PATOLOGI NEOPLASMA

SISTEM DIGESTIF,
HEPATOBILIER & PANKREAS

dr. Hermawan Istiadi, M.Si.Med

Bagian Patologi Anatomi FK UNDIP
085740148700
hermawanistiadi@yahoo.com
 CONTENT
1. Patologi Neoplasma Rongga Mulut
2. Patologi Neoplasma Kelenjar Saliva
3. Patologi Neoplasma Esofagus
4. Patologi Neoplasma Gaster
5. Patologi Neoplasma Hepatobilier
6. Patologi Pankreas
 SASARAN BELAJAR
Mahasiswa mampu :
• Menjelaskan asal sel dan sifat dari tumor pada sistema
digestif, hepatobilier dan pankreas
• Menjelaskan faktor resiko keganasan pada sistema digestif,
hepatobilier dan pankreas
• Menjelaskan gambaran klinis dari tumor pada sistema
digestif, hepatobilier dan pankreas
• Menjelaskan gambaran patologis dari tumor pada sistema
digestif, hepatobilier dan pankreas
 PATOLOGI NEOPLASMA
RONGGA MULUT

dr. Hermawan Istiadi, M.Si.Med

Bagian Patologi Anatomi FK UNDIP
085740148700
hermawanistiadi@yahoo.com
 Neoplasma Jinak
Fibroma
• Localized
proliferation of
fibrous
connective tissue
in response to
tissue irritation

• Painless and asymptomatic

• Submucosal nodules with limited growth
potential
 Neoplasma Jinak
Fibroma

Densely fibroblasts in a collagen-rich stroma

 Neoplasma Jinak
Squamous Papilloma
• Painless and
asymptomatic
• Warty
exophytic
growth
• Low Malignant
potential

• Exophytic warty proliferation of the squamous epithelium driven by

HPV serotypes 6 and 11
• Including Verruca and condyloma
Neoplasma Jinak
Squamous Papilloma
 Tumor & Lesi Pre-Kanker
Leukoplakia
Penebalan epidermis /
hiperkeratosis

Faktor resiko :
Tembakau, Iritasi konik,
alkoholik, makanan
iritan, infeksi HPV

Plak putih, tak dapat

dilepaskan dari dasarnya,
tak berhubungan dengan
penyakit tertentu 3 – 25% menjadi squamous
cell carcinoma
Tumor & Lesi Pre-Kanker
Leukoplakia

Penebalan epidermis / hiperkeratosis

s/d Displasia Berat
 Tumor & Lesi Pre-Kanker
Erythroplakia
• Plak merah, dapat
meninggi atau
tidak
• Tak dapat dilepas
dari dasarnya.

Displasia Berat – Ca.Insitu – Minimally invasive

Carcinoma
 Tumor & Lesi Pre-Kanker
Erythroplakia

Displasia Berat – Ca.Insitu – Minimally invasive

Carcinoma
 Karsinoma Sel Skuamus
Prevalensi : > 50 th Faktor resiko :
Lokasi : • Paparan UV
Lidah, faring, • Leukoplakia, erythroplakia
bibir, dasar mulut • Perokok
• Infeksi HPV 16/18
• Alkoholik
• Iritasi kronik
Prognosis : 5 years survival rates
:
90% (Stadium awal), 40%
(Stadium lanjut tanpa Gejala : Nyeri lokal,
metastasis), < 20% (dengan disfagia, ulserasi
metastasis)
 Karsinoma Sel Skuamus

• Lesi awal : plak (penebalan) Penyebaran :

berwarna putih-abu ▪ Mulut : Submandible node
• Lesi lanjut : Eksofitik, – cervival node
endofitik, ulseratif ▪ Lidah : cervical nood
 Karsinoma Sel Skuamus
Numerous nests and islands of malignant keratinocytes with keratin pearl, invading
the underlying connective tissue stroma and skeletal muscle
 Odontogenic Cysts and Tumors
Kista Odontogenik
Klasifikasi Kista Odontogenik
1. Inflmmatory
a. Periapical Cyst
b. Residual cyst
c. Paradental cyst
2. Developmental
a. Dentigerous Cyst
b. Odontogenic keratocyst
c. Gingival cyst
d. Adult Eruption cyst
e. Lateral periodontal cyst
Odontogenic Cysts and Tumors
Periapical (Radicular) Cyst
• Etiologi :
Inflamasi kronis
(ex : pulpitis
kronis)
• Lokasi : Apex
gigi -->
Periapical Abses
--> Jaringan
granulasi di apex
gigi --> kista
 Odontogenic Cysts and Tumors
Periapical (Radicular) Cyst
Kista Dilapisi Epitel Skuamous kompleks
 Odontogenic Cysts and Tumors
Dentigerous Cyst

