Alcian Blue Pas Special Stain Is Negative for Intestinal Metaplasia Cpt
Gut. 2003 Jun; 52(6): 807–812.
Gastric abdominal metaplasia as detected by a monoclonal antibody is highly associated with gastric adenocarcinoma
Z K Mirza
oneDepartments of Medicine and Pathology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ, USA
Chiliad Grand Das
1Departments of Medicine and Pathology, UMDNJ-Robert Wood Johnson Medical Schoolhouse, New Brunswick, NJ, United states
J Slate
aneDepartments of Medicine and Pathology, UMDNJ-Robert Forest Johnson Medical School, New Brunswick, NJ, The states
R North Mapitigama
2Muhlenberg Regional Medical Center, Plainfield, NJ, USA
P Due south Amenta
1Departments of Medicine and Pathology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ, The states
L H Griffel
1Departments of Medicine and Pathology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ, USA
L Ramsundar
1Departments of Medicine and Pathology, UMDNJ-Robert Forest Johnson Medical School, New Brunswick, NJ, United states of america
J Watari
iiiAsahikawa Medical College, Asahikawa, Nippon
K Yokota
3Asahikawa Medical College, Asahikawa, Japan
H Tanabe
3Asahikawa Medical College, Asahikawa, Nippon
T Sato
threeAsahikawa Medical College, Asahikawa, Japan
Y Kohgo
3Asahikawa Medical Higher, Asahikawa, Nihon
M M Das
oneDepartments of Medicine and Pathology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ, U.s.a.
Abstract
Groundwork: Some forms of gastric intestinal metaplasia (GIM) may be precancerous but the cellular phenotype that predisposes to gastric carcinogenesis is not well characterised. Mucin staining, as a means of differentiating GIM, is difficult. A monoclonal antibody, mAb Das-1 (initially called 7E12H12), whose staining is phenotypically specific to colon epithelium, was used to investigate this issue.
Methods: Using mAb Das-i, by a sensitive immunoperoxidase analysis, we examined histologically confirmed GIM specimens from 2 countries, the USA and Japan. A total of 150 patients comprised three groups: group A, GIM (fields away from the cancer area) from patients with gastric carcinoma (north=60); group B, GIM with chronic gastritis (without gastric carcinoma) (n=72); and group C, chronic gastritis without GIM (n=xviii).
Results: Fifty vi of 60 (93%) patients with GIM (both goblet and non-goblet metaplastic cells) from grouping A reacted intensely with mAb Das-1. Cancer areas from the aforementioned 56 patients besides reacted. In contrast, 25/72 (35%) samples of GIM from patients in group B reacted with mAb Das-1 (group A v B, p<0.0001). None of the samples from group C reacted with the mAb.
Conclusions: Reactivity of mAb Das-1 is clinically useful to simplify and differentiate the phenotypes of GIM. The colonic phenotype of GIM, as identified past mAb Das-1, is strongly associated with gastric carcinoma.
Keywords: monoclonal antibiotic, Das-i, colonic-blazon metaplasia, gastric carcinogenesis
Morphological changes in the mucosa of the tummy, resembling that of the intestine, constitute the condition known every bit intestinal metaplasia. Gastric abdominal metaplasia (GIM) is not a single entity but rather a heterogeneous group of metaplastic changes.1 Matsukura et al divided GIM into complete (minor intestinal) and incomplete (colonic) varieties using enzyme techniques.2 Another nomenclature categorised GIM into three types: I (complete), and Two and Three (incomplete).iii This is based on the fact that pocket-sized abdominal goblet cells produce sialoglycoprotein that stains with periodic acrid-Schiff (PAS) and alcian blue (AB), and colonic goblet cells produce sulphomucin that is detected past AB/high fe diamine (HID) staining.1, 4, 5
Incomplete GIM appears to carry the highest preneoplastic potential for the intestinal variety of gastric carcinoma, which is the most common type of gastric carcinoma; even though some studies have also linked complete GIM with gastric carcinoma.6 Using histological and histochemical mucin staining techniques, it has been hard to accurately ascertain the phenotypic differentiation of GIM due to observer dependent variability in identifying subtle colour differences.7 This state of affairs is often further complicated past the coexistence of unlike types of GIM and the presence of "mosaic cases", which have been reported to occur in 41% of patients. A biomarker(southward) to reliably differentiate various types of GIM, and identify patients who may exist at a higher risk of developing gastric carcinoma, would be clinically very useful.
