Neoplasia (Handout) Flashcards
(199 cards)
1
Q
Fundamental and shared characteristics of cancer
A
- Genetic disoder caused by DNA mutations
- Genetic alterations in cancer cells are heritable. As a results, cells harboring these alterations are subject to Darwinian selection.
- Mutations and epigenetic alternations impart to cancer cells a set of properties are referred collectively as cancer hallmarks.
2
Q
Four major classes of genes involved in cancer
A
Oncogenes
Tumor suppressor genes
Genes that regulate apoptosis
Genes that regulate interactions between tumor cells and host cells
3
Q
Genes that induce a transformed phenotype when expressed in cells by promoting increased cell growth
A
Oncogenes
4
Q
Genes that normally prevent uncontrolled growth and when mutated or lost, allow transformed phenotype to develop
A
Tumor suppressor genes
5
Q
Functions of tumor suppressor genes
A
Governors
Guardian
6
Q
Breaks on cell proliferation
A
Governors
7
Q
Senses genomic damage
A
Guardians
8
Q
Some these genes initiate and choreograph a complex “damage control response” that leads to the cessation of proliferation or apoptosis if the damage is too great
A
Guardian genes
9
Q
Enhances cell survival rather than stimulating proliferation per se
A
Genes that regulate apoptosis
10
Q
Genes that are recurrently mutated or functionally altered in certain cancers
A
Genes that regulate interactions between tumor cells and host cells
11
Q
Benign and malignant tumors are differentiated based on
A
degree of differentiation, rate of growth, local invasiveness and distant spread
12
Q
Benign or malignant.
Resemble the tissue of origin and are well-differentiatied
A
Benign
13
Q
Benign or malignant.
Poorly or completely undifferentiated (anaplastic)
A
Malignant
14
Q
Benign or malignant.
Tend to be slow growing
A
Benign
15
Q
Benign or malignant.
Grow faster
A
Malignant
16
Q
Benign or malignant.
Well circumscribed and have a capsule
A
Benign
17
Q
Benign or malignant.
Poorly circumscribed and invade the surrounding normal tissues
A
Malignant
18
Q
Benign or malignant.
Remain localized to the site of origin
A
Benign
19
Q
Benign or malignant.
Locally invasice and metastasize to distant sites
A
Malignant
20
Q
Mutations that alter the function of cancer genes and thereby directly contribute to the development or progression of a given cancer
A
Driver mutations
21
Q
Acquired mutations that are neutral in terms of fitness and do not affect cellular behavior
A
Passenger mutations
22
Q
Can either activate or inactivate the protein products of the genes depending on their precise position and consequence
A
Point mutations
23
Q
True or False.
Point mutations that convert proto-oncogenes generally produce a gain-of-function by altering amino acid residues ina domain that normally hold the person’s activity in check (RAS gene).
A
True
24
Q
True or False. Point mutations (also insertions and deletions) in tumor suppressor genes reduce or disable the function of the encoded proteins (TP53).
A
True
25
May be produced by chromosomal translocations or inversions
Gene rearrangement
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Some gene reaarangements result in overexpression of proto-oncogenes by removing then form their normal regulatory elements and placing them under control of an inappropriate hightly active promoter or enhancer
Gene rearrangements
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Other oncogenic gene rearrangments create fusion genes encoding novel chimeric proteins
Gene rearrangements
28
Another prevalent abnormality in tumor cells
| Removal of specific regions of chromosomes may result in the loss of particular tumor suppressor genes
Deletions
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Proto-oncogenes may be converted to oncogenes by ___________, with consequent overexpression and hyperactivity of otherwise normal proteins.
Gene amplification
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Two clinically examples of gene amplification
NMYC neuroblastoma
| HER2 gene in breast cancers
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Defines as a number of chromosomes that is not a mutiple of the haploid sate
Anueploidy
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In human, this is a chromosome that is not a multiple of 23
Aneuploidy
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This was remarkably common in cancers, paticularly carcinomas, and was proposed of carcinogenesis
Aneuploidy
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Effects of aneuploidy
Errors in mitotic checkpoint
| Increase the copy number of key oncogenes and decrease potent tumor suppressors
35
Noncoding single-stranded RNAs, approximately 22 nucleotides in legnth
MicroRNAs (miRNAs)
36
Negative regulators of genes
MicroRNAs
37
MiRNAs inhibit gene expression posttranscriptionally thru
Translation suppression
mRNA cleavage (in some cases)
38
Reversible/heritable changes in gene expression that may occur without mutation
Epigenetics
39
Epigenetics involve posttranslational modifications of __________ and ______________ both affecting gene expression.
