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Oncology > Oncology > Flashcards

Oncology Flashcards

1
Q

Visible symptoms of breast cancer?

A
  • inverted nipple
  • knot/lump
  • large lymph node
  • bloody discharge
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2
Q

Diagnosis of breast cancer?

A
  1. Clinical examination (palpation)
  2. Imaging (ultrasound, mammography, MRI, X-ray)
  3. Morphological (biopsy).
  4. Biobank research after pathology
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3
Q

Factors affecting outcome in breast cancer?

A
  • tumor size
  • spread to lymph nodes
  • distant metastasis
  • hormone receptors
  • HER2 expression
  • tumpr grade
  • proliferation rate
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4
Q

Subtypes of breast cancer?

A
  1. ER+/HER-. It is common, low prolifeation, good prognosis, bone metastasis
  2. HER2+. High prolifeation, good prognosis with HER2 blockade, brain metastasis, 10-20% of all cases
  3. Triple negtive. Poor prognosis, high proliferation, visceral metastasis.
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5
Q

Treatment of breast cancer?

A
  1. Surgery. Can dye the lymph nodes, to know which should be removed. If metatstatic: systemic treatment.
  2. Adjuvant therapy.
    - Radiotherapy. All patients. After surgery
    - chemotherapy. All high risk patients. ER+/HER2- may not need therapy
    - endocrine therapy ER+ patients
    - anti-her2 herapy
    - aromatase inhibitors (postmenopausal).
    - LHRH to induce postmenapausal state
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6
Q

Cells in the mammary gland?

A
  • epithelial cells (ductal/lobular)
  • myoepithelial cells. Barrier against invasion
  • fibroblasts
  • immune cells
  • adipocytes
  • endothelial cells
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7
Q

Morphological steps in breast cancer?

A
  1. Normal epithelium
  2. Hyperplasia
  3. Atypical hyperplasia
  4. Carcinoma in situ
  5. Invasive cancer
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8
Q

Morphological steps in breast cancer?

A
  1. Normal epithelium
  2. Hyperplasia
  3. Atypical hyperplasia
  4. Carcinoma in situ
  5. Invasive cancer
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9
Q

How do you investigate breast cancer?

A
  • biopsy. IHC (proteins), in situ hybridisation (DNA)

- surgical removal. Tumor tissue. RNA/DNA. NGS

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10
Q

Histological markers in breast cancer?

A
  1. Estrogen receptor. Target for endocrine therapy.
  2. Progesterone receptor. Majority of breast cancers. Not a target dor adjuvant endocrine therapy.
  3. HER2. Growth-promoting factor. Overexpressed.
  4. Ki67. Marker for proliferation. Expressed in all cell except G0.
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11
Q

What is the epidemiological transition?

A

Describes changing patterns of population, age distributions, mortality, fertility, life expectancy and cause of death.

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12
Q

Risk factor in breast cancer?

A 
HIGH:
 -female sex 
- age 
- BRCA1/2
- high breast tissue density 
MEDIUM: 
- history of cancer
- recent/long term use of hormone replacement therapy 
- nulliparity 
LOW: 
- late menopause
- recent use or oral contraceptives
- alcohol consumption
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13
Q

Factors influencing mammography?

A
  1. BMI
  2. Hormonal replacement therapy
  3. Parity
  4. Time since menopause
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14
Q

Neuroblastoma?

A
  1. Sympathetic nervous system. Often in adrenal glands, but also spinal cords and pelvis
  2. Growth regulations. Amplifiction of MYCN gene, ALK gene and TERT.
  3. Treatment with chemotherapy, surgery and immuno/ differentiation therapy (Macrophage colony stimulating facotr (GM-CSF). ALK inhibitors.
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15
Q

Osteosarcoma?

A
  1. Bone tumor. Physiological growth. Growth plate. Osteoblasts
  2. Sporadic mutations. Loss of tumor suppressor function. Disruptions in signalling pathway. TGF.
  3. Neodjuvant, adjuvant, surgery.
  4. Immunotherapy. GD-2 and CSF
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16
Q

Apoptosis 3 main requirements?

