35AF e 36AF Avaliacao Prognostica-copia 2

7/23/2019 35AF e 36AF Avaliacao Prognostica-copia 2

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Avaliao prognstica das

neoplasias

Prof. Ana FlixFaculdade de Cincias Mdicas30 de Novembro de 2015


2/110

PROGNSTICO


3/110

Prognstico

Diagnstico"

Tipo histolgico" Diferenciao

Estadiamento" Marcadores de prognstico

Consequncias do crescimentotumoral Leso e condio pre"malignas


4/110

Prognstico

Diagnstico"

Tipo histolgico" Diferenciao

Estadiamento"

Marcadores de prognstico

Consequncias do crescimentotumoral Leso e condio pre"malignas


5/110

TIPO HISTOLGICO


6/110

Melanoma maligno

Leiomiosarcoma

Carc pavimento celular Carcinoma ductal

Linfoma no Hodgkin

GIST

Carc. neuroendcrino

Linfoma Hodgkin

Seminoma


7/110

Tipohistolgicosegundo a

classificao daOMS


8/110

Tipo histolgico

Categorias de prognstico#dependentes do tipo histolgico e estdio $

Bom #80$aos 5 anos % Intermdio Mau #


9/110

Carcinoma do endomtrio &

tipos histolgico e o prognstico !"#$ !$&$' $' (')*&"$'

+,&$-()."/"&( !"#

%&'()'*+,-'*. !/#

0,1+(23*4(2( 56#

0(.$'$ 789:8#

123435' 635.5' :! 9 /"#

7,&"8(.(,6"5&$ (

9('&"8(.(,6"5&$6;#


10/110

COMO SE IDENTIFICA O

TIPO HISTOLGICO?


11/110

Tipo histolgico

Observao microscpica #cito ehistologia$em coloraes de rotina e em casosseleccionados dever ser complementada com:

imunohistoqumica"

Tumores pouco diferenciados"

Metstases reveladoras" Deteco de molculas com valor prognstico e

teraputico

diagnstico molecular"

Linfomas/leucemias; e Sarcomas; etc" Prognstico"

Doena mnima


12/110

Caso clnicoHomem, 63 anos com

queixas de rouquidoh 1 ano recorre aomdico por dispneia eperda de peso de 10kgnos ltimos meses.Refere hbitos

tabgicos e alcolicosdesde sempre.No exame objectivo

mau estado geral

emagrecimentoacentuado

perda de massasmusculares

tumor com 4 cm nalaringe


13/110

Imunohistoqumica Microscopia electrnica


14/110

DIAGNSTICOCarcinoma pavimento celular, tipo sarcomatide


15/110

MARCADORES IMUNO"

FENOTPICOS


16/110

Melanoma maligno

Leiomiosarcoma


Linfoma no Hodgkin

GIST

Carc. neuroendcrino

Linfoma Hodgkin

Seminoma

Cito-queratinas Cito-queratinas Cromogranina

Sinaptofisina

Vimentina

DesminaActina

CD45

CD20CD3

CD15

CD30CD20

pS100HMB45

CD117CD34

CD117PLAP


17/110

MARCADORES EM

MICROSCOPIAELECTRNICA


18/110

Melanoma maligno

Leiomiosarcoma


Linfoma no Hodgkin

GIST

Carc. neuroendcrino

Linfoma Hodgkin

Seminoma

DesmossomasFil. intermdios

LumesDesmossomas

Fil. intermdios

Grnulosneuro-

endcrinos

Fil. finos

Fil. intermdios!

Melanossomas

!

!!


19/110

MARCADORES

MOLECULARES


20/110

Melanoma maligno

Leiomiosarcoma


Linfoma no Hodgkin

GIST

Carc. neuroendcrino

Linfoma Hodgkin

Seminoma

! Status geneerBB2

!

! !

