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APP > APP Cancer I (from notes) > Flashcards

APP Cancer I (from notes) Flashcards

0
Q

Neoplasia

A
  • abnormal growth of tissue resulting from loss of responsiveness to growth control signals
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1
Q

Proto-Oncogene (vs. oncogene)

A
  • encode proteins which normally stimulate call proliferation
  • altered forms of proto-oncogenes are oncogenes
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2
Q

Carcinoma

A

Cancer of epithelial origin

EX: lung, breast, prostate, bladder

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3
Q

Sarcoma

A

Malignant neoplasms of mesenchymal origin

EX: Fat, bone, muscle

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4
Q

Prefix meaning: hemangio

A

blood vessels

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5
Q

Prefix meaing: adeno

A

gland

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6
Q

Hyperplasia

A

increase in the number of cells

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7
Q

Dysplasia

A
  • Abnormal tissue architecture
  • Cells retain their function
  • Some cellular and nuclear changes leading to loss of cell uniformity
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8
Q

Anaplasia

A
  • Undifferentiated cells
  • Variable in size and shape
  • Numerous and atypical mitoses
  • Lack of organized tissue architecture
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9
Q

Rhabdomyosarcoma is a tumor of?

A

Skeletal muscle malignant tumor

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10
Q

Benign

A
  • Well-differentiated cells with preserved specialized features of the parent cells
  • Usually well demarcated. Often encapsulated masses
  • NO invasion of the surrounding tissue
  • No distant metases
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11
Q

Malignant

A
  • Lack of differentiation, anaplasia
  • locally invasive, infiltrating
  • Frequently present in distant metastases
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12
Q

Normal Cell Growth

A
  • Bone Marrow myeloblasts
  • Immune cells
  • Epidermal cells
  • Epithelial cells
  • Regenerating tissues
  • cell division TIGHTLY regulated by both growth promothing and inhibitory regulators
  • Usually cell damage or disruptions of cell cycle leads to cell death (apoptosis)
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13
Q

Features of Cancer Cells

A
  1. self-sufficiency in growth signals
  2. insensitivity to growth-inhibitory signals
  3. evasion of apoptosis
  4. limitless replicative potential
  5. sustained angiogenesis
  6. ability to invade and metastasize
  7. Evasion of host immune response
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14
Q

Cell Growth Regulation involces these factors (5)

A
  • Growth factors (PDGF, EGF)
  • GF Receptors (Tyrosine kinase, EGFR - ERBB1, ERBB2 (HER2))
  • Signal-Transducing proteins
  • Transcription factors (change Gene expression)
  • Cell cycle check points
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15
Q

Oncogene

A
  • altered forms of proto-oncogenes
  • sustained gain-of-function alterations in cancers
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16
Q

3 mechanisms of Gain-of-Function Alterations

A
  • Point mutations
  • Chromosomal rearrangements
  • Gene amplifications
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17
Q

Mechanisms of oncogene activation

A

1) multiple copies of oncogene (called?)
2) gene amplification
3) point mutation
4) chromosomal translocation leading to overexpression

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18
Q

How can Chromosomal translocation cause oncogene activation?

A
  • oncogene can be traslocated adjacent to a gene that is constituitivelly on (change in transcriptional control elements)
  • or translocated to create a noval-fusion gene to create a Chimeric Protein
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19
Q

TGF-alpha in sarcomas – is an example of what kind of dysregulation? Another ex?

A
  • overexpression of Autocrine Growth Factor
  • PDGF in GBM (glioblastoma?)
20
Q

Tumor Suppressor

A
  • usually get inactivated
  • can be epigenetically altered (environmental control)
  • usually recessive (both alleles must be inactivated to lose function).
  • When inherited they lead to familial cancers –> inherited cancers develop in multiple locations EXAMPLE: Retinoblastoma; p53
21
Q

retinoblastoma gene

(recheck this)

A
  • a tumor suppressor gene, codes for DNA-binding protein, present in every single cell
  • usually controls cycle by preventing transition from G1 to S
  • Hypophosphorylation means active –> this prevents activation of S-phase genes
  • double deletion in each gene results in RB tumor (GF release results in Rb protein inactivation by cyclin-dependent phosphorylation)
22
Q

APC

A

adenomatous polyposis coli gene encodes protein regulating cell proliferation and adhesion APC protein interacts with beta-catenin, which is a signaling molecule in the WNT pathway With WNT stimulation, APC releases beta-catenin, and beta-catenin translocates to the nucleus and activates genes promoting cell-cycle progression In colon cancer these cause polyps which will 100% turn into malignant tumors transformation associated with loss of second APC allele occur in majority of sporadic colorectal cancers

23
Q

p53

A

Is a transcription factor Active in every single cell protects our cells –> called guardian of the genome normally bound to MDM2 genes under stress (hypoxia, UV) it is no longer bound to MDM2 gene which causes its degradation and short-half life active p53 leads to transcription of CDK inhibitor -p21 –> G1 growth arrest common in >70% of human cancers tetrameric transcription factor alterations usually in DBD

24
Q

Li-Fraumeni Syndrome

A

is a dominant syndrome caused by p53 issues other factors that contribute to LFS: mutations of CHK2 gene polymorphism of WT p 53