A
  1. development
  2. Miantenance
  3. defence
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17
Q

Morphology of apoptosis?

A
  1. Cytoplasm shrinks
  2. Blebbing membrane
  3. Chromatin condensation & fragmentation
  4. Apoptotic body formation
  5. Nuclear membrane shrinkage
  6. Removed by phagocytosis
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18
Q

Extrinsic pathway in apoptotic program

A
  • ligand binding (TRAIL, Fas receptor)
  • Intracellular adaptor protein FADD
  • create a complex DISC
  • Activation of procaspase 8/10. Self-cleavage
    Two ways:
    1. activation of BAX and BAK
    2. Activation of caspase 3/9
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19
Q

Intrinsic pathway apoptotic program?

A
  • lethal stimuli recognized by BH3-only proteins
  • activation of BAX and BAK
  • Induce MOMP in mitochondria
  • release cytochrome c
  • together with APF1 form apoptosome
  • activate procaspase 9
  • activate caspase3/7
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20
Q

What is SMAC?

A

release by mitochondria together with cytochrome C and inactivates IAP.

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21
Q

Where is BCL-2 located and how does it affect the apoptotic programme?

A
  • Mitochondria.
  • Anti and Pro
  • form pores or block them
  • can be regulated by BH3-only
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22
Q

How is the intrinsic pathway activated?

A
  • signalling: p53, MYC, ER stress
  • apoptotic signalling:
    1. nutrient deprivation
    2. growth factor deprivation
    3. reactive oxygen species
    4. DNA damage
    5. radiation
    6. chemotherapy
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23
Q

Another pathway of apoptosis?

A

Granzyme-mediated apoptosis. Triggered by cytotoxic T-lymphocytes or NK cells. Activate Fas or inject protease Granzyme B

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24
Q

How does phagocytosis occur?

A
  • recognition of PtdSr. Inner part of the membrane. Visible due to conformational changes of the cell
  • recognized by annexin receptor on macrophages
  • cytoskeletal rearrangements and apoptotic digestion
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25
Q

Evasion of apoptosis mechanisms

A
  1. Bcl-2 malfunctioning
    - loss/deregulation of proapoptotic BAK/BAX
    - downregulation of BH3
    - Upregulation of anti-apoptotic Bcl-2
  2. APAF1 pomoter methylation, no apoptosome
  3. Caspase not working. - Loss or downregulation
    - IAP upregulation
  4. Receptor not working
    - Expression of FLIP, block activation of FADD
    - mutation in receptor
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26
Q

Targeting apoptotic pathways

A
  1. BH3 mimetics
  2. SMAC-mimetics. IAP antagonist.
  3. TRAIL-receptor agonists
  4. MDM2 inhibitor
  5. BCL-2 blockers
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27
Q

What is autophagy?

A
  • normal process, self degradation
  • break down of organelles, catabolites recycled, used for energy metabolism,
  • induced in hypoxia/starvation/growth factor deprivation.
  • lysosomal activity
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28
Q

Detection of apoptosis?

A
  1. Gel electrophoresis. Due to fragmentation. Caspase cleave ICAD, disinhibition of CAD. fragments visible on ladder.
  2. Tunel essay. Specialiased polymerase attach dUTP analgoues with a marker. Mark 3-OH ends.
  3. Annexin/propidium iodide staining. Annexin bind PtdSr. PI color DNA. Visualize stage.
  4. Detection of caspase cleavage products on western blot
  5. Electron microscopy, fluorescence imaging
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29
Q

How is necrosis different?

A
  • not programmed
  • extrinsic
  • morphology: increase cell volume, fragmented chromatin, cell lysis
  • release of content
  • clearance and inflammation
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30
Q

Decrease/increase risk in colon cancer?

