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Quizzes > Science

Which Phrase Best Describes Cancer? Cell Cycle and Mitosis Quiz

Quick, free cell cycle and cancer quiz. Instant results.

Editorial: Review CompletedCreated By: Mikael BrorsonUpdated Aug 27, 2025
Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art illustration for cell cycle stages quiz on a golden yellow background.

This quiz helps you choose which phrase best describes cancer and review the cell cycle stages. Practice mitosis, from prophase to telophase and cytokinesis, then see what you missed with instant feedback. For more ways to study, try the which phrase best describes cancer quiz, explore a mitosis and cytokinesis quiz, or warm up with a cancer quiz.

Which phase of the cell cycle is characterized by the replication of DNA?
G2 phase
M phase
G1 phase
S phase
During the S phase of interphase, each chromosome is replicated to ensure both daughter cells receive identical DNA. This is a critical step before mitosis. Proper progression through S phase is tightly regulated to prevent genomic instability.
During which phase does the cell divide its cytoplasm to form two separate daughter cells?
Metaphase
Anaphase
Prophase
Cytokinesis
Cytokinesis is the final step of cell division, where the cytoplasm splits to form two distinct cells. In animal cells, a cleavage furrow pinches the cell membrane. In plant cells, a cell plate forms down the center.
Which checkpoint ensures the cell has no DNA damage before entering S phase?
G2 checkpoint
G1 checkpoint
Restriction checkpoint
Spindle checkpoint
The G1 checkpoint monitors cell size, nutrients, growth factors, and DNA integrity before DNA replication. If damage is detected, the cell can pause for repair or trigger apoptosis. This gating is crucial to prevent propagation of mutations.
What is the name of the phase when chromosomes condense and become visible under a microscope?
Telophase
Prophase
Anaphase
Metaphase
During prophase, chromatin fibers condense into discrete chromosomes. The nuclear envelope begins to break down and the mitotic spindle forms. This condensation is necessary for accurate segregation.
In which phase do sister chromatids align at the cell's equatorial plate?
Telophase
Anaphase
Metaphase
Prophase
During metaphase, motor proteins position sister chromatids along the metaphase plate. This alignment ensures equal separation of genetic material. The spindle assembly checkpoint monitors this alignment.
Which enzyme unwinds DNA during replication in S phase?
Polymerase
Topoisomerase
DNA ligase
Helicase
DNA helicase breaks hydrogen bonds between base pairs, unwinding the double helix ahead of the replication fork. This action allows DNA polymerases to synthesize new strands. Proper helicase function is vital to genome stability.
What is the end result of mitosis in a normal somatic cell?
Two haploid cells
One diploid cell
Four haploid cells
Two diploid cells
Mitosis produces two genetically identical diploid daughter cells from one diploid parent cell. Each daughter has the same chromosome number as the parent. This continuity is essential for tissue growth and repair.
Which structure forms in plant cells to initiate cytokinesis?
Spindle midzone
Cell plate
Cleavage furrow
Contractile ring
In plant cells, vesicles from the Golgi apparatus coalesce at the center to form the cell plate. This plate develops into a new cell wall, separating the two daughter cells. Animal cells use a cleavage furrow instead.
What term describes an uncontrolled, abnormal growth of cells?
Senescence
Apoptosis
Cancer
Metastasis
Cancer refers to the uncontrolled proliferation of cells due to failures in cell cycle regulation. Mutations in oncogenes or tumor suppressors disrupt normal checkpoints. This leads to abnormal growth and potential metastasis.
Which protein acts as a tumor suppressor by halting the cell cycle in response to DNA damage?
E2F
p53
Cyclin D
CDK2
p53 is activated by DNA damage and can induce cell cycle arrest at G1 to allow repair. If damage is irreparable, p53 can trigger apoptosis. Loss of p53 function is common in many cancers.
What is the primary role of cyclin-dependent kinases (CDKs) in cell cycle regulation?
Form the mitotic spindle
Degrade cyclins
Bind DNA directly
Phosphorylate target proteins
CDKs bind cyclins to form active complexes that phosphorylate key proteins for cell cycle progression. Different CDK - cyclin pairs act at specific checkpoints. Incorrect CDK regulation can contribute to uncontrolled division.
Which stage of mitosis is defined by the separation of sister chromatids?
Telophase
Metaphase
Anaphase
Prophase
In anaphase, cohesin proteins are cleaved, allowing sister chromatids to be pulled toward opposite poles. Microtubules shorten to move chromosomes. Accurate anaphase is vital to prevent aneuploidy.