• Lokasi : Korona gigi yang impaksi (ex : impaksi gigi molar 3)

• Lesi Unilokuler, dibatasi epitel skuamus
 Odontogenic Cysts and Tumors
Dentigerous Cyst

Kista dilapisi epitel Kuboid hingga kolumner

 Odontogenic Cysts and Tumors
Tumor Odontogenik
1. Ameloblastoma

Most common benign epithelial odontogenic tumor, which is slow

growing, but locally aggressive, persistent, and frequently recurrent,
80% in mandible, Uni/Multicystic
 Odontogenic Cysts and Tumors
Tumor Odontogenik
1. Ameloblastoma

Follicular pattern with peripheral columnar cells / pallisading

 Odontogenic Cysts and Tumors
Tumor Odontogenik
2. Odontoma

A tumor-like malformation (hamartoma) composed of enamel, dentin,

pulpal tissue, and cementum – Solid Tumor
 PATOLOGI NEOPLASMA
KELENJAR SALIVA

dr. Hermawan Istiadi, M.Si.Med

Bagian Patologi Anatomi FK UNDIP
085740148700
hermawanistiadi@yahoo.com
 TUMOR KELENJAR SALIVA
• Lokasi : 80% pada Parotis
• Age : 60 -70 th
• Pada Kel.Parotis : 70-80% Tumor jinak (pleomorphic
adenoma & Warthin tumor)
• Tumor Ganas : mucoepidermoid carcinoma (15% pada
parotis, 40% pada submandibula)
• Faktor risiko : radiasi, kemoterapi, virusEBV, familial.
TUMOR KELENJAR SALIVA
Pleomorphic Salivary Adenoma
• A benign neoplasm composed
of : ductal epithelial cells and
myoepithelial cells set within
a mesenchymal stroma
• > 90% salivary gland
neoplasm, all age.
• Asymptomatic, slowly
growing mass
• Well-circumscribed,
encapsulated
 Pleomorphic Salivary Adenoma

• Epithelial glandular ductal structures

• Myoepithelial cells
• Mesenchymal stroma either myxoid, mucochondroid, osseous, Fat
 Warthin Tumor
• Second most
common
salivary gland
tumor
• Asymptomatic,
slowly growing
mass, all age
• Multicystic,
well
circumscribed

Synonim: Papillary Cystadenoma Lymphomatosum /

Cystadenolymphoma
 Warthin Tumor

Dindingnya berbentuk papillary → stroma limfoid yang

dibatasi oleh 2 lapis sel kolumner
 Mucoepidermoid Carcinoma

• Most common malignant salivary gland tumor

• 60% in major salivary glands (parotid usually)
• Painless, fixed, slowly growing swelling, otorrhea, dysphagia, and
trismus
 Mucoepidermoid Carcinoma

Consists of Malignant mucous cell, intermediate cell, and

epidermoid/squomoid cells
 PATOLOGI NEOPLASMA
ESOFAGUS

dr. Hermawan Istiadi, M.Si.Med

Bagian Patologi Anatomi FK UNDIP
085740148700
hermawanistiadi@yahoo.com
 BARRETT’s ESOPHAGUS

Metaplasia Kolumner (Skuamus →

Kolumner)
BARRETT’s ESOPHAGUS
 BARRETT’s ESOPHAGUS

Prolonged
Inflamasi /
Gastroesophageal Re-epitelisasi
ulserasi
Reflux

Epitel Metaplasia Diferensiasi

Kolumner kolumner Sel
Bergoblet
Komplikasi :
1. Ulserasi
Tahan terhadap Asam
2. Striktur
Lambung
3. Adenokarsinoma
(30-100X)
BARRETT’s ESOPHAGUS
Barrett’s esophagus with dysplasia
 KARSINOMA ESOFAGUS

PREVALENSI Karsinoma Sel Skuamus (90%)

