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Saluran cerna/gastrointestinal (GI) tract
merupakan saluran yg dimulai dari
rongga mulut sampai ke anus, yg tda
segmen2 yg berbeda scr anatomi……
esofagus, gaster, usus halus, colon,
rectum, dan anus.

Secara klinis, Tumor/Neoplasia GI tract:
 benign
 malignant

Asal Tumor:
 Epitel >>>
 Otot polos dan sel stromal lainnya
 MALT (Mucosa-Associated Lymphoid
Lesi Premalignant
leukoplakia refers to a whitish, well-
defined mucosal patch or plaque caused by
epidermal thickening or hyperkeratosis.
WHO, leukoplakia is a white patch or
plaque that can not be scraped off and
cannot be characterized as any other

- older men.
- on the vermilion border of the lower
lip, buccal mucosa, the hard and soft palates.
- less frequently on the floor of the mouth and
other intraoral sites.
- localized, sometimes multifocal or even diffuse,
smooth or roughened, leathery, white, discrete
areas of mucosal thickening.
- microscopic: vary from banal hyperkeratosis
without underlying epithelial dysplasia to mild
to severe dysplasia bordering on carcinoma in

- Only histologic evaluation distinguishes
these lesions.
- Unknown cause
- Strong association with the use of tobacco,
particularly pipe smoking and smokeless
tobacco (pouches, snuff, chewing).
- More recently, HPV antigen has been
identified in some tobacco-related
lesions, raising the possibility that the
virus and tobacco act in concert in the
induction of these lesions.

- Oral leukoplakia is an important finding
because 3% to 25% (depending
somewhat on location) undergo
transformation to squamous cell

 Erythroplakia refers to red, velvety, often
granular, circumscribed areas that may
or may not be elevated, having poorly
defined, irregular boundaries.
Histologically, erythroplakia almost
invariably reveals marked epithelial
dysplasia (the malignant transformation
rate is >50%), so recognition of this
lesion becomes even more important
than identification of oral leukoplakia.
Figure:A, Leukoplakia of the tongue in a smoker.
Microscopically, this lesion showed severe dysplasia with
transformation to squamous cell carcinoma in the posterior
elevated portion (arrow). B, Leukoplakia with marked
epithelial thickening and hyperkeratosis.
Figure: Erythroplakia. A, Lesion of the maxillary
gingiva. B, Red lesion of the mandibular alveolar ridge.
Biopsy of both lesions revealed carcinoma in situ.

Figure : Clinical, histologic, and molecular progression of oral cancer. A,
The typical clinical progression of oral cancer. B, The histologic
progression of squamous epithelium from normal, to hyperkeratosis, to
mild/moderate dysplasia, to severe dysplasia, to cancer. C, The sites of the
most common genetic alterations identified as important for cancer
 SCC >>>
 3% dari semua kanker di US
 Sering usia >40 th
 Klinis: nyeri atau sulit mengunyah, relatif
asimptomatik sehingga sering diabaikan
 saat ditemukan sudah bermetastasis.
 Bila ditemukan pada stadium awal, 5-year
survival rate bisa >90%.
 80% pada kelj parotis.
 Laki-laki ≈ Perempuan.
 Usia pada dekade 6 atau 7.
 Benign: parotis 70% - 80%, kelj submaksila
 Benign parotis: > pleomorphic adenoma
(tumor campur yg berasal dari kelj liur), yg
agak jarang: papillary cystadenoma
lymphomatosum (Warthin tumor).
 Malignant kelj liur yg sering:
mucoepidermoid carcinoma, terutama di
 Pleomorphic Adenoma (Mixed Tumor of
Salivary Glands)
- >90%
- slow-growing, well-demarcated, encapsulated
lesion, rarely > 6 cm in greatest dimension.
- arising in the superficial parotid, painless
- despite the tumor's encapsulation, histologic
examination often reveals multiple sites where
the tumor penetrates the capsule. Adequate
margins of resection are thus necessary to
prevent recurrences. On average, about 10% of
excisions are followed by recurrence.
 Warthin Tumor (Papillary Cystadenoma
Lymphomatosum, Cystadenolymphoma)
- parotid gland.
- arise from heterotopic salivary tissue
trapped within a regional lymph node
during embryogenesis.
- small, well-encapsulated, round to ovoid
mass that on transection often reveals
mucin-containing cleftlike or cystic spaces
within a soft gray background.

