neoplasia

_____ of mitosis is not equal in different cell types

rate

some cells don’t undergo mitosis

• neurons

• skeletal muscle cells

• _____ muscle cells

cardiac

some cells undergo rapid rates of mitosis

• hair cells

• mucosal cells

• _______ cells

epithelial

proto-oncogenes and oncogenes are _____ genes

regulator

cancer cells that self produce growth factors leads to ______ signaling

• also, mutations in these receptors leads to ligand-independent activation in cancer = signals to themself to divide and grow

autocrine

during extrinsic signaling (signal comes from outside), when a ligand binds to a death receptor, it leads to a signaling cascade that activates ______

capcases

during extrinsic signaling, when caspases are activated, the capcases carry out _______

apoptosis

during extrinsic signaling, when caspases are activated, the capcases also causes the mitochondria to release _______ which then releases more capcases

cytochrome C

during extrinsic signaling, when caspases are activated, the capcases also causes the mitochondria to release cytochrome C, which then releases more capcases to carry out _____

apoptosis

during intrinsic signaling, the signal comes from ______

inside

all cells have GF receptor on surface

→ GF binds to receptor (can also be activated by cytokines)

→ signaling cascade is initiated

→ activates ______

→ phosphorylates

MAP kinases

to ensure that cancer cells survive and/or proliferate they:

• have an _____ number of GF receptors

increased

to ensure that cancer cells survive and/or proliferate they:

• _______ activation via GF receptor → always active receptor

ligand independent

to ensure that cancer cells survive and/or proliferate they:

• have mutated _______ factor → cannot bind to tumor suppressor protein

transcription

to ensure that cancer cells survive and/or proliferate they:

• release VGEF → ______ tumor blood supply

increase

to ensure that cancer cells survive and/or proliferate they:

• ______→ makes cancer resistant to drug by lowering uptake of drug that cancer gets

efflux transporters

to ensure that cancer cells survive and/or proliferate they:

• ____ = liquify tissue= cancer cells move easier = metasize

EMT

to ensure that cancer cells survive and/or proliferate they:

• have enzymes that inactivate/metabolize _____

chemotherapy

____ is new growth

• can be benign or malignant

neoplasia

Benign growth:

• ______ growth

local

Benign growth:

• ______ invade

do not

Benign growth:

• ____ margins

clear

Benign growth:

• _______ → membrane forms around it

encapsulated

Benign growth:

• _____ metastasize → no EMT = no enzymes to break down extracellular matrix

cannot

Benign growth:

• treatment is usually _______

surgical

Benign growth:

• very ____ differentiated

well

malignant growth:

• ____ invade

do

malignant growth:

• _____ have EMT → helps invade

do

malignant growth:

• can _______

metastasize

malignant growth:

• grow _______

relentlessly

malignant growth:

• causes _______ and inflammation

necrosis

malignant growth:

• releases _______ that affects the system

  • ex: hormones, increased clotting factor → leads to widespread symptoms such as neurological symptoms even if tumor is not in brain (paraneoplastic symptoms)

  • ex: substances that affect physiology = nonspecific symtoms

substances

tumor ____ equal growth

does

tumor ______ equal cancer (malignant only)

equal

if we remove benign tumors, it does not reoccur; malignant tumors ______ recur

can

benign ____ convert to malignant

can

____ is a a checkpoint during G1 phase that allows the cell cycle to continue to S phase

p53

the _____ phase is when cell is not dividing and is at rest (no DNA replication)

G0

the _____ phase is when cell is preparing for cell division → 1st cell growth phase

• proteins biosynthesized

G1

the _____ phase is when cell’s DNA are replicating

• most sensitive phase of cell cycle

S

the _____ phase is when cell grows again → 2nd growth phase

• post synthesis, pre-mitotic

G2

the _____ phase is when cell is undergoing the actual process of division

M

p53 and ____ are tumor suppressor proteins → prevents cell division

RB

transcription factors are ____ and _____

E2F, MYC

____ and ____ forms a complex that allows cell cycle to move forward

CD, CDK

CDK inhibitors and ____ → prevents CD and CDK from combining and allowing cell cycle to progress

p21

GF+ receptors activates ____

MAP kinase

kinases _____

phosphorylates

MAP kinase phosphorylates = increased ______

CD and CDK

phosphorylated Rb attached to E2F means ______ transcription → _____ translation → ______ cell division

no

______ activates transcription

• moves from G1 checkpoint over to S phase → cell cycle moves and cell divides

E2F

tumor suppressor proteins = police → checkpoints in cell cycle

• _____ (cyclin inhibitor)- activated upon DNA dmg to arrest cell cycle and induce apoptosis of cell

p53

regulatory proteins

• ____ = retinoblastoma protein (tumor suppressor protein)