Histones and DNA methylation
40
Along their course, cancers generally become more aggressive and acquire greater malignant potential, referred to as
Tumor progression
41
The acquisition of the genetic and epigenetic alterations that confer these hallmarks may be accelerated by ___________________________.
Cancer-promoting inflammation and by genomic instability
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These are considered as enabling characteristics because they promote cellular transformation and tumor progression
Cancer-promoting inflammation and by genomic instability
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True or False.
| All cancers display eight fundamental changes in cell physiology which are considered hallmarks of cancer.
True
44
Hallmarks of Cancer
1. Self-sufficiency in growth signals
2. Insensitivity to growth-inhibitory signals
3. Altered cellular metabolism
4. Evasion of apoptosis
5. Limitless replicative potential (immortality)
6. Sustained angiogenesis
7. Invasion and metastasis
8. Evasion of immune surveillance
45
Normal cellular genes whose products promote cell proliferation
Proto-oncogenes
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Mutant or overexpressed versions of proto-oncogenes that function autonomously w/o requirement for normal growth-promoting signals
Oncogenes
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Mechanisms of uncontrolled proliferation by oncogenes
a. Stimulus-independent expression of growth factors and their receptors (autocrine loop) (“self-stimulation”)
b. Mutation in genes encoding growth factor receptors/tyrosine kinases -> constitutive signaling
c. Amplification of EGF receptor family genes (such as HER2 in Breast Cancer)
d. Fusion of portions of ABL tyrosine kinase + BCR protein gene = BCR-ABL fusion gene that encodes a constitutively active tyrosine kinase (as seen in certain leukemias)
e. Mutations in genes encoding signaling molecules (RAS commonly is mutated in human cancers and normally flips between resting GDP-bound state and active GTP-bound state. Mutation block hydrolysis of GTP to GDP, leading to unchecked signaling)
f. Overproduction or unregulated activity of transcription factors
g. Translocation of MYC in some lymphomas leads to overexpression and unregulated expression of its target genes controlling cell-cycling
h. Mutations that inactivate cyclin genes or inactivate negative regulators of cyclins and cyclin-dependent kinases
48
Drive the cell cycle by phosphorylating various substrates and normally are controlled by CDK inhibitors.
Complexes of cyclins with CDKs
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True or False.
Mutations in genes encoding cyclins, CDKs, and CDK inhibitors result in uncontrolled cell cycle progression and are found in a wide variety of cancers including melanomas and brain, lung, and pancreatic cancers.
50
True or False.
It is now accepted that loss of normal cell cycle control is central to malignant transformation and that at least one of the four key regulators of the cell cycles is mutated in most human cancers.
True
51
Four key regulators of the cell cycle
p16, cyclin D, CDK4, RB
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Governor of the cell cycle
Rb
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One defective copy of RB gene is present in the germ line
Only one additional somatic mutation is needed to completely eliminate RB function
Familial retinoblastoma
54
Exerts anti-proliferative effects by controlling the G1 to S transition of the cell cycle
Rb gene
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In its active form, RB is ___________________ and binds to ______________________.
Hypophosphorylated; E2F transcription factors
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This interaction prevents transcription of genes like cyclin E that are needed for DNA replication, and so cells are arrested in G1.
Binding of RB to E2F transcription factors
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Inactivation of Rb gene
Growth factor signaling leads to cyclin D expression > activation of cyclin D-CDK4/6 complexes > inactivation of RB by phosphorylation > release of E2F
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Fundamental to malignant transformation
Loss of cell cycle control
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True or False.
Almost all cancers have a disabled G1 checkpoint due to mutation of either RB or genes that affect RB function such as cyclin D, CDK4, and CDKIs.
True
60
Many oncogenic DNA viruses (like ___________) encodes proteins (like __________) that bind RB and render it nonfunctional.