Using a colon epithelial protein, we adult a novel murine monoclonal antibody, mAb Das-1 (formerly known every bit 7E12H12, IgM isotype), that reacts with colonic epithelium.viii Using both immunoperoxidase and immunofluorescence assays, we and others have independently demonstrated that mAb Das-1 specifically reacts with colonic epithelium (both goblet and non-goblet absorbent cells) but not with small intestinal enterocytes (including goblet cells) from the jejunum or ileum, or normal epithelium from the residuum of the gastrointestinal tract.viii, 9 Although mAb Das-ane does not react with normal gastric and oesophageal epithelium, it reacts sensitively (95%) and specifically (100%) with Barrett'due south epithelium and adenocarcinoma of the oesophagus, indicating a strong association of its reactivity to this precancerous status.ten, xi
In the present study, we explored if mAb Das-one reactivity helps to identify the colonic phenotype of metaplasia in the stomach and its clan with gastric carcinoma. We examined the immunoreactivity of the mAb against the tissue with different histological spectra of chronic gastritis start at an early phase before the development of GIM, in the intermediate stage when GIM had developed but no cancer was detectable, and finally in the stage where GIM was associated with gastric carcinoma. As gastric carcinoma is more common in Japan, we compared the reactivity in the tissue specimens obtained from the USA (New Jersey, NJ) and Japan.
MATERIALS AND METHODS
Paraffin embedded tissue blocks were obtained from 150 patients from NJ and Nippon.
Grouping A (n=60)
Nosotros used the reckoner database of the pathology departments to randomly select 60 tissue blocks with a diagnosis of GIM associated with gastric carcinoma. 30 five patients from Nihon (group A1) and 25 from NJ (group Aii) were included. For each of these 60 patients, paired samples of stomach (surgical specimens) included both cancer areas and histologically proved GIM areas away from the cancer segments.
Group B (n=72)
Biopsy tissue specimens containing GIM without gastric carcinoma were obtained both from Japan (group B1, n=31) and NJ (group Btwo, n=41).
Group C (northward=eighteen)
Eighteen biopsy samples were obtained from Japan with chronic gastritis, without prove of GIM. The biopsy samples in groups B and C were obtained during routine upper endoscopy procedures for a diverseness of indications (usually dyspepsia and peptic ulcer disease) other than gastric carcinoma.
V serial 5 μm sections were obtained from all of the blocks. Haematoxylin-eosin (H&Due east) staining was performed on the first and terminal department cut from each cake and reviewed to ensure the presence of histological abnormalities in both of the sections from the aforementioned block. The 2d to fourth sections were used for immunohistochemical studies. All samples from groups A and B (excluding cancer blocks) had GIM that was observed in both the initial and final H&E sections. 1 of the sections from each patient was examined with mAb Das-ane using a sensitive immunoperoxidase assay, as described previously.10, 11 Each experiment also included at to the lowest degree 2 slides of normal colon and jejunal tissue sections as positive and negative controls, respectively. Reactivity to mAb Das-1 was considered positive if a crisp gilded brown staining of cells was present. Ii investigators (ZKM and KMD) and a single pathologist (PSA) reviewed each slide together. A substantial number of cells, and more than one gland, had to be reactive to mAb Das-one before a specimen was considered positive. If only an occasional goblet cell was stained, the sample was considered negative. There was understanding among the investigators more than than 95% of the fourth dimension.
Using standard protocols,12 76/132 GIM tissue samples (group A, 35; group B, 41) were too stained with AB (pH two.5)/PAS and AB (pH 2.5)/HID to further subcategorise GIM into various types or "mixed" varieties, based on different colours of mucins displayed by neutral versus sialo or sulphomucins. The remaining tissue samples were not bachelor for mucin staining considering of the small-scale size of the tissue in which deeper sections did not accept enough mucosa. "Mixed" diversity was defined equally the presence of both complete and incomplete GIM types in the same tissue section, without a articulate predominance of either type. A sample was considered having "predominantly" complete or incomplete if either variety represented more than than 75% of the GIM area. Coded slides of mucin staining were interpreted by the single pathologist (PSA). Subsequently, the code was broken and staining of mAb Das-1 and mucin stains were compared to identify the corresponding areas.