A

+ processed meat

    • ethanol intake
  • physical activity
  • whole grain
  • dairy products
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31
Q

Symptoms of colon cancer

A
  • anemia
  • change in bowel habits
  • blood/mucinous in stool
  • feeling of incomplete bowel evacuation
  • pain/fatigue/weight loss
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32
Q

Treatment on colorectal cancer?

A
  1. Surgery.
    - right sided hemicolectome
    - left sided hemicolectomy.
    - sigmoid resection
    - low anterior resection
    - abdominoperineal resection (lower rectal part)
  2. Adjuvant: chemotherapy. Radiotherapy in rectal.
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33
Q

Peritoneal carcinosis

A

ancer affecting the peritoneum, the thin membrane surrounding your abdominal organs. eritonectomy is a procedure used to remove cancerous tumors from the lining of the abdominal cavity. Together with Hyperthermic intraperitoneal chemotherapy (HIPEC). Chemotherapy intravenously during surgery.

34
Q

Other coloncancer treatment?

A
  1. imhibiting growth and survival of EGFR
  2. Binding circulating VEGF. Reduction of microvascular growth of blood vessels
  3. Block tyrosine kinases that are very active in angiogenesis
35
Q

CBio?

A

Cancer Genomic Portal. Exploration of multidimensional cancer genomics data sets. Biologic insights and clinical applications.

36
Q

Where does data from cBio come from?

A
  1. Cancer genome atlas
  2. PubMed
  3. Cancer cell encyclopedia
37
Q

What data is available a cBio?

A
  1. Clinical data (treatment, prognosis)
  2. Omic (mutations, copy numbers, fusion genes, mRNA expression, DNA methylation, protein levels)
  3. Predicted functional effect
  4. Variant reccurence
  5. Background biological data
38
Q

What is personalized cancer medicina?

A
  • medical model
  • using characterisation of genotypes/phenotypes
  • tailoring righ therapeutic strategy
  • predisposition to disease
  • deliver timely and targeted prevention
39
Q

What is P4 medicine?

A

Predictive
Preventive
Personlized
Participatory

40
Q

Transcriptomics?

A

all genes expressed as mRNA

41
Q

Single RNA sequencing?

A
  • cells fused in droplets with specific primers
  • identify cel
  • reconstruction of cell type in a tumor
42
Q

Specimen to investigate in PM?

A
  1. Biopsy.
  2. Circulating CTC. IHC.
  3. CtDNA. Fragmented genome release from dying cells.
  4. Normal tissue/Blood.
43
Q

Trial design?

A

Umbrella trials. Single disease. Multiple aberrations. Multiple targeted interventions.

Basket trials. Multiple disease. Single drug targeting. Multiple disease. Single aberration.

Drug repurposing

Genomic-guided. Find drugs targeting driver protein products.

44
Q

PM workflow?

A
  1. Consider patient
  2. Material
  3. Assays, analysis (FISH, NGS, IHC, karotyping)
  4. Bioinformatics/databases
  5. Action. Targeted therapy
  6. Monitoring
  7. Adjustments
45
Q

Prevention of infectious cancer?

A
  • risk groups for regular controls
  • screening of risk groups
  • therapeutic vaccination
  • antiviral treatment
46
Q

Type pf viral-host cell interactions?

A
  1. Lytic/replictive. Production of new virus particles
  2. Abortive. Virus do not complete the replication cycle
  3. Transformatio. Expression of selected viral particles. Changes of the cellular phenotype/morphology. Cell acquire features.
  4. Latent. Persists as its genome with limited expression of viral genes.
47
Q

Mechanism of carcinogenesis in HPV?

A
  • E6 bind p53. Inactivate. Block of apoptosis

- E7 bind Rb. Release G1 arrest and cell cycle progression.

48
Q

What does EBV cause?

A
  • Burkitt’s lymphoma

- Kaposi sarcoma

49
Q

Different types of oncogenes?

