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Cell Cycle and Cancer. Cancer Terms Neoplasm – new, abnormal growth of cells Benign – not cancerous Malignant - cancerous Cancer – cellular growth disorder.

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Presentation on theme: "Cell Cycle and Cancer. Cancer Terms Neoplasm – new, abnormal growth of cells Benign – not cancerous Malignant - cancerous Cancer – cellular growth disorder."— Presentation transcript:

1 Cell Cycle and Cancer

2 Cancer Terms Neoplasm – new, abnormal growth of cells Benign – not cancerous Malignant - cancerous Cancer – cellular growth disorder that results from the mutation of the genes that regulate the cell cycle Carcinogenesis – development of cancer

3 Characteristics of Cancer Cells Table 9.2 (page 159) Cancer cells – Lack differentiation, do not contribute to body – Have abnormal nuclei, enlarged, abnormal # of chromosomes – No apoptosis – Form tumors, no contact inhibition, disorganized and multilayered – Not encapsulated – Undergo metastasis and angiogenesis Telomeres – a region of repetitive DNA at the end of a chromosome, which protects the end of the chromosome from deterioration. Cancer cells have longer regions so they can continue to reproduce.

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5 Prognosis (probable outcome) 1.Whether the tumor has invaded surrounding tissue 2.Whether there is lymph node involvement 3.Whether there are metastatic tumors in distant parts of the body

6 Proto-oncogenes specify proteins that directly and indirectly promote the cell cycle Found at the end of a stimulatory pathway A mutated proto-oncogene = oncogene

7 Tumor-suppressor genes At the start of inhibitory pathway Directly or indirectly inhibit the cell cycle When mutates, inhibitory proteins fail to be active and cell cycle is unchecked. Ex. P53, mutated mostly in human cancers, works to turn on the expression of other genes who inhibit cell cycle and stimulates apoptosis.

8 oncogenes Cancer causing genes Cause acceleration of the cell cycle by coding for a faulty receptor protein or specify an abnormal protein product that stimulates the cell cycle to begin. Can bring about excess cyclin and excess inhibitors of p53 so that apoptosis does not occur. Ex. rasK, rasN, BRCA1


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