What name is given to the non-dividing phase of the cell cycle?
Telophase
Prophase
G0 phase
Interphase
G0 is a quiescent state where cells are metabolically active but not proliferating. Many differentiated cells enter G0 instead of dividing. Cells can re-enter G1 from G0 under certain conditions.
Which structure is responsible for separating chromosomes during cell division?
Golgi apparatus
Nucleolus
Centromere
Spindle apparatus
The spindle apparatus, composed of microtubules, orchestrates chromosome movement. Kinetochore microtubules attach to centromeres and pull chromosomes apart. Proper spindle function is critical for genomic stability.
What triggers the transition from metaphase to anaphase?
Activation of APC/C complex
Phosphorylation of cyclin D
Binding of CDK4 to cyclin B
Expression of E2F
The anaphase-promoting complex/cyclosome (APC/C) ubiquitinates securin, allowing separase to cleave cohesin. This leads to sister chromatid separation. APC/C regulation ensures proper timing.
Which of the following best describes telophase?
Chromosome condensation
Nuclear envelope re-forms
DNA replication
Chromatids separate
In telophase, separated chromosomes arrive at poles and de-condense into chromatin. The nuclear envelope reassembles around each set. This readies the cell for cytokinesis.
What is the hallmark phrase that best describes the uncontrollable nature of cancer cells?
Divide and conquer
Stop at will
Grow without checks
Pause for repair
The phrase "grow without checks" captures how cancer cells ignore regulatory checkpoints and proliferate abnormally. Normal cells respond to signals that halt growth when needed. Loss of checkpoint control is central to tumor development.
Which protein complex targets cyclins for degradation to regulate cell cycle progression?
APC/C
Origin recognition complex
Cohesin
DNA Pol ?
The anaphase-promoting complex/cyclosome (APC/C) is an E3 ubiquitin ligase that marks cyclins for proteasomal degradation. This ensures proper exit from mitosis. Dysregulation can contribute to cancer progression.
Which modification activates cyclin-dependent kinases during the cell cycle?
Methylation
Acetylation
Phosphorylation
Ubiquitination
Phosphorylation of specific residues on CDKs by CAK (CDK-activating kinase) activates the kinase. This allows CDKs to phosphorylate downstream targets. Misregulation can lead to uncontrolled cell division.
Which tumor suppressor protein inhibits cyclin-CDK complexes and can induce senescence?
RB
p21
Cyclin E
Aurora B
p21 binds to and inhibits multiple cyclin-CDK complexes, enforcing G1 and G2 arrest in response to p53 activation. This can lead to cellular senescence. Loss of p21 function permits proliferation of damaged cells.
What is the role of retinoblastoma (Rb) protein in the G1/S transition?
Degrades DNA polymerase
Sequesters E2F until phosphorylated
Phosphorylates cyclin D
Activates E2F transcription factors
Hypophosphorylated Rb binds E2F transcription factors, preventing transcription of S-phase genes. Cyclin D/CDK4 phosphorylates Rb, releasing E2F. Dysfunctional Rb leads to unscheduled S-phase entry.
Which signaling pathway is frequently mutated in cancer and involves Ras proteins?
MAPK/ERK
Notch
PI3K/Akt
Wnt/?-catenin
The MAPK/ERK pathway is activated by Ras GTPases and regulates cell proliferation and differentiation. Mutations in Ras prevent GTP hydrolysis, leading to constitutive signaling. This contributes to oncogenesis.
How does telomerase contribute to the immortality of cancer cells?
Triggers senescence
Induces apoptosis
Increases DNA repair
Elongates telomeres
Telomerase adds telomeric repeats to chromosome ends, counteracting the shortening that occurs during replication. Most somatic cells lack telomerase and undergo senescence. Cancer cells reactivate telomerase to become immortal.
Which DNA repair mechanism corrects single-strand breaks often caused by UV light?
Nucleotide excision repair
Mismatch repair
Base excision repair
Non-homologous end joining
Nucleotide excision repair removes bulky lesions like thymine dimers from UV damage. An endonuclease excises the damaged segment, and DNA polymerase fills the gap. Defects in this pathway cause xeroderma pigmentosum.
Which oncogene product is a transcription factor upregulated in many cancers?
Myc
Caspase-3
BRCA1
p21
c-Myc is a transcription factor that promotes genes involved in proliferation and metabolism. Overexpression drives uncontrolled cell growth. Many cancers show Myc amplification.
What is the function of the spindle assembly checkpoint?
Ensure DNA replication is complete
Initiate cytokinesis
Activate CDK1
Prevent anaphase until all kinetochores are attached
The spindle checkpoint delays anaphase onset until all chromosomes are properly attached to the spindle microtubules at their kinetochores. This ensures accurate chromosome segregation. Mutations can lead to aneuploidy in cancer.
