When the cell cycle goes wrong: checkpoints and cancer
Grade 9 Science Worksheet - Challenge Me
Circle the best answer.
Read this first
Notebook on the regulators (model data)
line what it says 1 Cyclin levels rise and fall as the cell moves through the cycle 2 A Cdk needs a cyclin partner to be fully active 3 p53 is a tumor suppressor that can halt the cycle at the G1 gate 4 p53 is a positive regulator that pushes cells past the G1 gate Bo proofreads a classmate's notebook. Exactly one line is wrong. Which line, and why?
- Line 2, because a Cdk is fully active with no partner
- Line 1, because cyclin levels stay steady through the cycle
- Line 3, because tumor suppressors push cells to divide
- Line 4, because p53 is a negative regulator that halts the cycle
Use this
Notebook on mutations and cancer (model data), 4 rows. Columns: line, what it says. 1, Cancer starts with changes in genes that control how cells grow and divide. 2, UV rays from sunlight can damage DNA and change genes. 3, Proto-oncogenes are normal genes; some mutations turn them into oncogenes. 4, One mutation in one gene is enough to turn a healthy cell into a cancer cell.
Esme proofreads a classmate's notebook. Exactly one line is wrong. Which line, and why?
- Line 4, because a healthy cell needs more than one DNA change
- Line 1, because gene changes cannot affect how cells divide
- Line 2, because damaged DNA means the cell is already a cancer cell
- Line 3, because a normal gene cannot become an oncogene
NCI card (from the National Cancer Institute)
topic what NCI says changes needed a healthy cell needs two or more DNA changes before it turns cancerous as cells divide cancer cells gain more DNA changes over time Jun claims that one mutation in the p53 gene turns a healthy cell into a cancer cell. Does the card support this?
- No: a healthy cell needs two or more DNA changes, so one is not enough
- No: p53 has no part in controlling cell division
- Yes: a change in any gene makes a cell cancerous
- Yes: p53 is a brake gene, so losing it alone makes a cell cancerous
Use this
NCI card (from the National Cancer Institute), 2 rows. Columns: topic, what NCI says. most genetic changes, are not harmful on their own. genes linked to cancer, tend to be proto-oncogenes, DNA repair genes or tumor suppressor genes.
Kira says that every mutation in a cell leads to cancer. Does the card support this?
- Yes: a mutation changes a protein, so the cell loses control of its cycle
- No: a mutation does not change the proteins a cell makes
- No: most genetic changes are not harmful on their own, and cancer-linked ones tend to hit certain genes
- Yes: a mutation in a division gene turns a cell cancerous on its own
Gene card (model)
gene before the mutation after the mutation Q a go signal that tells cells to divide when needed a go signal that stays on R a protein that halts the cycle when DNA is damaged no working protein Luz compares two mutated genes on the card. Which statement fits the card?
- Q is a stuck accelerator and R is a failed brake; either can lead to uncontrolled division
- Q is a failed brake and R is a stuck accelerator; neither can lead to uncontrolled division
- Q is a failed brake and R is a stuck accelerator; either can lead to uncontrolled division
- Q is a stuck accelerator and R is a failed brake; neither can lead to uncontrolled division
Use this
Cells in a dish after each round (model data), 6 rows. Columns: round, working gate, broken gate. 0, 5, 5. 1, 5, 10. 2, 5, 20. 3, 10, 40. 4, 20, 80. 5, 40, 160. In this model, a working gate holds damaged cells for 2 rounds of repair, then they divide each round; a broken gate holds none.
Milo reads the table. After round 5, how many more cells does the broken-gate dish hold than the working-gate dish?
- 40 cells
- 200 cells
- 60 cells
- 120 cells
If both dishes keep doubling each round, how many cells will Noah count in the working-gate dish after round 7?
- 50 cells
- 80 cells
- 160 cells
- 640 cells
If the broken-gate dish keeps doubling each round, how many cells will Pia count in it after round 6?
- 35 cells
- 320 cells
- 160 cells
- 80 cells
Use the table
Cycle wheel (model, not to scale), clockwise from the top: G1, S, G2, mitosis (M), cytokinesis. Three gates (checkpoints) stand on the wheel: the G1 gate near the end of G1, the G2 gate before mitosis, and the M gate in mitosis, before the sister chromatids are pulled apart. A gate drawn open lets a cell pass, a gate drawn closed holds the cell, and a gate drawn broken no longer checks. The G1 gate is drawn broken; the G2 gate and the M gate are drawn open. A cell with damaged DNA is entering S. Gene card (model)
gene protein job J halts the cycle at G1 when DNA is damaged K moves the cell on past a gate Ren combines the wheel and the gene card. The G1 gate is broken and a damaged cell is entering S. Which mutation explains the wheel?
- Gene J no longer makes a working protein, so the cell stops dividing for good
- Gene K no longer makes a working protein, so nothing halts the damaged cell
- Gene J no longer makes a working protein, so nothing halts the damaged cell
- Gene J now makes extra protein, so the gate holds the cell longer
Zee combines the wheel and the card. The cell's reserves are low, yet the G1 gate is drawn open. Which statement explains the wheel?
- The Cdk change breaks the gate, so the cell stops in G1 for good
- The gate works as usual, so the cell has met the checks
- The Cdk change is a stuck accelerator that pushes the cell past the gate too early
- The Cdk change is a failed brake that lets the gate stay open