A
  1. Growth factors and receptors
  2. Signal transducers
  3. Nuclear oncoprotein
  4. Anti-apoptotic regulators
50
Q

What do you know about Myc?

A
  • TF
  • regulate genes involved in cell cycle progression, protein synthesis, metabolism
  • activated by EGFR-Ras
  • Burkitt lymphoma. translocation from 14 to 8 chromosome
  • Neuroblastoma. Amplified.
51
Q

What do you know about c-abl?

A
  • nuclear tyrosine kinase
  • role in DNA damage-induced apoptosis
  • Chromsome 22 to 9 translocation.
  • fusion protein bcr-abl give a constitutive tyrosine kinase activity.
  • found i leukemia
52
Q

Ways of oncogene actiation?

A
  1. Retroviral transduction
  2. Promoter inserion. cMyc
  3. Fusion protein. bcr-abl
  4. Chromosomal translocation. cmyc
  5. Amplification. cmyc neuroblastoma
  6. Point mutation. p53
53
Q

EGF?

A
  • tyrosine kinase
  • lung cancer
  • point mutatiosn
  • trigger cell devision
  • known as HER1
  • Ras-MEK-MAPK pathway
54
Q

Ras?

A
  • signal transducer
  • point mutations
  • signalling trough three pathways
    1. MAPK. Ras-GTP binds and activates the kinase Raf. Activate MEK-MAPK. MAPK enters the nucleus. Activate AP1 transcription factor. Activate cyclin D. c-Jun and c-Fos are components of AP-1.
    2. PI3K pathway. Cell survival. Production of second messenger PIP3 and recruiting PDK-1. Akt also recruits and phosphorylates transcription factors.
    3. Ral-GEF/Rac pathway Cell motility.
55
Q

Bcl-2?

A
  • antiapoptotic genes
  • translocation 14/18
  • not alone (need more mutations for cancer progression)
56
Q

IDH1

A
  • glioblastoma
  • enzyme
  • conversion of isocitrate (ICT) to Ⲁ-ketoglutarate
  • On chromosome 2q34.
57
Q

Rb?

A
  • bone, soft tissue sarcoma and retinoblastoma
  • bind E2F
  • released when phosporylated by cyclin D ad Cdk2
  • E2F activate genes required for S phase
58
Q

PTEN?

A
  • inhibit PI3K7/Akt pathway
59
Q

VHL?

A
  • chromosome 3
  • hydroxylate an send HIF 1 for degradation
  • regulates expression of VEGF
60
Q

Mutations in colon cancer?

A
  1. Adenoma.
    - Wnt signaling. APC
    - MAPK signaling. RAS
    - PI3K signaling. PTEN, SMAD4, TGF
    - p53 signaling
  2. Serrated polyps.
    - Wnt signaling catening
    - MAPK. RAS and BRAF
    - PI3K signalling
    - TGF
61
Q

Vogelgram?

A
  • multistep cancer progression model
  • progressive accumulation of genetic alteration involving tumor supressor genes and oncogenes
  • series of steps
62
Q

Finding cancer associated genes?

A

Linkage: large effect, low frequency
Association: small effect, most common disease

63
Q

Mouse models pros/cons?

A 
\+ genetically similar 
\+ same organs 
\+ similar histological features
- higher metabolic rate 
- different cancer susceptibility 
- different microbiome and pathogens 
- difference in immune system
64
Q

Cancer model?

A
  1. Non genetic
    - spontaneous. long wait. proper environement. unspecified tumor development
    - carcinogen induced. known carcinogen but unkown effect. faster.
    Xenograft (inject into mice) Orthotopic(inject into tissue origin)
  2. Genetically engineered GEEM
65
Q

Types of immunodeficient mice?

A
  1. NOD/SCID. Decreased number of NK, macrophages and dendritic cells. No T/B cells.
  2. NOD/SKID gamma. Lack of NK cells. Xenografts.
  3. NOG. Truncated IL-2 receptor. Lack of NK cells. Xenografts.
  4. PDX. Personalized medicine. Cultivate individual patient’s tumor cells/tissue in mice. Histopathological features and genetic profile of the original patient tumours.

second generation PDX:
Partial humanization of the murine immune system and stroma.