! cKit iso12

Marcadorescromossmicosclonalidade


21/110

DO INFORMAO DE

ALVOS E DE RESPOSTA TERAPUTICA


22/110

Melanoma maligno

Leiomiosarcoma


Linfoma no Hodgkin

GIST

Carc. neuroendcrino

Linfoma Hodgkin

Seminoma

! Status geneerBB2

! !

BRAF, cKIT cKit, PDGF,Succinil

!

!


23/110

:(;$34,$3$?"(' @(65-( 8(5'"@3(

A6$') 5,& $3( ?(,$-( D ?(,$-(

?

+,


24/110

Journal of Pathology

J Pathol2010;220: 307315

Published online17 November 2009 in Wiley InterScience

(www.interscience.wiley.com)DOI:10.1002/path.2636

Invited Review

Does massively parallel DNA resequencing signify the endof histopathology as we know it?

Samuel AJR Aparicio1,2,3* and David G Huntsman2,3

1Molecular Oncology, BC Cancer Agency, 675 W10th Avenue, Vancouver V5Z 1L3, Canada2Centre for Translational and Applied Genomics, BC Cancer Agency, Vancouver V5Z 1L3, Canada3Department of Pathology, University of British Columbia, G227-2211 Wesbrook Mall, Vancouver, BC V6T 2B5 Canada

*Correspondence to:Samuel AJR Aparicio, MolecularOncology, BC Cancer Agency,675 W10th Avenue, VancouverV5Z 1L3, Canada.E-mail: [email protected]

No conflicts of interest weredeclared.

Received: 1 September 2009

Revised: 23 September 2009

Accepted: 26 September 2009

Abstract

Next-generation DNA sequencing devices have revolutionized cancer genomics by bringing

whole genome resequencing of patients tumours within practical and economic reach.

We present an overview of the techniques involved and review early results from the

resequencing of cancer genomes. The possible impacts of whole-genome and trancriptome

resequencing in clinical cancer research and the practice of pathology are discussed.

Copyright 2009 Pathological Society of Great Britain and Ireland. Published by John

Wiley & Sons, Ltd.Keywords: DNA sequencing; mutational heterogeneity; cancer genome; transcriptome;tissue sampling; mutational landscape; tumour evolution

"/


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"6


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Table 1

Some milestones in the clinical research of circulating cell-free DNA in the blood.

Year Event

1948 Discovery of cell-free DNA in blood

1965 Circulating DNA as a possible factor in oncogenesis

19661973 Detection of high levels in patients with systemic lupus erythematosus, rheumatoid arthritis, leukemia, and other diseases

1972/1975 Methodical aspects of determining in normal plasma samples1977 Detection of increased values in cancer patients depending on tumor stage and treatment

1989 Evidence of similar characteristics between circulating DNA and tumor DNA in cancer patients

19941999 Evidence of further tumor-related genetic alterations in circulating DNA

1997 Presence of fetal DNA in plasma of pregnant women

1998 Description of plasma DNA chimerism after transplantation

20002010 Circulating DNA in diagnosis and prognosis of numerous diseases (tumors, trauma, heart infarction, stroke etc.)

2010 Oncogenic transformation of cultured cells by circulating DNA in plasma

Biopsia lquida


27/110

L:GMANIG0B

9"'


28/110

AB0


29/110

F+NRSG0I D 9+M7F7!7NF

Benign tumorAn abnormal proliferation ofcells driven by at least onemutation in an oncogene ortumor suppressor gene.These cells are not invasivewhich distinguishes themfrom malignant cells.

Vogelstein B, Papadopoulos N, Velculescu VE, Zhou S, Diaz LA Jr, Kinzler KW.Cancer genome landscapes.Science. 2013 Mar 29;339(6127):1546-58.

Malignant tumor

An abnormal proliferation of cellsdriven by mutations in oncogenesor tumor suppressor genes thathas already invaded theirsurrounding stroma.

It is impossible to distinguish an isolated benign tumor cell from

an isolated malignant tumor cell. This distinction can be made

only through examination of tissue architecture.