Which phase of mitosis immediately follows the separation of sister chromatids?
Anaphase
Telophase
Metaphase
Prophase
Telophase succeeds anaphase when chromatids have reached the poles. The nuclear envelope re-forms and chromosomes de-condense. This sets the stage for cytokinesis.
Which type of cell death is commonly activated by severe DNA damage when repair fails?
Autophagy
Senescence
Apoptosis
Necrosis
Apoptosis is programmed cell death triggered by irreparable DNA damage. It prevents propagation of mutated cells. p53 plays a central role in activating apoptotic pathways.
Which enzyme seals nicks in the sugar-phosphate backbone during DNA replication?
DNA ligase
Helicase
Primase
Topoisomerase
DNA ligase catalyzes the formation of phosphodiester bonds, sealing breaks between Okazaki fragments on the lagging strand. This completes strand synthesis. Inhibition of ligase can cause genomic instability.
Which protein complex activates the G2/M transition by phosphorylating target proteins?
Cyclin E - CDK2
Cyclin D - CDK4
Cyclin A - CDK2
Cyclin B - CDK1
The Cyclin B - CDK1 complex, also known as Maturation Promoting Factor (MPF), triggers entry into mitosis by phosphorylating multiple substrates. Activation requires removal of inhibitory phosphates. Dysregulation can lead to mitotic errors.
Which mechanism contributes directly to chromosome shortening in normal somatic cells?
Excessive DNA ligase activity
Continuous topoisomerase action
Incomplete lagging-strand replication
Hyperactive telomerase
The end-replication problem means DNA polymerases cannot fully replicate 3' ends of chromosomes on the lagging strand. Each division shortens telomeres. Telomerase counteracts this in germ and stem cells.
Which process describes the spread of cancer cells from the original tumor to distant sites?
Angiogenesis
Metastasis
Invasion
Hyperplasia
Metastasis involves cancer cells invading the bloodstream or lymphatic system and colonizing distant organs. It's responsible for most cancer-related deaths. Multiple molecular changes enable this process.
Which ubiquitin ligase regulates the degradation of cyclin E and its dysfunction can lead to deregulated S phase entry?
Proteasome 26S
CDK7 complex
APC/C
SCF complex
The SCF (Skp1 - Cullin - F-box) complex ubiquitinates cyclin E, targeting it for proteasomal degradation. Loss of SCF function results in cyclin E accumulation and unscheduled S-phase entry. This contributes to genomic instability in cancers.
Which histone modification is commonly associated with active transcription of cyclin genes?
H4K20me1
H3K4me3
H3K27me3
H3K9me3
Trimethylation of histone H3 on lysine 4 (H3K4me3) is linked to promoters of actively transcribed genes, including cyclins. This epigenetic mark recruits transcriptional machinery. Altered histone modification patterns are seen in cancer.
Which component of the shelterin complex protects telomeres and its loss can trigger DNA damage responses?
WRN
TRF2
RAD51
Ku70
TRF2 binds double-stranded telomeric DNA, maintaining the T-loop structure that conceals chromosome ends. Loss of TRF2 exposes telomeres, eliciting ATM-mediated DNA damage signaling. This can lead to end-to-end fusions.
Which transcription factor directly upregulates expression of cyclin D in response to mitogenic signals?
E2F1
NF-?B
STAT1
AP-1
AP-1, formed by Fos/Jun heterodimers, binds promoter regions of acute response genes including cyclin D. Mitogenic signals like growth factors activate MAPK pathways that increase AP-1 activity. Dysregulated AP-1 contributes to oncogenesis.
Which mechanism allows cancer cells to bypass replicative senescence besides telomerase activation?
Alternative lengthening of telomeres (ALT)
Enhanced mismatch repair
Upregulation of p16INK4a
Increased DNA methylation
ALT is a telomerase-independent mechanism using homologous recombination to elongate telomeres. About 10 - 15% of cancers utilize ALT. It enables continued proliferation despite telomere shortening.
Which CDK inhibitor is often deleted or silenced in cancers, leading to G1 checkpoint failure?
p16INK4a
p53
p21
p27Kip1
p16INK4a inhibits CDK4/6, preventing Rb phosphorylation and progression into S phase. Deletion or silencing by methylation of CDKN2A (p16) is common in many cancers. Loss of p16 removes a critical G1 checkpoint.
How does the oncogenic BCR-ABL fusion protein promote uncontrolled cell division in chronic myeloid leukemia?
Constitutively active tyrosine kinase
Inhibits CDK2
Activates Ras indirectly
Phosphorylates p53
BCR-ABL is a fusion protein with constitutive tyrosine kinase activity that activates multiple downstream mitogenic pathways such as Ras/MAPK and PI3K/Akt. This drives uncontrolled proliferation of myeloid cells. Targeted therapies inhibit its kinase domain.
