Cancer and Cell Division Mitosis

what is cancer

disease of the cell cycle

what gene types being mutated cause cancer

tumor supressors and protocongens

tumor supressors include

genes that pause cell cycle, apoptosis genes, dna repair genes

protooncogens contain

genes that promote cell cycle and respond to growth hormones

sources of mutation

dna replication, non disjuntion, exposure to mutagens

nondisjuntion

when sister chromatids dont separate in anaphase

cell division 2 types

mitosis and meiosis both have cytokinesis

cell theory

all cells come from preexisting cells

haploid

one chromosomes of each type, one centromere

diploid

two of each chromosome type, 2 centromeres

why do normal cells need to divide

to grow and develop the body, cell replacement, heal wounds

size of genome is expressed in

base pairs

levels of chromatin packing

double helix, nucleosome bead nucleosome, looped domains, metaphase chromosome

chromosome distribution in mitosis

duplication to make pairs, separation into chromatids

does ploidy change in mitosis

no

human female has what chromosome

xx and no y

male has what chromosome

xy

phases of cell cycle

interphase and M phase

interphase

G1, S, G2

what happens in interphase

normal functioning of cell and prep for division

M phase

mitosis phase: prophase, prometaphase, metaphase, anaphase, telophase, cytokinesis

What is majority of cell cycle

Interphase

G1

• The cell grows larger.

• The cell produces proteins and organelles.

• The cell carries out its normal functions.

• It prepares for DNA replication. (S)

G1 lasts

7-9 hrs

S phase

stage where DNA replicates

S lasts

6-8 hr

G2

• The cell grows more.

• The cell makes proteins and other materials needed for mitosis.

• The cell checks the replicated DNA and repairs damage when possible.

• It prepares to enter mitosis (M phase).

G2 lasts

4-5 hr

interphase

each chromosome is made of sister chromatids

prophase

chromosomes condense spindles form

prometaphase

nuclear envelope breaks, microtubules attach to middle of chromosome

metaphase

chromosomes go to middle of cell

anaphase

sister chromatids separate and pulled apart

telophase

nuclear envelope reforms and chromosomes de condense

cytokinesis

actin myosin ring causes membrane to pinch in and cells to split into two daughters

cytokinesis in plants

as vesicles are transported from golgi to cell, vesicles fuse to form cell plate

cytokinesis in animals, fungi, slime mold

actin myosin ring makes cleavage furrow

do bacteria undergo cytokinesis

no

how do bacteria divide

binary fission

stuctures involved in mitosis

• Chromosome

• Chromatin

• Sister chromatids

• Centromere

• Kinetochores (middle of cell)

• Microtubule-organizing center

• Centrosome

• Centrioles

why does skin peel when too long in sun

apoptosis of cells

control of cell cycle

internal controls can cause cell cycle length to vary

variation in what leads to differences in cell cycle

G1

in rapidly dividing cells

basically no G1

in nondividing cells

permenantly stuck in G1, called G0

What's involved in regulating the cell cycle?

protein complexes

How many distinct cell cycle checkpoints are there?

4

What happens if regulatory molecules are defective?

Checkpoints may fail. Cells may start dividing in an uncontrolled way.

how do cancers vary

Time of onset, growth rate, seriousness, cause

How is cancer caused?

All cancers arise from failure of cell cycle checkpoints.

If a cell has accumulated DNA damage, it is unlikely to pass which checkpoint?

G2

What are some internal controls?

Cyclins, protein kinases, proto-oncogenes, tumor suppressors

External controls

Growth factors like hormones, density-dependent inhibition(if too crowded no division), and anchorage dependence(needs smt to attach to)

What is required to pass the G1 checkpoint?

Adequate cell size, nutrients are sufficient, social signals present, undamaged DNA.

Requirements to pass G2

Replicated chromosomes successfully. DNA is undamaged. Activated MPF is present.

MPF does what

signals cell to start mitosis

MPF made from

Cyclin B binds to CDK1, forming MPF.

What's required to pass M-phase checkpoints?

Chromosomes have attached to spindles. Chromosomes have properly segregated. MPF is absent.

Metastasis

spread of cancer cells throughout body

How many mutations are typically required to produce a cancer cell?

4 or more somatic mutations

Properties of cancer cells

Malignant; invasive, cancerous, spread through blood or lymph, initiates secondary tumors.

Benign versus malignant

Continue to divide, but not invasive versus divide and spread through adjacent tissues.

What are proto-oncogenes?

They promote cell division.

Example of a proto-oncogene

RAS

What are tumor suppressor genes?

Inhibit cell division.

Example of tumor suppressor genes

BRCA1, BRCA2, p53.

What other types of genes regulate cell division?

Ones that regulate apoptosis, ones involved in DNA repair

If DNA is physically damaged, what protein pauses the cell cycle?

p53 or another tumor suppressor

How is the cell cycle paused?

DNA repair pathways are activated. The protein can stop the cell cycle at G1 or S.

What happens when there is too much dna damage?

Apoptosis

A damaged tumor suppressor could lead to what?

Uncontrolled growth

Where are BRCA1 and BRCA2 found?

Localized at the midplane during cell division, helps to repair DNA, and works with repair proteins.

What is immunoprecipitation?

A way to isolate a protein using an antibody

BRCA1 and BRCA2 are considered to be tumor suppressor genes because

Their normal products participate in the repair of DNA damage.

Oncogenes

The dangerous gene can be made from viral genes or mutated proto-oncogenes.

How can a proto-oncogene be promoted to an oncogene?

• Mutation causing increased protein activity

• Increased number of gene copies, making more proteins

• Change in location, putting the gene under control of a new promoter- more transcription, more protein

all protein-related

What is a RAS protein?

A proto-oncogene that controls cell division by switching on and off. When it's mutated, it can lead to uncontrolled cell division and cancers.

The product of the P53 gene

Inhibits the cell cycle.

Regulatory proteins that prevent a cell from entering the next phase of the cell cycle under conditions of DNA damage are also known as

Tumor suppressors

Are internal and external controls related?

Yes, they have to work together for cell division to function.

Normal cells: external controls

Anchorage dependence and density-dependent inhibition

Do cancer cells exhibit anchorage dependence and density-dependent inhibition?

No, they've escaped those mechanisms and are transformed.

What do normal cells look like when contained in a dish versus cancer cells?

Normal cells form a single layer, and they do not move up or down. Cancer cells don't exhibit anchorage dependence or density-dependent inhibition, so they can create a mountain.

What is chemotherapy?

Attacks the rapidly dividing cells, interferes with mitotic spindle formation and DNA replication.

What does radiation do?

Damages the DNA and breaks the double strands. Triggers apoptosis

What is immunotherapy?

New approach to fighting cancer where T cells are inserted into the patient's blood and then reinjected into the patient

What is a mutagen?

Cancer-causing agents that damage DNA and promote cell division

What are some examples of mutagens?

X-rays, UV radiation, tobacco

During what phase in the cell cycle would you expect there to be large changes in polymerization or depolymerization of microtubules?

Mitosis, because microtubules are used to create spindle fibers and allow for the fibers to pull chromosomes apart

Which checkpoint likely causes cells to arrest when spindle microtubules are inhibited?

M checkpoint because during this check, cells make sure chromosomes are attached to spindles correctly before moving on. This is right before mitosis.