"!


30/110

DIFERENCIAO


31/110

Graduao da diferenciao dasneoplasias malignas

Grau de semelhana com o tecido

normal Caractersticas das clulas

Pleomorfismo

Dimenses dos ncleos

Actividade mittica


32/110

Diferenciao

normal

G1

G3

G2

Semelhana com onormal %morfo"

funcional


33/110

Anaplasia


34/110

Mitoses


35/110

grau de diferenciao

definido pelo grau de semelhanado tumor com o tecido que lhe dorigem

pode ser subdividido em: "bem, mdio ou pouco diferenciado" Graus 1, 2 e 3 #eventualmente 4$

"

baixo grau e alto grau" ou, em casos especficos, tem um

sistema prprio


36/110

exemplos

adenocarcinoma do clon e recto" Baixo e Alto grau

adenocarcinoma do endomtrio " Grau 1, 2 e 3

adenocarcinoma da prstata" Gleason

H critrios especficos para cada neoplasia


37/110

Adenocarcinoma do endomtrio

Grau 1 a 5% e de 50% de

reas slidas

Avaliao da morfologia de ncleos por fazer up gradings


38/110

score combinado de GleasonAdenocarcinoma da prstata


39/110

score combinado de Gleason

3

Adenocarcinoma da prstata


40/110

score combinado de Gleason

3

4

3+4=7



41/110

3+4=7 4+3=7!

o predomnio de

reas de grau

histolgico 4 pode

retirar a indicao

operatria



42/110

Prognstico

Diagnstico" Tipo histolgico"

Diferenciao

Estadiamento



43/110

ESTADIAMENTO


44/110

Estadiamento

Avaliao clnica de pacientes com neoplasiaincide sobre a

Extenso local e disseminao tumoral

" Histria e exame fsico " Estudo analtico #bioqumico, hormonal,$"

Estudo imagiolgico " ESTUDO ANTOMO"PATOLGICO


45/110

T Tumor

N Gnglios linfticos

M Metstases a distncia


46/110

Crescimento invasivo do Adenocarcinoma

do clon


47/110

Estadiamento

De acordo com os elementosT - Tumor

N - Gnglios linfticosM Metstases a distncia


48/110

ADENOCARCINOMA DO

ENDOMTRIO


49/110

Prognstico

Diagnstico" Tipo histolgico"

Diferenciao

Estadiamento



50/110


Vrios tipos de elementos clnico emorfolgicos que so teis paraestimar grupos de doentes com umaevoluo clnica e que so utilizadosna seleco da teraputica


51/110

OUTROS PARAMETROS

MORFOLGICOS DEPROGNSTICO

Carcinoma endometriide do endomtrio


52/110

Factores de prognstico

com utilidadecomprovada

Tipo celular

Grau histolgico

Invaso vascularlinftica

Estdio da FIGO

p53 Ploidia tumoral

marcadores com utilidadeprovvel

Receptores deestrognios

Bcl2 Ki67 ErbB2

Densidademicrovascular


53/110

Dados morfolgicos #que no entram noestadiamento na maioria dos tumores%

ex. Invaso linfo&vascular

Factor de prognstico independente da presena demetstases em gnglios linfticos


54/110

Marcadores tumorais#ver tabela Robbins%

Protenas indicadoras da presena

de tumorescom possibilidade deserem usadas no diagnsticoe naorientao teraputica

SEROLGICOS

IMUNOHISTOQUMICOS


55/110

IsoenzimasAntignios onco-fetais

Marcadores tumorais

" alfa"fetoprotena" antignio carcino"

embrionrio

" fosfatase cida prosttica" NSE


56/110

Hormonas

Marcadores tumorais

" Tiroglobulina" Calcitonina" HCG " Catecolaminas

Mucinas

Ca 125

Ca 19-9

Ca 15-3


57/110

Marcadores tumorais

Protenas especficas

" Imunoglobulinas" Antignio

especfico daprstata #PSA$

Figado

PSA


58/110

Marcadores tumorais

Marcadores moleculares

"

