Telomeres & Cancer Overview

<p>APC interacts with microtubules to maintain spindle stability. (D)</p> Signup and view all the answers

<p>Absence of Wnt signaling leads to B-catenin breakdown through ubiquitination. (D)</p> Signup and view all the answers

<p>Stabilizes vascular integrity (D)</p> Signup and view all the answers

<p>A transition from angiogenic quiescence to an active formation of blood vessels (B)</p> Signup and view all the answers

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

<p>They break down the ECM, creating invasive pathways (D)</p> Signup and view all the answers

<p>Metastasis (B)</p> Signup and view all the answers

<p>It activates FAK leading to downstream signaling (D)</p> Signup and view all the answers

<p>They inhibit growth factors like VEGF (D)</p> Signup and view all the answers

<p>RhoA (B)</p> Signup and view all the answers

<p>Ang2 (D)</p> Signup and view all the answers

<p>Inhibit MMP activity and ECM remodeling (C)</p> Signup and view all the answers

<p>Replicative senescence (C)</p> Signup and view all the answers

<p>Inactivation of cell cycle checkpoints (A)</p> Signup and view all the answers

<p>By deletion of p16INK4A (A)</p> Signup and view all the answers

<p>Cells become prone to chromosomal instability (A)</p> Signup and view all the answers

<p>Breakage-fusion-bridge cycles (B)</p> Signup and view all the answers

<p>It stabilizes p53 by inhibiting MDM2 (C)</p> Signup and view all the answers

<p>Hypo-phosphorylated Rb (B)</p> Signup and view all the answers

<p>Induced expression of TERT (C)</p> Signup and view all the answers

<p>Complex non-reciprocal translocations (D)</p> Signup and view all the answers

<p>Line blood vessels and lymphatics (A)</p> Signup and view all the answers

<p>Cell adhesion (C), Cell polarity (D)</p> Signup and view all the answers

<p>It creates a novel fusion protein BCR-ABL. (B)</p> Signup and view all the answers

<p>It causes uncontrolled proliferation of myeloid cells. (A)</p> Signup and view all the answers

<p>Mutations in the APC gene and other factors. (A)</p> Signup and view all the answers

<p>It provides essential growth factors for tumor survival. (A)</p> Signup and view all the answers

<p>Blastic phase (C)</p> Signup and view all the answers

<p>Human tumor cells rarely grow in mice. (B)</p> Signup and view all the answers

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

<p>Chronic phase (B)</p> Signup and view all the answers

<p>Interferon alpha and STI-571 (A)</p> Signup and view all the answers

<p>Facilitate faithful replication, prevent degradation, and prevent fusion of DNA ends. (A)</p> Signup and view all the answers

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

<p>T-loop structure (A)</p> Signup and view all the answers

<p>It extends the 3’ overhang of telomeres for replication. (D)</p> Signup and view all the answers

<p>The irreversible loss of the ability to divide in vitro. (A)</p> Signup and view all the answers

<p>They shorten gradually. (A)</p> Signup and view all the answers

<p>The maximum number of divisions a normal somatic cell undergoes before senescence. (C)</p> Signup and view all the answers

<p>Senescence-associated secretory phenotype (SASP). (A)</p> Signup and view all the answers

Telomeres protect chromosome ends from degradation, fusion, and ensure accurate replication.

Telomeres have a characteristic structure: a short, repeated sequence (e.g., TTAGGG in humans), and a single-stranded 3' overhang. The structure is stabilized by t-loops and G-quadruplexes.

Normal somatic cells shorten their telomeres with each division. Cancer cells and germ cells do not.

An enzyme that adds telomere sequences to the ends of chromosomes, preventing shortening.

The phenomenon where cells stop dividing due to shortened telomeres.

The limited number of cell divisions a normal cell type can undergo.

Telomerase activity is often activated in cancer cells, allowing them to divide indefinitely and contributing to cancer growth.

FISH is a technique for locating and visualizing telomeres or other specific DNA sequences within cells, using fluorescent probes.

Cancers can avoid replicative senescence by activating telomerase or using alternative mechanisms.

Senescence can occur due to telomere attrition or cellular stress.

Cellular mechanisms that verify the integrity of DNA before cell division, inducing senescence when needed.

A state where cells with severely damaged chromosomes can't avoid cell death.

Formation of new blood vessels from pre-existing ones.

A network of vessels that drain fluids and carry immune cells.

The process of creating new blood vessels during embryonic and adult life.

Major signaling molecule for angiogenesis

Regulate vascular integrity; Ang1 stabilizes, Ang2 destabilizes

Cancer cell spread to new sites

Cancer cell's ability to penetrate surrounding tissue

Matrix Metalloproteinases; break down extracellular matrix

Cell-matrix adhesion molecules

Cell-cell adhesion molecules

The material surrounding cells; provides support & structure

Transition from inactive to active blood vessel formation

APC (Adenomatous Polyposis Coli) is a protein that helps regulate cell division. It interacts with β-catenin, a protein that promotes cell growth. APC normally keeps β-catenin levels low, preventing excessive cell growth.

When APC function is lost, β-catenin accumulates, leading to uncontrolled cell growth. This can contribute to the development of colorectal cancer.

Wnt signaling is a pathway that promotes cell growth. When Wnt proteins bind to their receptors, they activate β-catenin, allowing it to stimulate cell division.

TGF-β signaling is a pathway that regulates cell growth and can either promote or inhibit cell division, depending on the context. In colorectal cancer, loss of TGF-β signaling can contribute to tumor development.

APC plays a role in maintaining the stability of chromosomes during cell division. Loss of APC can lead to chromosomal instability (CIN), where chromosomes are miscopied or lost, contributing to cancer development.

The spread of cancer cells from their original location to other parts of the body.

A process where epithelial cells (tightly packed, forming sheets) transform into mesenchymal cells (more mobile, able to migrate).

EMT allows cancer cells to break free from the original tumor, invade surrounding tissue, and travel through the bloodstream to distant sites.

The first stage of CML characterized by a slow and gradual increase in white blood cells, mostly neutrophils. Patients may have few symptoms.

A more advanced stage where the number of white blood cells increases rapidly and there are abnormalities in the blood cells.

The most advanced stage with very rapid growth of immature blood cells. This phase is often resistant to treatment.

A specific chromosomal abnormality found in CML where a piece of chromosome 9 is swapped with a piece of chromosome 22 creating a new fusion gene.

The Philadelphia chromosome is a hallmark of CML and leads to the production of a fusion protein (BCR-ABL) that drives uncontrolled cell growth.

A targeted drug that specifically inhibits the activity of the BCR-ABL fusion protein, effectively stopping the uncontrolled growth of CML cells.

APC is a tumor suppressor gene. When it is mutated, it no longer effectively controls cell division, leading to the formation of polyps and eventually colorectal cancer.