- Microscopically, 2 characteristic features:
(1) two-tiered epithelial layer lining the
branching, cystic, or cleftlike spaces.
(2) an immediately subjacent, well-
developed lymphoid tissue sometimes
forming germinal centers.
- Recurrence rate:10% is attributed to
incomplete excision, multicentricity, or a
second primary tumor.
- Malignant transformation is rare; about half
of reported cases have had prior radiation
Figure: Warthin tumor. A, Low-power view
showing epithelial and lymphoid elements.
Note the follicular germinal center beneath the
epithelium. B, Cystic spaces separate lobules
of neoplastic epithelium consisting of a double
layer of eosinophilic epithelial cells based on a
reactive lymphoid stroma. 23
 Mucoepidermoid carcinoma
- terutama pd kelj liur mayor
- mucus-secreting cells, cells showing
squamous differentiation
 Adenoid cystic carcinoma
- terutama pd kelj liur minor
- cendrung menginvasi selubung saraf/
perineural spread
- small epithelial cells arrange in
islands showing micocystic change
Figure: A, Mucoepidermoid carcinoma showing islands
having squamous cells as well as clear cells containing
mucin. B, Mucicarmine stains the mucin reddish-pink.

Figure. Adenoid cystic carcinoma in a salivary gland. A,
Low-power view. The tumor cells have created a cribriform
pattern enclosing secretions. B, Perineural invasion by

- The replacement of the normal distal stratified
squamous mucosa by metaplastic columnar
epithelium containing goblet cells.
- A complication of long-standing
gastroesophageal reflux, occurring in as many
as 5% to 15% of persons with persistent
symptomatic reflux disease.
- male : female = 4:1
- > whites race

- Prolonged and recurrent gastroesophageal
reflux  inflammation, ulceration of the
squamous epithelial lining  healing occurs
by ingrowth of progenitor cells and re-
- In the microenvironment of an abnormally low
pH in the distal esophagus caused by acid
reflux, the cells differentiate into columnar
Metaplastic columnar epithelium is thought to
be more resistant to injury from refluxing
gastric contents

- Complication : ulcer and stricture.
- The risk for the development of
- Persons with Barrett esophagus have a
30- to 100-fold greater risk of
developing esophageal
adenocarcinoma than do normal
populations, the greatest risk being
associated with high-grade dysplasia.
Figure. Barrett esophagus. A, B, Gross view of distal esophagus (top)
and proximal stomach (bottom), showing A, the normal
gastroesophageal junction (arrow) and B, the granular zone of Barrett
esophagus (arrow). C, Endoscopic view of Barrett esophagus showing
red velvety GI mucosa extending from the gastroesophageal orifice.
Note the paler squamous esophageal mucosa.

Figure. Barrett esophagus. Microscopic view showing squamous mucosa
and intestinal-type columnar epithelial cells (goblet cells) in a glandular
 Intramural or submocosa:
- leiomyoma, fibroma, lipoma,
hemangioma, neurofibroma,
 Mucosal:
- Squamous papilloma,
fibrovascular polyp, inflamatory

 Squamous cell carcinoma
- Worldwide: 90% of esophageal cancers,
- More common in blacks
- Men > Women
- > 50 years old

- Morphology : epithelial dysplasia 
carcinoma in situ  invasive cancer.
Early: small, gray-white, plaquelike
thickenings or elevations of the mucosa.
In months to years,
(1) polypoid exophytic masses
(2) ulcerations
(3) diffuse infiltrative neoplasms
Whichever the pattern, about 20% arise
in the cervical and upper thoracic
esophagus, 50% in the middle third, and
30% in the lower third.
 Adenocarcinoma
- Associated with Barrett esophagus
- More common in whites
- Men > Women
- > 40 years old

- Morphology:
* arise from dysplastic mucosa in the setting
of Barrett esophagus.
* distal 1/3 of the esophagus and may invade
the subjacent gastric cardia.
* Initially appearing as flat or raised patches
on an otherwise intact mucosa  large
nodular masses or show deeply
ulcerative or diffusely infiltrative
- Micr: mucin-producing glandular tumors
showing intestinal-type features, in keeping
with the morphology of the preexisting
metaplastic mucosa.
 Clinical features
• Insidious in onset and produces dysphagia and
obstruction gradually and late
• Weight loss, anorexia, fatigue, and weakness
appear, followed by pain, usually related to
• Diagnosis is usually made by imaging
techniques and endoscopic biopsy

