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Medical Genetics > Lab 10 - Oncogenesis 1 > Flashcards

Lab 10 - Oncogenesis 1 Flashcards

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USMLE® Step 1 flashcards Biology 101 flashcards
1
Q

Oncogenetic transformation/Carcinogenesis- Definition and what does it results from?

A

The way a physiological cell changes into a cancerous cell

Result from the action of one or a combination of chemical, physical, biologic and/ or genetic insults to cells.

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2
Q

Stages of Carcinogenesis

A

1) Initiation
2) Promotion
3) Transformation
4) Progression

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3
Q

Initiation

A

Exposure of cells to appropriate doses of carcinogens, either by environmental factors or due to hereditary traits.

Results from an irreversible genetic alteration, most likely one or more simple mutations, transversions, transitions, and/or small deletions in DNA.

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4
Q

Promotion

A

Reversible stage, does not involve changes in the structure of DNA but rather in the expression of the genome mediated through promoter-receptor interactions

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5
Q

Transformation

A

Conversion stage when it’s transformed to malignant cells

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6
Q

Progression

A

Irreversible stage characterized by karyotypic instability and malignant growth.

Angiogenesis
Metastasis

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7
Q

Angiogenesis

A

Formation of new blood vessels. Stimulates growth, induce malignancy and induce metastasis

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8
Q

Metastasis

A

Is a pathogenic agent’s spread from a primary site to a secondary site within the host body.

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9
Q

Two phases of metastasis:

A
  1. Invasion and growth: invades the extracellular matrix:
    - Detachment of tumor cells from each other
    - Degradation of ECM and basement membrane
    - Attachment of tumor cells to matrix components
    - Migration of tumor cells/locomotion/intravasation
  2. Spread, dissemination, metastasis
    - lymphatic spread
    - Diret seeding of body cavities and surfaces
    - Hematogenous spread
    - CSF spread
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10
Q

Molecular targets during the stages of oncogenesis include

A

Protooncogenes
Cellular oncogenes
Tumor suppressor genes

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11
Q

5 Cancer cell characteristics

A
  1. Evasion of apoptosis
  2. Limitless replicative potential
  3. Sustained angiogenesis
  4. Ability to invade and metastasize
  5. They are tumorgenic
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12
Q

Warburg effect

A

Cancer cells obtain their energy through aerobic glycolysis and not oxidative phosphorylation

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13
Q

Does cancer cells induce autophagy?

Definition of autophagy

A

No

A process where the cell itself stops their own growth and cannibalizes their own organelles and membranes due to severe nutrient deficiency

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14
Q

What does the cancer cells do with the normal stromal cells

A

The cancer secretes signal proteins and proteolytic enzymes that alter the stromal structure. The stroma then secretes signal proteins that stimulate cancel cell growth and division. The stroma also secretes proteases that remodel the ECM in favour of the tumor

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15
Q

Cancer cells show mutations in genes that are important for

A

Mismatch repair
Nucleotide excision repair
Base excision repair

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16
Q

Maintence of which enzyme is one of the most important characteristics for cancer cells?

A

Telomerase

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17
Q

Cancer cells can elongate telomeres in two ways

A
  1. Telomerase: is an enzyme that uses RNA as a template to restore the telomeres
  2. Alternative lengthening of telomeres: elongates the telomeres by DNA recombination
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18
Q

Tumors are describes by terms derived from

A

Appearance of the neoplasm, tissue of origin and degree of differentiation

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19
Q

Classification of tumors according to biological properties

A

Benign, malignant, locally malignant/ semimalignant.

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20
Q

Oma, carcinoma and sarcoma - suffix

A

Oma: benign
Carcinoma: malignant of epithelial or glandular origin, most common. Sarcoma: malignant of mesenchymal origin (connective tissue)

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21
Q

Lipo, Leiomyo, rhabdomyo, osteo, chondro, adeno, cholangio – prefix

A 
Lipo: adipose tissue 
Leiomyo: smooth muscle 
Rhabdomyo: striated muscle 
Osteo: bone
Chondro: cartilage
Adeno: glandular 
Cholangio: bile duct.
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22
Q

Classification of tumors by grade

A

Increasing abnormality to respect for the surrounding tissues increases the grade.

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23
Q

Classification of tumors by stage

A

Staging is a way of describing or classifying a cancer based on the extent of cancer in the body. Based on size and metastasis, from where it started and where it spread to. Ex: TNM staging.

24
Q

TNM stands for

A

T: size of primary tumor
N: lymph nodes involved
M: metastasis.

25
Q

Benign vs malignant tumor

A

Cancerous: Benign tumor is not cancerous while malignant is cancerous.

Growth rate: Benign has slow, malignant has fast growth.

Recurrence: Benign tumors is less likely to recur while malignant are more likely.

Protective sac: Benign tumors is surrounded by a protective sac that restricts its growth and makes it easier to remove, malignant tumors does not have this sac.

Treatment: Benign tumors respond well to treatment and prognosis is favourable.

Invasive: Benign tumors are non-invasive while malignant are invasive. Benign tumors can be serious if they are pressing a primary nerve, main artery or compress brain matter.

Metastasize: Malignant tumors can multiply uncontrollably, metastasize and invade surrounding tissue, this is not happening with benign tumors.

Malignant tumors are formed from abnormal cells that are highly unstable and travel via the blood stream, circulatory system and lymphatic system.

26
Q

Apoptosis- Definition and why it happens

A

Programmed cell death (death of damaged cells). When a cell becomes mutated and does not repair itself, it can be sacrificed to prevent that mutation from being passed on to the next generation of cells. Causes cell to shrink, develop belbs, undergoes degradation of genetic and protein materials in the nucleus, and have their mitochondria breakdown, thus releasing cytochromes.

