Cancer videos 1&2

cells collaborate

• send, retrieve, interpret signals to tell each other how to act

• cells are socially responsible, resting, dividing, differentiating, drying for good of the organism

• disturbances can trouble the harmony

cell signaling

cells get a multitude of signals at a time

cancer definition

• disease in which an individual mutant clone of cells prospers at the expense of its neighbors

• mutations that promote this destructive duplication can jeopardize the organism

• by the time a tumor is detected, already 1bilion cancer cells produced

cancerous cells

• They don’t listen to signals that tell them how to coordinate

• They don’t need a series of signals for division

• They can turn on signal transduction pathways without a signal

socially respocible cell division

1. repair

2. fight infection

3. growth of an organism

4. replace

2 main signals responsible for cell growth/division

mitogen, growth factors

mitogen

• initiates/cmtinues mitosis 

• stimulatory signal (stimulates mitosis)

• extracellular signals (comes from other cells) usually neighbors

• mitogen binding to a receptor is the activation needed to drive the cell cycle

Growth factors

• stimulates increase of cell mass

• promotes synthesis of macromolecules + inhibits their degradation

• growth factor binding to receptor is the activation needed fot nutrient uptake and utilization

cell divsion quality control

• cells have to monitor its progression throughout the cycle

• they have checkpoints to check if the cellular conditions are appropriate to keep mitosis going

• if it doesn’t pass through the checkpoints, it will apoptose

g1 checkpoint

The cell will pass G1

1. Mitogens are present (cells can’t progress from G1 to S unless mitogens have been secreted on the cells to tell it to continue to go through mitosis)

2. the cell should be large enough

3. There should be enough nutrients in the cell’s surroundings to support mitosis

4. Its DNA should not be damaged. 

G2 checkpoint

The cell will continue mitosis if

1. Cell size is adequate

2. Chromosome replication is successfully completed (if chromosomal replication is not accurate, it will not continue mitosis)

Metaphase checkpoint

happens during mitosis

continues to go to anaphase if all the chromosomes are attached to a mitotic spindle

causes of tumors

loss if internal balance (homeostasis):

increased cell division can cause tumors

decreased apoptosis can cause tumors

increased cell division + decreased apoptosis can cause tumors (most cancers have this combo)

what causes uncontrolled cell division

Different cancers are caused by different defects that lead to uncontrolled cell division

All cancers come from mutations that cause defects in proteins that regulate the cell cycle and are involved in maintaining chromosomal stability. Mutations knock out the functions of key genes

development of cancer

1. Initiating mutation - a mutation causes one cell to act abnormally. The mutated cell has a proliferation (offspring producing) advantage

2. mutated cell abnormally divides a few times (faster than the speed of the unmutated cells) so now there’s copys of this mutated cell

3. another mutation happens to one of the copies (this cell is now two mutations away from a regular healthy cell)

4. The second mutation causes the cell to have a bigger proliferation advantage

5. progression- more mutations accumulate. Cells that divide or survive faster/better are selected for

mutation

A mutation is a change in the DNA sequence of an organism. It can occur at any point in the genome and can involve the addition, deletion, or alteration of nucleotides. 

how many mutations linked to cancer

cancer doesn’t arise from 1 mutation

cancer is an accumulation of mutations

normal cell response

1. They respond to growth factors and mitogens 

2. They respond to growth factors and mitogen inhibitors

3. They respond to apoptosis signals 

properties shared by many cells capable of cancerous growth

1. disregard external and internal signals

2. altered responses to apoptotic signals 

3. they get around limitations on proliferation→example: gets passed replicative senescence

4. genetically unstable. Their DNA can have extra chromosomes, fewer chromosomes, or fused chromosomes

5. They can escape from their home tissues and be invasive

6. Some can survive and proliferate in foreign sites (known as metastasizing and is not an easy process),

7. Many induce help from nearby cells (angiogenesis) and modify nearby cells

replicatice senescence

normal cells permanently stop dividing after a certain number of divisions (replicative senescence) because With every cell division, telomeres get shorter. eventually The critically short telomeres trigger a DNA damage response, signaling to the cell that it can no longer divide. The cell enters a permanent state of cell cycle arrest called replicative senescence, where it stops dividing but remains alive. 

Normal cells require grwoth factors mitogemn

In basic growth medium plus PDGF (growth factor), normal cells proliferate. In a growth medium alone, cells fail to divide

• Some cancer cells can be grown in basic growth media alone

density dependent inhibition of cell division

NORMAL CELLS

• many cells require a surface for divison

• if you plate them, they attach to the surface and form a monolayer (Anchorage dependence)

• each cell is getting signals from the cells around it whixha llowa it to know the density of the cells around it

• this gives a negative signal (telling it to not divide)

• so if you scared a part of the monolayer the cells around the scrape would divide again and then stop when its filled (density dependent inhibition)

CANCER CELLS

• cancer cells do not exhibit Anchorage dependence (they can grow and divide without being attached to a solid surface or extracellular matrix)

• they don’t exhibit density dependent inhibition