FAKTOR RESIKO :
• Penyakit Esofagus
(Akalasia, Esofagitis,
plummer vinson syndrome)
• Alkoholik
• Perokok berat
Adenokarsinoma (10%)
• Defisiensi vitamin &
FAKTOR RESIKO : mineral
• Barrett’s Esofagus • Kontaminasi jamur dalam
makanan
• Intake nitrosamin tinggi
KARSINOMA ESOFAGUS
Adenokarsinoma

Karsinoma sel
Displasia
skuamus
 KARSINOMA ESOFAGUS
Squamous Cell Carcinoma

• 20% pada 1/3 atas, 50% pada 1/3 tengah, 30% pada 1/3 bawah
• Stadium awal : seperti plak penebalan mukosa, kecil, abu-putih
• Stadium lanjut : (1) masa polypoid (2) nekrosis & ulserasi (3)
infiltratif difus
KARSINOMA ESOFAGUS
Squamous Cell Carcinoma
 ESOPHAGEAL CARCINOMA
Adenocarcinoma

• Lokasi umumnya 1/3 distal & dapat menginvasi cardia gaster

• Masa noduler besar/ ulseratif/ infiltratif difus
• DD/ : Gastric Cardiac Adenocarcinoma
• If Barrett esophagus is detected, cancers at esophagogastricjunction
are labeled as esophageal cancers (IHC : TTF1)
• If bulk of neoplasm is in stomach, lesion is regarded as gastric cancer.
ESOPHAGEAL CARCINOMA
Adenocarcinoma
44
 PATOLOGI NEOPLASMA
GASTER

dr. Hermawan Istiadi, M.Si.Med

Bagian Patologi Anatomi FK UNDIP
085740148700
hermawanistiadi@yahoo.com
46
 TUMOR JINAK GASTER
HYPERPLASTIC POLYP
• 50 - 60 th, 2nd most common Gastric polyp
• 25-75% associated w/ HP
• Dapat mengecil setelah bacterial eradication
• Ukuran >1.5 cm - reseksi – Resiko dysplasia
• Lokasi : Antrum > corpus
• Gejala : = chronic gastritis
• Malignant potential <2%

Tumor Jinak Gaster

 TUMOR JINAK GASTER

Hyperplastic Polyp
• Marked elongation of pits
• Branching and cystic
dilatation of foveolae
• Edematous lamina propria
with mixed inflammatory
infiltrate
• Adjacent Mucosa : Chronic
Gastritis

Tumor Jinak Gaster

 TUMOR JINAK GASTER
Fundic gland polyps
• Most common type of gastric polyp
• Solitary or multiple polypoid lesions
• Limited to body/fundus
• Patient mean age is 50-60 years
• May be sporadic or familial
• Berhubungan dengan Familial Adenomatosus Polip (FAP)
• Berhubungan dengan terapi PPI – Pertumbuhan kelenjar
• Gejala : nausea, vomiting, epigastric pain

Tumor Jinak Gaster

 TUMOR JINAK GASTER
Fundic gland polyps
• Cystically dilated
glands – oxyntic gland
• Stroma minimal
• Adjacent mucosa
normal

Tumor Jinak Gaster

 TUMOR JINAK GASTER
ADENOMA / DYSPLASIA GASTER
• Noninvasive, neoplastic gastric epithelium / Polypoid gastric
dysplasia
• Etiology : HP gastritis with intestinal metaplasia / Fundic gland
polyps / hyperplastic polyps / Familial adenomatous polyposis /
Peutz-Jeghers / juvenile polyposis
• 50 - 60 th
• 30% menjadi Adenokarsinoma
• Lokasi : Antrum > Corpus
• Gejala : = chronic gastritis

Tumor Jinak Gaster

 TUMOR JINAK GASTER

ADENOMA
Tumor – Low Grade Dysplasia
Jinak Gaster
 TUMOR JINAK GASTER
ADENOMA – High Grade
Dysplasia
• Severe architectural
alterations &marked
nuclear atypia.
• Note irregular nuclei,
nuclear overlapping and
stratification

Tumor Jinak Gaster

 ADENOKARSINOMA GASTER
Intestinal Type Diffuse Type
• Gastritis kronis → • Tidak berhubungan
metaplasia intestinal dengan Gastritis
• Differensiasi baik kronis
• Lebih sering • Differensiasi buruk
• > 50 thn • Lebih jarang
• < 50 thn

• Lokasi : pylorus and antrum (50-60%); cardia (25%)