RESULTS
Demographic data of patients in group A (GIM from patients with gastric carcinoma), group B (GIM without associated gastric carcinoma), and group C (chronic gastritis tissue without GIM) are shown in table 1▶. There were no statistically significant differences amid the three groups. Within group A, mean age (SD) for Japanese patients (group Aone) was 65.v (9) years (range 43–82) and mean historic period of patients from NJ (grouping Atwo) was 78.4 (5.nine) years (range 69–91) (p<0.002). Yet, in group B, in that location were no meaning differences in historic period; hateful (SD) historic period of patients from Japan (group B1) was sixty (14) years (range xviii–76) and in patients from NJ (group B2), 63 (19) years (range 31–92).
Table 1
Patient demographics
| Grouping* | Mean (SD) age (y) | Males (%) |
|---|---|---|
| Group A (north=60) | 68.8 (10.0) | 60 |
| Grouping B (north=72) | 64.nine (17.5) | 53 |
| Group C (n=18) | 62.8 (xv) | 72 |
Fifty vi of 60 (93%) samples of GIM from carcinoma patients, away from the cancer expanse (group A), reacted intensely with mAb Das-1. These included 33/35 (94%) patients from Japan (grouping Ai) and 23/25 (92%) patients from NJ (grouping A2) (fig one▶). Both goblet and non-goblet metaplastic cells only in the GIM areas clearly reacted with mAb Das-1 (fig two▶). The residuum of the gastric tissue was negative. In contrast with group A, but 25/72 (35%) GIM samples from patients without gastric carcinoma (group B) reacted with mAb Das-1 (fig 3C▶) while 65% did not react (fig 3F▶). None of the samples with chronic gastritis without GIM (group C) reacted with the antibody. The difference betwixt the immunoreactivity of mAb Das-one against GIM in grouping A versus group B and group B versus C was highly statistically significant (p<0.0001 and p<0.003, respectively) (fig 1A▶). The cancer area from each of the 56/60 patients from grouping A, whose GIM tissue samples (away from the cancer area) were positive with mAb Das-i, also reacted with the mAb (fig 4▶).
Grouping A represents gastric intestinal metaplasia (GIM) tissue from patients with gastric carcinoma located away from the cancer area, group B represents GIM tissue from patients without gastric carcinoma, and grouping C represents gastric mucosal biopsies (with no GIM) obtained during routine upper endoscopy (used as controls). (A) Statistical analyses amidst the total patient groups from Nihon and New Jersey (NJ). (B) Differences in each group and between the two countries. Aone versus Bane, p<0.0001; A2 versus B2, p<0.0001; A1 versus Aii, non significant; B1 versus Btwo, p<0.01.
Various stainings of the serial sections from the antrum of the stomach with gastric abdominal metaplasia (GIM) (away from the gastric carcinoma area) from group A (original magnification 160× for each function except (E) (250×)). (A) Haematoxylin-eosin staining showing preponderance of goblet cells indicating the presence of GIM. (B) Immunoperoxidase staining with the monoclonal antibody mAb Das-one showing specific reactivity of the metaplastic glands. Reactivity is clearly axiomatic both in goblet and non-goblet cells. Notation there is no reactivity with the balance of the tummy mucosa. (C) College magnification of the boxed area from (B). Intense reactivity of mAb Das-1 against the glandular epithelium, including both non-goblet and goblet cells is evident. Reactivity is intense along the basolateral and upmost domains. (D) Immunoperoxidase staining of normal colon mucosa with mAb Das-i equally a positive control. The reactivity (golden brown colour) is seen in both goblet and non-goblet cells with no reactivity of the lamina propria. Reactivity is more than intense in the crypt area along the basolateral domain. (E) Immunoperoxidase staining of the jejunal mucosa with mAb Das-1 and counterstained with toluidine blue. mAb Das-1 did non react with the jejunal enterocytes.
Serial sections of formalin fixed paraffin embedded biopsy tissue from two patients with gastric intestinal metaplasia (GIM) without carcinoma (group B). Haematoxylin-eosin staining (A, D), alcian bluish/loftier iron diamine staining (B, Eastward), and immunoperoxidase analysis with the monoclonal antibiotic mAb Das-1 (C, F). (A–C) is from the same patient and (D–F) from the second patient. mAb Das-1 stained both goblet cells (shorter arrow) and metaplastic non-goblet cells (longer arrow) in the glands (C). While GIM is conspicuously evident with the presence of goblet cells (D, E), mAb Das-1 did non stain the glands (F). The arrow shows the unstained goblet cells (original magnification 160× for each part).