66
Q

Type of trials?

A
  1. Screening trials
  2. Prevention trials Action/Agent studies.
  3. Treatment trials.
67
Q

Trial phases

A

Phase 0. Preclinical. Animal model.
Phase I. First in Man. Very low dose to one patient. Close Monitoring. After that Phase I trials can start. Safety and pharmacokinetics. Healthy volunteers or oncological patients, 30-40 participants.
Phase II. A homogenous group, 100 participants. Examines the efficacy, safety and appropriate dose.
Phase III. Randomized control trials. Broader patient group, 1000’s participants. Frequent comparative studies. Confirming efficacy and adverse reaction patterns.
Phase IV. Long-term follow up, post-authorisation of FDA/EMA. Long term effects and rare side effects

68
Q

Lung cancer treatment?

A

Early stage:

  • surgery/radiotherapy
  • post operative radio treatment is no longer recommended. Maybe for stage II/III

Locally advanced:
- no surgery
- downstaging with chemo/radio than surgery
- or only chemo (carboplatin + vinolrebin)
- IT works bad. Maybe mucin 1 cancer antigen?
Oncogene addicted:
TKIs
EGFR: Osimertinib
ALK: Crizotinib
IT: checkpoint inhibitor, PDL-1 expression, anti-CTLA4

69
Q

Lung cancer and sex

A
  • tobacco increased in females
  • metabolic detoxification is different
  • estrogen effects
  • genomic driver (EGFR) more common in women
70
Q

Resistance in TKIs?

A
  1. EGFR dependent
    amplification
    mutation. change the affinitity for TKI
  2. EGFR independent.By passing
    HER2 or MET amplifiction
    - IGF1R activation
71
Q

transition to mesenchymal factors?

A 
Intrinsic: 
- morphological changes 
- metabolic changes 
- epigenetic changes 
- genetic aberrations
Extrinsic factors: 
- degree of inflammation 
- signalling
- secreted factors
- cell-cell communication
72
Q

Seven steps of metastatic cascade?

A
  1. Primary tumor formation
  2. Migration. Localized invasion. Through basement membrane. Protrusions and contractions. Chemically degrade the matrix.
  3. Intravasate in the blood vessels. Macrophages. Angiogenesis. Vasculature immature and hyperpermeable.
  4. Transport through the circulation. Survive in the bloodstream. Proliferate. May migrate in different forms:
    - solitary
    - non transformed + leader cells
    - transformed + leader cells.
  5. Extravasate. Through adhesion.
  6. Colonize. Tumor environment important
73
Q

Proteins upregulated and deregulated in EMT?

A 
\+ N-cadherin
\+ SNAIL 
\+ SLUG 
\+ twist
\+fibronectin/vimentin

E-cadherin
beta/alfa-catenin

74
Q

Receptor complexes that regulate the switch from E to N?

A
  1. IGF/HGH. growth factor receptors. Enable transcription of snail, twist and Zeb. Downregulate E-cad.
  2. TGF. Concentration of receptor is important. Induce N-cad transcription. Crosstalk with other pathways. RHO-like gtpases.
75
Q

Two important signalling pathways regulating cell reorganization in EMT?

