Histology and histopathology Vol.17, nº 1 (2002)

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Effects of chronic administration of either ethanol or pentanol on rat duodenum morphology
(Murcia : F. Hernández, 2002) Vaquera, J.; Vaquera, A.; Girbes, T.
The morphology of the rat duodenum after chronic treatment with 15% (v/v) ethanol and 4% (v/v) pentanol was studied. Male Wistar rats of experimental groups were given ethanol and pentanol for 15 weeks with food and fluid freely available. Ethanol-15% and 4% pentanol-fed rats showed a significantly reduced fluid and food intake as compared with control rats. The study of the mucosa indicated that the number of chronic inflammatory infiltrating (mononuclear cells) and goblet cells was higher in the groups of the ethanol- and pentanol-fed rats than in the control group. There was an increase in the thickness of the brush border in pentanolfed rats. Intervillus adhesion was concurrently observed in the pentanol-fed rats but not in the control or ethanolfed rats. After ethanol feeding many of the villi developed blebs at the apex of the villus or laterally on its upper half. These blebs generally remained intact. In contrast, after pentanol feeding no bleb formation was appreciated. The intake of ethanol and other short chain alcohols present in alcoholic beverages leads to mainfold disturbances on the rat duodenum. These findings suggest that the chronic ingestion of pentanol seems to promote cellular changes but less important than those observed after chronic ethanol ingestion.
Open Access
IIThe glycoconjugate sugar residues of the sessile and motile cells in the thymus of normal and Cyclosporin-A-treated rats: lectin histochemistry
(Murcia : F. Hernández, 2002) Gheri, G.; Gheri Bryk, S.; Riccardi-Arbi, R.; Sgambati, E.; Cirri Borghi, M.B.
It is well known that cell surface glycoconjugates play a determinant role in cellular recognition, cell-to-cell adhesion and serve as receptor molecules. T-lymphocytes are in strict contact with the thymic epithelial cells, which control their process of maturation and proliferation. On the other hand the normal maturation of the epithelial cells is believed to be induced by T-lymphocytes. For these reasons we have studied the glycoconjugates saccharidic moieties of the sessile and motile cells in the thymus of normal male albino Wistar rats and their changes following cyclosporin-A treatment, using a battery of seven HRPlectins. Cytochemical controls were performed for specificity of lectin-sugar reaction. Some sections were pre-treated with neuraminidase prior to staining with HRP-lectins. Our results have demonstrated, in the control rats, a large amount and a variety of terminal and subterminal oligosaccharides within and/or on the epithelial thymic cells and in macrophages. After cyclosporin-A treatment, among the thymic epithelial cells, the subcapsular, paraseptal and perivascular cells showed the loss of some sugar residues, which characterized the same cells in the intact thymus. Some hypotheses are reported on the role played by the glycoconjugate sugar residues in control and cyclosporin-A treated rats.
Open Access
Morphological changes in the mink area postrema during growth and under different stages of sexual activity
(Murcia : F. Hernández, 2002) Aleman, N.; Cerutti, P.; Guerrero, F.
The histological features of the area postrema (AP) of mink brains of both sexes were investigated at different ages and physiological conditions with light and electron microscopy. The mink AP was a twin-winged structure located at the dorsal surface of the medulla oblongata and consisted of neurons, glial cells, and both continuous and fenestrated capillaries enmeshed in a rich neuropil. The ventricular surface of the mink AP was covered by a single layer of tanycytes except at its most caudal part that was covered by a basal membrane derived from the pia mater. Supraependymal cells and intraventricular axons were also a common finding over the apical poles of tanycytes. However, our study demonstrates that the mink AP acquires the above general features at an advanced postnatal time and that, once fully developed, it undergoes morphological changes that can be directly linked to the aging process and sexual activity of the animals.
Open Access
Influence of light-dark, seasonal and lunar cycles on the nuclear size of the pinealocytes of the rat
(Murcia : F. Hernández, 2002) Martínez Soriano, F.; Armañanzas, E.; Ruíz Torner, A.; Valverde-Navarro, A.A.