• Stadium awal : terbatas pada mukosa and submukosa,
• Stadium Lanjut : menyebar lebih dalam dan luas.
54
Adenokarsinoma Gaster
 ADENOKARSINOMA GASTER
Intestinal Type Diffuse Type
• Infeksi H pylori • Tidak berhubungan
• Intake nitrosamin >> dengan infeksi H
• Intake buah/sayur << pylori
• Anemia perniciosa

Tipe Morfologi : Gejala klinik :

1. Exofitik / fungating 1. Cachexia, Anemia
2. Endofitik / flat 2. Abdominal discomfort,
3. Exkavasi 3. Disfagia
55
Adenokarsinoma Gaster
Endoscopic
Classification
Early Gastric
Cancer
• I : Protruded
• II.Superficial
• IIa :elevated type
• IIb : flat type
• IIc :mimics
benign ulcer
• III : Excavated

56
 ADENOKARSINOMA GASTER
Intestinal Type
• Infeksi H pylori
• Intake nitrosamin >>
• Intake buah/sayur <<
• Anemia perniciosa

Struktur tubulo-papillary; epitel kolumner mensekresi musin

 ADENOKARSINOMA GASTER
Diffuse Type
• Tidak berhubungan
dengan infeksi H
pylori

Signet ring cell Carcinoma; Linitis Plastica

 ADENOKARSINOMA GASTER
• Age : 5th decade
• M:F 2:1
• Prognosis
– Early adenocarcinomas have (T1) good prognosis
– > 90% survival at 5 years for mucosal tumors & 80% for
submucosal tumors
– T2: 65%
– T3: 35%
– T4: 16%
ADENOKARSINOMA GASTER
ADENOKARSINOMA GASTER
 LIMFOMA PADA GASTER

Limfoma Gaster
• Mucosa-associated lymphoid tissue
(MALT) lymphoma
• Most gastric MALT lymphomas
associated with gastritis caused by
Helicobacter pyloriinfection
• GI tract is the most common site of
MALT lymphoma
• 85% of all GI MALT lymphomas
occur in stomach
• Gejala : dyspepsia, epigastric pain,
Hematemesis, melena, weight loss
 NEUROENDOCRINE TUMOR

• Definition : Neuroendocrine neoplasms arising from

enterochromaffin-like (ECL) cells / neuroendocrine cell / kulchitsky
cell
• GI is the largest endocrine system in the body)
NEUROENDOCRINE TUMOR
0,3% all gastric neoplasm
Carcinoid syndrome :
- Gastrin
- ACTH
- Serotonin
- Histamin
65
 NEUROENDOCRINE TUMOR

NET NET NEC

66
 Contoh Kasus
Seorang Pria 50 tahun, mengeluh lemah, letih, lesu, sulit menelan.
Pasien juga mengeluh nyeri ulu hati, yang sudah dirasakannya sejak 5
bulan terakhir dan sering mendapat pengobatan dokter. Berat badan
turun 10 Kg dalam 3 bulan tanpa sebab yang jelas. Hasil pemeriksaan
biopsi melalui endoskopi, didapatkan struktur tubulo-papillary;
dilapisi epitel kolumner mensekresi musin, dengan inti pleiomorfik,
mitosis abnormal (+). Apakah Diagnosisnya?
A. Polip hiperplastik
B. Fundic Gland Polyp
C. Adenoma Gaster
D. Adenokarsinoma tipe intestinal
E. Adenokarsinoma tipe difus

67
 PATOLOGI NEOPLASMA
HEPATOBILIER

dr. Hermawan Istiadi, M.Si.Med

Bagian Patologi Anatomi FK UNDIP
085740148700
hermawanistiadi@yahoo.com
 PATOLOGI TUMOR HEPAR
1. Tumor Jinak
a. Hemangioma
b. Adenoma hepatoselulare
c. Fokal nodular hiperplasia
2. Tumor Ganas Primer
a. Karsinoma hepatoselulare
b. Cholangiokarsinoma
3. Tumor Ganas Sekunder
(Metastasis, Terutama colon)

Patologi Tumor Hepar

 PATOLOGI TUMOR HEPAR
1. Tumor Jinak
a. Hemangioma
b. Adenoma hepatoselulare
c. Fokal nodular hiperplasia

Patologi Tumor Hepar

 PATOLOGI TUMOR HEPAR
1. Tumor Jinak
a. Hemangioma
b. Adenoma hepatoselulare
c. Fokal nodular hiperplasia