A
  1. Tumor Cell- Tumor Cell Adhesion. Support epithelial polarity and constitute a barrier for water. Cadherin forms bridges to other cells. Upon signalling the cells might lose cell polarity and adhesion. Upon cytokine binding, signalling cascade, proteases degrade E-cad. E-Cad ( cell to cell), N-Cad (cell to membrane). Interact via catenins with the cytoskeleton. Catenins also bind to transcription factors. Downregulation of E-Cad. Upregulate N-Cad. Melanoma cells leave keratinocytes: bind to macrophage, stromal cells and to other cancer cells. FGF and PDGF signaling via N-cadherin enhances tumor cell proliferation and survival in the bloodstream. N Cad can bind to other receptors. Enable EMT. Become not dependent on cell to cell contact. Cells lose shape, become spindle-like.
  2. Tumor Cell - Extra Cellular Matrix Interaction. Macrophages release proteases. Extrinsic factors. Cleaves extracellular matrix (collagen, laminins, fibronectins). Ligands for integrins. The expression of different integrins determines where the cell can adhere as the integrins have different ligands. Integrins are zip codes and regulate the remodelling of actin filaments upon binding. Cells start to express filopodia (spike-like extensions) and lamellipodia (sheet-like protrusions). Cdc42, Rac and Rho have an important role. Detach from the basal membrane and penetrate the tissue barriers. Further remodelling of actin filaments and focal adhesion.
76
Q

Actin filaments plasticity?

A
  1. Rho. Contraction. Allows cancer cells to penetrate the tissue barriers surrounding tumors.
  2. Rac. Control leading edge. Actin polymerization. Lamellipodium.
  3. Cdc42. Contraction. Nuclear positioning and cell body translocation.
77
Q

VEGF role in EMT?

A

ngiogenesis is highly dependent on the VEGF signalling pathway. Cause integrin expression for interaction with ECM. Regulated by the hypoxia inducible factor HIF-1. VEGF increases vascular permeability. Endothelial cells in tumor vessels are abnormally aligned, leaky, immature, irregular flow, hypoperfused and promote tumor cell invasion. HIF can be degraded with the help of VHL, however, often mutated in cancer.

78
Q

Metabolic reprogramming in EMT?

A

pregulation of glucose transporters GLUT1 and GLUT3 is further promoting glycolysis. GLUT3 correlates with poor prognosis and EMT activation, mediated by activation of ZEB1.In addition to carbohydrate pathways, EMT‐associated changes in fatty acid, lipid and glycosphingolipid metabolisms. The morphological changes of cancer cells during EMT are accompanied by alterations in membrane fluidity and lipid composition.

79
Q

Therapies for EMT?

A
  1. Target pro-metastatic TAMs, Tumor associated macrophages. Can be reprogrammed to a M-2 state, considered pro-tumorigenic. Together with TGF signalling they may induce co-migration of tumor cells towards blood vessels. Macrophages regulate vascular function. Can express proteases that allow cancer cells to pass endothelial lining. Sit close to the blood vessels. Reprograming includes factors, e.g. EGFR, CSF -1 (from cells) and EFG, CSFR1 (from macrophages). Macrophages form a gradient that facilitates chemotaxis.
  2. Metalloproteinase inhibitors. Migration and colonization.
  3. Immune check-point inhibitors. Blocks proteins called checkpoints that are made by some types of immune system cells, such as T cells, and some cancer cells. These checkpoints help keep immune responses from being too strong and sometimes can keep T cells from killing cancer cells.
  4. mprove vessel functionality. Monoclonal antibody to VEGF. Integrin peptide inhibitors. Or target receptors.
  5. Ligand-neutralizing antibodies, decoy receptor or inhibitors to TGF, EGFR, WNT etc. Reduction in SNAIL, TWIST and ZEB levels.
80
Q

What does low pH lead to?

A
  1. Obstacle for efficient cancer therapy. RT: radicals can not be form. CT: diffusion barrier. IT: over production of adenosine. Supressor of T cells
  2. Inflammation, fibrosis
  3. EMT & metastasis
  4. Resistance to apoptosis/autophagy
  5. Genomic instability & unfolded protein response
81
Q

What does VEGF do in angiogenesis?

A
  1. Activate growth factor transcription
  2. Angiogenic sprouting. VEGF is the guiding gradient
  3. Overexpression lead to bad vessels
82
Q

p53?

A
  • induced in damage and stress
  • tf
  • express p21 that inhibit cdk
  • express pro-apoptotic bcl-2

Oncology (1 decks)

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