Morphological and physiological studies suggest a possible division of the pineal parenchyma into an external or “cortical” and another central or “medullar” layer. We have studied the possible influence of the light/dark, seasonal and lunar cycles on the nuclear size of the pinealocytes of the rat in both the hypothetical “cortical” and “medullar” layers. Forty male Wistar rats were used. Experiment was carried out in two seasons, winter and spring, two lunar phases, full moon and new moon, and the two circadian phases, photophase and scotophase. The nuclear volume of the pinealocytes, calculated from the Jacobj’s formula, was the karyometric parameter used as measurement of the nuclear size. Main results showed that nuclear volume of the cortical pinealocytes was greater than that of the medullar pinealocytes only during the photophases of winter new-moon days and spring full moon days, whereas in all the remaining situations, the greater nuclear sizes were found in the pinealocytes of the medullar layer. These results support the existence of independent morphological variations of the pinealocyte in the central and peripheral zones of the pineal gland.
Open Access
Alzheimer ß-amyloid peptides normal and abnormal localization
(Murcia : F. Hernández, 2002) Takahashi, R.H.; Nam, E.E.; Edgar, M.; Gouras, G.K.
Alzheimer's disease (AD) neuropathology is characterized by accumulation of “senile” plaques (SPs) and neurofibrillary tangles (NFTs) in vulnerable brain regions. SPs are principally composed of aggregates of up to 42/43 amino acid ß-amyloid (Aß) peptides. The discovery of familial AD (FAD) mutations in the genes for the amyloid precursor protein (APP) and presenilins (PSs), all of which increase Aß42 production, support the view that Aß is centrally involved in the pathogenesis of AD. Aß42 aggregates readily, and is thought to seed the formation of fibrils, which then act as templates for plaque formation. Aß is generated by the sequential intracellular cleavage of APP by ßsecretase to generate the N-terminal end of Aß, and intramembranous cleavage by g-secretase to generate the C-terminal end. Cell biological studies have demonstrated that Aß is generated in the ER, Golgi, and endosomal/lysosomal system. A central question involving the role of Aß in AD concerns how Aß causes disease and whether it is extracellular Aß deposition and/or intracellular Aß accumulation that initiates the disease process. The most prevalent view is that SPs are composed of extracellular deposits of secreted Aß and that Aß causes toxicity to surrounding neurons as extracellular SP. The recent emphasis on the intracellular biology of APP and Aß has led some investigators to consider the possibility that intraneuronal Aß may directly cause toxicity. In this review we will outline current knowledge of the localization of both intracellular and extracellular Aß.
Open Access
Expression of E-cadherin-catenin complex in human benign schwannomas
(Murcia : F. Hernández, 2002) Hasegawa, M.; Muramatsu, N.; Tohma, Y.; Fukaya, K.; Fujisawa, H.; Hayashi, Yoshihiro; Tachibana, Osamu; Kida, S.; Yamashita, J.; Saito, K.
The Ca2+-dependent cell adhesion molecule E-cadherin has been known to express in normal and reactive Schwann cells in rodents, and to play an important role in Schwann cell-Schwann cell adhesion and maintenance of peripheral nervous tissue architecture. However, little is known about expression of E-cadherin in schwannomas. The aim of the present study was to investigate the cellular expression and localization of E-cadherin, and its associated protein, alpha E-, alpha N- and beta-catenins in human schwannomas, which are supposed to derive from Schwann cells. We tested the hypothesis that these proteins might show an altered expression/distribution in schwannoma cells which correlates with their neoplastic behavior, including sparse cell-cell contact, as seen those in meningiomas and various carcinomas. In human schwannomas, however, E-cadherin, alpha E-catenin, and beta-catenin were detected by western blotting and i m m u n o h i s t o c h e m i s t r y, whereas alpha N-catenin was not. Immunoprecipitation using anti-E-cadherin antibody resulted in alpha E-catenin forming a complex with Ecadherin. SSCP analysis revealed no mutations in the transmembrane domain or in intracellular cateninbinding site of E-cadherin. These data suggest that the Ecadherin- alpha E-catenin complex is well preserved in human schwannoma cells, which is compatible with its benign behavior, and these molecules might be used as additional cell markers of Schwann cell-derived tumors.
Open Access
Changes in the peptidergic innervation in the carotid body of rats chronically exposed to hypercapnic hypoxia: an effect of arterial CO2 tension
(Murcia : F. Hernández, 2002) Kusakabe, T.; Hirakawa, H.; Matsuda, H.; Yamamoto, Y.; Nagai, T.; Kawakami, T.; Takenaka, T.; Hayashida, Y.
