Introduction to Cancer Biology

<p>15-25% (A)</p> Signup and view all the answers

<p>Gliomas (A)</p> Signup and view all the answers

<p>Abnormal and disorganized cell growth forming distinct masses. (D)</p> Signup and view all the answers

<p>Impaired immune response and resultant infections. (C)</p> Signup and view all the answers

<p>Increased cell numbers while maintaining normal morphology. (D)</p> Signup and view all the answers

<p>They are typically mutated to be 'always on' contributing to tumorigenesis. (A)</p> Signup and view all the answers

<p>Raf-MAPK pathway (D)</p> Signup and view all the answers

<p>By promoting cell cycle progression and blocking differentiation. (A)</p> Signup and view all the answers

<p>Metabolic activation systems (A)</p> Signup and view all the answers

<p>Point mutations in prokaryotic cells (D)</p> Signup and view all the answers

<p>It may yield false positives for certain mutagens. (B)</p> Signup and view all the answers

<p>A single mutated precursor cell (A)</p> Signup and view all the answers

<p>Leukemia (D)</p> Signup and view all the answers

<p>Gene amplification or chromosomal translocation (D)</p> Signup and view all the answers

<p>Both copies of a tumor suppressor gene must be inactivated for tumorigenesis. (C)</p> Signup and view all the answers

<p>They promote apoptosis by binding to pro-survival Bcl-2 proteins. (C)</p> Signup and view all the answers

<p>It stimulates glucose metabolism and inhibits apoptosis. (A)</p> Signup and view all the answers

<p>Blockade of apoptosis and cell survival promotion. (D)</p> Signup and view all the answers

<p>p53 interacts more effectively with arrest genes than apoptotic genes. (A)</p> Signup and view all the answers

<p>It augments the cytochrome c signal by inhibiting IAP function. (B)</p> Signup and view all the answers

<p>Accelerated cell cycle progression (B)</p> Signup and view all the answers

<p>Both hits must occur in the same retinal cell (B)</p> Signup and view all the answers

<p>Triggers apoptosis and cell cycle arrest (B)</p> Signup and view all the answers

<p>Formation of a dominant negative protein that can disrupt function (B)</p> Signup and view all the answers

<p>Preventing the transition from G1 to S phase (B)</p> Signup and view all the answers

<p>Inhibition of MDM2-mediated degradation (C)</p> Signup and view all the answers

<p>Immortalization of cells (D)</p> Signup and view all the answers

<p>Thymidylate synthase (C)</p> Signup and view all the answers

<p>It phosphorylates Rb, leading to E2F release (C)</p> Signup and view all the answers

<p>Activation of DNA repair pathways (C)</p> Signup and view all the answers

<p>PI3K (A)</p> Signup and view all the answers

<p>It inhibits MDM2. (C)</p> Signup and view all the answers

<p>Embryonic stem cells are totipotent. (A)</p> Signup and view all the answers

<p>Death receptors can induce apoptosis in specific target cells. (A)</p> Signup and view all the answers

<p>Cancer stem cells may resist traditional treatments more effectively. (D)</p> Signup and view all the answers

<p>Inhibits caspase activation by interfering with FADD. (A)</p> Signup and view all the answers

<p>Environmental signals from stromal cells. (B)</p> Signup and view all the answers

<p>Accumulation of mutations. (B)</p> Signup and view all the answers

<p>Extrinsic pathway (A)</p> Signup and view all the answers

A group of diseases affecting multicellular species, characterized by unregulated tissue growth forming tumors.

Spread of cancer cells to and growth in foreign sites, a key feature in many cancers.

Cancer cells growing beyond normal tissue boundaries in their original location.

Excessive cell growth where cells look normal and form normal tissue.

Replacement of one cell type with another not normally present.

Cytologically abnormal cells, showing changes in size, shape, greater division, and lack of normal cell characteristics.

Abnormal, disorganized tissue growth forming masses, can be benign or malignant.

Classifying cancer based on its size and extent in the body to estimate prognosis (survival probability).

Cancer development requires multiple genetic mutations, not just inherited ones.

Cancer arising from a single ancestral cell.

Benign tumors of uterine wall showing X-chromosome inactivation pattern.

Cancers involving B cell precursors.

A test measuring back mutations in Salmonella to detect mutagens.

A gene that, when mutated, promotes cancer development.

A gene that, when mutated, loses its ability to prevent cancer.

A small G-protein involved in cell signaling; mutations lock it in active state.

Transcription factor that regulates cell growth; over-expression is a common cancer driver.

A crucial intracellular signaling cascade often disrupted in cancer, many proteins involved.

Apoptosis pathway initiated within the mitochondria, involving release of cytochrome c and other proteins.