Hemangioma 
Blood-filled vascular
channels separated by
dense fibrous stroma

Patologi Tumor Hepar

 PATOLOGI TUMOR HEPAR
1. Tumor Jinak
a. Hemangioma
b. Adenoma hepatoselulare
c. Fokal nodular hiperplasia
Gejala :
• Abdominal pain (rapid growth – menekan kapsul hepar /
nekrosis krn penurunan suplai darah)
• Ruptur adenomas – perdarahan intraabdomen - emergency
• Resiko transformasi maligna
Faktor Resiko :
• Kontrasepsi oral dan anabolic steroids

Patologi Tumor Hepar

 PATOLOGI TUMOR HEPAR
1. Tumor Jinak
a. Hemangioma
b. Adenoma hepatoselulare
c. Fokal nodular hiperplasia

Patologi Tumor Hepar

 PATOLOGI TUMOR HEPAR
1. Tumor Jinak
a. Hemangioma
b. Adenoma hepatoselulare
c. Fokal nodular hiperplasia
• Soliter / multiple nodul hiperplastik dari hepatosit,
Pada hepar nonsirosis
• Young to Middle-aged
lobulated contours and a
central stellate scar, broad
fibrous scar, chronic
inflammation present within
parenchyma
Patologi Tumor Hepar
 PATOLOGI TUMOR HEPAR
2. Tumor Ganas Primer
a. Karsinoma hepatoselulare (Hepatoma)
b. Cholangiokarsinoma

Patologi Tumor Hepar

 PATOLOGI TUMOR HEPAR
2. Tumor Ganas Primer
a. Karsinoma hepatoselulare (Hepatoma)
b. Cholangiokarsinoma
Faktor resiko :
• Penyakit Hepar
Kronik, Sirosis
Hepatis, fatty liver,
metabolic disease
• HBV, HCV and toxic
injuries (aflatoxin,
alcohol)

Patologi Tumor Hepar

 PATOLOGI TUMOR HEPAR
2. Tumor Ganas Primer
a. Karsinoma hepatoselulare (Hepatoma)
b. Cholangiokarsinoma
Gejala dan Tanda :
• Gejala PHK
• Upper abdomi nal pain,
malaise, fatigue, weight
loss, hepatomegaly,
abdominal mass or fullness
• Serum α-fetoprotein >>,
USG, CT, MRI
• Metastasizes to the lungs
Patologi Tumor Hepar
 PATOLOGI TUMOR HEPAR
2. Tumor Ganas Primer
a. Karsinoma hepatoselulare (Hepatoma)
b. Cholangiokarsinoma
Penyabab Kematian pasien :
• Cachexia
• Ruptur varises esofagus
• Liver failure - hepatic coma
• Ruptur tumor - fatal bleeding
Mayoritas : meninggal setelah 2
tahun didiagnosis

Patologi Tumor Hepar

 PATOLOGI TUMOR HEPAR
2. Tumor Ganas Primer
a. Karsinoma hepatoselulare (Hepatoma)
b. Cholangiokarsinoma

Malignancy of the biliary tree

(Intrahepatik / ekstrahepatik)
Risk factor :
• Chronic inflammation
• Cholestasis
• Clonorchis sinensis

Patologi Tumor Hepar

 PATOLOGI TUMOR HEPAR
2. Tumor Ganas Primer
a. Karsinoma hepatoselulare (Hepatoma)
b. Cholangiokarsinoma

• 50-60% : Perihilar (Klatskin

tumor)
• 20-30% : distal tumor
(common bile duct)

Gejala :
• Biliary obstruction
• Cholangitis
• Right upper quadrant pain /
Fullness
 PATOLOGI SALURAN EMPEDU - Tumor
Tumor pada Kandung empedu :
1. Tumor Jinak
Adenoma, papilloma (tunggal / multipel)
2. Tumor Ganas
Karsinoma kandung empedu(Adenokarsinoma)
Faktor Resiko : gallstones (95% of cases)
Gejala : Ikterus obstruktivus & pembesaran kandung empedu