The abundance of neuropeptide Y (NPY)-, vasoactive intestinal polypeptide (VIP)-, substance P (SP)-, and calcitonin gene-related peptide (CGRP)- immunoreactive nerve fibers in the carotid body was examined in chronically hypercapnic hypoxic rats (10% O2 and 6-7% CO2 for 3 months), and the distribution and abundance of these four peptidergic fibers were compared with those of previously reported hypocapnicand isocapnic hypoxic carotid bodies to evaluate the e ffect of arterial CO2 tension. The vasculature in the carotid body of chronically hypercapnic hypoxic rats was found to be enlarged in comparison with that of normoxic control rats, but the rate of vascular e n l a rgement was smaller than that in the previously reported hypocapnic- and isocapnic hypoxic carotid bodies. In the chronically hypercapnic hypoxic carotid b o d y, the density per unit area of parenchymal NPY fibers was significantly increased, and that of VIP fibers was unchanged, although the density of NPY and VIP fibers in the previously reportetd chronically hypocapnic and isocapnic hypoxic carotid bodies was opposite to that in hypercapnic hypoxia as observed in this study. The density of SP and CGRP fibers was decreased. These results along with previous reports suggest that d i fferent levels of arterial CO2 tension change the p e p t i d e rgic innervation in the carotid body during chronically hypoxic exposure, and altered peptiderg i c innervation of the chronically hypercapnic hypoxic carotid body is one feature of hypoxic adaptation.
Open Access
Expression of parathyroid hormone-related protein (PTHrP) in parathyroid tissue under normal and pathological conditions
(Murcia : F. Hernández, 2002) Kitazawa, R.; Kitazawa, S.; Maeda, S.; Kobayashi, A.
Parathyroid hormone-related protein (PTHrP), a factor responsible for malignancy associated hypercalcemia, plays a physiological roles such as bone development and placental calcium transport. The expression of PTHrP in adult human parathyroid tissues under normal and pathological conditions was analyzed. By immunohistochemistry, PTHrP expression was detected in 86% of normal parathyroid (12/14 cases), 74% of adenomas (14/19) and 89% of hyperplasia secondary to chronic renal failure (16/18). PTHrP protein was observed mainly in the cytoplasm of oxyphil cells, consistent with the localization of its mRNA demonstrated by in situ hybridization. The rate of PTHrP-positive cells was higher in areas consisting of oxyphil cells than in those of non-oxyphil cells, regardless of whether the parathyroid was normal or pathological. In the normal parathyroid, an age-related increase in PTHrP expression was observed with a relative increase in oxyphil cells, reflecting aging and deterioration of parathyroid tissue. In adenoma, cases with a predominance of oxyphil cells expressed PTHrP, whereas clear cell adenoma did not. In secondary hyperplasia, the rate of PTHrP-expressing cells was higher than in normal parathyroid or adenoma, with varying levels of expression among nodules. We speculate that PTHrP could act through the paracrine/ autocrine mechanism to regulate proliferation and d i fferentiation of normal and neoplastic parathyroid cells.
Open Access
Genetic and epigenetic alterations of tumor suppressor and tumor-related genes in gastric cancer
(Murcia : F. Hernández, 2002) Tamura, G.
Both genetic and epigenetic alterations of tumor suppressor and tumor-related genes involved in the pathogenesis of gastric cancer are reviewed here, and molecular pathways of gastric carcinogenesis are proposed. Gastric carcinomas are believed to evolve from native gastric mucosa or intestinal metaplastic mucosa that undergoes genetic and epigenetic alterations involving either the suppressor pathway (defects in tumor suppressor genes) or mutator pathway (defects in DNA mismatch repair genes). Methylation of E - c a d h e r i n in native gastric mucosa results in undifferentiated carcinomas (suppressor pathway), while methylation of hMLH1 results in differentiated foveolartype carcinomas (mutator pathway). The majority of d i fferentiated gastric carcinomas however, arise from intestinal metaplastic mucosa and exhibit structural alterations of tumor suppressor genes, especially p 5 3. They appear to be related to chronic injury, perhaps due to Helicobacter pylori infection. Approximately 20% of differentiated carcinomas (ordinary-type) have evidence of mutator pathway tumorigenesis. Mutations of E - c a d h e r i n are mainly involved in the progression of d i fferentiated carcinomas to undifferentiated tumors. The molecular pathways of gastric carcinogenesis depend on the histological background, and gastric carcinomas show distinct biological behaviors as a result of discernible cellular genetic and epigenetic alterations.
Open Access
Diabetic nephropathy: The central role of renal proximal tubular cells in tubulointerstitial injury
(Murcia : F. Hernández, 2002) Phillips, A.O.; Steadman, R.
