bild 2 midterm 2

tumor suppressors:

Normally repress growth, so when inactivated will promote cancer.

proto-oncogenes

Normally encourage growth, so when over-activated (or inappropriately activated) will promote cancer.

genes that promote differentiation

Normally turned on

to promote differentiation and turn off growth, so with

inactivated will promote growth and spread of cancer.

dna repair genes

Normally fix errors in DNA, so when inactivated will promote mutations and therefore cancer.

genes that promote angiogenesis:

Normally promote

growth of blood vessels, so when over-activated or

inappropriately activated will promote tumor growth and spread of cancer.

depolarization

membrane potential gets more positive (less negative)

hyperpolarization

membrane potential gets more negative (less positive

oncogene

promotes cell growth and division (stuck accelerator)

over-activation of proto-oncogene

more cancer

inactivating, inhibiting or suppressing tumor suppressor

more cancer

inactivating, inhibiting, or suppressing oncogene

less cancer

promoting tumor suppressor

less cancer

tumor suppressor

suppress cancer (brake) -> promote apoptosis

apoptosis

cell death, repair DN, slow down cell division

cancer

uncontrollable growth (cell division) of body cells -> form a mass (tumor); arises from mutations in genes -> multiple mutations accumulated

promotes cancer

- more cell division = more chance for mutation

- more undifferentiated cells = more division so more mutation

- impaired or defective DNA repair mechanisms = more chance for mutation

- more growth signaling

- more blood vessels (angiogenesis) = for tumor growth

- more capaable of metastasis

why do fully differentiated cells not promote cancer

because they undergo less cell division -> so there is less of a chance for mutation

angiogenesis

more blood vessels = allows for tumor growth.as tumor grows larger, its volume increases faster than surface area = > low surface area/volume ratio => less nutrients exchange, tumor cannot grow more 1-2mm => need blood vessels

metastasis

spread of cancer cells from primary tissue to distant organs through blood

cancer promoting changes chart

know gene type, normal funciton, cancer-promoting change

chemotherapy

systemic drug treatment that kills rapidly dividing cells by damaging DNA or disrupting cell division

radiation therapy

local treament that uses high-energy radiation to damage DNA and destroy cancer cells in a specific area

Immunotherapy

treatment that stimulates or modifies the immune system to recognize and attack cancer cells.

localized treatment (solid tumor, localized)

radiation, surgery (most effective)

localized treatment (blood cancer - systematic, ex: leukemia)

no radiation, no surgery

systematic treatment (solid tumor, localized)

chemotherapy, immunotherapy (yes, but depends)

systematic treatment (blood cancer - systematic, ex: leukemia)

chemotherapy (most effective), immunotherapy

rapid proliferation

rapid increase, spread, or multiplication of something, often referring to a high rate of growth or reproduction in numbers

Why does cancer and embryonic development share these characteristics of rapid proliferation, ability to migrate, and reduced sprecialization.

both cancer cells and embryonic cells activate gentic programs that promote cell division, migration, and reduced differentiation.

endocrine system (hormones, chemical messengers) - long distance communication within the mammalian body (nervous system)

- gland releases hormone into bloodstream

- hormone circulates everywhere

- ONLY cells with the right receptor respond

- slow duration

- long-lasting effects

- broad targets (cells throughout body)

nervous system (neurons) - long distance communication within the mammalian body (nervous system)

- electrical signal travels down a neuron (action potential)

- chemical signal crosses synapse (neurotransmitter)

- signal reaches a specific target cell

- extremely fast (milliseconds

- short-lived effects

- precise target (muscles, neurons, and glands)

neurotransmitter

chemical signal crosses a synapse

nervous system

electrical impulses are the messengers in the nervous system

endocrine system

Hormones are the chemical messengers in the endocrine system that target cells through the bloodstream

parts of the nervous system

brain, spinal cord, peripheral nervous system, ganglion, nerve

parts of the endocrine system

Pituitary gland,

Pineal gland,

Thyroid gland,

Thymus,

Adrenal glands,

Pancreas, ovary (female), testis (male)

neurons

- electrical signaling

- generate action potentials

- carry information

- communicaton

glia

do everything neurons don't

- support and protection

- do not fire action potentials

astrocyte function

Deliver nutrients from blood to neurons Maintain ion balance (K+, Na+) Help repair damage

astrocyte location

CNS

microglia function

destroy pathogens, clean cellular debris

microglia location

CNS

oligodendrocytes function

Wrap axons in myelin One cell → wraps many axons

oligodendrocytes location

CNS

schwann cells location

Wrap axons in myelin One cell → one axon

schwann cells location

PNS

central nervous system

- brain and spinal cord

- decision making

- integration system

peripheral nervous system

- all nerves outside of the CNS

- sends info TO and FROM CNS

dendrites

receive signals

soma

integrates signals

axon

transmits signal

axon terminals

release neurotransmitter

nucleus

gene expression (not signaling)

information flow through a neuron

dendrites > soma > axon > axon terminals

what happens when Na+ channels are blocked

- You do not get a normal AP

- no sharp rising phase; at most a small subthreshold bump

what does rising phase depend on

Na+ influx

what happens when Na+ channels open less well (reduced function) ?

