83 research outputs found
Sequential morphological characteristics of murine fetal liver hematopoietic microenvironment in Swiss Webster mice
Embryonic hematopoiesis occurs via dynamic development with cells migrating into various organs. Fetal liver is the main hematopoietic organ responsible for hematopoietic cell expansion during embryologic development. We describe the morphological sequential characteristics of murine fetal liver niches that favor the settlement and migration of hematopoietic cells from 12 days post-coitum (dpc) to 0 day post-partum. Liver sections were stained with hematoxylin and eosin, Lennert’s Giemsa, Sirius Red pH 10.2, Gomori’s Reticulin, and Periodic Acid Schiff/Alcian Blue pH 1.0 and pH 2.5 and were analyzed by bright-field microscopy. Indirect imunohistochemistry for fibronectin, matrix metalloproteinase-1 (MMP-1), and MMP-9 and histochemistry for naphthol AS-D chloroacetate esterase (NCAE) were analyzed by confocal microscopy. The results showed that fibronectin was related to the promotion of hepatocyte and trabecular differentiation; reticular fibers did not appear to participate in fetal hematopoiesis but contributed to the physical support of the liver after 18 dpc. During the immature phase, hepatocytes acted as the fundamental stroma for the erythroid lineage. The appearance of myeloid cells in the liver was related to perivascular and subcapsular collagen, and NCAE preceded MMP-1 expression in neutrophils, an occurrence that appeared to contribute to their liver evasion. Thus, the murine fetal liver during ontogenesis shows two different phases: one immature and mainly endodermic (<14 dpc) and the other more developed (endodermic-mesenchymal; >15 dpc) with the maturation of hepatocytes, a better definition of trabecular pattern, and an increase in the connective tissue in the capsule, portal spaces, and liver parenchyma. The decrease of hepatic hematopoiesis (migration) coincides with hepatic maturation
Review of chromophobe renal cell carcinoma with focus on clinical and pathobiological aspects
In recent years, the concept of chromophobe
renal cell carcinoma (RCC) has been established.
Chromophobe RCCs account for about 4-6% of all renal
tumors. Macroscopically, the cut surface of the tumor is
generally grey-beige in color. Histologically, there are
two variants (typical and eosinophilic). In the typical
variant, large tumor cells with architecture of a compact
tubulo-cystic pattern proliferate. The cytoplasm is
abundant and shows a fine reticular translucent pattern.
The cell border is thick, prominent and eosinophilic. In
the eosinophilic variant, tumor cells are smaller and
markedly eosinophilic, and a perinuclear halo is often
seen. Histochemically, the tumor cells generally show a
diffuse and strong reaction for Hale's colloidal iron
staining. Ultrastructurally, tumor cells contain many
cytoplasmic microvesicles (150-300 nm). In
chromosomal analysis, a low chromosome number is
characteristic of chromophobe RCCs, due to the frequent
occurrence of a combined loss of chromosomes 1, 2, 6,
10, 13, 17, and 21. In differential diagnosis, histological
distinction from oncocytomas, which share a common
phenotype (intercalated cells of the collecting duct
system), is most important. In this diagnostic setting,
recent studies have given rise to several problems.
Firstly, some cases of coexistent chromophobe RCC and
oncocytoma (so-called renal oncocytosis) or cases of
oncocytoma with metastasis have recently been reported.
Secondly, the existence of chromophobe adenoma, which is the benign counterpart of chromophobe RCC,
and an oncocytic variant of chromophobe RCC has
recently been suggested. Therefore, further studies are
needed to elucidate the relationship between
chromophobe RCCs and oncocytomas, to confirm
whether chromophobe adenoma actually exists or not,
and to identify the key gene that causes chromophobe
RCCs
Review of sarcomatoid renal cell carcinoma with focus on clinical and pathobiological aspects
In sarcomatoid renal cell carcinoma (RCC),
it is generally accepted that the sarcomatoid portion is
derived from metaplastic transformation of carcinoma.