Haematoxylin-eosin (A) and immunoperoxidase (B) staining of the serial sections from a gastric carcinoma specimen. Intense cytoplasmic staining of the cancer cells with monoclonal antibody mAb Das-ane is clearly evident (original magnification 160×).
Although the reactivity of mAb Das-1 confronting GIM associated with cancer was similar in patients from Japan (Ai) and NJ (A2), in patients with GIM without cancer (grouping B) the reactivity in Japanese patients (subgroup B1) was higher (52%) compared with NJ patients (22%) (subgroup B2). This difference was statistically meaning (p<0.01) (fig 1B▶). The difference between patients in subgroups B1 and B2 may be due to a higher prevalence of Helicobacter pylori infection in Japanese patients. H pylori status was available for each of 31 Japanese patients (group B1) but non for the NJ grouping (B2). Nineteen of 31 (61%) patients were H pylori positive whereas 12 were negative. Indeed, amid these Japanese patients, mAb Das-1 reactivity was higher (13/xix; 68%) in the GIM associated with the H pylori positive group compared with the H pylori negative grouping (3/12; 25%). This difference was highly statistically pregnant (p<0.001).
Each of the samples of GIM that reacted positively with mAb Das-1 showed intense, more often than not cytoplasmic, staining in the goblet cells. In not-goblet metaplastic cells, reactivity was more intense in the basolateral and upmost areas (fig 2B, 2C▶), with calorie-free cytoplasmic staining. In the cancer tissue, staining with mAb Das-1 was intense, lengthened, and mostly cytoplasmic (fig 4▶). Portions of the normal gastric mucosa, including the stroma, did not react with mAb Das-one (figs 2B, 2C, 3C, 3F, and 4B▶ ▶ ▶).
On reviewing mucin stains (AB/PAS and AB/HID), the majority of the slides showed coexistence of "complete" and "incomplete" GIM phenotypes, with a predominance of either variety, or clearly a "mixed" pattern of staining (table 2▶). Mapping of selected areas of stained slides showed a consistent correlation between the predominantly "incomplete" type of GIM (type II or III) and mAb Das-i immunoreactivity (table 2▶).
Table 2
Comparing of monoclonal antibody mAb Das-one and mucin staining (alcian blue/periodic acrid-Schiff and alcian blue/loftier iron diamine) in gastric abdominal metaplasia (GIM)*
| GIM blazon on the basis of mucin stain | ||||
|---|---|---|---|---|
| GIM | MAb Das-ane reactivity | Complete | Incomplete | Mixed |
| Grouping A†(due north=35) | Positive (n=33) | 9‡ | 6 | 18 |
| Negative (n=ii) | 2 | 0 | 0 | |
| Total | xi | 6 | 18 | |
| Group B (north=41) | Positive (n=9) | 3‡ | 3 | 3 |
| Negative (due north=32) | 27 | ane | 4 | |
| Full | 30 | 4 | 7 | |
Irrespective of group A or group B, 9/10 (xc%) of the "incomplete" type of GIM reacted with mAb Das-1 (tabular array 2▶). Nonetheless, 12/41 (29%) "complete type" (type I, or pocket-sized intestinal phenotype) of GIM too reacted with mAb Das-1, suggesting the difficulty in articulate separation of incomplete versus complete types of GIM. Nine of these 12 "complete" types that were reactive to mAb Das-1 belonged to group A (GIM associated with cancer) and the remaining three were from grouping B (GIM without cancer). This departure between groups A and B (9/eleven (82%) 5 three/30 (10%)) was highly pregnant (p<0.0001) (table two▶). Thus it is clearly evident that mAb Das-1 reactivity is strongly associated with GIM in the presence of gastric cancer, irrespective of "complete" (type 1) or "incomplete" (types 2 or Three) types, with 82% and 100% positivity, respectively (table 2▶). The cancer areas from each of the same patients (paired samples) besides reacted with mAb Das-1.
Eighteen of 35 (51%) GIM samples in group A and seven/41 (17%) in group B were of "mixed" multifariousness, as divers by mucin histochemistry. Of these, 18/18 (100%) samples in group A and three/7 (43%) in grouping B were positive with mAb Das-one, further supporting the assertion of the ability of mAb Das-i to identify the "high run a risk" phenotype in the "mixed" group.