HPV; E7
61
Guardian of the Genome
TP53
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This encode p53
TP53
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Central monitor of stress in the cell
TP53
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TP53 is activated by
Anoxia, inapporpriate oncogene signalling or DNA damage
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Activated p53 ontrols the expression and activity of genes involved in
Cell cycle arrest, DNA repair, cellular senescence, and apoptosis
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Mechanism of p53 activation
DNA damage – activation of p53 by phosphorylation – transcription of CDKN1A (P21) - prevention of RB phosphorylation – G1-S block in cell cycle
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Main effect of the G1-S block in cell cycle
Allows the cell to repair DNA damage
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True or False.
| In unrepairable DNA damage, p53 induces cellular senescence or apoptosis.
True
69
Individuals inherit one defective copy of TP53 in the germ line, wherein only one additional mutation is required to lose normal p53 functioning
Li-Fraumeni syndrome
70
Patients with Li-Farumeni syndrome are prone to develop a
Wide range of tumors
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Incapacitation of p53 by HPV is achieved by
Binding to the proteins encoded by these viruses
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True or False.
| 70% of human tumors demonstrate biallelic mutations in TP53.
True
73
Inhibits proliferation of cells by activation of growth-inhibiting genes and suppression of growth-promoting genes
TBG-Beta
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Growth inhibiting genes
CDKI
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Growth promoting genes
MYC
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Function of TGF-beta is compromised in tumors by
Receptor mutations (Colon, stomach, endometrium) and mutational inactivation of SMAD genes that transduce TGF–Beta signaling in the pancreas
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Maintains contact inhibition that is lost in malignant cells
E-cadherin
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Possess anti-proliferative capabilities that regulate the destruction of beta catenin proteins
APC gene
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When APC is lost, ______________ will not be destroyed leading to its translocation to the nucleus where it acts as a growth-promoting transcription factor
Beta–catenin
80
Inherited presence of a germ line mutation in the APC gene and sporadic loss of sole normal allele leading to the development of colonic polyps at a young age.
Familial Adenomatous Polyposis Syndrome
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Polyps in the FAPS evolve into _____________.
Colon cancers
82
True or False.
| Somatic loss of the APC gene is seen in approximately 70% of sporadic colon cancers.
True
83
Even in the presence of ample oxygen, cancer cells demonstrate a distinctive form of cellular metabolism characterized by high levels of glucose uptake and increased conversion of glucose to lactose (fermentation) via the glycolytic pathway.
Warburg effect
84
Number of ATP produced by Warburg effect
2 ATP
85
True or False.
Even though it yields only 2 ATP, the multiple number of cancer cells making those ATP create enough energy to continue living and replicating.
True
86
This explains why tumor cells are glucose hungry
Warburg effect
87
Form of pro-growth metabolism that favors glycolysis over oxidative phosphorylation, provides rapidly dividing cells with metabolic intermediates needed for synthesis of cellular components (while oxidative phosphorylation does not)
Warburg effect
88
True or False.
Warburg effect is not cancer-specific, and is induced in normal cells by exposure to growth factors and becomes fixed in cancer cells.
True
89
Triggers warburg effect
Metabolic reprogramming is produced by signaling cascades downstream of growth factor receptors, the very same pathways that are deregulated by mutations in oncogenes and tumors suppressor genes in cancers
90
Inducers of warburg metabolism
Oncoproteins - RAS, MYC, mutated growth factor receptors
91
Oppose warburg metabolism
Tumor suppressors - PTEN, NF1, P53
92
State of severe nutrient deficiency in which cells arrest their growth and cannibalize their own organelles, proteins, and membranes as carbon sources for energy production
Autophagy
93
True or False.
Cancer cells may accumulate mutations to avoid autophagy, or may corrupt the process to provide nutrients for continued growth and survival.
True
94
Some oncoproteins such as mutated IDH act by causing the formation of high levels of “_______________” that alter the epigenome, thereby leading to changes in gene expression that are oncogenic.
Oncometabolites
95
Tumors may be resistant to programmed cell death, as a consequence of inactivation of _____ or activation of _______________.
P53; anti-apoptotic genes
96
Evasion of cell death by cancers mainly involves acquired abnormalities that interfere with the
intrinsic (mitochondrial) pathway of apoptosis
97
Most common apoptotic abnormalities involve
Loss of TP53 function
98
Mechanism of loss TP53 function
TP53 mutations or overexpression of MDM2
Prevents upregulation of PUMA
99
A p53 inhibitor
MDM2
100
Another cause of evasion of apoptosis
Overexpression of anti-apoptotic members of the BCL2 family (BCL2, BCL-XL, and MCL1)
101
Protect cells from the action of BAX and BAK, the proapoptotic members of the BCL2 family
BCL2, BCL-XL and MCL-1
102
True or False.