A group of proteins that regulate apoptosis. Pro-survival Bcl-2 proteins prevent cell death, while BH3-only proteins promote apoptosis.

The observation that cancer cells have higher rates of glycolysis and lactate production than normal cells, despite the presence of oxygen.

A protein kinase that promotes cell growth, glucose metabolism, and inhibits apoptosis.

A complex formed by Apaf-1, cytochrome c, and pro-caspase-9, leading to caspase activation and apoptosis.

p53 is a tumor suppressor protein that is regulated by MDM2, an oncoprotein. MDM2 binds to p53 and promotes its degradation, decreasing p53 levels in the cell. This interaction is disrupted by phosphorylation of p53 on its N-terminal residues (S15, S20) by kinases like ATM, ATR, Chk1, and Chk2, which are activated by DNA damage.

p19ARF is a tumor suppressor protein that inhibits MDM2, leading to increased levels of p53. It acts as a 'protector' of p53, preventing MDM2 from degrading it.

Myc and Ras are oncogenes that promote cell proliferation. When overexpressed, Myc and Ras can lead to increased levels of p19ARF, which in turn upregulates p53. However, oncogenic forms of Myc and Ras create strong pressure for loss of p53 function.

Stem cells have two defining characteristics: 1) They can divide indefinitely, potentially throughout the life of the organism. 2) They are capable of self-renewal, meaning each daughter cell can either remain a stem cell or become a progenitor cell that can further differentiate.

When a stem cell divides, the daughter cells can either retain their stem cell identity or become committed progenitor cells. Progenitor cells are restricted in their proliferation and differentiation potential compared to stem cells.

Pluripotency refers to the ability of a stem cell to differentiate into many different cell types. Multipotency describes the ability of a stem cell to differentiate into a limited number of cell types. Embryonic stem cells are pluripotent, while adult stem cells are usually multipotent.

Mutations affecting the c-kit receptor tyrosine kinase or its ligand, SCF (stem cell factor), can disrupt stem cell function. These mutations lead to defects in various cell lineages, including melanocytes, hematopoietic cells, and neural structures, highlighting the importance of c-kit signaling for stem cell maintenance.

Stem cells exhibit two mechanisms of division: 1) Environmental asymmetry: stem cell fate is influenced by signals from surrounding cells. 2) Divisional asymmetry: asymmetric distribution of molecules (like Numb) during cell division determines the fate of each daughter cell.

Hematopoietic stem cells (HSCs) found in bone marrow provide an excellent model to study stem cell biology. HSCs can form all blood cell types, and their differentiation can be studied using techniques like FACS sorting and adoptive transfer.

Cancer stem cells (CSCs) are thought to arise from either: 1) Alterations in normal stem cells due to mutations, acquiring a partially transformed character. 2) 'Dedifferentiation' of committed progenitor cells, where they gain self-renewal capacity and contribute to the formation of tumors.

A model explaining how mutations in tumor suppressor genes, like Rb, lead to cancer. It proposes that two hits (mutations) are needed to inactivate both copies of a tumor suppressor gene, allowing uncontrolled cell growth.

The loss of one copy of a gene, often due to mutations or deletions, leaving only one functional copy. This is a key event in the two-hit hypothesis, especially for tumor suppressor genes.

Rb is a key cell cycle regulator that binds to E2F transcription factors, preventing their activation of genes needed for cell growth. This acts as a break on cell proliferation. Loss of Rb's function removes this break, leading to uncontrolled cell division.

E2Fs are transcription factors that control the expression of genes required for cell cycle progression. They are bound and inactivated by Rb but activated upon Rb phosphorylation, driving cell cycle entry and growth.

Cyclin/Cdk complexes phosphorylate Rb, causing a conformational change that releases E2Fs. This allows E2Fs to activate genes necessary for cell cycle progression, ultimately driving cell growth.

When Rb is inactivated, E2Fs are constitutively active, leading to uncontrolled cell cycle progression and increased cell proliferation. This can contribute to the development of cancer.

p53, a tumor suppressor, acts as a 'watchdog', monitoring cellular stress. It can trigger cell cycle arrest or apoptosis in response to DNA damage or other cellular imbalances, preventing uncontrolled proliferation.

p53 functions as a tetramer, and mutations in one allele can drastically disrupt its activity. It regulates the expression of various target genes involved in cell cycle control, apoptosis, and DNA repair.

Inactivation of p53 allows cells to bypass checkpoints and continue dividing despite damage. This can contribute to cancer formation by allowing damaged cells to proliferate unchecked.

p53's activity is tightly regulated to prevent its unchecked activation, which can be lethal. Regulation involves protein stability, nuclear localization, and post-translational modifications that modulate its transcriptional activity.