Lectures 1-2 Flashcards

1
Q

What is a tumor?

A

A group of cells which display unregulated proliferation. Also known as a neoplasm.

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2
Q

What is metastasis?

A

Metastasis is the ability of a malignant tumor to form 2 degree tumors (metastases) at other sites in the body.

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3
Q

How does Metastasis occur?

A

It occurs when small clusters of cancerous cells dislodge from the primary tumor to invade the blood or lymphatic vessels and are carried to distant sites, taking up residence and proliferating.
The potential to do this is called Metastatic potential.

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4
Q

Tumor arise from what kind of tissues?

A

Either epithelial tissues or non-epithelial tissues.

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5
Q

Epithelial tumors:

A

-Are called Carcinomas.
-They make up 80-90% of cancers eg. Breast, colon, prostate, lung, stomach, skin, oesophagus, liver, ovary, gallbladder and urinary.

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6
Q

Non-epithelial tumors:

A

-Leukemia, Lymphoma and multiple myeloma (9% of all cancers) are malignant tumors of hematopoietic cells derived from bone marrow.
-Sarcoma (1% of cancers) arise from a variety of mesenchymal cell types.
-Cells that form part of the central and peripheral nervous systems. Includes gliomas, glioblastomas, neuroblastomas, medulloblastomas. Makes up 1.3%.

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7
Q

Oncogenes vs Tumor suppressor genes:

A

-Oncogenes are usually “gain of function mutations” generally dominant eg cMYC
-Tumor suppressor genes (TSGs) are usually “loss of function mutations” generally recessive eg Rb

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8
Q

What are proto-oncogenes?

A

Genes that encode elements of the cell’s signal transduction network and parts of the cell cycle control system. When mutated they can allow cancer to occur.

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9
Q

Proto-oncogenes can encode:

A

-Growth Factors
-Growth Factor Receptors
-Signal Transduction Molecules
-Nuclear Proteins

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10
Q

2 types of Signal Transduction Molecules:

A
  1. Cytoplasmic membrane associated proteins:
    src (tyrosine kinase)
    ras (GTP-binding protein)
  2. Soluble signal transduction proteins:
    raf (serine/threonine kinase)
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11
Q

2 nuclear proteins:

A
  1. c-myc (gene regulatory protein, HLH family)
  2. jun + fos (form AP-1)
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12
Q

What does activation of oncogenes lead to

A

Generally lead to increased cell division and growth, lack of apoptosis, increased cell
motility, invasion and loss of differentiation i.e Cancer

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13
Q

How can oncogenes become activated.

A

-genetic/point mutations
-chromosomal translocations
-gene amplification
-epigenetic factors
-Increased protein stability

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14
Q

Point mutation:

A

Results in gene being constitutively active or increased activity e.g Hras

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15
Q

Gene Amplification:

A

Normal protein is overproduced e.g HER2

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16
Q

Chromosome translocation:

A

Gene moves to a strong enhancer which leads to increased protein expression e.g c-myc in Burkitt’s lymphoma

17
Q

2 observations that suggest tumors derived from a single abnormal cell:

A
  1. Karyotyping/DNA Analysis
  2. X Chromosome inactivation
18
Q

Multistep Nature of Cancer:

A

The tendency of untreated tumors to develop from benign or small to malignant, large tumors over time.

19
Q

What happens to tumor cells during lag phase?

A

They undergo a succession of changes.(multiple genetic/epigenetic changes)