In a large majority of follicular B-cell lymphomas, BCL2 levels are high because of a (14;18) (q32;q21) translocation that fuses the BCL2 gene with the regulatory elements of the transcriptionally active immunoglobulin heavy chain gene.
True
103
Induce the death of cancer cells by stimulating the intrinsic pathway of apoptosis and are being developed as therapeutic agents
Inhibitors of the MDM2 (which activate p53) and inhibitors of BCL2 family members
104
Most normal human cells have a capacity of at most _____ doublings.
70 doublings
105
After the 70th doubling, cells lose the ability to divide and enter replicative senescence.
Progressive shortening of telomeres at the ends of chromosomes
106
activate cell cycle checkpoints, leading to senescence
Shortened telomeres
107
DNA repair pathways are inappropriately activated by shortened telomeres, leading to massive chromosomal instability and mitotic crisis.
Disabled checkpoints
108
True or False.
| Telomere maintenance is seen in virtually all types of cancers.
True
109
Enzyme that is upregulated in 85-95% of cancers which keeps the telomere count of cancer cells.
Telomerase
110
When tumor cells reactivate telomerase, they
Stave off mitotic catastrophe and achieve immortality
111
A few tumors use other mechanisms to lengthen their telomeres which depend on DNA recombination.
Alternative lengthening of telomeres
112
Vascularization of tumors is controlled by the balance between ____________________________________ that are produced by tumor and stromal cells.
angiogenic and anti-angiogenic factors
113
Triggers angiogenesis
Hypoxia
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Growth factors involved in angiogenesis
HIF-1α acts on the transcription of the proangiogenic factor VEGF
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Mechanism of angiogenesis
Hypoxia ➡️ stabilized HIF-1α ➡️ activated transcription of VEGF ➡️ angiogenesis
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p53 induces synthesis of the angiogenesis inhibitor
thombospondin-1
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upregulate VEGF expression and stimulate angiogenesis
RAS, MYC, and MAPK signaling
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used to treat a number of advanced cancers and prolong clinical course, but not curative
VEGF inhibitors
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Ability to invade tissues, a hallmark of malignancy
Invasion and metastasis
120
Four steps of invasion and metastasis
1. Loosening of cell–cell contacts
2. Degradation of ECM
3. Attachment to novel ECM components
4. Migration of tumor cells.
121
lost by the inactivation of E-cadherin through a variety of pathways
Cell-cell contacts
122
Basement membrane and interstitial matrix degradation is mediated by proteolytic enzymes secreted by tumor cells and stromal cells, such as
MMPs and cathepsins
123
release growth factors sequestered in the ECM and generate chemotactic and angiogenic fragments from cleavage of ECM glycoproteins
Proteolytic enzymes
124
True or False.
The metastatic site of many tumors can be predicted by the location of the primary tumor. Many tumors arrest in the first capillary bed they encounter (lung and liver, most commonly).
True
125
True or False.
Some tumors show organ tropism, probably due to activation of adhesion or chemokine receptors whose ligands are expressed by endothelial cells at the metastatic site.
True
126
True or False.
| Cells can be recognised by the immune system as non-self and are destroyed.
True
127
True or False.
| Anti-tumor mechanism are mediated predominantly by cell-mediated mechanisms.
True
128
Presented on the cell surface by MHC class I molecules and are recognized by CD8+ cells
Anti-tumor activity
129
Different classes of tumor antigens includes products of
Mutated genes
Overexpressed or aberrantly expressed proteins
Tumor antigens produced by oncogenic viruses
130
True or False.
Immunosuppressed patients have an increased risk for cancer development, particularly types caused by oncogenic DNA viruses.
True
131
Mechanisms by which tumors may avoid the immune system
Selective outgrowth of antigen-negative variants
Loss or reduced expression of histocompatibility molecules
Immunosuppression mediated by expression of certain factors (e.g., TGF-β, PD-1 ligands) by the tumor cells
132
True or False.
Antibodies that overcome some of these mechanisms of immune evasion are approved for treatment of patients with advance forms of cancer.
True
133
Etiology of cancer:
| _________________ inflict genetic damage, which lies at the heart of carcinogenesis.
Carcinogenic agents
134
Three classes of carcinogenic agents:
Chemicals
Radiant energy
Microbial products
135
Chemical carcinogens have ________________________________ that directly damage DNA, leading to mutations and eventually cancer.