Amplificao de genes


59/110

Marcadores tumorais

ndice de proliferao Receptores hormonais Expresso de alvos

teraputicos Doena residual mnima

ERBB2 - CISH


60/110

CARCINOMA DA MAMAexemplo


61/110

Biomarcadores prognstico e de orientaoteraputica com utilidade comprovada

Tipo histolgico Grau histolgico Invaso vascular

linftica

Estdio ganglionar axilar a distncia

Receptores deestrognios eprogesterona

ERBB2

Utilidade em gruporestricto Ki"67

SEM utilidade comprovada em uso clnico h mais de 5anos mas onde so depositadas grandes esperanas Testes moleculares tipo Oncotype DX test ; MammaPrint test


62/110

CARCINOMA DA MAMA


63/110

com utilidade comprovada

Tipo histolgico Grau histolgico Invaso vascular

linftica Estdio

ganglionar axilar a distncia

Receptores deestrognios eprogesterona

ERBB2 Utilidade em grupo

restricto

Ki"67


64/110

Outros

Oncotype DX test

Em casos seleccionados Custo aproximado 3000&


65/110

RECIDIVA

Manifestao de novo de uma neoplasia maligna apstratamento e aps um perodo de tempo durante o qual aneoplasia no era detectvel


66/110

PROGRESSONeoplasia maligna em disseminao ou agravamento local


67/110

Tipos de recidiva

Local / Regional

No mesmo local Em gnglios

linfticos loco"

regionais

A distncia

Noutra localizao /rgo


68/110

Como se avalia o risco de recidiva?

diferente em todos os doentes Depende de factores de prognstico

No possvel garantir a cura


69/110

Sobrevivncia

Avalia"se habitualmente:" Taxa de sobrevivncia aos 5 anos" Taxa de sobrevivncia relativa

" Na comparao com a populao sem doena


70/110

Caractersticas clnicas das neoplasias

efeitos dos tumores sobre o hospedeiro" Efeitos locais" Efeitos a distncia

Sndromes paraneoplsicas

Caquexia Metstases

causas de morte em doentes com neoplasia


71/110

Efeitos das neoplasias benignas

Pela sua localizao N de tumores

Produo hormonal Alteraes gastro"intestinais Tamanho

Torso e enfarte


72/110


Pela sua localizao Adenomas pituitrio

comprimem a pituitria normale o quiasma ptico

Craniofaringiomas comprimem

e invadem o hipotlamo Mixoma auricular %bloqueia a

circulao intra"cardaca Meningiomas comprimem o

crebro Quistos colides bloqueiam o

fluxo do liquor

Adenomas pleomrficos

comprimem o nervo facial

MENINGIOMA


73/110


N de tumores Lipomas na "adiposis

dolorosa

Tumores neurais no

Sndrome de VonRecklinghausen's; Hamartomas na

esclerose tuberosa,etc.$


74/110

Produo hormonal

Adenomas dapituitria, adrenais,

insulinomas,vipomas, reninomas,outros$

Alteraes gastro"intestinais

Hemorragia Obstruo

Intussuspeco Perda de potssio



75/110


Tamanho cistadenomas

mucinosos do ovriocom 20 kg, etc.

Torso e enfarte tumores do ovrio


76/110

Efeitos das neoplasias malignas

Invaso das estruturas normais e/ou

" Leso cerebral e herniao"

Edema pulmonar

"

Fracturas sseas" Trombocitopenia, granulocitopenia, anemia" Hemorragia #trombocitopenia e invaso vascular$"

Obstruo do ansas gastro"intestinais" Derrame peural

"

lceras e fstulas" Caquexia"

..