 Tumor yg berasal dari mukosa >>
 Tumor yg berasal dari mukosa
diklasifikasikan pada polip dan

 Gastric Polyps
- polyp: any nodule or mass that projects
above the level of the surrounding
- generally restricted to mass lesions
arising in the mucosa
- uncommon as compared with colonic

- (1) hyperplastic polyps (80% to 85%),
arise from an exuberant reparative
response to chronic mucosal damage and
hence are composed of a hyperplastic
mucosal epithelium and an inflamed
edematous stroma. They are not true

Gastric hyperplastic polyp. Low-power microscopic view of the
polyp showing hyperplastic foveolar epithelium and inflammation.
- (2) fundic gland polyps (∼10%),
are small collections of dilated corpus-
type glands thought to be small
- (3) adenomatous polyps (∼5%).
an adenomatous polyp harboring

 Gastric Carcinoma
- the second leading cause of cancer-
related deaths in the world
- Japan and South Korea have the highest
- a favored location is the lesser
curvature of the antropyloric region
- two morphologic types:
intestinal and diffuse
- The intestinal type:
 arise from gastric mucous cells 
intestinal metaplasia in the setting of
chronic gastritis.
 tends to be better differentiated
 more common type in high-risk
 occurs primarily after age 50 years
with a 2 : 1 male predominance,
- The diffuse variant:
 arise de novo from native gastric
mucous cells,
 is not associated with chronic gastritis,
 tends to be poorly differentiated.
 occurs at an earlier age with female

 Chronic inflammation induced by H.
pylori may release reactive oxygen
species, which eventually cause DNA
damage, leading to an imbalance
between cell proliferation and apoptosis,
particularly in areas of tissue repair

 Gastric carcinoma is classified on the
basis of depth of invasion, macroscopic
growth pattern, and histologic subtype.
 The morphologic feature having the
greatest impact on clinical outcome is the
depth of invasion.

 depth of invasion:
 Early gastric carcinoma: a lesion
confined to the mucosa and submucosa,
regardless of the presence or absence of
perigastric lymph node metastases.
 Advanced gastric carcinoma : a
neoplasm that has extended below the
submucosa into the muscular wall and
has perhaps spread more widely.
 macroscopic growth patterns:
(1) exophytic, with protrusion of a tumor
mass into the lumen;
(2) flat or depressed, in which there is no
obvious tumor mass within the mucosa;
(3) excavated, whereby a shallow or
deeply erosive crater is present in the
wall of the stomach.

Diagram of growth patterns and spread of gastric carcinoma. In early
gastric carcinoma (A), the tumor is confined to the mucosa and
submucosa and may exhibit an exophytic, flat or depressed, or
excavated conformation. Advanced gastric carcinoma (B) extends into
the muscularis propria and beyond. Linitis plastica is an extreme form
of flat or depressed advanced gastric carcinoma.
Gastric carcinoma. Gross photograph showing an ill-defined,
excavated central ulcer surrounded by irregular, heaped-up borders
 histologic appearances:
 The intestinal variant ... malignant cells
forming neoplastic intestinal glands
resembling those of colonic adenoca.
 The diffuse variant ...gastric-type mucous
cells that generally do not form glands but
rather permeate the mucosa and wall as
scattered individual "signet-ring" cells or
small clusters in an "infiltrative" growth
Krukenberg tumor (ovaries)

Gastric carcinoma. A, Intestinal type demonstrating
gland formation by malignant cells, which are
invading the muscular wall of the stomach. B,
Diffuse type demonstrating signet-ring carcinoma
cells. 57
 Less common gastric tumors
 MALT lymphoma (mucosa-associated
lymphoid tissue)
- 5% of gastric malignancy
- associated with H. Pylori infection
- AB treatment can induce tumor

Gastric MALT lymphoma. Note the lymphoepithelial lesions
(arrows). 59
 - a solid tumor of the gastric
submucosa or wall with
unpredictable malignant potential.
- epithelioid or spindle cells feature
- c-kit gene mutations (c-KIT is the
stem cell factor receptor)
- PDGF receptor α mutations
- both receptors have cytoplasmic
tyrosine kinases that activate
downstream signaling pathway
- responsive to TKI 60
Gastrointestinal stromal tumor. A, Gross photograph of the tumor arising from the
muscularis propria of the gastric wall. B, Microscopic view of the tumor showing
spindle cell feature. C, Immunohistochemical stain showing the tumor cell c-KIT
 >> colon
 Benign : epithelial,
25-50% of older adults