25
Q

Consequences of p53 mutations

A

altered does not bind to DNA, loss of function and dominant negative mutant and gain of function

26
Q

ERBB1

A

Epidermal Growth Factor Receptor 1 truncated receptors in glioblastoma

27
Q

Proto-oncogenes - Growth Factor Recptors

A

1) Mutated or truncated forms of the receptors so that they are constitutively on - ex:glioblastoma 2) Overexpression of growth factor receptors - ex: ERBB1 in squamous cell carcinomas of lung -ex: ERBB2(HER2) in breast cancer

28
Q

Proto-oncogenes - Signal Transducing Proteins

A

Examples of 2nd messenger systems which may be altered in CA: 1) RAS 2) SRC 3) ABL 4) RAF 5) MAPK

29
Q

Ras in cancer

A
  • Encodes p21 G-protein, which transmits mitogenic signal through phosphorylation
  • Point mutations (that affects GTP binding site/GTP hydrolysis) can cause RAS (and RAF-MAPK pathwy) to be constitutively active
  • Most common abnormalities in human CA (particularly, pancreatic and colon)
30
Q

ABL

A

Non-receptor tyrosine kinase promotes apoptosis in CML, translocation of chromosome 22 where it fuses with part of BCR gene –> this forms aberrant chromosome, and therefore aberrant protein

31
Q

Chromosome Philadelphia

A

Formed as a result of ABL translocating to BCR gene and fusing, creating an aberrant chromosome 22

32
Q

What does the BCR-ABL protein do?

A

This fusion protein retains in the cytoplasm Has high tyrosine kinase activity –> stimulates multiple pathways including RAS-RAF mitogenic cascade

33
Q

What is MYC?

A

The most commonly involved TF in human CA EX: 1) overexpression in Burkitt’s Lymphoma 2/2 translocation to the chromosome 14 in close proximity to Ig gene 2) Gene amplification in lung and breast 3) Similar genes such as N-MYC and L-MYC are gene amplified in NEUROBLASTOMA and NSCLC, respectively

34
Q

Examples of nuclear Transcription Factors

A

MYC MYB JUN FOS REL

35
Q

Cell Cycle Regulation

A

Progression of cell cycle is driven by cyclins and cyclin-dependent kinases (CDKs) Cell cycle is tightly controlled by CDK inhibitors

36
Q

Most common perturbations in cell cycle regulation are?

A

G1 to S phase transition 2/2: 1) overexpression of cyclin D in breast, liver, esophagus, and lymphomas 2) Amplification of CDK4 in melanomas, sarcomas, and glioblastomas

37
Q

Tumor Suppressor Genes

A

Tumor suppressor genes code for Growth inhibitory signals –> INHIBIT CELL PROLIFERATION or stimulate apoptosis upon damage Inactivation of tumor suppressor genes can result an insensitivity to growth-inhibitory signals

38
Q

What may cause an inactivation of tumor suppressor genes?

A

1) mutations 2) truncation 3) deletions 4) methylation (epigenetic changes) of the promotor

39
Q

Mutations of tumor suppressor genes

A
  • Must be recessive meaning two alleles must be altered in order to lose their function inherited forms
  • contribute to familial cancers and develop earlier in age
40
Q

Retinoblastoma Cancer

A

pediatric tumor deletion of Rb tumor suppressor gene

sporadic form: both mutations in Rb acquired after birth –> tumor frequency is low

familial form: 1 mutation is already inherited, and 1 more needs to occur after birth –> frequency of retinoblastoma is very high and tumors arise bilaterally

41
Q

BRCA1

A
  • tumor suppressor genes
  • encode nuclear proteins involved in response to DNA damage and DNA repair
  • germline mutations cause 85% and 50% increased risk of breast and ovarian cancers
42
Q

BRCA2

A
  • germline mutations lead to increased risk of breast cancer 80%, while ovarian cancers are not as common but still risk of 10%
  • associated with increased risk 6% of male breast cancer
43
Q

HNPCC

A

hereditary nonpolyposis colorectal cancer

  • associated with defects in mismatch repair genes
44
Q

xeroderma pigmentosum

A

increased risk of UV-induced skin cancers due to the defects in the nucleotide excision repair system responsible for removal of UV-cross-linked residues

45
Q

ALK

A
  • anaplastic lymphoma kinase
  • ALK is a receptor tyrosine kinase preferentially expressed in the CNS and PNS germline
  • activating mutations of ALK have been associated with familial neuroblastoma, which segregates as autosomal-dominant disease
  • also occur in sporadic cases of neuroblastoma

**This would be an oncogene and an alteration in it will be beneficial to the cell

46
Q

miRNAs

A

oncogenic miRNA target tumor suppressors tumor suppressor miRNA target oncogenes

47
Q

How does deregulation of apoptosis cause cancer?

A
  • Leads to survival/propagation of damaged, mutated cells
  • reduced levels of CD95 result in inactivation of death-induced signaling complex by FLIP protein
48
Q

Telomerase activity

A

shorten telomeres 60-70 doublings and then cells enter non replicative senescence Telomerases is an enzyme which maintains normal length telomerases upregulated in CA which allows for unlimited cell divisions

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