Sarcomatoid RCCs account for about 1-8% of all renal
tumors. Macroscopically, tumors generally form
encapsulated masses and show invasive growth.
Sarcomatoid RCCs originate from all subtypes of RCCs,
including conventional, papillary, chromophobe, and
collecting duct carcinomas. With regard to the growth
pattern of the sarcomatoid component, malignant fibrous
histiocytomatous, fibrosarcomatous and unclassified
sarcomatous patterns are frequently seen.
Immunohistochemically, sarcomatoid RCCs are
generally positive for AE1/AE3, epithelial membrane
antigen (EMA) and vimentin and negative for desmin,
actin and S-100. Little is know about genetic alterations
in sarcomatoid RCCs. Further studies are therefore
needed to identify the key gene involved in sarcomatoid
transformation of RCCs
Review of metanephric adenoma of the kidney with focus focus on clinical and pathobiological aspects
The concept of metanephric adenoma has
become established in recent years. Metanephric
adenoma is a rare neoplasm. Macroscopically, the cut
surface of the tumor displays a tan to gray or yellow
color, and tumors generally form well-circumscribed
masses. Histologically, tumors are composed of small
epithelial cells that form small acini. Glomeruloid
bodies, which are composed of lobulated papillary
projections, are occasionally seen. Although there have
been few studies using chromosomal analysis, two
recent studies have shown partial monosomy or LOH of
2p. On the other hand, the concept of metanephric
tumors has recently become broadened. These tumors
include metanephric adenomas, adenofibromas and
stromal tumors, and they compose a continuous
histological spectrum. Therefore, further studies on
various aspects are needed to identify the gene
responsible for the occurrence of metanephric tumors
and, furthermore, to clarify the association among the
three types of metanephric tumors
High molecular weight caldesmon positive stromal cells in the capsule of hepatocellular carcinomas
Aims: To investigate the smooth muscle nature of the stromal cells in the capsule of hepatocellular carcinomas. Methods: Immunohistochemical analysis using monoclonal antibody to high molecular weight caldesmon (HCD), a highly specific marker for smooth muscle cells, was performed in 33 encapsulated hepatocellular carcinomas and adjacent hepatic tissues. Results: HCD positive stromal cells were detected in the capsule of 21 of the 33 hepatocellular carcinomas examined. Conclusions: The capsule of hepatocellular carcinomas contains smooth muscle cells
Review of papillary renal cell carcinoma with focus on clinical and pathobiological aspects
Recent studies have shown that papillary
renal cell carcinoma (RCC) is clinically and
genotypically a distinct entity. Papillary RCCs account
for about 10-15% of renal parenchymal neoplasms.
Macroscopically, the cut surface is yellow or brown in
color and large tumors frequently show cystic change.
Hemorrhage and necrosis are common. Histologically,
Delahunt and Eble have classified papillary RCCs into
type 1 (small cells, single layer) and type 2 (large cells,
pseudostratification) according to the cytoplasmic
volume and thickness of the lining cells. In
chromosomal analysis, gain of chromosomes 7 and 17,
loss of Y chromosome and additional gains
(chromosome 3q, 8p, 12q, 16q and 20q) are frequently
found in type 1 papillary RCCs, but the chromosomal
aberration of type 2 papillary RCCs seems to be more
heterogenous than that of type 1 papillary RCCs.
Mutations of MET proto-oncogenes in some cases of
both hereditary and sporadic papillary RCCs have
recently been detected. Furthermore, all hereditary and
sporadic papillary RCCs with MET proto-oncogene
show type 1 histological features. Type 1 papillary RCCs
generally seem to have a favorable prognosis, but type 2
tumors have a worse prognosis than do type 1 tumors.
Papillary RCCs with involvement of the X chromosome
and cancer syndrome with predisposition to
cutaneous/uterine leiomyomas and papillary RCCs, the
histological features of which are basically different
from those of usual papillary RCCs, have also been
recently reported. Since papillary RCCs seem to
constitute clinically, histologically, and even genetically
more heterogenous groups than previously thought,
further investigations are needed to characterize the
subtype of papillary RCC
- …