Tumor Saluran Empedu

82
 A 41-year-old, previously healthy woman has noted abdominal
discomfort for the past month. On physical examination, she is afebrile.
Her stool does not have occult blood. Laboratory studies show normal
serum total protein, albumin, AST, ALT, and bilirubin, but her alkaline
phosphatase is elevated. Serologic testing for hepatitis A, B, and C
viruses is negative. Abdominal CT scan shows a 9-cm right hepatic lobe
mass with irregular borders. The lesion is resected and grossly has a
central stellate scar with radiating fibrous septa that merge into
surrounding hepatic parenchyma. On microscopic examination, the
mass has prominent arteries in dense connective tissue along with
lymphocytic infiltrates and bile duct proliferation. What is the most
likely diagnosis?
 (A) Cholangiocarcinoma
 (B) Focal nodular hyperplasia
 (C) Hepatic adenoma
 (D) Hepatocellular carcinoma
 (E) Macronodular cirrhosis 83
A 61-year-old man has had ascites for the past year. After
paracentesis with removal of 1 L of slightly cloudy,
serosanguineous fluid, physical examination shows a firm,
nodular liver. Laboratory findings are positive for serum HBsAg
and anti-HBc. He has a markedly elevated serum α-fetoprotein
level. Which of the following hepatic lesions is most likely to be
present?
 (A) Hepatocellular carcinoma
 (B) Massive hepatocyte necrosis
 (C) Marked steatosis
 (D) Wilson disease
 (E) Autoimmune hepatitis

84
 PATOLOGI PANKREAS

dr. Hermawan Istiadi, M.Si.Med

Bagian Patologi Anatomi FK UNDIP
085740148700
hermawanistiadi@yahoo.com
 PHYSIOLOGY OF PANCREAS
Normal Protection Mechanisms :
• Most digestive enzymes are synthesized as inactive
proenzymes (zymogens)
• Most proenzymes are activated by trypsin (activated by
duodenal enteropeptidase (enterokinase))
• Acinar and ductal cells secrete trypsin inhibitors - limit
intrapancreatic trypsin activity

PANCREATITI
S
 ACUTE PANCREATITIS
• Reversible pancreatic parenchymal injury associated with
inflammation
• Etiologies : toxic (e.g., alcohol) & Biliary tract disease - 65%,
pancreatic duct obstruction (e.g., biliary calculi) - 60%,
inherited genetic defects, vascular injury, and infections
• Other Triggers : Metabolic disorders, Genetic, Medications
(Furosemide, azathioprine) , Traumatic injury, Ischemic injury
, Infections (Mumps)
• Clinical Features : include acute abdominal pain (referred to
the upper back – left shoulder), systemic inflammatory
response syndrome, and elevated serum lipase and amylase
levels
• Sequelae : pancreatic abscess and pancreatic pseudocyst
 Acinar cell Injury

Interstitial inflammation and edema + Proteolysis + Fat Necrosis + Vessel Damage, Hemorhage

ACUTE
PANCREATITIS
 ACUTE PANCREATITIS

fat necrosis and focal pancreatic parenchymal necrosis

ACUTE PANCREATITIS
 CHRONIC PANCREATITIS
• Prolonged inflammation of the pancreas - irreversible
destruction of exocrine parenchyma, fibrosis, in the late
Stages : destruction of endocrine parenchyma
• Etiology : Alcohol abuse, Long-standing obstruction, Repeated
bouts of acute pancreatitis, Autoimmune, Hereditary
• Clinical features : Abdominal pain, intestinal malabsorption,
and diabetes, 10% develop Pancreatic pseudocysts
CHRONIC PANCREATITIS
CHRONIC PANCREATITIS

Extensive fibrosis and atrophy

 PSEUDOCYSTS

localized collections of necrotic and hemorrhagic material that are rich in pancreatic
enzymes and lack an epithelial lining
 CARCINOMA PANCREAS
• Cigarette smoking is the leading preventable cause of
pancreatic cancer.
• Mostly : ductal adenocarcinomas
• Clinical Features : Pain, Obstructive jaundice, Weight loss,
anorexia, and generalized malaise, weakness, Migratory
thrombophlebitis (Trousseau sign), Elevated carcinoembryonic
antigen and CA19-9 antigen, 70% DM
• Prognosis :
– Ductal Ca : 3-5 Months if untreated, 10-20 months after
resection
– NEC : 1-12 months after treatment
 CARCINOMA PANCREAS

Moderately to poorly differentiated adenocarcinoma forming abortive

tubular structures or cell clusters and showing aggressive, deeply infiltrative growth
pattern
SELAMAT BELAJAR