1) Breast :

· Introduction
· Risk factors
·
Etiology
·
Patrogenisis
·
clarificativ
·
morphology
·
C M
.

· Treatment

INTRODUCTION :
-

*
mmm
of f
- Abr is mos commones and deadly malignancy

CAbr
-
rd deaths of diagnosed

-
ER =
Estrogen Receptor
PR =
progestine Receptor
Factor respir <
HERL = human endomecial growth
3-kinase
inveint bes prophets
PIK3CA = Phosphatidye

TP53 are tho imp genes here

- BRCA2 ,
BRLA2 , genes

FACTORS
-

RISIL
un u
men)

=
Women) (Y .
-
* All the Molewloe variants (luminas
%
->
Gender (99
women ER tre ·
TN) Forms DCIS only
-

Age colder

breast feeding (ABr causes

prolonged
↑ thus all of Familial
-

DCIS except CDU1 >

- lobular
-
expone to estrogen

-
Br SPORADIC CA Br
FAMILIAL CA
conce cause is sporadic
25-33 %· of cares are due
to -
of

genetic predisposition -

Expone 1 Estrogen
80-90 % BRCA 1 E BRLA2 menache
(13) Early
-

[17) ↓
↓ &
-late menopause
lumnal
Triple-re to cried
morphology Absent breafeeding
Morphology -

CDU TP53
- other -
PTEN , , 1

.
etc
 FAMILIAL CARLINOMA
:-

PATHOGENISIS
OF
mum
m
en

mmm 80-gr%. of CABR

BRCA1 G
BRLA2 be
to came
- required
-

em ↓ tho is
mutations Es gene
multiple
·

CABU
Fam .

(V imps
Ideification of carriers
.

↓ treatment

Masterlomy
musations of
CABr cares
>
-
gentine
risk
-
high
other PIEN ·
TB53
mmm ·

~ CDU I
·
PlICBLA

- Midrate (10-30 % prevailance).

-

Emeka

· the there genes

- maintains genomic integrity
ATM - mutation occus
·
gene
Ataxia Telangetaria
DNA damage due to

↓
Detected by ATM

↓
TP53
Informs
-
- IfI PRs fails
to corner

is succeeds An DNA damage

↓ ↓
CELL CYCLE ARREST Apop TUSIS

IS BRLA1 BFLAL CHER2

* REPAIR MECHENISM REGULATED BY , ,
 BRLAI BRCA2
,
mmm e

recombinations
A repairs DNA viamologous
d
Sister chromad is need as

template to repair the DNA

WHY BRCA1 92 related to CABW so strongly?

--- BRLA1 and 2

muttalion
BRCA1 BRLAZ
-

of Br and oies
has
loss y finerians
ordian mesions
↓ epi ces
Huan
DNA
are more prone
Idiopanic repair which
~
Los a specific Discubed
musations can be
type of Dont
repair only
BRCA can gil
.
 MA
:-
PATHOGEMSIS OF
~

--triple& the
re
Here m
bunmat ~
m
C50-6 04 . )

Expore).
(Mamls due t ↑ Echogen
LUMINAL
:

-
levels
Estrogen
.

PR4
ERP ,
,
are appl
(other types
-

-
well dif ,
slow growing

-
Estogen
a I proliferative
Breas becoz-
· I dangerous for

a proliferation in Dr already
↓

↑ Esmgen Expose .

↓
DNA damage
↑ proliferation >
-

↓
DNA repair
=
no time for
TUMOUN & HER , <Pr
CAD -

↓
-are some population
arise
ER , PRA furores

luminat
--B .
Chigh geodel
A Clow grade 2 T B5 3
the

· TBAS -
Ve
· can arise frm A

· also BRCA2
murarich
 ·
Treatment
z
-

amiesongen therapy

programs
·
:

m
reuneme .
rates
-

good .
"I

:
BRLA1)
the CHER-2-17) (same dur As
&
were
L-FRAUMANI

3
AKA ERBB2
-
SYNDROME
↓ APOPTOS IS Lu
- a cell proliferation ,

TP53 gene mut

LABr im
- 20 %
O G
Tp = Frown Mani
- HER-2 Gene - - - - -
---

AMPLIFICATION
10) VIA P13K -AKT
Curally =

↓ signalling

↑ Action of VER
- ↓
and NECF) human
zausor
Endo grows ↑ proliferation of

-
cells and ↓ Apophonis

L
un
SCANCER - TUMOUR
mmm

ON
DEPENDS
LEVEL Of HER-2 EXPRESSION
*
EXPRESSED
Amt of ER

Arti HER-2 AnliBedy turapy

TREATMENT
: -

-
↓

can blid revitance to

it
crarely) mostly good
PROGNOSIS :

prognosis
 TN BC
-
:

independent pathway
-
Estogen

COMPALIVESTUDY :
-

mo

FACOPIANA-
1) SEROS em
m

GRENOMA
SEROUS TUBAL INTRAEPITHELAL
-
Similar #
f
TUMOUR of FACCOPIAN TUBE]
ESEROUS
BNLA1 mutation
- Also genuine
:

OF BREAL
-

CARONOMA
2) LUMINA mmm
ver

~
INBL
UMI mammography
X
MAMMOGRARLY
-

as a
presents just
-

X
LA IDENTIFY mas

/gld response
-

A
-good prognosis
To Amicancer turapy
↑ wimim
-Renence
- Recurrence rarl
first Gyrs
 TYPES Of CABr -
-

u
~

-- invasive
Carinoma in sit
(Breaches Myoep-
Craw do evic imecial BM).
+

brea
BM)
myoepimeral
+

- All Car ar ADENOCtroMAS

-

u
Lobular :
"any Casinoma mar progresses

"
Arm Leis

oier CA that can't

-
ductal--"every
um

a
special histological diagnosis"
processed
as
be
 I
LCIS
DCIS
to duet
· DEF :-
epithelial proliferation
· proliferation of alls unfined
duits and and lobules but grows in a dyscohesive
that is engined to

