, Cancer development
both are needed
Cancer is uncontrolled cel It disease
growth .
is a
genetic to form
-
Cancer
different
signauingpathways
→
mutati ons aan occur in > Causes Cancer
lifestyle
→
role
Plays
a
transformation from
charge Norma I cells into
=
tumor cells .
>
driver mutations mutations in / tumor
norm at cells
gain oncogen
es
supressorgenes
:
>
for fail transformation mutati ons deed to somatic
pas angermutations happen in cells
:
,
Cancer Critical
genes
-
>
Proto mutated active or over expressie become
oncogen e over
genes oncogen
es ,
causing
- :
a tumor .
→ RAS RAF EGFR SRC
, , , ,
MYC , TGFB ,
Smad 4
>
Tumor supressor of function mutation Cancer →
P 52 PTEN APC
gene
:
loss can ca use .
, ,
TGFB ,
retinobastoma ,
P 53 mutated in almost alt
-
Intra / inter tumor
Heterogeen eity >
human cameras .
Inter breast different peopu DNA Maintenance mutations result in
genomic Stability
>
Cancer in in
genes
: :
.
caused different
can be
by mutati ons
>
Intra : one tumor can have different tumor 611 behaviour
mutations in multiple
genes
Benigni goedaardig
Malignant kwaadaardig
:
Tumor Development Angiogenese
Primary Tumor : The tumor reeds 02 Food
>
benign
> abnormal cells +
,
'
↳ treat with radiation to prevent spread
'
The tumor Secret es compounds Minps
Ing such as
This
degrade the basat membrana of the
>
tumor
locatyinuades tissues to blood Vessel
> >
Further of the
Angiogeneseis : the tumor attiacts biooduessds
growth tumor into the blood Vessel
for nourishment is in daad tumor factors ✓ OEF DFGF
b :
,
PDGF ,
>
Metastasio : From >
When the tumor increas.es
cells moue
awag primary
tumor
Migration into the vessel , it
and inuade other
body parts via blooduessels and becomes
Matignon tand spreads to other
Organ
s .
lymph Uessels . .
Matignon
→
the tumor becomes t
ij
, Tumor
Migration how is it controlled ? EMT epithetial to
mesenchym
at transition mediates metastasio
: - →
In from
important is
going
>
tissue : to metastatic tumor
norm al Cev
organization is controlled
by primary
( faal adhesions)
adherentjunctions)
>
E- cadherins ( and
integrins makes the cells Mobile ,
they can moue
>
E cadherins Connect cells left from epitheta l Squares polarised
the cells Morpho
1099 90 stretohy
s
Changes
: >
and to each other =
allows them to enter the blood Vessel
right cells .
.
>
upldown ÎF
Integrins : Connect cells controlled
by that
downregu late adhesions and
cytoskelet on and increase
to extracellulair matrix other cells at Components
mesenchym
+ . .
These adhesions are connected to
kinases + acties to Control Movement of the cells inside .
See video Notes
In Cancer of remoued.to Onenote
attachment cells deed to be in Crease
Migration in
:
.
cadherinsaredownregulated "" ""
>
>
integrins shift as wal ( connect to Ecm and uinau.FINÏ integiins
> This win make it possible for the cells to move .
50
EMT of Cancer cells
induces
Migration
into the
Circulatie n !
A 7th Hallmark In 2022 : New hallmark 5
Tumor Micro environment =
tumor eens internet with
many
(
Ground them epitheta This continuous
19
cells :
,
immune cells .
from of
phenotypicplasticity
>
Changes primary to
malignant
tumor in
dynamic the
=
. Cancer cells are a constant
Changing cells
☐
> This
term to described the cells surround
Ing the Cancer cells .
Seems to be
Party
controlled
by no nmutational
epigenetic
( neutropnils Fibroblasten
macro
pnages , , Muscle cells , ,
lymphatic cells , re
Programming
epitheta cells) >
New info about the Micro bio mes of Cancer cells
>
New info about series cent Cancer cells
'
.
