoxicity

266
Q

Pyrimidine Analogue drug

A

Anitmetabolite-5-Flurouracil

267
Q

Antimetabolite-5-Fluoruracil anti-cancer method

A

pyrimidine analogue, activates dUMP to inhibit thymidylate synthase to inhibit DNA synthesis and promote apoptosis

268
Q

What cancers is Antimetabolite-4-fluorouracil use for?

A

Gi malignancies, Breast, H/N, ovarian

269
Q

Resistant mechanisms in Antimetbolite-4-flurouracil?

A

Alterations to drug target, adaptive response (increased Thymidine synthase)

270
Q

How do cancer cells after drug target for Antimetabolite-4-flurouracil?

A

reduced affinity of FdUMP

271
Q

Adaptive response for Antimetabolite-4-fluroruacil resistance?

A

increased level of thymidine synthase

272
Q

Toxicity of Antimetabolite-5-fluorurical

A

Toxic to rapidly dividing cells; myelosuppresion, alopecia, dermatological problems

273
Q

Topoisomerase interacting agents - anti-cancer method

A

stabilize cleavage complex between toposimerase and DNA; relegation to leave DNA breaks and promote apoptosis

274
Q

Topoisomerase interacting agents cancer uses

A

breast, ALL, lymphoma, sarcoma

275
Q

Topo interacting agents resistance methods

A

Increased efflux, mutations in topoisomerase (alterations to drug target)

276
Q

Topo interacting agents - toxicity

A

myelosuppresive, cardiotoxicity - risk of cardiomyopathy, CHF, secondary malignancies -AML

277
Q

Anti-microtubule interacting agents - anticancer method

A

targets Alpha and Beta tubular to prevent cell division, motility, secretion, adhesion, signal transduction and apoptosis

278
Q

Vinca Alkaloids - anti-cancer method

A

bind to tubulin to cause depolarization

279
Q

what are vinca alkaloids used for?

A

Pediatric malignancies, hematopoietic tumors, solid tumors

280
Q

Resistance mechanisms of vinca alkaloids

A

Increase efflux, mutation at target (tubulin)

281
Q

Toxicity of vinca alkaloids?

A

neurotoxicity, myelosuppresion, neutropenia

282
Q

Microtubule targeted agents - anti-cancer method

A

taxanes, bind to interior surface of MT to stabalize and block mitosis and promotes apoptosis

283
Q

Microtubule targeted agents -cancer uses

A

breast, ovarian lung, solid tumors

284
Q

Microtubule targeted agents - resistance

A

increased efflux, altered target (tubulin binding), dysfunctional apoptosis

285
Q

Toxicity of microtubule targeted agents

A

myelosuppresion, neutropenia, peripheral neuropathy, alopecia

286
Q

Hormonal Agents - cancer types

A

hormonally responsive cancers - breast, prostate, endometrial

287
Q

Tamoxifen

A

estrogen receptor inhibitor; blocks ability of native estrogen to stimulate gene expression

288
Q

Antiandrogens

A

bind to androgen receptor to inhibit function as TF

289
Q

Letrozole

A

aromatase hormon agent, catalyzes synthesis of estrogen from androgens

290
Q

Gondadoprophin-releasing hormone

A

leuprolide - inhibit testosterone production

291
Q

Hormone/steroid agent - resistance

A

mutations in receptors to alter drug response; activation of receptor by other mechanism (phosphorylation)

292
Q

Hormonal agents - toxicity

A

assocations with altered steroid hormone binding - hot flashes, decreased bone density, gynecomastia

293
Q

Antibodyies as Anti-Cancer

A

Inhibiting function at target, cell mediated toxicity, delivery of toxins, chemotherapeutic drugs, radioisotopes

294
Q

Rituximab

A

Anti-Cd20 antibody used to treat B-cell tumors

295
Q

Herceptin

A

Anti-Her2 breast cancer

296
Q

Avastin

A

Anti VEGF colon cancer

297
Q

Kinase Inhibitor - anti-cancer

A

traget that causes route of tumor development

298
Q

Imatinib - anti-cancer action

A

binds to active site where ATP binds of BCR-ABL to inhibit tyrosine kinase function

299
Q

Resistance to Imatinib

A

activation of secondary TK, oncogenic independence, extracellular sequestration, BCR-ABL overexpression, inhibitor insensitive BCR-ABL allels

300
Q

Immune Checkpoint Inhibitors

A

circumvent immune system and take advantage of checkpoints. CTLA-1 and PDL-1

301
Q

CTLA-4

A

reduces T-cell activation

302
Q

how can CTLA-4 be used as anti-cancer?