Diabetic nephropathy is now the commonest cause of end stage renal disease and accounts for 30- 40% of all patients requiring renal replacement therapy. Furthermore, the incidence of diabetic nephropathy continues to increase, in part due to the improved survival of type 2 diabetic patients as the cardiovascular mortality in this group declines (Ritz and Stefanski, 1996). Clinically incipient nephropathy is first manifest by the onset of persistent microalbuminuria, after which, overt diabetic nephropathy is heralded by the appearance of persistent proteinuria. Subsequently, there is a progressive decline in glomerular filtration rate (GFR) resulting, within 5 years, in end stage renal disease in 50% of patients (Hasslacher et al., 1989). The pathology of the renal lesions are similar in type I and II diabetes ( Taft et al., 1994), although it has been suggested that there is more heterogeneity in type II diabetes (Chihara et al., 1986). Studies analysing structural-functional relationships have demonstrated that the development of proteinuria correlates with the degree of mesangial expansion (Mauer et al., 1984; White and Bilous, 2000). Although diabetic nephropathy was traditionally considered a primarily glomerular disease, it is now widely accepted that the rate of deterioration of function correlates best with the degree of renal tubulointerstitial fibrosis (Mauer et al., 1984, Bohle et al., 1991). This suggests that although in the majority of patients the primary event is a condition manifest by glomerular changes resulting in proteinuria, the long-term outcome is determined by events in the renal interstitium. Wi t h the increasing awareness of the importance of these pathological interstitial changes, interest has focused on the role of cells, such as the epithelial cells of the proximal tubule (PTC) or the interstitial myofibroblast, in the initiation of fibrosis. The aim of the present review is to analyse the available data supporting the role for the PTC in orchestrating renal interstitial fibrosis in diabetic nephropathy as a result of glucose-dependent alterations in PTC function. The potential for subsequent e ffects on PTC-fibroblast cross-talk will also be considered.
Open Access
Histological study of timing and embryology of notochordal abnormalities in rat exposed in utero to Doxorubicin
(Murcia : F. Hernández, 2002) Menegola, E.; Broccia, M.L.; Di Renzo, F.
Experimental Doxorubicin-exposure in utero is correlated with foetal oesophageal atresia, tracheooesophageal fistula, axial alterations. While gastrointestinal and respiratory defects have been larg e l y investigated, only sporadic data have been published to date on notochordal and vertebral defects. The aim of this work was the study of the genesis of chordal and vertebral abnormalities in rat embryos and foetuses exposed to Doxorubicin and the study of their correlation with oesophageal and tracheal defects. For this purpose, pregnant rats were i.p. injected with saline (control) or with 4mg/Kg b.w. Doxorubicin on days 9.5 and 10.5 of gestation. Embryos and foetuses were morphologically analysed on days 10.5-15 and 16, 18, 20 of gestation respectively, fixed in formaldehyde and histologically processed. Slides were routinely stained with haematoxylin-eosin (11-15 days post coitum embryos and all foetuses) or specifically stained with aniline blue for the staining of basal laminae (10.5 days post coitum embryos). Moreover, some foetuses at term (20 days post coitum) were processed for bone and cartilage staining. The data obtained in the present work confirm the specificity of Doxorubicin in inducing gastro-intestinal and tracheal defects, describe the genesis of these defects step by step, describe the type and the genesis of notochordal abnormalities and their fate and exclude the role of Doxorubicin in inducing axial skeletal malformations.
Open Access
Ultrastructural abnormalities of muscle spindles in the rat masseter muscle with malocclusion-induced damage
(Murcia : F. Hernández, 2002) Bani, D.; Bergamini, M.
Human temporomandibular disorders due to disturbed occlusal mechanics are characterized by sensory, motor and autonomic symptoms, possibly 1 related to muscle overwork and fatigue. Our previous study in rats with experimentally-induced malocclusion due to unilateral molar cusp amputation showed that the ipsilateral masseter muscles undergo morphological and biochemical changes consistent with muscle hypercontraction and ischemia. In the present study, the masseter muscle spindles of the same malocclusionbearing rats were examined by electron microscopy. Sham-operated rats were used as controls. In the treated rats, clear-cut alterations of the muscle spindles were observed 26 days after surgery, when the extrafusal muscle showed the more severe damage. The fusal alterations affected predominantly capsular cells, intrafusal muscle fibers and sensory nerve endings. These results suggest that in the malocclusion-bearing t rats, an abnormal reflex regulation of the motor activity of the masticatory muscles may take place. They also allow us to hypothesize that muscle spindle alterations might be involved in the pathogenesis of human temporomandibular disorders.