Which epigenetic alteration is most commonly seen in promoter regions of tumor suppressor genes?
H2A ubiquitination
miRNA binding
Histone acetylation
CpG island hypermethylation
Hypermethylation of CpG islands in promoters leads to chromatin compaction and gene silencing. This frequently inactivates tumor suppressor genes in cancer. It's a reversible modification targeted by epigenetic therapies.
Which cyclin-CDK complex is primarily responsible for initiating DNA replication origin firing?
Cyclin A - CDK2
Cyclin E - CDK1
Cyclin D - CDK4
Cyclin B - CDK1
Cyclin A - CDK2 activity during S phase phosphorylates components of the pre-replication complex to initiate DNA synthesis at licensed origins. Proper timing prevents re-replication. Deregulation causes genomic instability.
What is the molecular consequence of a BRCA1 loss-of-function mutation in cells?
Uncontrolled telomerase activity
Loss of mismatch repair
Impaired homologous recombination
Defective base excision repair
BRCA1 is essential for homologous recombination repair of double-strand breaks. Mutations lead to reliance on error-prone repair pathways, causing genomic instability. This predisposes cells to breast and ovarian cancers.
Which microRNA family negatively regulates cyclin D1 expression and is often downregulated in tumors?
miR-21
miR-200
miR-15/16
let-7
miR-15/16 targets cyclin D1 mRNA for degradation, reducing G1/S progression. Loss of these miRNAs correlates with overexpression of cyclin D1 in cancers. MicroRNA dysregulation is a hallmark of tumorigenesis.
Which adenovirus protein can inactivate both p53 and Rb to drive host cell cycle progression?
E6
E1A
E2F
E7
Adenovirus E1A binds Rb, releasing E2F, while E1B-55K cooperates to degrade p53. This hijacks host checkpoints to promote viral replication. Viral proteins inform cancer biology by showing checkpoint vulnerabilities.
What is the effect of hyperactivation of the PI3K/Akt pathway on the cell cycle?
Enhanced G1 arrest
Increased apoptosis
Promotion of G1/S transition
Inhibition of DNA replication
PI3K/Akt signaling promotes cell survival and growth by activating mTOR and inactivating GSK3?, leading to cyclin D accumulation. This pushes cells past the G1/S checkpoint. Mutations here are common in cancers.
Which structural feature of cyclin-dependent kinase inhibitors (CKIs) allows them to bind and inhibit multiple CDKs?
A SH2 domain
An alpha-helix motif
A zinc-finger region
A Cdk-binding domain
CKIs like p21 possess a binding domain that interacts with the catalytic cleft of various CDKs. This broad specificity allows them to halt multiple cell cycle transitions. Understanding this helps target CDK regulation in cancer therapy.
Which feedback loop ensures irreversibility of the metaphase-to-anaphase transition?
APC/C - Cdc20 activation by Cdk1
Wee1 kinase activation
Cyclin B synthesis
p53 stabilization
Active Cdk1 - cyclin B phosphorylates and activates APC/C - Cdc20, leading to cyclin B degradation. This creates a positive feedback loop that makes anaphase entry irreversible. It ensures unidirectional cell cycle progression.
What consequence does ATR kinase activation have during replication stress?
Promotes telomere shortening
Inhibits p53
Activates Chk1 and halts cell cycle
Triggers mitotic entry
ATR senses replication stress and phosphorylates Chk1, which then inhibits Cdc25 phosphatases. This prevents activation of CDK1/2, pausing the cycle until replication is restored. Failure leads to genome instability.
Which metabolic adaptation in cancer cells supports rapid proliferation under hypoxic conditions?
Warburg effect
Oxidative phosphorylation
Fatty acid oxidation
Gluconeogenesis
The Warburg effect describes increased glycolysis even in the presence of oxygen, allowing lactate production for rapid ATP and biosynthetic intermediates. This supports proliferation in hypoxic tumor microenvironments. It's a hallmark of cancer metabolism.
How does mutation of the spindle checkpoint protein Mad2 contribute to aneuploidy?
Enhances cohesin binding
Stabilizes microtubules
Weakens checkpoint, allowing premature anaphase
Inhibits APC/C activation
Mad2 inhibits APC/C - Cdc20 until all kinetochores are attached. Mutations reduce its function, permitting anaphase before proper chromosome alignment. This missegregation leads to aneuploidy.
Which cancer therapy targets the enzyme PARP and exploits DNA repair deficiencies?
PARP inhibitors
CDK4/6 inhibitors
Proteasome inhibitors
mTOR inhibitors
PARP inhibitors prevent single-strand break repair, causing accumulation of double-strand breaks. In BRCA-deficient tumors that lack homologous recombination, this leads to synthetic lethality. It's an emerging targeted therapy.
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Study Outcomes

