Tumour Pathology 4 and 5 Flashcards

1
Q

Mitosis

A

Mechanism of cellular replication. A diploid cell becomes 2 diploid cells.

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2
Q

Cell cycle

A

The time interval between mitotic divisions.
G2 = preparation for mitosis and cell growth.
M = mitosis and cell division
G1 = synthesis of components required for DNA synthesis and a checkpoint.
S = DNA synthesis.
G1, S and G2 are known as the interphase.
There are approximately 25 x 10^(6) cell divisions per second.

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3
Q

Number of cells in body

A

Approximately 10^(13)

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4
Q

Carcinogenesis

A

Caused by a mutation of genetic material that upsets the normal balance between proliferation and apoptosis. Only mutations in genes regulating cell division, apoptosis and DNA repair cause a cell to lose control of proliferation.

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5
Q

Abnormal cell cycle

A

The primary defect in cancer is uncontrolled proliferation via cell cycle dysregulation

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6
Q

Cell pathways disrupted

A
  1. Cyclin D-pRb-E2F
  2. p53
    - Virtually all cancers are dysregulated at G1-S because of mutation in one of four genes; Rb, CDK4, cyclin D, p16.
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7
Q

Aetiological cancer agents

A

Chemicals, radiation, oncogenic viruses, age, inherited.

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8
Q

How do aetiological agents cause abnormalities

A

The purine and pyramidine bases in DNA are critical cellular targets for damage by radiation and various oxidising and alkylating agents. Chemical carcinogens/active metabolites react with DNA to form adducts. Adduct formation at particular sites in DNA leads to the activation of oncogenes and suppression of tumour suppressor genes.

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9
Q

Tumour formation

A

More than one mutation is necessary for carcinogenesis. All sporadic cancers harbour multiple genetic abberations and abnormalities which accumulate with time. Activation of several oncogenes and loss of 2 or more anti-oncogenes occurs in most cancers.

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10
Q

Genetic changes in cancer

A

Mutations can be sporadic and/or inherited and they accumulate over time. Loss of cell cycle control leads to malignant transformation. Key regulators include; p16, cyclin D, CDK4 and Rb and are mutated in majority of cancers. Loss or mutation of p53 allows genetically damaged cells to proliferate forming malignant neoplasms.

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