Highly reactive electrophile groups
136
do not require metabolic conversion to become carcinogenic
Direct-acting agents
137
not active until converted to an ultimate carcinogen by endogenous metabolic pathways.
Indirect-acting agents
138
may influence carcinogenesis by altering the conversion of indirect-acting agents to active carcinogens.
Polymorphisms of endogenous enzymes such as cytochrome P-450
139
Examples of direct-acting agents
alkylating agents used for chemotherapy
140
Examples of indirect-acting agents
benzo(a)pyrene, azo dyes, aflatoxin
141
act by stimulating cell proliferation. Increased proliferation may occur through direct effects of tumor promoters on target cells or may be secondary to tissue injury and regenerative repair
Tumor promoters
142
Because malignant transformation results from mutations, most chemical carcinogens are mutagenic acting as ________________ (induction of cell proliferation is a sine qua non of tumor promotion) which can be augmented by non-tumorigenic ___________________.
Initiators; promoters
143
True or False.
Application of an initiator may cause mutational activation of an oncogene, such as RAS, but with subsequent application of promoters leads to clonal expansion of initiated (mutated) cells.
True
144
True or False.
| Initiated clone cells accumulates additional mutations, developing eventually into a malignant tumor.
True
145
True or False.
| Sustained cell proliferation increases the risk for mutagenesis, and hence promotes neoplastic transformation.
True
146
Whatever its source, ___________is an establish carcinogen.
Radiation
147
Sources of radiation
UV rays of sun, radiographs, nuclear fission, radionuclides
148
Three causes of ionizing radiation
o chromosome damage
o chromosome rearrangement
o point mutations (less frequently)
*any of which may affect cancer genes and thereby drive carcinogenesis
149
UV rays in sunlight induce the formation of ____________ within DNA, leading to mutations that can give rise to _________________________________ of the skin.
pyrimidine dimers; squamous cell carcinomas and melanomas
150
Oncogenic RNA viruses
HTLV-1
| HCV
151
Another term for Human T-cell leukemia/Lymphoma Virus
Human T-Lymphocytic virus
152
causes adult T-cell leukemia/lymphoma (ATLL) that is endemic to Japan and the Caribbean
HTLV-1
153
a viral protein found in a unique region called pX encoded in the HTLV-1 genome
Tax gene
154
Stimulates proliferation, enhances cell survival, and interferes with cell cycle controls; essential for viral replication, because it stimulates transcription of viral RNA from the 5’ long-terminal repeat
Tax gene
155
alters the transcription of several host cell genes and interacts with certain host cell signaling proteins. By doing so, this gene contributes to the acquisition of several cancer hallmarks.
Tax gene
156
Although this proliferation initially is _______________, the proliferating T cells are at increased risk for secondary mutations that may lead to the outgrowth of a ___________________.
polyclonal; monoclonal leukemia
157
True or False.
| All types of hepatitis are RNA viruses except for HBV, which is a DNA virus.
True
158
Another type of oncogenic RNA virus
Hepatitis C Virus (HCV)
159
Oncogenic DNA virus
HPV
EBV
HBV
160
Associated with benign warts, as well as cervical cancer (Squamous Cell Carcinoma of the Cervix)
Human Papilloma Virus (HPV)
161
Oncogenicity of HPV is related to expression of two viral oncoproteins:
E6 and E7
162
Action of E6 and E7
E6 binds to p53
E7 binds RB tumor suppressors
Neutralizes the action of the genes
163
True or False.
E6 and E7 from high risk strains of HPV (which gives rise to cancers) have higher affinity for their targets than do E6 and E7 from low risk strains of HPV (gives rise to benign warts).
True
164
EBV is implicated in the pathogenesis of
```
Burkitt’s lymphomas
Lymphomas in immunosuppressed patients
Hodgkin lymphoma
Uncommon T-cell and NK cell tumors
Nasopharyngeal carcinoma
subset of Gastric Carcinoma
sarcomas (rarely)
```
165
Certain EBV gene products contribute to oncogenesis by stimulating _______________________________________. Concomitant compromise of immune competence allows ________________________, leading eventually to development of lymphoma.
normal B-cell proliferation pathways
| sustained B-cell proliferation
166
True or False.
| Between 70% to 85% of hepatocellular carcinomas worldwide are caused by HBV or HCV
True
167
The oncogenic effects of HBV and HCV are _________________, but the dominant effect seems to be _____________________________________, with hepatocellular injury, stimulation of hepatocyte proliferation, and production of reactive oxygen species that can damage DNA.
multifactorial; immunologically mediated chronic inflammation
168
The _______________ of HBV and the HCV core protein can activate a variety of signal transduction pathways that also may contribute to carcinogenesis.
