The Cell Cycle and Cancer

Transcription

1 The ell ycle and DN Transcription (Nucleus) Transcription DN Nuclear envelope RN Protein Translation (Ribosomes) RN Processing mrn Translation Polypeptide Pre-mRN Nuclear pores Ribosome Transcription Translation RN is synthesized from DN in the nucleus mrn (messenger) is created as a copy of the gene onverts base sequence of nucleic acids into the amino acid sequence of proteins Involves mrn, trn, and rrn Occurs at the ribosome in the cytoplasm enetic ode Each three-base sequence on DN (triplet) is represented by a codon on mrn One gene one mrn strand one polypeptide product EOND BE Phe Tyr ys er top top Leu top Trp Leu Ile et or tart Val Pro Thr la His ln sn Lys sp lu rg er rg ly Figure

2 TRNRIPTION 3 DN Functions of ell Division RN RN 5 transcript polymerase RN PROEIN Exon RN transcript (pre-mrn) Intron minoacyl-trn synthetase NLE FORTION OF mino INITITION OPLEX acid INO ID TIVTION YTOPL trn mrn rowing polypeptide ctivated amino acid 3 rowth Replacement Repair Reproduction E P Ribosomal subunits 5 TRNLTION E nticodon odon Ribosome The ell ycle n illustration of the life cycle of a cell onsists of four major phases 1 phase phase 2 phase phase Interphase (preparation for cell division) 1 checkpoint (restriction point) 1 rowth rowth and DN synthesis 2 rowth and final preparations for division 2 checkpoint opyright 2010 Pearson Education, Inc. Figure 3.31 The ell ycle ummary Interphase 1 Prepare for division DN replication 2 Last minute preparation before division begins phase itosis eparation of replicated DN ytokinesis plitting of the cell 1 checkpoint (restriction point) 1 rowth rowth and DN synthesis 2 rowth and final preparations for division 2 checkpoint Figure

3 DN replication Preparing for ell Division Takes place during (synthesis) phase of cell cycle Occurs in the nucleus DN replication overview hromosome Old DN Helicase unwinds the double helix and exposes the bases denine Thymine ytosine uanine Free nucleotides Replication fork DN polymerase Old strand acts as a template for synthesis of new strand Leading strand Two new strands (leading and lagging) synthesized in opposite directions Lagging strand DN polymerase Old (template) strand opyright 2010 Pearson Education, Inc. Figure 3.32 DN Replication The Process of ell Division End result is two complete sets of DN ssures appropriate chromosome number in daughter cells Includes two distinct events 1. itosis division of chromatin Prophase naphase Telophase 2. ytokinesis division of cytoplasm by cleavage furrow The Process of ell Division itotic () phase of the cell cycle Essential for body growth and tissue repair Does not occur in most mature cells of nervous tissue, skeletal muscle, and cardiac muscle Early Prophase Early mitotic spindle ster Early Prophase hromosome consisting of two sister chromatids entromere We will come back to cancer 3

4 Prophase Late Prophase Polar microtubule pindle pole Fragments of nuclear envelope DN is condensed centromere Late Prophase Kinetochore Kinetochore microtubule ister chromatids LE µm hromosome duplication (including DN synthesis) pindle entromere ister chromatids eparation of sister chromatids plate entromeres ister chromatids naphase Telophase and ytokinesis Nuclear envelope forming Nucleolus forming ontractile ring at cleavage furrow naphase Daughter chromosomes Telophase 4

5 The Process of ell Division ytokinesis Problems during mitosis ay or may not be fatal Examples Non-disjunction Down syndrome X and Y chromosomes ell movement ells actually divide Follows nuclear division LE 12-9a ytokinesis Begins during late anaphase Ring of actin microfilaments contract to form a cleavage furrow Two daughter cells are pinched apart Each contains a nucleus identical to the original leavage furrow 100 µm ontractile ring of microfilaments Daughter cells leavage of an animal cell (E) econd most common cause of death in.. ctually just became the most common in Kansas Prostate cancer Estimated 217,730 men will be diagnosed Breast cancer 12.2% women will be diagnosed ost common types Prostate (men) Breast (women) Lung olorectal 5

6 LE checkpoint Damage control exists in the cell cycle of normal cells Example: proto-oncogenes, tumor suppressor genes (P53) ontrols do not function properly in cancer cells Results in uncontrolled cell division bsence of or defective regulatory proteins cells compete with and crowd out normal cells 1 ontrol system 2 checkpoint 2 checkpoint enes coding for checkpoint proteins utation of genes results in uncontrolled cell division nything that can alter these genes can trigger cancer cells form tumors asses of abnormal cells within otherwise normal tissue Benign tumor ells are encapsulated and remain at original site alignant tumor Invades surrounding tissue and may metastasize LE LE olon Tumor Lymph vessel landular tissue cell Blood vessel etastatic tumor Loss of tumorsuppressor olon wall gene P (or other) ctivation of ras oncogene Loss of tumorsuppressor gene p53 tumor grows from a single cancer cell. cells invade neighboring tissue. cells spread through lymph and blood vessels to other parts of the body. small percentage of cancer cells may survive and establish a new tumor in another part of the body. Normal colon epithelial cells mall benign growth (polyp) Loss of tumorsuppressor gene D Larger benign growth (adenoma) dditional mutations alignant tumor (carcinoma) 6

7 lassification REEBER THEE FOR LL 3 TER 1. arcinoma Epithelium 2. arcoma onnective tissue, bone or muscle 3. yeloma Plasma cells in bone marrow 4. Lymphoma Lymph tissue 5. Leukemia bnormal white blood cells ymptoms vary with type nusual bleeding or discharge lump that does not go away sore that does not heal within two weeks change in bowel or bladder habits Persistent hoarseness or cough Indigestion or difficulty swallowing hange in a wart or mole auses arcinogens Oncogenic viruses Examples: Human Papilloma Virus (HPV can infect cervical cells) Epstein Barr virus (can infect B-cells and lead to lymphoma) Hepatitis B virus (can infect liver cells) Hereditary factors 7