77/110

Sndrome paraneoplsica

Podem ser a 1 manifestao de umaneoplasia

Podem provocar problemas clnicosgraves e letais Podem simular doena disseminada#metstases$e perturbar o raciocnio

para a teraputica


78/110

Sndrome paraneoplsica

Sinais e sintomas no relacionadosdirectamente com a progresso localou a distncia da neoplasia

Sinais e sintomas no relacionadoscom secreo tumoral

ocorre em cerca de 10(

dosdoentes portadores de neoplasiamaligna


79/110

Efeitos das neoplasias malignas

Sndromes paraneoplsicas" Febre" Sndrome de CUSHING" Virilizao " Feminizao" Hiponatrmia

"

Hipoglicmia


80/110

Efeitos dos tumores malignos

" Sndrome carcinide #flushing, asma ediarreia$

" Policitmia"

Trombocitose " Anemia hemoltica auto"imune" Sndrome de hiperviscosidade " Neuropatia perifrica" Miastenia gravis


81/110

Causas de morte por neoplasia

PNEUMONIA uma das causas mais frequentes de morteem pacientes com cancro. NEUTROPENIA #invaso da MO por clula sneoplsicas$ IMMUNOSUPPRESSO NO ESPECFICA OBSTRUO DAS VIAS EREAS #derrame pleural,

acamado$ ATELECTASIAS por dificuldade em tossir, acumulao de

secrees com colapso alveolar e infeco ASPIRAO de alimentos e de VMITO NARCTICOS suprimem o estmulo respiratrio

SPSIS#habitualmente bacilos gram#"$com choque #no facilmente identificvel uma origem da infeco %pulmo,bexiga, tumor necrosado$


82/110

Causas de morte por neoplasia

HEMORRAGIA#crebro, intestino, outro local$ comum

em pacientes com trombocitopnia #invaso da MO$ TROMBOEMBOLISMO PULMONAR#acamados e

alguns pacientes ambulatrios$

FALNCIA RENAL #infiltrao tumoral, obstruoureteral$

SNDROMES PARANEOPLSICAS DOENA IATROGNICA espervel em doentes que

foram submetidos a cirurgia, radioterapia e quimioterapiamesmo se forem curados Ann. Int. Med. 111: 411, 1989

SUICDIO E a EUTANSIA

Menos comuns so: falncia de rgos como o fgado,tamponamento cardaco, etc.


83/110

Sndrome da lse tumoral

A morte celular em massa pode levar morte dos doentes #tipos$" Hipercalimia

Paragem cardaca

" Hiperfosfatmia" Hiperuricmia

Insuficincia renal crnica

" Hipocalcmia


84/110

REGRESSO

ESPONTNEA

1 em cada 140 000 casos #?$


85/110

Regresso espontnea de tumores

Hemangioma em crianas" 2,6(dos recm nascidos" Incio s 2 a 4 semanas" Regresso ocorre pelos 10

anos#80"90($" Mecanismo

desconhecido


86/110

Regresso tumoral

Carcinomas de clulas renais Neuroblastoma

Melanoma maligno Coriocarcinoma Hepatocarcinoma Carcinoma da bexiga


87/110

Neuroblastoma

Sistema nervososimptico" Neuroblastoma" Ganglioneuroblastoma"

Ganglioneuroma

Mecanismos"

Diferenciao Hipometilao do ADN Diminuio da actividade da

telomerase


88/110

Melanoma maligno

Primrio pode regredir" Estudo de 5000 melanomas malignos

2,2 casos em 1000 com regresso total do

primrio

Mecanismo" Imunolgico #CD4+$

World J. Surg. 19, 352-358, 19 95

WORLD

Journal of

SURGERY

9 995 by the Soci~t~

International e de Chirurgie

Spontaneous Regression of Human Melanoma/Nonmelanoma Skin Cancer:

Association with Infiltrating CD4 T Cells

Gary M. Halliday, Ph.D, Anita Patei, M.B., B.S., Michelle J. Hunt, M.B., B.S., M.Med.,

Frances J. Tefany, M.B., B.S., M.Med., Ross St.C. Barnetson, M.D.