HBx protein
169
H. pylori infection has been implicated in both
gastric adenocarcinoma and MALT lymphoma
170
The mechanism of H. pylori–induced gastric cancers is ___________________, including immunologically mediated chronic inflammation, stimulation of gastric cell proliferation, and production of ______________________ that damage DNA.
Multifactorial; reactive oxygen species
171
It is thought that H. pylori infection leads to ______________________________ and that eventually _______________________________ emerges as a result of accumulation of mutations.
polyclonal B-cell proliferations; monoclonal B-cell tumor (MALT lymphoma)
172
Effects of tumor on host
1. Location of tumor
2. Paraneoplastic syndrom
3. Cancer cachexia
173
Location of tumor
Ulceration
Obstruction
Loss of blood supply
174
systemic symptoms that cannot be explained by tumor spread or by hormones appropriate to the tissue, are caused by the ectopic production and secretion of bioactive substances
Paraneoplastic syndrome
175
Symptom complexes that occur in patients with cancer and that cannot be readily explained by local or distant spread of the tumor or by the elaboration of hormones indigenous to the tissue of origin of the tumor
Paraneoplastic syndrome
176
Bioactive substances that are secreted in paraneoplastic syndrome
ACTH, PTHrP, or TGF-α
| E.g. lung cancer producing ACTH
177
Progressive loss of body fat and lean body mass, accompanied by profound weakness, anorexia, and anemia; draining the body’s nutrients for it to survive
Cancer cachexia
178
Clinical aspects of neoplasia
1. Effects of tumor on host
2. Grading
3. Staging
179
Determined by cytologic appearance/differentiation; behavior and differentiation are related, with poorly differentiated tumors having more aggressive behavior
Grading
180
True or False.
| The closer it looks like the original epithelium, the lower the grade.
True
181
Grading levels of neoplasia
```
Well-differentiated (Grade I)
Moderately differentiated (Grade II)
Poorly differentiated (Grade III)
```
182
Extent of tumor
Staging
183
Determined by surgical exploration or imaging based on size, local and regional lymph node spread, and distant metastases
Staging
184
True or False.
| Staging has greater clinical value than grading because it is the better prognosticating factor.
True
185
TNM (Tumor, Nodes, Metastasis) system
STAGE 1: 0-2cm, non-palpable, non-recognizable tumor
STAGE 2: 2-5cm
STAGE 3: > 5cm
STAGE 4: metastasis, even if not palpable
186
Laboratory diagnosis of cancer
Morphologic methods
Immunohistochemistry
Flow cytometry
187
Clinical and radiologic data are invaluable for optimal pathologic diagnosis.
The specimen must be adequate, representative, and properly reserved.
Morphologic methods
188
Morphologic methodology
Cytologic preparations
| Tissue preparations
189
Cytologic preparations
Pap smear
| FNAB
190
Tissue preparations
```
Frozen sections
Tissue core needle biopsy
Incision biopsy
Excision biopsy
Radical resection biopsy
```
191
Immunohistochemistry includes
Detection of cytokeratin
Hormone production
Enzyme production
192
Fluorescently labeled antibodies against cell surface molecules and differentiation antigens used to obtain the phenotype of malignant cells
Flow cytometry
193
Molecular diagnostics of cancer
1. Diagnosis of malignancy
2. Prognosis and behavior
3. Detection of minimal residual disease
4. Diagnosis of hereditary predisposition to cancer
5. Therapeutic decision-making
194
Molecular profiling of tumors
“OMICS”
195
complete draft of the sequence of the human genome, released in 2003
Advances have enabled the systematic sequencing and cataloging of the genomic alterations in various human cancers, and effort sponsored by the National Cancer Institute called the Cancer Genome Atlas
Human Genome Project
196
assess epigenetic modifications genome-wide
Epigenetic
197
quantify all of the RNAs expressed in a cell population
Transcriptome
198
measure many proteins simultaneously
Proteome
199
take a snapshot of all the cell’s metabolites
Metabolome