27
Q

What happens if DNA repair fails?

A

P53 protein activated the transcription of pro-apoptotic genes like BAX and PUMA

28
Q

What genes are activated when the amount of pro-apoptotic proteins outweight the amount of anti-apoptosis?

A

BAX and BAK

29
Q

Role of BAX

A

Punches holes in the mitochondrial membrane, which makes the mitochondria leak cytochrome c which leads to a series of events that initiate the apoptosis.

30
Q

Loss of p53 function leads to what?

A

DNA damage goes unrepaired, mutations accumulate in oncogenes and other cancer genes, and the cell goes in a path leading to malignant transformation.

31
Q

Necrosis- Definition and Cause

A

Premature death of cells and living tissue. Caused by factors external to the cell or tissue, such as infection, toxins or trauma. Cells may swell or forms vacuoles on their surface, with interior structures either distending or shrinking rapidly, destroying the cell’s process and chemical structures.

32
Q

Unregulated release of cytochrome and cell membrane’s phospholipid during necrosis causes what?

A

Immediate reactions in surrounding tissue, leading to swelling (inflammation) and edema.

33
Q

Macrophage-cleaning occurs in apoptosis or necrosis?

A

Apoptosis

34
Q

Where does oncogenes originate from?

A

Proto-oncogenes, which are genes involved in the four basic regulators of normal cell growth:
Growth factors, growth factor receptors, signal transduction molecules and nuclear transcription factors

35
Q

When mutation occurs in proto-oncogenes

A

It can become an oncogenes, a gene whose excessively product can lead to unregulated cell growth and differentiation

36
Q

How are the oncogenes activated?

A

Typically by gain-of-function mutation, gene amplification (increased number of genes), hypomethylation of oncogene’s 5’ region (increases transcription), or chromosome rearrangements that upregulate the oncogene

37
Q

Oncogenes are typically found in which tumors?

A

Sporadic tumors

38
Q

Most oncogenes induce growth through the

A

Receptor tyrosine kinase pathway

39
Q

Less common pathways for oncogenes growth

A

WNT pathway
Notch pathway
JAK/STAT pathway

40
Q

Tumor suppressor gene

A

Is a gene that protects a cell from one step on the path to cancer.

When this gene mutates to cause a loss or reduction in its function, the cell can progress to cancer, usually in combination with other genetic changes.

41
Q

Categorization of tumor suppressor genes

A
  1. Inhibitors of mitogenic signaling pathways
  2. Inhibitors of cell cycle progression
  3. DNA repair factors
  4. Inhibitors of “pro-growth” programs of metabolism and angiogenesis
  5. Inhibitors of invasion and metastasis
  6. Enablers of genomic stability
42
Q

Inhibitors of mitogenic signaling pathways

A

NF1 (neurofibromin-1): neurofibromatosis type 1, neuroblastoma, juvenile myeloid leukemia

NF2: neurofibromatosis type 2, schwannoma, meningioma

APC (adenomatous polyposis coli protein): carcinoma of the stomach, colon and pancreas

43
Q

Inhibitors of cell cycle progression

A

CDKN2A: INK4A and ARF: melanoma and different carcinomas

RB (retinoblastoma protein): retinoblastoma

44
Q

DNA repair factors

A

BRCA1 and 2: breast and ovarian cancers

MSH2 and 6, and MLH1: colon carcinoma

45
Q

Inhibitors of “pro-growth” programs of metabolism and angiogenesis

A

VHL: von vippel lindau protein

46
Q

Inhibitors of invasion and metastasis

A

CDH1: E-cadherin: gastric carcinoma and lobular breast carcinoma

47
Q

Enablers of genomic stability

A

TP53: p53 protein: Li-Fraumeni syndrome and most human cancers

48
Q

Function of microRNA

A

Inhibit RNA and protein-coding RNA molecules themselves. Regulate cellular processes; cellular proliferation, differentiation and survival. Some function as tumor suppressor genes (Let-7), while others function as oncogenes (Mi-372 and mi-373).

49
Q

How does the tumor cells affect miRNA?

A

They exhibit dramatic changes in miRNA expression. Loss/silencing or overexpression of miRNA is observes in many tumors. May therefore promote abnormal tumor cell survival.

50
Q

Angiogenesis is controlled by a balance between what?

A

Angiogenesis promoters and inhibitors.

51
Q

Angiogenesis promoters:

A

Basic fibroblast growth factors (bFGFs), VEGFs, proteases

52
Q

Angiogenesis inhibitors:

A

angiostatin and endostatin

53
Q

Angiogenic switch:

A

Increased production of angiogenic promoters and/or loss of angiogenic inhibitors

54
Q

Angiogenic switch activated by:

A

Lack of oxygen, mutations in TSGs or oncogenes, gain-of-function mutations in RAS or MYC (RAS-MAP kinase pathway).

55
Q

What are the effects of angiogenic switch on the tumor?

A

1) Stimulate growth: delivery of nutrients induces the secretion of growth factors by endothelial cells, IGFs and PDGFs.
2) Induce malignancy: newly synthesized blood vessels have an irregular pattern of connection –> irregular blood flow within the tumor, hypoxia in several areas within the tumor, areas of hypoxia favours the growth of mutant cancer cells seeing as they are more suitable to survive under harsh conditions.
3) Induce metastasis: tumors have access to the circulatory system and are able to metastasize.

56
Q

What leads to permanent inactivation of tumor suppressor genes?

A

Loss-of-function mutation in RB1, deletion of the gene, hypermethylation of it’s 5’ region

Medical Genetics (10 decks)

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