Department o f Dermatology, University of Sydney, Royal Prince Alfred Hospital, Missenden Road, Camperdown, New South Wales 2050,

Australia

Abstract. Spontaneous re gression occurs in some human malignant

melanomas a nd basal cell carcinomas (BCCs). We have compared the

cellular infiltra te in regressing and nonregressing tumors in order to

analyze the mechanism by which regression occurs. Regressing primary

melanomas and BCCs were infiltrated with a larger number of CD4*, but

no CD8 +, T lympho c~es t han were seen in nonregressing tumors. The

number of interleukin 2 receptor-positive (eariy activation marker) but

not transferrin receptor-posi tive ( intermediate ac tivation marker ~ T cells

was increased, indic ating that the infiltrating T cells were activated. Large

numbers of Langerhans cells, macrophages , and other class II major

histocompatibi lity complex (MHC)-expre ssing cell s were present but were

no increased in the regressing tumors. There were no detectable B

lymphoeytes, and the regressing tumor cells displaye d levels of HLA-DR

expressio n similar to those of the nonregressing tumors. Compari son of

sqnamous cell carcinoma (SCCs) with keratoacanthomas (KAs), which

are likely to be a spontaneously r egressing form of SCC, also showed

increased i nfiltration of activat ed CD&-, but not CD8 +, T cells within the

KA. A murine ultraviol et ((W)-induced squamous tumor that spontane-

ously regresses when transplanted into immunocompeten t syngeneic mice

was also infiltrated with incr eased numbers of activated CD&-, but not

CD8 +. T cells prior to and during rejection. These results i ndicate that

spontaneous regressi on of human skin tumors is likely to be immunolog-

ically mediated, and that CD4 + T lymphocytes seem to mediate this

regression.

There is Considerable experimental evidence that skin tumors can

induce effective immune responses in mice. Epithelial skin tumors

[1] and melanomas [2] are able to immunize syngeneic mice

against subsequent Challenge with the same tumor line. Addition-

ally, some ultraviolet UV) light-induced skin tumors in mice,

which grow progressively in immunosuppressed hosts, regress

when transplanted into syngeneic immunocompet ent mice. This

result implies that the immun e system is responsible for this tumor

regression [1, 3]. As transplantation experiments cannot be per-

formed in humans, evidence that the immune syst em plays a role

in controlling the growth of human tumors is less direct. The

antigen MAGE-1, which i capable of causing rejection of human

melanomas, has been clon ed [4]. This antigen, associated with

HLA-A1, is recognized by cytotoxic T lymphocytes, which are

capable of destroying MAGE-l-posit ive tumor cells [5]. Studies of

Correspondence to G. Halliday, Ph.D.

cellular infiltrates and other markers of immunologic activation,

as well as isolation of cytotoxic lymphocytes from patients,

suggests that the immune system at least limits growth of human

melanomas and n onmelanoma skin cancers [6, 7].

Analogous to the UV-induced regressor tumors in mice, a

number of human skin tumors regress spontaneously. Most

studies on the role of the immune system in controlling human

skin cancers have used progressively growing tumor material,

where tumor growth is outpacing tumor destruction. In contrast,

tumor cell death exceeds tumor growth in regressing human

tumors, providing valuable material for analysis of the biologic

process that can lead to tumor destruction. Lit tle is known about

spontaneously regressing human skin tumors. We have been

studying spontaneous regression of human primary malignant

melanoma [8], basal cell carcinomas BCCs) [9], and keratoacan-

thomas KAs) [10] over the past 5 years, and here we contrast and

review these findings.