A polyp is a mass that protrudes into the
gut lumen; they may be pedunculated
(with a stalk) or sessile (without a stalk).
 They may be non-neoplastic or

 Non-neoplastic polyps
- result from abnormal mucosal maturation,
inflammation, or architecture.
- have no malignant potential.
- represent 90% of colonic epithelial

Hyperplastic polyps
- small (<5 mm in diameter), nipple-like,
hemispherical, smooth protrusions of the
- singly, multiple.
- anywhere in the colon, well over half are
found in the rectosigmoid region.
- histologically : crypts lined by well-diff
goblet or absorptive epithelial cells,
separated by a scant lamina propria.
 Although the vast majority of hyperplastic
polyps have no malignant potential, it is now
being recognized that some "hyperplastic
polyps," the so-called sessile serrated
adenomas, located on the right side of the
colon, may be precursors of colorectal
carcinomas. They may be solitary or
multiple ("hyperplastic polyposis"). These
polyps show microsatellite instability and
can give rise to colon cancers by the
mismatch repair pathway

Juvenile polyps
- focal, hamartomatous proliferations
- frequently in children < 5 years old but also
are found in adults of any age (retention
- usually large in children (1-3 cm
indiameter) but smaller in adults
- rounded, smooth, or slightly lobulated and
sometimes have a stalk as long as 2 cm
- singly and in the rectum
- have no malignant potential.

Peutz-Jeghers polyps
- This syndrome is caused by germ-line
mutations in the LKB1 gene, which
encodes a serine threonine kinase
- hamartomatous polyps that involve the
mucosal epithelium, lamina propria, and
muscularis mucosa
- singly or multiply
- rare autosomal dominant syndrome

Peutz-Jeghers polyps
- characterized by multiple hamartomatous
polyps scattered throughout the entire GI
tract and melanotic mucosal and cutaneous
pigmentation around the lips, oral mucosa,
face, genitalia, and palmar surfaces of the
- patients with this syndrome are at risk for
intussusception, which is a common cause of
- tend to be large and pedunculated with a
firm lobulated contour
Non-neoplastic colonic polyps. A, Hyperplastic polyp; high-
power view showing the serrated profile of the epithelial
layer. B, Peutz-Jeghers polyp; low-power view showing
the splaying of smooth muscle into the superficial portion
of the pedunculated polyp.

 Neoplastic polyps (adenomas)
- range from small, often pedunculated, tumors to
large lesions that are usually sessile.
- incidence in the small intestine <<, in the colon
- the prevalence of colonic adenomas is 20% to
30% before age 40, rising to 40% to 50% after
age 60
- males and females are affected equally
- well-defined familial predisposition to sporadic

 Alladenomatous lesions arise as the result
of epithelial proliferation and dysplasia,
which may range from mild to so severe as
to represent transformation to carcinoma.
Furthermore, there is strong evidence
that most sporadic invasive colorectal
adenocarcinomas arise in preexisting
adenomatous lesions.

 Tubular adenoma : tubular glands,
smooth surface
 Villous Adenoma: villous frondlike
projections of epithelial surface
 Tubulovillous adenoma: mix
 Serrated adenoma: features of both
hyperplastic polyp and adenoma

A, Pedunculated adenoma showing a fibrovascular stalk lined by normal colonic mucosa and a
head that contains abundant dysplastic epithelial glands, hence the blue color
with the H & E stain. B, A small focus of adenomatous epithelium in an otherwise normal
(mucin-secreting, clear) colonic mucosa, showing how the dysplastic columnar epithelium
(deeply stained) can populate a colonic crypt and create a tubular architecture.
A, Sessile adenoma with villous architecture. Each frond is lined by
dysplastic epithelium. B, Portion of a villous frond with dysplastic
columnar epithelium on the left and normal colonic columnar
epithelium on the right.
Familial adenomatous polyposis in an 18-year-old woman. The
mucosal surface is carpeted by innumerable polypoid adenomas
 Clinical Features
- The smaller adenomas: asymptomatic, until
such time that occult bleeding leads to
clinically significant anemia.
- Villous adenomas: more frequently
symptomatic because of overt or occult
rectal bleeding. The most distal villous
adenomas may secrete sufficient amounts of
mucoid material rich in protein and
potassium to produce hypoproteinemia or

 98% of all cancers in the large intestine
are adenocarcinomas.
 They almost always arise in adenomatous
polyps that are generally curable by
 With an estimated 134,000 new cases per
year and about 55,000 deaths, this
disease accounts for nearly 15% of all
cancer-related deaths in the US.
 Epidemiology
- The peak incidence: 60 to 70 years of age;
fewer than 20% of cases occur < the age of
50 years.
- Adenomas are the presumed precursor
lesion for most of the tumors; the frequency
with which colorectal cancer arises de novo
from flat colonic mucosa remains undefined
but appears to be low.
- Males > females.

- genetic and environmental (diet)
- When colorectal cancer is found in a young
person, preexisting ulcerative colitis or one of
the polyposis syndromes must be suspected. In
addition, individuals with hereditary
nonpolyposis colorectal cancer syndrome
(HNPCC, also known as Lynch syndrome),
caused by germ-line mutations of DNA mismatch
repair genes, are at a high risk of developing
colorectal cancers. (HNPCC patients are also at
risk of developing other tumors, such as

Schematic of the morphologic and molecular changes in the
adenoma-carcinoma sequence. It is postulated that loss of one normal
copy of the tumor suppressor gatekeeper gene APC occurs early.
Indeed, individuals may be born with one mutant allele of APC,
rendering them extremely likely to develop colon cancer. This is the
"first hit," according to Knudson's hypothesis. The loss of the normal
copy of the APC gene follows ("second hit"). Mutations of the
oncogene K-RAS seem to occur next. Additional mutations or losses
of heterozygosity inactivate the tumor suppressor gene p53
(on chromosome 17p) and SMAD2 and SMAD4 on
chromosome 18q, leading finally to the emergence of
carcinoma, in which additional mutations occur. It is
important to note that while there seems to be a temporal
sequence of changes, as shown, the accumulation of
mutations, rather than their occurrence in a specific order, is
more important.
Carcinoma of the cecum. The fungating carcinoma projects into the
lumen but has not caused obstruction.
Carcinoma of the descending
colon. This circumferential
tumor has heaped-up edges
and an ulcerated central
portion. The arrows identify
separate mucosal polyps.

Invasive adenocarcinoma of colon, showing malignant
glands infiltrating the muscle wall
 Clinical Features
- fatigue, weakness, and iron deficiency
- occult bleeding, changes in bowel habit,
or crampy left lower quadrant
- iron deficiency anemia

- Spread: adjacent structures and by metastasis
through the lymphatics and blood vessels.
- the favored sites for metastasis are the regional
lymph nodes, liver, lungs, and bones, followed by
many other sites including the serosal
membrane of the peritoneal cavity.
- Carcinomas of the anal region are locally
invasive and metastasize to regional lymph
nodes and distant sites
- Almost 80% of malignant tumors of the anal canal
are squamous cell carcinomas.

Pathologic staging of colorectal cancer. Staging is based on
the depth of tumor invasion.
 only 3% to 6% of GI tumors, >> benign tumors.
 smooth muscle origin, adenomas, and lipomas,
followed by various neurogenic, vascular, and
hamartomatous epithelial lesions.
 adenocarcinomas and carcinoids have a roughly
equal incidence.
 GISTs have received much attention recently,
because they have an activating mutation
affecting KIT, a tyrosine kinase receptor that is
the target of new therapeutic agents

 Adenocarcinoma of the Small Intestine
- similar to colonic cancers.
- Most small bowel carcinomas arise in the
duodenum (including the ampulla of Vater).
- Cramping pain, nausea, vomiting, and
weight loss
- anemia or rarely intussusception or
- Adenomas in the immediate vicinity of the
ampulla of Vater may produce biliary
obstruction causing jaundice.

- In the past, these tumors were considered to be
smooth muscle tumors, either benign
leiomyomas or malignant leiomyosarcomas,
sometimes with a spindle cell composition.
- However, on the basis of a molecular marker
common to these tumors, they are classified as
- With the use of IHC markers, GISTs are now
subdivided into (a) tumors that show smooth
muscle cell differentiation (the most common
type); (b) tumors with neural differentiation
(often called GI autonomic nerve tumors; (c)
tumors with smooth muscle/neural dual
differentiation, and (d) tumors lacking
differentiation toward these lineages..
- GISTs constitute the majority of
nonepithelial tumors of the stomach but
can be present in the small and large
- most GISTs have a somatic mutation in the
c-KIT (CD117) gene, which encodes a
tyrosine kinase receptor. Mutations in this
receptor (generally in exon 11) lead to
consitutive signaling from the receptor,
without the need for a ligand.
GIST. A, GIST from the stomach wall.
B, Histology of the tumor showing
spindle cells with elongated nuclei
with fine chromatin, and eosinophilic
fibrillar cytoplasm. C, KIT stain
showing strong and uniform
reactivity of the tumor cells. Note KIT
staining of mast cells in the adjacent
normal muscle wall.
 GI Lymphoma
 MALT lymphoma.
- originates in B cells of the MALT of the GI
- affects adults, lacks a sex predilection, and
may arise anywhere in the gut: stomach
(55% to 60% of cases), small intestine (25%
to 30%), proximal colon (10% to 15%), and
distal colon (≤10%). The appendix and
esophagus are only rarely involved.

 Carcinoids

Carcinoid tumor. A, Multiple protruding tumors are present at the ileocecal

junction. B, The tumor cells exhibit a monotonous morphology, with a delicate
intervening fibrovascular stroma. C, Electron micrograph showing dense core
bodies in the cytoplasm.
- Cells generating bioactive compounds, particularly peptide
and nonpeptide hormones, are normally dispersed along
the length of the GI tract mucosa and have a major role in
coordinated gut function.
- Endocrine cells are abundant in other organs, but most of
the tumors that develop from these cells arise in the gut.
Tumors arising from these endocrine cells are called
carcinoid tumors; they may develop in the pancreas or
peripancreatic tissue, lungs, biliary tree, and even liver. The
term carcinoid is an old reference to "carcinoma-like," which
has persisted through the decades. The peak incidence of
these neoplasms is in the sixth decade, but they may appear
at any age. They compose less than 2% of colorectal
malignancies but almost half of small intestinal malignant

 Although all carcinoids are potentially malignant
tumors, the tendency for aggressive behavior
correlates with the site of origin, the depth of
local penetration, and the size of the tumor. For
example, appendiceal and rectal carcinoids
infrequently metastasize, even though they may
show extensive local spread. By contrast, 90% of
ileal, gastric, and colonic carcinoids that have
penetrated halfway through the muscle wall have
spread to lymph nodes and distant sites at the
time of diagnosis, especially those larger than 2
cm in diameter.

 Aswith normal gut endocrine cells, the
cells of carcinoid tumors can synthesize
and secrete a variety of bioactive
products and hormones. Although
multiple hormones may be synthesized
by a single tumor, when a tumor secretes
a predominant product to cause a clinical
syndrome, it may be called by that name
(e.g., gastrinoma, somatostatinoma, and
 Gastric MALT lymphomas arise in the setting of
mucosal lymphoid activation, as a result of
Helicobacter-associated chronic gastritis. With H.
pylori infection, there is an intense activation of T
and B cells in the mucosa. This leads to
polyclonal B-cell hyperplasia and eventually to
the emergence of a monoclonal B-cell neoplasm.
MALT lymphoma cells are CD5 and CD10
negative, and a t(11;18) translocation is common
(the translocation creates a fusion gene between
the apoptosis inhibitor BCL-2 gene in
chromosome 11 and the MLT gene in
chromosome 18).

 Primary GI lymphomas generally have a
better prognosis than do those arising in
other sites, because combined surgery,
chemotherapy, and radiation therapy
offer reasonable hopes of cure. About
50% of gastric lymphomas can regress
with antibiotic treatment for H. pylori.
Those that do not regress usually contain
the t(11;18) translocation or other genetic
 Benign
 Malignant

Hepatocellular carcinoma. A, Autopsied liver showing a unifocal, massive
neoplasm replacing most of the right hepatic lobe in a noncirrhotic liver; a satellite
tumor nodule is directly adjacent. B, In this microscopic view of a well-
differentiated lesion, tumor cells are arranged in nests, sometimes with a central
lumen, one of which contains bile (arrow). Other tumor cells contain intracellular
bile pigment.
Cholangiocarcinoma. A, Autopsied liver showing a massive neoplasm
in the right hepatic lobe and innumerable metastases permeating the
entire liver. B, Microscopic view showing tubular glandular structures
embedded in a dense sclerotic stroma.
Pathologic Basis of Disease
Pathology Illustrated