Open Access
Identification of dendritic cells in aortic atherosclerotic lesions in rats with diet-induced hypercholesterolaemia
(Murcia : F. Hernández, 2002) Ozmen, J.; Bobryshev, Y.V.; Lord, R.S.A.; Ashwell, K.W.S.
We have previously identified dendritic cells (DCs) in the intima of human large arteries. These vascular DCs are common in atherosclerotic lesions but their immature forms are also present in normal arterial intima. Pathophysiological studies on vascular DCs are limited because they have only been studied in human specimens obtained at operation or post-mortem. The aim of the current study was to determine whether DCs participate in the development of atherosclerotic lesions in hypercholesterolemic rats. Male Wistar rats were divided into a control (n=13) and experimental cohort (n=48). The experimental animals were fed an atherogenic diet and 1% saline, while the controls were fed standard rat cubes and water. The aortas were obtained from both groups at 10, 20, and 30 weeks following commencement of the diet. An en face immunohistochemical technique, routine section i m m u n o h i s t o c h e m i s t r y, and transmission electron microscopy were used to detect the presence of DCs in the aortas. Examination of the aortas showed that S100+ cells with dendritic cell morphology were present in the aortic intima of hypercholesterolemic rats. The S100+ DCs displayed immunopositivity for OX-62 and MHC Class II antibodies. Within various types of atherosclerotic lesions, these cells were clustered throughout the intima but were especially prominent around arterial branch-points where they co-localized with various cell types, including T-cells and macrophages. Ultrastructural analysis confirmed the presence of cells with characteristics typical of DCs. These features included the presence of a welldeveloped tubulovesicular system, dendritic processes, and a lack of secondary lysosomes and phagosomes. This study establishes the presence of DCs in the aortic intima of rats with diet-induced atherosclerosis. The presence of DCs in this model of experimental atherogenesis could provide a new approach to investigating the function of DCs and may help clarify the immune-inflammatory mechanisms underlying atherosclerosis.
Open Access
Gelatinases and their inhibitors in tumor metastasis: from biological research to medical applications
(Murcia : F. Hernández, 2002) Giannelli, G.; Antonaci, S.
The involvement of matrix metalloproteinase (MMPs)-2 and -9, also known as gelatinases, in cancer cell migration and invasion has been well documented, although it is not yet clear how they facilitate metastasis formation in the course of malignancies. The idea that gelatinases are responsible for degradation of extracellular matrix (ECM) components and breakdown of basement membrane (BM) tissue boundaries has turned out not to be entirely correct. An action by remodelling the ECM components of the BM exposing new cryptic sites, or releasing growth factors, cytokines, or active ECM proteolysed fragments seems to be nearer to the truth. On the other hand, tissue inhibitors of gelatinase activity (TIMP-2), are involved both in the MMP-2 activation process, in concert with membrane type 1-MMP (MT1-MMP), and in the inhibition of gelatinolytic activity. Therefore proteolysis, the central step for cancer metastasis, should occur as a result of an imbalance between MMP-2 and TIMP-2. Many studies have reported the importance of this balance in patients with different malignancies, and considerable effort is currently being spent on the study of molecules that can shift the balance in favour of inhibition of MMP proteolytic activity. In this review we focus on the role of gelatinase activity in cancer invasion, addressing the following issues: how and where proteolysis occurs in cancer tissues, how it can be regulated, what the clinical implications are of the studies reported in literature so far, and finally what the future developments in this field that could have an impact on the management of patients affected by malignancies may be.
Open Access
Chronic hypoxia induced ultrastructural changes in the rat adrenal zona glomerulosa
(Murcia : F. Hernández, 2002) Lorente, M.; Mirapeix, R.M.; Miguel, M.; Longmei, W.; Volk, D.; Cervós-Navarro, J.
The adrenal cortex plays an important role in adaptation to various forms of stress, including hypoxia. While physiological changes in the aldosterone metabolism during hypoxia have been extensively described, few studies have focused on the morphological changes in the adrenal glands under chronic hypoxia. We studied the ultrastructure of the z o n a g l o m e ru l o s a of 6-month-old Wistar rats exposed to chronic normobaric hypoxia. Animals were divided into two groups: control (n=12) and hypoxic (n=12). In this latter group, the animals were kept at 7% O2 concentration after a gradual adaptation (21, 15, 12, 10, 8, 7 vol% O2 ). The duration of the study was 112 days. In comparison with normoxic rats, body weight and adrenal gland weight of hypoxic animals was significantly reduced by 18.5% (p=0.006) and 14.7% (p=0.001) respectively. The thickness of the z o n a glomerulosa decreased due to atrophy of cells. The main ultrastructural changes observed were: 1) a decrease in, or complete elimination of, lipid droplet content; 2) a marked increase in lysosome number; and 3) the presence of giant mitochondria. Our findings show that rats fail to adapt to severe chronic hypoxia. The ultrastructural changes in the zona g l o m e ru l o s a found in the present study could reflect changes in the aldosterone pathway.