It has been recognized for a number of years that some human

melanomas regress spontaneously. Spontaneously regressing hu-

man melanomas are infiltrated with large numbers of lymphocytic

cells [11], and cytotoxic T cell clones have been est ablished from

a regressing melanoma [12], suggesting that regression may be

immunologically mediated. The prognos tic significance of mela-

noma regression, however, remains obscure as metastasis still

occurs in these patients [13, 14]. Melanoma regression could often

escape detection and hence may be more common than is

reported. It is also likely that within a regressing lesion individual

tumor cells progress and change their tumor antigens so they

cannot be recognized by the ongoing immune response. These

cells may therefore survive regression and form metastases. BCCs

also spontaneously regress, although this subject has undergone

even less study than melanoma regression. BCCs are more

numerous in immunosuppressed patients [15], and regressing

BCCs are infiltrated with large numbers of inflammatory cells

[16], suggesting that the i mmune response may play a role in

regression of BCCs.

Keratoacantho ma is another example of a regressing human

skin tumor. KAs can be compared with squ amous cell carcinomas

SCCs), which generally run a progressive course that leads

Clnical data


89/110

i l i l i

ill l i l i li l i l i illi

l li li i i l i il i l i

li i i i i li i li i i l i i l i l i

i i i l i i i ill l i i

i li i i I l li i l i l

li i l li i l i ili I i i i i li i l i ili

l l i i i l i i

li i l l i li i i l i l

Good et al. Genome Biology 2014, 15:438Organizing knowledge to enable personalization of medicine in cancer

Tissue

Increase value

AP report

Clinical decision

;!


90/110

LESO E CONDIO PRE"

MALIGNA

Precursores clnicos


91/110

provavelmente

todas as neoplasias desenvolvem"se apartir" condio e leso pr"maligna"

neoplasias benignas " outras


92/110

leso pr&malignacondio pr&maligna


93/110

condio pr&maligna

condio pr"maligna uma doenaque condiciona risco aumentado dedesenvolvimento de uma neoplasiamaligna

uma condio pr"maligna umantecedente ou um precursor temporal

de neoplasia maligna


94/110

condio pr&maligna

no"hereditria" hiperplasia do endomtrio" colite ulcerosa

"

metaplasia pavimentosa do brnquio " metaplasia de Barrett" cirrose heptica" gastrite atrfica


95/110

condio pr&maligna

hereditria" PAF "polipose adenomatosa familiar

#APC$" HNPCC "sndrome de Lynch" MEN "neoplasia endcrina mltipla


96/110

condio pr&maligna

RISCO aumentado dedesenvolvimento de neoplasiamaligna


97/110

leso pr&maligna

leso pr"maligna uma leso oualterao histolgica que antecede odesenvolvimento de uma neoplasiamaligna = DISPLASIA

a leso pr"maligna o antecedentelocal ou o precursor lesional de

malignidade


98/110

condio =precursor temporal

leso = precursor lesional


99/110

colite ulcerosa

Doena inflamatria crnicaintestinal

Processo inflamatrio recurrente, de etiopatogenia

desconhecida, limitado ao clon e recto commanifestaes extra&intestinais

Homem 44


100/110

Homem, 44anos

Episdios dediarreia commuco esangue

Desconfortoabdominal


101/110


102/110

Inflamao activa

Inflamao quiescente


103/110

durao da doena" < 10 anos #


104/110

leso pr&maligna

displasia


105/110

displasia

termo impreciso mas PRTICO alteraes celulares muito irregulares que

ultrapassam a hiperplasia mas ainda no

so suficientes para serem chamadas deneoplasia

nos epitlios, h um grau de displasia quese mistura com o carcinomain situ


106/110

CONDIO PR"MALIGNA

LESO PR"MALIGNA

NEOPLASIA INVASIVA

#METAPLASIA DE BARRETT$

#DISPLASIA EM METAPLASIA DE BARRETT$

#ADENOCARCINOMA$


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NEOPLASIAS BENIGNAS


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OUTRAS LESES


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outras

restos embrionrios" rim" maxilar

leses inflamatrias crnicas"lceras crnicas da pele " osteomielite e fistulizao


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35AF e 36AF Avaliacao Prognostica-copia 2

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Transcript of 35AF e 36AF Avaliacao Prognostica-copia 2