CCDU 1 genes (E-cadherini)

.
libules .
Farim

Mammography
Mammographic Findings
via
· & can't be identified
via mammography
can be identified [Anidental Findings).
%) Thierry.
bur
very rarely [5
is Invasive CABr).
X very .
race
·

AND SECRETIONS
-
CALLIFICATION
Necrosis I
is used
(which to diagnose pus)
Lis o more
bilateral (20-n0Y)
less bilateral (10-20
% ) ·

· DCIS s
· MOSTLY TRUE PRECURSOR
a Nor a re processor.
cells in Dusim
identical
1bez
and invasive caminoal

I
.
MORPHOLOCY

has
peomorphic cells
since
signer ring appearance
·

·
has

in E-cadherin
fault
· Ir is HERI 44 and ER-re ·
ER4 PR the but HERL e

· THERE ARE O 14PES · PALETOID SPREAD bur no pager disease

1) Com 2) CRIBRFORM

>
- CENTRAL
AREA UF
NECRESIS
3) MILROPAPILAM u) Papillary

R
oNUFBR
CORES

FIBROVASLULAR
-
LORES
G CACKS MYEP1
LAYER

ROBBINS.
2) soud (not gries in
PAGETS LIS A TYPE PCIS)
PE OF
-
:
·

· UNILATERAL

DIFF PLAUNOSIS
: -

- ELZEMA
MYOEPITHEA
I
BREACH BM OR
DOESN'T
O

- has pruriris
-
Surface Breaching
of .
avinoma

beim
Frymamarons
-

must formation
-
 INVASIVE CARLLNOMA :
-

um
~

--
2) SPECIAL TYPES
1) No special type mine

CNOSS
· There are no
other types
in were

ductal adenocarcinoma
-only

① Ngi
masses (2-3cm in size)
o
They are
palpable
mass radiodense
· can we mammography (irregular ,

chestnut).
o
while
witting >
-
grating sound (water
due to demoplastic sha and foci of calification
.

histo- ·
desmoplastic smal realtimes
u

Fibro lisme
less shimal reaction but we fatty
·
rarely was

wit scoring
scoring
nu
: --
Nottingam
GRADE1 : -

(well diff
ulters
·
fubular/cribrigon pattern Ccookie
·
small uniform nussei

· o provisation .

GRADEC :
(mid diff)
-

·
solid clusters of cells
·
pleomorphic mulei
o a proliferation
CURADE 3 : (purely diff)
· RACKED NESTS / SOLD SHEETS OFELLS
·
enraged pleomorphic unei

o
puliferation
· NECROTIC AREAS ARE SEEN DAD
 SPECIAL TYOE : -

u m
are there
-
many special types
- CAEWONZED AS

-
% a com
TNBC (A)
OTHERE)
HERZ the ES
LUMINAL (a) INFLAMMATORY

mean
O

· LOBULAR
·

·
APOCRINE
MICROPAPILLARY
s CA

· MUCINOUS · METASTATIL
CARLINOMA
·
TUBULAR CA M)
.

· SECRETORY
· PAPILLARY CARLINOMA
zam
MALLU
↓ -

↓
MALLU PATV -
grade nucricies and libular
Now

ITUBULAR
- -

↓
monious f PAPILLARY
botn are so

↓ demo plasia
gr and

huner &
↓
HARD TO DETECT
:
Ubulae
-

1) ·

-
CDUI , dyscolerive infilterates
recoperitoneum :

-
melamatizes to peritoneum ,

⑭ meninges (depromeninges)
mammography
⑧ -
hand to delect via imaging -
*
a

signer ringue demo practic

E
ADD
Fails t pedure
minimal rucims
demopearia
munin droplets
.
appearance >
-

-signer ring
:
a munimous
~
-

soft i rubbery
-
appr pace gray-bene
- min filled alls.
 · Tubular

lesion
-

diff diagnosis
:
-

Bening sclerosing

ibrigor pattern
SNOUTS
-
Apowine
↑

papelary
· :

num

Fibrovascular sma
-
forms the papillae >
- stoma wi

APOCRINE
-
:

2) ·

swear gland
⑳music-reembles
>
- melei

(hyperpigmented

·
nucei a mulcioli
-
large
-GRANULAR cytoplasm .

·
MICROPAPILLARY
wi

- misnomer (no papilne formed)

ECF
that
years
on
-unow dlls
balls of

MARY
:
-

3)
mulation has this pattern
- > WOY . A BRCA1
-

Luypermetrylarims

page
ine ,
BRLAI Nd

↓
unfilterates Tumore
.

un

brus SoF) and had to

minimal dennoplaria
-
-

detest

nulei & muleirti lympho-plasmacytic

3) infilteration
FEATURES :
- 1) pleomorphic large
Border
2)↑ mirotic figures
u) on Infiltrative pushing
 METAPLASTIC CARLINOMA-
m
um

D- spindle shaped and manix producing

**

celles similar
are to myrepiterial cells .

*A*
gene expression of
-
f
-

gene expression

INFLAMMATORY CARLINMA
u)

↓ Gossi
·
novascular spaces
plugs
↓
failure y lymphatic diamage
misnomer
↓ ↓
-

edematous skin
>
- PEAU'D ORANGE
no
inflammation stock to Like Of COOPER
APPEARANCE

is present
· no palpable mass

PROCNOSTIC D PICTIVE FR
mum