The interaction between an these cells with the
tumour
very important
are .
lonenote)
Macrophage double
=
agent
L
protect Cancer cells + make portals for them to enter bood Wessels .
both are needed
Cancer is uncontrolled cel It disease
growth .
is a
genetic to form
-
Cancer
different
signauingpathways
→
mutati ons aan occur in > Causes Cancer
lifestyle
→
role
Plays
a
transformation from
charge Norma I cells into
=
tumor cells .
>
driver mutations mutations in / tumor
norm at cells
gain oncogen
es
supressorgenes
:
>
for fail transformation mutati ons deed to somatic
pas angermutations happen in cells
:
,
Cancer Critical
genes
-
>
Proto mutated active or over expressie become
oncogen e over
genes oncogen
es ,
causing
- :
a tumor .
→ RAS RAF EGFR SRC
, , , ,
MYC , TGFB ,
Smad 4
>
Tumor supressor of function mutation Cancer →
P 52 PTEN APC
gene
:
loss can ca use .
, ,
TGFB ,
retinobastoma ,
P 53 mutated in almost alt
-
Intra / inter tumor
Heterogeen eity >
human cameras .
Inter breast different peopu DNA Maintenance mutations result in
genomic Stability
>
Cancer in in
genes
: :
.
caused different
can be
by mutati ons
>
Intra : one tumor can have different tumor 611 behaviour
mutations in multiple
genes
Benigni goedaardig
Malignant kwaadaardig
:
Tumor Development Angiogenese
Primary Tumor : The tumor reeds 02 Food
>
benign
> abnormal cells +
,
'
↳ treat with radiation to prevent spread
'
The tumor Secret es compounds Minps
Ing such as
This
degrade the basat membrana of the
>
tumor
locatyinuades tissues to blood Vessel
> >
Further of the
Angiogeneseis : the tumor attiacts biooduessds
growth tumor into the blood Vessel
for nourishment is in daad tumor factors ✓ OEF DFGF
b :
,
PDGF ,
>
Metastasio : From >
When the tumor increas.es
cells moue
awag primary
tumor
Migration into the vessel , it
and inuade other
body parts via blooduessels and becomes
Matignon tand spreads to other
Organ
s .
lymph Uessels . .
Matignon
→
the tumor becomes t
ij
, Tumor
Migration how is it controlled ? EMT epithetial to
mesenchym
at transition mediates metastasio
: - →
In from
important is
going
>
tissue : to metastatic tumor
norm al Cev
organization is controlled
by primary
( faal adhesions)
adherentjunctions)
>
E- cadherins ( and
integrins makes the cells Mobile ,
they can moue
>
E cadherins Connect cells left from epitheta l Squares polarised
the cells Morpho
1099 90 stretohy
s
Changes
: >
and to each other =
allows them to enter the blood Vessel
right cells .
.
>
upldown ÎF
Integrins : Connect cells controlled
by that
downregu late adhesions and
cytoskelet on and increase
to extracellulair matrix other cells at Components
mesenchym
+ . .
These adhesions are connected to
kinases + acties to Control Movement of the cells inside .
See video Notes
In Cancer of remoued.to Onenote
attachment cells deed to be in Crease
Migration in
:
.
cadherinsaredownregulated "" ""
>
>
integrins shift as wal ( connect to Ecm and uinau.FINÏ integiins
> This win make it possible for the cells to move .
50
EMT of Cancer cells
induces
Migration
into the
Circulatie n !
A 7th Hallmark In 2022 : New hallmark 5
Tumor Micro environment =
tumor eens internet with
many
(
Ground them epitheta This continuous
19
cells :
,
immune cells .
from of
phenotypicplasticity
>
Changes primary to
malignant
tumor in
dynamic the
=
. Cancer cells are a constant
Changing cells
☐
> This
term to described the cells surround
Ing the Cancer cells .
Seems to be
Party
controlled
by no nmutational
epigenetic
( neutropnils Fibroblasten
macro
pnages , , Muscle cells , ,
lymphatic cells , re
Programming
epitheta cells) >
New info about the Micro bio mes of Cancer cells
>
New info about series cent Cancer cells
'
.
The interaction between an these cells with the
tumour
very important
are .
lonenote)
Macrophage double
=
agent
L
protect Cancer cells + make portals for them to enter bood Wessels .