- harder to reach threshold

- if it fires, peak may be reduced or AP may fial to fully develop

what happens when Na+ channels fail to inactivate

- the AP stays depolarized longer (plateau-ish)

- repolarization is delayed

- neuron may be prone to repeated firing/seizures

repolarization

the biological process where excitable cells (neurons or muscle) restore their negative internal charge after depolarization. It is a critical "reset" phase of the action potential—often described as cellular relaxation or recharging—where sodium channels close and potassium channels open, allowing positive potassium ions to leave the cell

what happens if K+ channels are blocked (ex: TEA)

- falling phase is slower

- repolarization delayed

- undershoot reduced or missing

- AP is "wider" = takes longer to return to rest

- key: AP propagation can still occur because propagation depends on Na+ driven depolarization to trigger the next segment

what happens when K+ channels open more easily/earlier

- faster repolarization

- bigger undershoot (more hyperpolarization)

- peak might be cut short (because K+ "fights" Na+ sooner)

how lack of myelination would affect the propagation of the action potential

- AP regenerated at every patch of membrane

- slower conduction

- more ion dissipate

how myelination would affect the propagation of the action potential

- AP "jumps" between nodes = saltatory conduction

- faster, energy-efficient

what is the shape of AP when myelinated or not

- AP shape is identical from unmeyelinated and myelinated, only arrival time changes.

how does AP change when demyelinated

becomes slower, less efficient, or fails

neurotransmitter release

- controlled by Ca2+ entry and vesicle fusion

- more release . more receptors activted . stronger signaling

- less release . weaker signaling

whether receptors can respond

- nt only works if receptors are present and functional

- blocked or absent receptors = no signaling, even with normal release

- more receptors or higher sensitivity = stronger response

length nt stays in synapse

- clearance (reuptake, degradation, diffusion), ends the signal

- slower clearance = longer, stronger signaling

- faster clearance = shorter, weaker signaling

if nt release increases

- predictions: more nt in the synaptic cleft, more receptors bind nt, stronger postsynaptic response, greater chance the postsynaptic cell reaches threshold and fires an AP

if nt release decreases

- predictions: less nt available to bind receptors, weaker postynaptic response, postsynaptic neuron less likely to reach threshold

no matter how healthy the postsynaptic cell is, less NT = ....

less signaling

examples from lecture about nt signaling

- black widow spider toxin creates Ca2+ pores

- more Ca2+ enters presynaptic neuron

- more vesicle fusion > more NT relesed

↑ NT release

↑ signaling

↓ NT release

↓ signaling

↑ receptors

↑ signaling

Block receptors

↓ or no signaling

Slower clearance

↑ duration & strength of signaling

Faster clearance

↓ duration & strength of signaling

clearance

(reuptake, degradation, diffusion), ends the signal

water-soluble molecules bind....

to receptors on the cell membrane

lipid-soluable molecules bind....

to receptors inside the cell

two mechanisms for how different target cells exposed to the same hormone can respond in different ways

1. Different target cells may have different receptors for the hormone

2. Different target cells use the same receptor but different signal transduction pathways inside the cells to turn the receptor's response into a cellular response

how do different signal transduction pathways inside cells turn the receptor's response into a cellular response?

-activate certain enzymes

- release of ions like calcium

- gene expression

hypothalamus

receives information from brain and initiates reponse

pituitary

responds to hypothalamus to secrete hormones into the blood

anterior pituitary

1. hypothalamus secretes first hormone ex: GnRH

1. Hormone acts on anterior pituitary to release second homrone ex: LH, FSH

is the anterior pituitary direct or indirect?

indirect

posterior pituitary

1. hypothalamic axons project onto pituitary blood vessels and release hormone directly to the body ex: ADH, oxytocin

is the posterior pituitary direct or indirect?

direct

If hypothalamus is overactivated, how does that affect the eventual release of Thyroid-Stimulating Hormone (TSH)?

High TRH > High TSH release > high thyroid release > more inhibition on hypothalamus and more inhibition of anterior pituitary > less TSH is made

what does the thyroid hormone contain nd require?

iodine

If someone has low CRH levels, does that mean there is definitely something wrong with their hypothalamus?

No. This can also be because of high cortisol levels