Rb

regulatory protein

• ______ cell proliferation mediator

myc

Rb binds to and inhibits the action of _____

myc

once Rb is phosphorylated → myc is released from Rb= synthesis of _______

CD and CDK

increased rates of mitosis = increased risk of errors in ______

• associated with tissue trauma/ other stimuli

DNA replication

______ mutations → affects only one or few nucleotide → cause break or kink in double helix

point

____ Cellular growth no longer responding to normal mitotic controls

• No longer responds to contact inhibition

• Ignores the cell’s growth inhibiting signals

• Is resistant to apoptosis

• This excessive growth deprives other cells of nutrients 

neoplasm

neoplasm = expanding mass that creates _______ and/or pain in surrounding structure

pressure

neoplasms are usually immature cells

• lack ______ → lose function → impaired organ function

differentiation

____= neoplastic mass of cell

tumor

poorly differentiated cells are ________ agressive

more

_____ embryonic stem cells can be any tissue

totipotent

_____ embryonic stem cells can be

• endoderm line

• mesoderm line

• ectoderm line

pluripotent

_____ embryonic stem cells can be specialized

• develops into lung, pancreas (endoderm line), heart muscle and red blood cells (mesoderm line) or even skin and neurons (ectoderm line)

multipotent

pleomorphism is ↑ variation in cellular shape/size 

cellular

______ pleomorphism is ↑ variation in nuclear shape/size 

nuclear

↑ nuclear density is nuclear ______

• Disproportionally large size of nucleus relative to whole cell (increased nuclear/cytoplasmic ratio) 

hyperchromatism

what suffix is usually associated with benign tumors

• closely resembles tissue of origin

• Margins of tumor are well defined

• May be encapsulated

• Cells grow locally, and not in an aggressive manner

• Does NOT invade surrounding tissue 

• does not metastasize

-oma

two main effects of benign tumors:

• ____ of adjacent tissue

• _______ of hormone (uncontrolled)

• Rare systemic effects

  • Unless, a significant portion of the organ is made up of these cells

• Good prognosis (generally not life-threatening) depending on anatomical location

• Treatment: usually only involves surgical excision 

compression, secretion

suffix _____ and ____ for malignant tumors

• Malignant tumors= cancer

• Margins are poorly defined

• Tumor grows relentlessly → may cause obstruction

• Invades and destroys surrounding tissue

• The expanding mass compresses nearby blood vessels, leading to:

  • Necrosis

  • Impaired organ function

  • Inflammation around the tumor

  • ↑ pressure on surrounding structures 

• Systemic effects often present late: weight loss, fever, loss of appetite, anemia, unusual bleeding, paraneoplastic syndrome, etc.

• Major cause of death 

-carcinoma, -sarcoma

_______ syndrome are Additional complications as a result of substances released from tumor cells such as

• Neurologic function

• Blood clotting

• Hormonal effects

  → Complicate diagnosis and monitoring of patient 

Paraneoplastic

____ are Portion (%) of cells actively dividing 

growth fraction

_____ are time for a tumor to double in size

• Rapid vs. slow

• ex) Rapid: small cell lung cancer

• ex) Slow: prostate

mass doubling time

cancer is _____ cell proliferation

uncontrolled

cancer is _______ cellular differentiation

decreased

the _____ of cancer is deprived of nutrients and die

• increased inflammation and infection

necrotic core

cancer cells secretes Gf → _____ → angiogenesis → increased tumor growth

VEGF

VEGF also allows new _____ to form = more blood to cancer

blood vessels

a ____ is the only way to get a cancer diagnosis

biopsy

grade _ = differentiated cells similar to original cells

I

grade ____________ = differentiated cells similar to original cells

I

grade _______________________ - undifferentiated cells vary in size/shape → highly malignant

IV

TMN system → staging used as indicator of prognosis/therapy

• _______________________ stands for size of tumor

T

TMN system → staging used as indicator of prognosis/therapy

• _______________________ stands for extent of lymph node

M

TMN system → staging used as indicator of prognosis/therapy

• _______________________ stands for extent of metastasis

N

Stage _______________________ - small tumors and well localized = easy to treat, good prognosis

1

Stage _______________________ - are well advanced= diffuscult to treat, poor prognosis

4

type of therapy: _______________________

• intended to remove neoplasm

curative

type of therapy: _______________________

• to control symptoms, provide comfort, and improve the patient’s quality of life if cure is not achievable

palliative

type of therapy: _______________________

• Chemotherapy administered to reduce the tumor burden before surgery or radiation

neoadjuvant

type of therapy: _______________________

• Prophylactic treatment given as an additional treatment to prevent the formation of a secondary tumor

Adjuvant

type of therapy: _______________________

• Low-dose cytotoxic drugs given on a long-term basis to patients who are in complete remission to delay regrowth of residual cancer cells 

Maintenance

chemotherapy is administered in repeated doses at ____________ that maximize tumor cell kill but minimize the effects on normal tissues

intervals

Chemotherapy interferes with malignant cells _______________________ synthesis/activity

DNA

Chemotherapy interferes with malignant cells most active _______________________ cells

proliferating

Chemotherapy drugs are not __________________ specific→ lots of side effects

tumor

Chemotherapy interferes with malignant cells _______________________

cell cycle

during chemotherapy → drugs to attack cells in ____________ phase(s)of the cell cycle 

multiple