  1. Recall Cell Cycle Stages -

    Sequence and describe each phase tested in the cell cycle stages quiz, from interphase through cytokinesis.

  2. Analyze Mitosis Mechanisms -

    Identify key events and structural changes during mitosis questions to deepen your understanding of nuclear division.

  3. Differentiate Cytokinesis and Telophase -

    Explain the distinct roles covered in cytokinesis trivia and the telophase quiz, highlighting where they overlap and diverge.

  4. Interpret Cell Division Differences -

    Compare and contrast mitosis with other forms of division using the cell division differences test to reinforce core concepts.

  5. Determine Which Phrase Best Describes Cancer -

    Evaluate various descriptions to pinpoint the phrase that accurately captures cancer's hallmark of uncontrolled growth.

  6. Assess Implications of Dysregulated Growth -

    Evaluate how errors in cell cycle control lead to tumor formation and inform strategies for cancer prevention and research.

Cheat Sheet

  1. Understanding the Cell Cycle Phases -

    The cell cycle is divided into interphase (G1, S, G2) and mitotic phase (M), with DNA replication in S and division in M (NIH). Use the mnemonic "IPMAT" (Interphase, Prophase, Metaphase, Anaphase, Telophase) to recall mitosis order. Remember that checkpoints at G1 and G2 ensure DNA integrity before progression.

  2. Key Features of Mitosis -

    Mitosis distributes duplicated chromosomes equally into two daughter nuclei, maintaining chromosome number (2n→2n). In metaphase, chromosomes align on the metaphase plate, and the spindle assembly checkpoint prevents progression if attachments aren't correct (Nature Reviews). Think "M" for "Middle alignment."

  3. Cytokinesis: Splitting the Cell -

    Cytokinesis follows mitosis, cleaving the cytoplasm to form two cells; animal cells use a contractile ring to pinch in (cleavage furrow), whereas plant cells build a cell plate from Golgi-derived vesicles (ScienceDirect). A handy mnemonic is "Furrow for fauna, Flower plate for flora." Ensure you can contrast these mechanisms.

  4. Telophase and Nuclear Reassembly -

    During telophase, nuclear envelopes reform around separated chromosome sets and chromatin decondenses to resume normal gene expression (Cell Biology by Alberts). Spindle fibers disassemble, marking the close of nuclear division. Recall "tele" means "end," signifying the end of mitosis.

  5. Which Phrase Best Describes Cancer? -

    Cancer is best described as "uncontrolled cell proliferation due to checkpoint failure," reflecting loss of growth regulation (American Cancer Society). Another concise phrase is "growth without brakes." Link this concept back to failed G1/S or G2/M checkpoints to solidify understanding.

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