A

Block CTLA-4, so we can activate T-cells

303
Q

PD1

A

inhibits thea ability of the T-cell to kill the cancer cell

304
Q

how do we utilize PD1 as an anti-cancer

A

block PD1 from binding to PD-L1 to promote killing of cancer cells

305
Q

CTLA-4 block occurs in what phase

A

Priming phase in lymph node

306
Q

PDL-1 block occurs in what phase

A

Effector phase in peripheral tissue

307
Q

Problems of promoting immune response in cancer?

A

generating auotimmune diseases

308
Q

Primary Induction Chemotherapy

A

drug is primary treatment strategy, no surgery or radiation

309
Q

when is primary induction chemo curative?

A

adults: hodgkins (and non-hodgkins) lymphoma, germ cells cancers. Children: acute lymphoblastic lyphoma, films,

310
Q

What is primary chemo used for?

A

curative cancers, palliative care with no treatment options,

311
Q

Neoadjuvant Chemotherapy

A

use of chemo with localized cancer which useful therapies (surg/rad) may not be completely effective; before treatment to spare vital organs

312
Q

Goal of neoadjuvant chemo

A

increase effectivenesss of surgery or addition

313
Q

Neoadjuvant chemo is used for…

A

anal, breast, esophageal, N/H, gastric rectal, osteogenic and soft tissue sarcoma

314
Q

Adjuvant chemo

A

chemo after local treatment modalities;

315
Q

goal of adjuvant chemo

A

reduce incidence of localized and systemic recurrence by killing metastatic tumor cells; increase effectiveness of surgery/radaition

316
Q

uses of adjuvant

A

breast, colorectal, gastric, non-small cell lung cancers, melanoma

317
Q

how large is the therapeutic window in chemo?

A

smallest - due to balance between killing tumor and killing self

318
Q

Parmacokinetics of chemo

A

incredible varability due to differences in renal/hepatic function, age, prior surgery

319
Q

Efficacy and toxicity of chemo

A

incredibly variable between patients

320
Q

pharmacogenetics in chemo

A

very important due to polymorphisms

321
Q

are single drugs curative?

A

not likely. Need 3 or more drugs that are less tolerable

322
Q

Darwinian selection in tumor

A

tumor cells contain mutations and those that are resistant to treatment may exist in the tumor and become stronger with time

323
Q

Probability of resistance cell is based on?

A

tumor size and inherent mutation rate

324
Q

Principles for combining chemo drugs

A

1) drugs partially effective against same tumor should be combined 2) select drugs whose toxicities do not overlap 3) use drugs at optimal dose and schedules 4) keep treatment intervals short to allow recovery of normal tissue 5) avoid removal or dose reduction to prevent resistant lines

325
Q

tumor cell death is most often caused by

A

apoptosis that is triggered by DNA damage

326
Q

Maximally tolerated dose

A

as much as can be tolerated by patient; what you should try to treat at.

327
Q

Apoptosis triggers

A

activation of cytochrome C in mito, activating cystiene proteases called capsizes

328
Q

BH3 profiling

A

BH3 Activates mitochondria release CytoC. BH3 measures proximity of cancer to cell death.

329
Q

MOMP

A

Mitochondrial out membrane permebilization, signaled by BH3 to cause apoptosis

330
Q

What results for BH3 profiling for primed fro cell death?

A

High MOMP and low Bh3

331
Q

What results for BH3 profiling are not ready fo cell death

A

low MOMP and high BH3

332
Q

why does chemo work?

A

while cancer treatments utilized apoptosis, death is hallmark of cancer. Tumor cells are closer to cell death thatn normal cells and this creates the narrow therapeutic window and why chemo works

333
Q

optimal biolgical dose

A

in new cancer therapy that is used to inhibit biological target, most likely different than MTD

334
Q

Hallmarks of cancer

A

1) evading growth suppressors 2) avoid immune destruction 3) enable replicative immortality 4) tumor promoting inflammation 5) activating invasion and metastasis 6) inducing angiogenesis 7) genome inability and mutation 8) resisting death 9) deregulting metabolism 6) sustaining proliferation

335
Q

Mechanisms of chemoresistance

A

enhanced efflux, drug inactivation, alterations to drug target, adaptive repsonse, dysfunctional apoptosis

336
Q

Chemotherapy does..

A

DNA damage, toposimerase interacting agents, antimetabolites, MT interaction, Hormonal agents, antibodies, kinase inhbitor, immune chekpoint inhibitors

Disease And Defense (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions