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Clinicopathological analysis of pulmonary sclerosing hemangioma.Ann
Thorac Surg. 2004 Dec;78(6):1928-31.
BACKGROUND:
Sclerosing hemangiomas of the lung are uncommon tumors and are thought
to be benign. However, the histogenesis and clinicopathological
features of these tumors have not been elucidated. METHODS: We
analyzed the clinicopathological features of 26 sclerosing hemangiomas.
The immunoreactivity for Ki-67 and p53 of sclerosing hemangiomas was
determined and compared with that of pathological stage 1 pulmonary
papillary adenocarcinomas. RESULTS: The patients of sclerosing
hemangioma were predominantly female. Eighteen patients were detected
as a result of routine medical examinations and 15 were nonsmokers.
Seven patients underwent tumor enucleation, 10 underwent a wedge
resection, and 9 underwent a lobectomy. The mean tumor size was 2.2 cm
(range 1 to 5 cm). Pathological findings demonstrated a papillary
pattern in 23 cases, sclerotic pattern in 26 cases, hemorrhagic
pattern in 22 cases and a solid pattern in 25 cases. Twenty-five cases
had an excellent prognosis with no evidence of recurrence following
surgery. However, 1 patient who had undergone a wedge resection
developed a local recurrence and required an additional wedge
resection. The Ki-67 labeling index of sclerosing hemangiomas was
significantly lower than that of adenocarcinomas, whereas the Ki-67
labeling index of the recurrent case was 0.4%. No significant
immunohistochemical staining for p53 was observed in sclerosing
hemangioma cases. CONCLUSIONS: Sclerosing hemangioma exhibits various
histologic findings. Although we experienced one case with a recurrent
tumor, sclerosing hemangiomas did not exhibit malignant behavior.
Expression of E-cadherin, beta-catenin and p120(ctn) in the pulmonary
sclerosing hemangioma. Lung
Cancer. 2007 Jul;57(1):54-9.
BACKGROUND:
The major two types of cells in pulmonary sclerosing hemangiomas (PSH)
may be not equally maturity, but this viewpoint needs more evidences.
AIM: To determine E-cadherin, beta-catenin and p120(ctn) expression
phenotype in cuboidal and polygonal cells, which are the two major
cell types in pulmonary sclerosing hemangiomas. METHODS: Specimens
were obtained from 25 patients with PSH and 8 patients with pulmonary
inflammatory pseudotumors. The expression levels of E-cadherin, beta-catenin
and p120(ctn) were detected using a streptavidin peroxidase (SP)
immunohistochemical method. RESULTS: E-cadherin, beta-catenin and
p120(ctn) were expressed strongly on the cuboidal cell membranes,
while beta-catenin was also expressed the cuboid cytoplams in 25 PSH
patients. However, in the polygonal cell membranes, the expression
levels of these molecules were decreased, and mainly cytoplamic.
Specifically, E-cadherin, beta-catenin and p120(ctn) were expressed in
both the cytoplasm and on the cell membranes in the intracavitary
lining cells of the hemorrhagic regions. The expression phenotype in
proliferating type II pneumocytes in the eight pulmonary inflammatory
pseudotumors was similar to that in the cuboidal cells in PSH
patients. CONCLUSION: The cuboidal cells, resembling inflammatory
proliferative type II pneumocytes, display several characteristics of
epithelial cells, including normal expression of E-cadherin and
catenin. Comparatively, polygonal cells are not as mature as cuboidal
cells and lack of expression of E-cadherin and catenin.
Sclerosing
hemangioma of the lung: a rare lesion with a difficult diagnosis.Rev
Pneumol Clin. 2006 Dec;62(6 Pt 1):390-4.
Sclerosing
hemangioma of the lung is a rare lesion described for the first time
in 1956 by Liebow. We report a case in a 45 year-old woman who was
admitted for exploration of chronic cough. The chest x-ray revealed a
round opacity, well delimited in the left pulmonary parenchyma.
Surgical resection enabled the histopathological diagnosis of
sclerosing hemangioma. We review progress in our knowledge of the
histogenesis and diagnosis of this tumor. Immunohistochemistry has
been highly contributory although numerous points remain
controversial.
A case of
multiple sclerosing hemangiomas of both lungs.Nihon
Kokyuki Gakkai Zasshi. 2006
Nov;44(11):848-52.
A 16-year-old
Chinese girl was found to have abnormalities on chest roentgenography
at a school health checkup in 2004, and she visited our outpatient
clinic for the first time on July 2. Based on the imaging, there were
multiple nodules ranging in size up to 5cm in the longest dimension,
with regularly shaped clear margins, in both lungs. We considered lung
metastases of a malignant neoplasm as the most likely diagnosis and
performed a systemic workup but failed to make a clinical diagnosis.
We therefore performed an open lung biopsy on November 8.
Microscopically, the tumors consisted of a mixture of areas with a
papillary pattern, a solid pattern and a sclerosing pattern. Component
tumor cells were of two types: epithelial-like cells that covered the
surface of the papillary structures and round or polygonal cells that
showed a solid pattern of growth underneath. Immunohistochemical
examinations revealed that these tumor cells were positive for an
alveolar epithelium marker. From these results, we made a diagnosis of
sclerosing hemangioma. Here we report a rare case of multiple
sclerosing hemangiomas together with a review of the literature.
Radiology-pathology conference: sclerosing hemangioma of the lung.Clin
Imaging. 2006 Nov-Dec;30(6):409-12.
Sclerosing
hemangioma (SH) is a relatively rare, benign neoplasm of the lung.
Although there are relatively characteristic imaging findings, biopsy
remains the definitive diagnostic test. We report the radiology and
pathology of a patient with a SH, with emphasis on the computed
tomographic and (18)F-fluorodeoxyglucose positron emission tomography
findings, and review the literature on this unusual tumor.
Sclerosing
hemangioma of the lung: a benign tumour with potential for malignancy?Ann
Thorac Cardiovasc Surg. 2006
Oct;12(5):352-4.
Pulmonary
sclerosing hemangioma represents a rare neoplasm with variable
potential for progression. This case report of a 35-year-old female
with left-sided thoracic pain. Computed tomography revealed a
centrally located, well-circumscribed and partially calcified lesion.
Intraoperative findings were suggestive of a carcinoid tumour. The
tumour was completely removed by lobectomy followed by systematic
lymphadenectomy. The histopathological analysis revealed a sclerosing
hemangioma, a rare benign neoplasm. Sclerosing hemangiomas (SHs) are
true neoplasms derived from alveolar pneumocytes. However, little data
is available on the potential malignant behaviour, such as lymphnode
metastases, local recurrence, and the appearance of SH's. Generally,
wedge resection is justified in the majority of cases, but in cases of
uncertain intraoperative diagnosis, anatomic resection with systematic
lymphadenectomy is recommended.
Study of
androgen receptor and phosphoglycerate kinase gene polymorphism in
major cellular components of the so-called pulmonary sclerosing
hemangioma.Zhonghua
Bing Li Xue Za Zhi. 2006;35(5):267-71.
OBJECTIVE: To study the clonality of polygonal cells and surface
cuboidal cells in the so-called pulmonary sclerosing hemangioma (PSH).
METHODS: 17 female surgically resected PSH were found. The polygonal
cells and surface cuboidal cells of the 17 PSH cases were
microdissected from routine hematoxylin and eosin-stained sections.
Genomic DNA was extracted, pretreated through incubation with
methylation-sensitive restrictive endonuclease HhaI or HpaII, and
amplified by nested polymerase chain reaction for X chromosome-linked
androgen receptor (AR) and phosphoglycerate kinase (PGK) genes. The
length polymorphism of AR gene was demonstrated by denaturing
polyacrylamide gel electrophoresis and silver staining. The PGK gene
products were treated with Bst XI and resolved on agarose gel.
RESULTS: Amongst the 17 female cases of PSH, 15 samples were
successfully amplified for AR and PGK genes. The rates of polymorphism
were 53% (8/15) and 27% (4/15) for AR and PGK genes respectively.
Polygonal cells and surface cuboidal cells of 10 cases which were
suitable for clonality study, showed the same loss of alleles (clonality
ratio = 0) or unbalanced methylation pattern (clonality ratio < 0.25).
CONCLUSIONS: The polygonal cells and surface cuboidal cells in PSH
demonstrate patterns of monoclonal proliferation, indicating that both
represent true neoplastic cells.
Pulmonary
sclerosing hemangioma: report of 15 cases and review of the
literature.Zhonghua
Jie He He Hu Xi Za Zhi. 2006
Mar;29(3):164-6.
OBJECTIVE: To improve the understanding of pulmonary sclerosing
hemangioma (PSH). METHODS: The clinical data of 15 cases of PSH were
analyzed, and the literature was reviewed. The etiology, clinical
manifestations, differential diagnosis, treatment and outcome of PSH
were described. RESULTS: The etiology and histological origin of PSH
were unclear. Most cases were asymptomatic or only with mild symptoms.
The radiology of PSH often showed isolated nodule with distinct margin
in the lung field. The characteristics of its pathological
manifestation were as follows: (1) background of cell gathering or
mucin matrix with scattered white blood cells; (2) proliferation of
hemangioma with sclerosis of vessel wall; (3) papillary proliferation
of small vessels intruding into the air space; (4) existence of
hemorrhage or sclerosis zone. Immunohistological studies had not
defined the correct histological origin of PSH. A pre-operation
diagnosis of PSH was difficult. Thirteen cases had been misdiagnosed
as malignancy. The outcome of the disease was good when early surgical
resection was performed. CONCLUSIONS: PSH is an uncommon disease, and
can be easily misdiagnosed. More attention should be paid to its
clinical features and management.
Expression patterns of markers
for type II pneumocytes in pulmonary sclerosing hemangiomas and fetal
lung tissues.Arch
Pathol Lab Med. 2005 Jul;129(7):915-9.
CONTEXT:
Although the histogenesis of sclerosing hemangioma is currently not
well understood, the tumor has been characterized by its 2
histologically different types of cells, namely, surface and polygonal
cells. OBJECTIVE: To elucidate the origin of these cells, we analyzed
samples from 15 cases of sclerosing hemangioma and 15 specimens of
fetal lung tissue. DESIGN: We immunostained specimens from 15 cases of
sclerosing hemangioma and 15 samples of fetal lung tissue using
antibodies against thyroid transcription factor 1, MUC1, Thomsen-Friedenreich
antigen, and CD44v6, known as markers for type II pneumocytes, and a
panel of antibodies against cytokeratin, epithelial membrane antigen,
synaptophysin, CD56, estrogen receptor, and progesterone receptor.
RESULTS: In fetal lung tissue, MUC1 and thyroid transcription factor 1
were expressed throughout all developmental stages of airway
epithelium, whereas Thomsen-Friedenreich antigen and CD44v6 were
expressed by type II pneumocytes of saccular and alveolar origin.
Thomsen-Friedenreich antigen was expressed in the bronchial bud of the
pseudoglandular stage. MUC1, thyroid transcription factor 1, and
epithelial membrane antigen were observed in both surface and
polygonal cells of sclerosing hemangioma. Only the surface cells in
all cases of sclerosing hemangioma showed positivity for cytokeratin
and CD44v6. Thomsen-Friedenreich antigen was expressed in the surface
cells of 11 of 15 cases of sclerosing hemangioma. Epithelial membrane
antigen was expressed in both types of tumor cells, whereas
cytokeratin was not detected on polygonal cells, but was reactive with
surface cells. CONCLUSIONS: Our results suggest that the 2 types of
cells in sclerosing hemangioma may derive from a common precursor cell
through divergent differentiation toward the type II pneumocyte during
tumorigenesis.
"Pneumocytoma"
or "sclerosing hemangioma": histogenetic aspects of a rare tumor of
the lung.Pathologe.
2005 Sep;26(5):367-77.
Aspects of
histogenesis and nomenclature of so called "sclerosing hemangioma" of
the lung (WHO 1999) are discussed and compared with
immunohistochemical findings in eight examined operation specimen. The
lesion is characterised by the presence of typical surface cells,
which can be related to type II pneumocytes. Progesterone-receptor
positive stromal cells may derive from primitive mesenchymal cells.
Endothelial proveniance of tumor cells could not be confirmed by
immunohistochemistry. Therefore, this rare usually benign pulmonary
neoplasm should be entitled "pneumocytoma" analogous to the suggestion
of several other authors.
Bilateral
multiple pulmonary sclerosing hemangioma.Jpn
J Thorac Cardiovasc Surg. 2005
Mar;53(3):157-61.
We
present herein a rare case of bilateral pulmonary sclerosing
hemangioma, for which a differential diagnosis was made from
metastatic lung tumors. A 32-year-old asymptomatic woman was referred
to our hospital for further evaluation of abnormal chest shadows. A
chest computed tomogram revealed two round, well-circumscribed masses
in both sides of the lungs. Metastatic lung tumors were suspected,
however, a primary lesion was not detected by several examinations.
Thus, simultaneous video-assisted thoracic surgery for the bilateral
tumors was performed. The tumors, measuring 16x13x12 mm in the left
lung and 27x24x20 mm in the right lung, were resected, and then
pathological examination confirmed the diagnosis of sclerosing
hemangioma. Her postoperative course was uneventful and she has been
doing well without any sign of recurrence.
Expression of the estrogen
receptor beta in 37 surgically treated pulmonary sclerosing
hemangiomas in comparison with non-small cell lung carcinomas.Hum
Pathol. 2005 Oct;36(10):1108-12.
Sclerosing
hemangioma (SH) of the lung is an uncommon tumor with a predilection
for middle-aged women. This special phenomenon prompted us to examine
SH for the expression of ERalpha (human estrogen receptor) and ERbeta
(a second isoform of estrogen receptor). To investigate the staining
pattern of these tumors, we also stained lung tissues from patients
with non-small cell lung carcinomas and nonneoplastic type II
pneumocytes for comparison. Thirty-seven pulmonary SHs and 301
non-small cell lung cancers specimens were explored. Expression of
ERalpha and ERbeta was immunohistochemically measured. The overall
frequency of overexpression for ERbeta was 91.9%. It was detected in
both female (in 91.4% of 35 cases) and male (in 100.0% of 2 tumors
from men) patients. There was ERbeta overexpression in all 9 tumors of
solid pattern, 6 of 7 tumors of papillary pattern, all 4 tumors of
sclerotic pattern, 12 of 13 tumors of hemorrhagic pattern, and 3 of 4
tumors of mixed pattern. The staining pattern of the neoplastic cells
of the SH was similar to that of type II pneumocytes adjacent to the
tumor rather than that of non-small cell lung cancers, in which the
frequency of ERbeta overexpression was 45.8%. However, there was no
ERalpha detectable in these neoplasms. Estrogen receptor beta
overexpression is very frequent in pulmonary SHs, which is similar to
that of alveolar cells but quite different from non-small cell
carcinoma.
Huge benign
lung tumor in a female smoker.Rev
Pneumol Clin. 2005 Dec;61(6):379-81.
Pulmonary
sclerosing hemangioma is a rare, slow-growing, benign tumor. Its
potential for progression and its histiogenesis remains controversial.
CASE REPORT: A routine chest X-ray revealed a right abdominal mass in
41-year-old woman. Search for a cause was negative. The patient
underwent posterolateral thoracotomy for tumorectomy. Intraoperative
pathology analysis revealed the benign nature of the tumor. No
complication was observed postoperatively. The final pathological
conclusion was sclerosing hemangioma of the lung. Pulmonary sclerosing
hemangioma is a parenchymal tumor of the lung. The latest
immunohistochemical studies of this lesion suggest a pneumocyte
origin. Prognosis is good, but extension to lymph nodes may occur.
Surgery is always required for cure, and must be associated with lymph
node dissection for large tumors.
Immunohistochemical
and ultrastructural markers suggest different origins for cuboidal and
polygonal cells in pulmonary sclerosing hemangioma.
Hum Pathol. 2004 Apr;35(4):503-8.
We report the
morphological characteristics of 30 cases of sclerosing hemangioma (SH)
of the lung and explore the histological origin of the major cells in
these tumors. In addition to routine light and electron microscopy,
immunohistochemistry was performed by using 12 monoclonal primary and
5 polyclonal primary antibodies. These included surfactant protein B
(SP-B), thyroid transcription factor-1 (TTF-1), mast cell trypsin,
CD68, epithelial antigen markers (high molecular weight cytokeratin,
low molecular weight cytokeratin [CK-L], epithelial membrane antigen [EMA],
cancer embryonic antigen), mesothelial antigen, neuroendocrine markers
(neuron-specific enolase [NSE], chromogranin A, synaptophysin,
calcitonin, adrenocorticotropic hormone, human growth hormone [hHG]),
vimentin, and CD34. Surface cuboidal cells have short microvilli and
have lamellar bodies in their cytoplasm. They can sometimes merge into
multinuclear giant cells. Immunohistochemical results showed that
these cells are strongly positive for SP-B, TTF-1, CK-L, EMA, and
cancer embryonic antigen, whereas polygonal cells, previously also
described as round or pale cells, were strongly positive for vimentin
and TTF-1, and positive or weakly positive for 2 to 3 kinds of
neuroendocrine markers. Sparse neuroendocrine granules and abundant
microfilaments were observed in their cytoplasm. Some cell clusters in
the solid regions were positive for SP-B and EMA. Mast cells existed
sparsely in almost every field. Both cuboidal and polygonal cells were
negative to CD34 and mesothelial antigen staining. We conclude that
cuboidal cells of SH originate from reactive proliferating type II
pneumocytes, which can fuse into multinuclear giant cells. Polygonal
cells, as true tumor cells, likely originate from multipotential
primitive respiratory epithelium and possess the capability for
multipotential differentiation. The antibodies of SP-B, TTF-1,
vimentin, and CK-L are very helpful to diagnosis and differential
diagnosis of SH.
A case of
sclerosing hemangioma surrounded by emphysematous change.
Radiat Med. 2004 Mar-Apr;22(2):123-5.
A
44-year-old woman presented with high-grade fever. Chest radiography
showed a 30 mm solitary pulmonary mass in the left lower lobe. Chest
CT revealed a well-defined solid mass in the left lower lobe. On
contrast-enhanced CT, the mass showed homogeneity and mild
enhancement. There was an emphysematous portion in the surrounding
lung parenchyma. The patient underwent partial lobectomy of the left
lower lobe. The final diagnosis of sclerosing hemangioma with abundant
vasculature was confirmed pathologically. Pulmonary sclerosing
hemangioma is a rare benign neoplasm. Some cases have been reported in
which sclerosing hemangioma is surrounded by air spaces. We suggest
that the air spaces around the tumor were formed by not only
peritumoral bleeding but also a check-valve effect of the compressed
bronchus.
Type-II
pneumocyte differentiation in pulmonary sclerosing hemangioma:
ultrastructural differentiation and immunohistochemical distribution
of lineage-specific transcription factors (TTF-1, HNF-3 alpha, and
HNF-3 beta) and surfactant proteins.Virchows
Arch. 2004 Jul;445(1):45-53. Epub 2004
May 11.
Sclerosing
hemangioma (PSH) is a rare pulmonary tumor, in which two types of
tumor cells could be histologically discerned--surface and stromal
tumor cells. Nine tumor-tissue specimens from six female Japanese
patients were studied, focusing on the distribution of several
transcription factors related to lung epithelial development and
surfactant proteins and comparing the ultrastructural features of the
tumor cells. The immunohistochemical analysis revealed that the
surfactant proteins of surfactant apoprotein A, surfactant protein B,
and prosurfactant protein C were distributed in many of the
surface-lining cells and in a small number of stromal-tumor cells. In
addition, the nuclei of the tumor cells stained positive for thyroid
transcription factor 1 (TTF)-1, hepatocyte nuclear factor (HNF)-3
alpha, and HNF-3 beta. In situ hybridization staining for TTF-1 showed
similar positive signals. Ultrastructurally, two types of tumor cells
showed similar features, but stromal tumor cells lost the definitive
apico-lateral differentiation compared with the surface tumor cells
and showed restricted surface differentiation between the adjacent
tumor cells, forming small lumina accompanied by microvilli and
occasional multi-vesicle or multi-lamellar bodies. Conclusively, the
real tumoral population being undifferentiated stromal cells,the
lining cells are fully differentiated type-II pneumonocytes. PSH is a
proliferation of rather fetal type-II pneumonocytes (pneumocytoma or
pneumoblastoma?).
Sclerosing
hemangioma presenting as a solitary lung nodule. Report of one case.Rev
Med Chil. 2004 Jul;132(7):853-6.
Lung
sclerosing hemangioma is an uncommon tumor that presents as a solitary
asymptomatic nodule and that affects middle age women. It derives from
type II pneumocytes. We report a 52 years old female with a solitary
lung nodule detected in a chest X ray requested for the diagnosis of
an acute respiratory disease. The nodule was excised by video
thoracoscopy and the frozen section biopsy was informed as a non small
cell undifferentiated carcinoma. Therefore an inferior right lobectomy
with lymph node resection was performed. The definitive biopsy was
informed as a lung sclerosing hemangioma.
Loss of
heterozygosity patterns of sclerosing hemangioma of the lung and
bronchioloalveolar carcinoma indicate a similar molecular
pathogenesis. Arch
Pathol Lab Med. 2004 Aug;128(8):880-4.
CONTEXT: The
histogenesis and origin of sclerosing hemangioma (SH) of lung were
uncertain for many years. Many immunohistochemical, ultrastructural,
and recent molecular studies support the hypothesis that SH is a
neoplasm originating from the cells of the terminal lobular unit,
similar to the nonmucinous variant of bronchioloalveolar carcinoma (BAC).
Most cases of SH are benign, but they can metastasize to the regional
lymph nodes. OBJECTIVE: To compare the patterns of allelic loss of
tumor suppressor genes in SH and BAC by microdissection-based
genotypic analysis. DESIGN: Microdissection-based loss of
heterozygosity analysis of 9 cases of SH and 14 cases of BAC, using a
panel of 7 polymorphic microsatellite markers located on 1p, 5q, 9p,
10q, and 17p. Microsatellite marker and chromosomal arm-based
fractional allelic loss (FAL) were calculated in each case. RESULTS:
Our results showed similar patterns of allelic loss between the 2
groups of tumors on an individual case basis. Chromosomal arms 5q and
10q showed frequent allelic loss in SH (66.7% and 62.5%,
respectively), whereas in BAC, chromosomal arm 17p (52.6%) was
frequently affected. A statistically significant difference in allelic
loss between SH and BAC was located only on chromosomal arm 5q (P
=.04). Microsatellite marker D5S615 was significantly more frequently
affected in SH than in BAC (66.7% vs 28.6%; P =.04). CONCLUSION: Our
molecular data support the hypothesis of common origin of SH and BAC.
A putative tumor suppressor gene that might play a role in
tumorigenesis of SH may be located on the chromosomal arm 5q.
Thyroid
transcription factor-1 in the histogenesis of plumonary sclerosing
hemangioma.Zhonghua
Zhong Liu Za Zhi. 2002 Jul;24(4):384-7.
OBJECTIVE: To
investigate the significance of thyroid transcription factor-1 (TTF-1)
in the histogenesis of pulmonary sclerosing hemangioma (PSH). METHODS:
With clinicopathologic data of 36 PSH patients obtained, all specimens
were stained by immunohistochemical method with a panel of antibodies
including TTF-1, SpA, CK, EMA, F-VIII, CD34, Claretinin, HBME,
synaptophsin, chromogranin, actin and S-100. RESULTS: The patients
were mostly women with a mean age of 46.7 years and a median age of 48
years. All lesions were solitary and well circumscribed with a mean
size of 3.3 cm and a median size of 3 cm. No multiple or metastasis
was found. Surface cells (SC) and round cells (RC) were showed in PSH,
with more than 90% showing TTF-1 and EMA by immunohistochemical
method. CK and SpA were showed in SC, which were not showed in RC.
Neuroendocrine cells scattered within RC of PSH were detected in a few
cases. Mesothelial, vascular endothelial, neuroendocrine, and
myoepithelial markers by immunohistochemical method were negative.
CONCLUSION: Pulmonary sclerosing hemangioma, a benign tumor,
originates from the alveolar pneumocytes. Its surface cells are more
mature, while the round cells, being primitive respiratory epithelia,
may undergo phenotypic differentiation and evolve into mucinous glands
or neuroendocrine structure among other components.
Expression of
thyroid transcription factor-1 and other markers in sclerosing
hemangioma of the lung.Arch
Pathol Lab Med. 2001 Oct;125(10):1335-9.
CONTEXT:
Sclerosing hemangioma of the lung is well characterized histologically,
but the line of differentiation expressed by the tumor cells has been
unclear. Despite the implication by its name of a vascular neoplasm,
sclerosing hemangioma is considered by most authorities to be an
epithelial tumor, possibly related to the pulmonary epithelium.
OBJECTIVES: To determine the line of differentiation of the tumor
cells with immunohistochemistry and to review the related literature.
DESIGN: Nine cases of histologically typical pulmonary sclerosing
hemangioma were studied with pan-epithelial (epithelial membrane
antigen [EMA] and CAM 5.2), endothelial (CD31), neuroendocrine (chromogranin
A), and pulmonary epithelial markers (thyroid transcription factor-1
and PE10). Staining intensity was separately evaluated in the pale
cells of the solid areas and the cells lining the papillary
structures. RESULTS: Both cell types were positive for thyroid
transcription factor-1 and EMA in all cases (100%). Thyroid
transcription factor-1 showed diffuse strong staining, and EMA
staining varied from focal weak to diffuse strong. The pale cells
showed focal staining for keratin (CAM 5.2) in 2 (28%) of 7 cases, and
for PE10 in 5 (62%) of 8 cases. The papillary lining cells were at
least focally positive with CAM 5.2 and PE10 in all cases (100%).
Reactions for chromogranin and CD31 were negative in both cell types
in every case. The number of PE10- or CAM 5.2-positive papillary
lining cells was less than the number of EMA-positive papillary lining
cells. CONCLUSION: The uniform positivity for EMA is consistent with
the notion that the tumor cells of sclerosing hemangioma are
epithelial, and the strong thyroid transcription factor-1 positivity
suggests differentiation toward pulmonary epithelium. The papillary
lining cells expressing EMA as well as PE10 or CAM 5.2 likely
represent entrapped metaplastic alveolar epithelium, whereas the
papillary lining cells expressing only EMA more likely constitute true
neoplastic cells similar to those in the solid areas.
A
clinicopathologic study of 100 cases of pulmonary sclerosing
hemangioma with immunohistochemical studies: TTF-1 is expressed in
both round and surface cells, suggesting an origin from primitive
respiratory epithelium.Am
J Surg Pathol. 2000 Jul;24(7):906-16.
Pulmonary
sclerosing hemangioma (SH) is a lung neoplasm of uncertain
histogenesis that is composed of two major cell types: surface and
round cells. The authors studied 100 cases of pulmonary SH that
presented as a peripheral (95%), solitary (96%) mass of less than 3 cm
in diameter (74%) in asymptomatic patients who were mostly women (83%)
with a mean age of 46.2 years. Immunohistochemistry of multiple
epithelial, mesothelial, pneumocyte, neuroendocrine, and mesenchymal
markers was performed on 47 cases to investigate the histogenesis of
this neoplasm. Both surface and round cells stained with epithelial
membrane antigen (EMA) and thyroid transcription factor-1 (TTF-1) in
more than 90% of cases; however, the round cells were uniformly
negative for pancytokeratin and positive for cytokeratin-7 and CAM 5.2
in only 31% and 17% of cases, respectively. Surfactant proteins A and
B as well as Clara cell antigen were positive in varying numbers of
surface cells but they were negative in the round cells.
Neuroendocrine cells either as isolated scattered cells or as a
tumorlet within the center of SH were detected (chromogranin, Leu-7,
synaptophysin positive) in three cases. The expression of TTF-1 in the
absence of surfactant proteins A and B and Clara cell antigens in the
round cells of SH suggests that they are derived from primitive
respiratory epithelium. The alveolar pneumocytes and neuroendocrine
cells may either represent phenotypic differentiation of a primitive
respiratory epithelial component or they may correspond to non-neoplastic
entrapped or hyperplastic elements. The concomitant positivity of both
cell types in SH for TTF-1 and EMA, and the negativity of round cells
for pancytokeratin and neuroendocrine markers, provide useful clues
not only for histogenesis but also for the diagnosis of this lung
neoplasm.
Sclerosing
hemangioma of the lung--benign sclerosing pneumocytoma.
Pol J Pathol.
1999;50(2):99-106.
Three cases of
sclerosing hemangioma of the lung were studied. All developed in women
aged 28, 32 and 59 years. They had been discovered on routine chest
roentgenograms and then surgically removed. In two cases the tumours
were solitary, in one case there were six tumours varying in size. The
histology of this rare tumour and its various types as well as the
results of immunohistochemical studies have been described, partly
indicating its epithelial origin.
Neuroendocrine
differentiation in 32 cases of so-called sclerosing hemangioma of the
lung: identified by immunohistochemical and ultrastructural study.Am
J Surg Pathol. 1997 Sep;21(9):1013-22.
Thirty-two
cases of so-called sclerosing hemangioma of the lung observed by light
microscopy were further studied by electron microscopy and/or
immunohistochemistry. Three histologic patterns were seen: hemangioma-like,
papillary, and solid. The only significant component representing the
nature of the lesion is characteristic round cells within the stroma
in all these patterns, whereas the surface cells lining the papillary
projections or cystic spaces are normal or are hyperplastic
bronchioloalveolar cells with a few neuroendocrine cells.
Immunohistochemical findings showed that the "stromal cells" (tumor
cells) were positive for neuroendocrine markers, namely, chromogranin
A (19 of 22 cases), neuron-specific enolase (24 of 24), synaptophysin
(six of 10), adrenocorticotropic hormone (14 of 15), growth hormone
(14 of 15), calcitonin (11 of 15), and gastrin (11 of 14). Besides,
some tumor cells were positive for epithelial membrane antigen (four
of four), carcinoembryonic antigen (one of four), and vimentin (one of
one). All tumor cells were negative for polyclonal antikeratin
antibody (25 cases), AE1 (one case), and AE3 (one case). However, in
contrast to the "stromal cells," the surface cells of the cystic
spaces stained positively for keratin (25 of 25 cases), AE1 (one of
one), AE3 (one of one), epithelial membrance antigen (four of four),
and carcinoembryonic antigen (four of four); only a few of them
expressed neruoendocrine markers. Both surface and tumor cells were
negative for factor VIII-related antigen (25 cases), CD31 (one case),
and alpha1-antitrypsin (25 cases). Ten cases further studied by
electron microscopy and six examined by ultrastructural morphometry
showed that the surface cells were mainly type 2 pneumocytes
containing many lamellar bodies in the cytoplasm. Lying among them,
neuroendocrine cells were occasionally seen. The stromal tumor cells
had no lamellar body, but dense core granules (neurosecretory
granules) and microtubules. In six cases, 92.3% (345 of 374) of tumor
cells contained neurosecretory granules, which were pleomorphic and 73
to 1056 nm in diameter (mean, 302 nm). Two to 193 (mean, 12)
neurosecretory granules were found in each tumor cell. Both
immunohistochemical findings and ultrastructural evidence indicate
that so-called sclerosing hemangioma of the lung is a benign lesion
composed of neoplastic neuroendocrine cells with areas of sclerosis. A
suggested name for this tumor is benign neuroendocrine tumor of the
lung. The differentiation between this tumor and papillary adenoma,
bronchioloalveolar carcinoma, or carcinoid tumor of the lung is
discussed.
Papillary
pneumocytoma of the lung. An immunohistochemical and electron
microscopic study. Pathol
Res Pract. 1994 Feb;190(2):194-200.
Papillary
pneumocytoma, so-called sclerosing hemangioma of the lung, is a benign
pulmonary neoplasm. In the present study, clinical aspects,
immunohistochemical characteristics, and ultrastructural findings of
two cases of such tumors are described. Using a panel of various
antibodies, the authors found that cytokeratin, Leu-M1 and Ber-EP4
were expressed only in papillary areas. Similarly, apocrine epithelial
antigen was positive in cells lining papillary stalks. In contrast,
epithelial membrane antigen (EMA) stained cells both in solid and
papillary areas. CD 31, Ulex 1 and factor VIII-related antigen were
positive only in stromal vessels, as desmin and muscle actin. Vimentin
was positive in stromal cells and in papillary areas in one case. KP 1
staining was negative in neoplastic cells. Ultrastructurally, both
neoplastic cell types showed features of epithelial cells, and the
cells lining papillary stalks contained lamellar bodies characteristic
to type II pneumocytes. The evidence obtained clearly shows that the
neoplastic cells of this tumor are of epithelial type; one cell type
represents neoplastic type II pneumocytes, and another cell type
represents the heterogeneous group of epithelial cells, also sharing
features of type I pneumocytes.
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