Open Access
Expression, function and clinical relevance of MIA (Melanoma Inhibitory Activity)
(Murcia : F. Hernández, 2002) Bosserhoff, A.K.; Buettner, R.
Despite its ambiguous name the protein melanoma-inhibitory-activity (MIA) was identified as a key molecule involved in progression and metastasis of malignant melanomas. Therefore, in this review we intend to update the current knowledge on expression patterns, transcriptional regulation, function and clinical relevance of MIA. Furthermore, we will cover the recently discovered MIA homologous proteins OTOR/MIAL, MIA 2 and TANGO. In order to identify autocrine growth-regulatory factors secreted by melanoma cells, MIA was purified and cloned. Subsequent analyses of non-neoplastic tissues revealed specific MIA expression patterns in cartilage. In neoplastic tissues MIA expression was detected in malignant melanomas, in chondrosarcomas and less frequently in a variety of diff e r e n t adenocarcinomas including breast and colon cancers. For melanoma cells and chondrocytes it was shown that regulation of expression pattern was controlled on the level of mRNA transcription by defined transcription factors. Evidence obtained from in vitro and in vivo experiments indicated that MIA plays an important functional role in melanoma metastasis and invasion. A number of studies from different laboratories evaluated MIA as a highly specific and sensitive marker, clinically useful for follow-up and therapy-monitoring of patients with malignant melanomas. In addition, preliminary data suggests a further potential application as a surrogate marker for measuring cartilage damage in rheumatoid arthritis. Recently, it has become evident that MIA belongs to a gene family of four homologous proteins, MIA, OTOR (FDP, MIAL), MIA 2 and TANGO. Determination of the three-dimensional structure in solution identified MIA as the first member of this novel family of secreted, extracellular proteins adopting an SH3 domain-like fold. The data suggest specific protein-protein interactions with components of the extracellular matrix and possibly
Open Access
Immunoreactivity of Lewis blood group and mucin peptide core antigens: Correlations with grade of dysplasia and malignant transformation in the colorectal adenoma-carcinoma sequence
(Murcia : F. Hernández, 2002) Baldus, S.E.; Hanisch, F.G.; Pütz, C.; Flucke, U.; Mönig, S.P.; Schneider, P.M.; Thiele, J.; Hölscher, A.H.; Dienes, H.P.
Previous studies on the immunoreactivity of various mucin peptide and carbohydrate antigens in neoplastic colorectal tissues led to at least in part contradictory results. Therefore, we investigated a series of 42 adenomas and 44 carcinomas applying monoclonal antibodies (mabs) directed against Lewis blood group antigens (sialyl-Lea, Lex, sialyl-Lex, Ley) as well as mucin peptide cores (MUC1, MUC2 and MUC5AC) by i m m u n o h i s t o c h e m i s t r y. A statistically significant positive correlation between the development of highgrade dysplasia in colorectal adenomas and the immunoreactivity of Le y and MUC1 epitopes was observed, whereas MUC2 exhibited a significant negative correlation. The reactivity of the other epitopes did not show an association with the progression of malignant transformation. Colorectal carcinomas were subdivided according to their histopathological subtype. The immunohistochemical staining resulted in a significantly stronger MUC2 reactivity of mucinous vs. tubular adenocarcinomas. Immunoreactivity of the MUC1-specific mab, which does not react with the fully glycosylated peptide core, showed a statistically nonsignificant inverse tendency, whereas all carbohydrate antigens displayed a strong expression in both tumor subtypes. Furthermore, correlations between mucin peptide and carbohydrate epitope labelling were evaluated. Progression of the adenoma-carcinoma sequence was accompanied by an increase of Ley as well as MUC1 antigen and an increase of all Lewis antigens compared to MUC2 immunoreactivity. On the other hand, mucinous carcinomas exhibited an inverse pattern. In conclusion, these results demonstrate that Ley a n d MUC1 immunoreactivity correlate with malignant transformation in the colorectum, whereas MUC2 represents a marker for low-grade dysplasia and the subtype of mucinous carcinomas.

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