Give-and-take
In this study, we accept described a monoclonal antibody (mAb Das-1) that showed immunoreactivity in 93% of specimens of GIM associated with gastric carcinoma (grouping A) simply away from the cancer areas. Furthermore, the gastric carcinoma areas from the same 56/sixty patients besides strongly reacted with mAb Das-1. Immunoreactivity of mAb Das-1 in this group was similar in both Japanese and NJ patients. Withal, immunoreactivity was significantly (p<0.0001) higher in group A compared with GIM in non-cancer (group B) patients, both from Japan and NJ. Using patients from Japan who were at a higher risk than those from NJ, the data besides showed complete lack of reactivity of mAb Das-1 in chronic gastritis in the absenteeism of GIM (group C). These data demonstrate that GIM recognised by mAb Das-1, including both incomplete or colonic-type and complete or pocket-size intestinal-type, carries a risk of developing gastric carcinoma.
Gastric adenocarcinoma is the second most common malignancy and crusade of cancer related death worldwide.13 The prognosis of patients with surgically treated early gastric carcinoma, defined as carcinoma bars to the mucosa or submucosa, is fantabulous, with reported five twelvemonth survival rates of 90–95%.half-dozen, fourteen This survival rate can but be achieved if gastric carcinoma is detected at an early phase.
Epidemiological long term follow up studies and histological data support the notion that GIM and intestinal-type gastric carcinoma are closely linked.6, fifteen, 16 Colonic-type GIM carries the highest gamble for the abdominal-type of gastric carcinoma.6, 17 At the present fourth dimension, GIM (all various types) is recognised past the presence of goblet cells on H&E, or by AB staining, if goblet cells are not readily credible past routine histology. The significance of the latter stain has likewise been a source of some controversy because of its staining of normal neck cells and a "blueish blush" in some of the not-goblet epithelial cells.18 A combination of mucin stains (AB/PAS and AB/HID) is currently used to differentiate GIM into complete or incomplete varieties, or into types I, Two, and 3. Subtle changes in the colour shades of these stains—for case, blue, magenta, and regal—are the basis of recognition of these subtypes of GIM. Relying on these colour differences can be labour intensive and largely subjective, with significant interobserver variation. In addition, normal gastric tissue that should show the presence of neutral mucins only may show traces of acid mucins. For instance, in the body of the stomach, the base of operations of the glandular pits usually stains a faint bluish, and the mucous gland cells a faint gray, suggesting secretion of sialomucin and possibly sulphomucin, respectively.4 Electron microscopy and quantification of histochemical staining by image analysis take too been used in the past with variable results.19
Immunoperoxidase staining with mAb Das-i can be performed easily using a series section from a paraffin cake, along with routine histology. Equally mAb Das-1 does not react with small intestinal epithelium,eight– x its reactivity to GIM demonstrates the presence of a true colonic phenotype of GIM. Furthermore, reactivity with mAb Das-1 results in a well-baked golden brown colour restricted to intestinal glandular and goblet cells. These are easy to identify compared with multiple shades of a similar color in the example of complex mucin histochemistry.
In our experience, a "pure" single type of GIM is less common and, in fact, the bulk of our specimens in the carcinoma associated GIM group showed coexistence of both complete and incomplete types of GIM in the same section, with a predominance of ane or the other. Eighty ii per cent of "complete" blazon GIM from the gastric cancer grouping (grouping A) and but ten% of the "complete" type from the not-cancer group (grouping B) reacted with mAb Das-1 (p<0.0001). This suggests the difficulty of authentic separation of "consummate" blazon of GIM by mucin histochemistry in relation to the predisposition to gastric carcinogenesis. Furthermore, these data indicate the difference in the cellular phenotype of GIM betwixt the cancer and non-cancer groups, and a strong clan of mAb Das-1 reactive epitope in GIM associated with gastric carcinoma.
The significant departure in mAb Das-ane staining between groups A and B was evident, irrespective of the location of tissue, such equally in the body or antrum of the stomach. Nonetheless, information technology is intriguing that the reactivity of mAb Das-1 against GIM from the overall Japanese patients with no history of gastric carcinoma (grouping Bone) was significantly (p<0.01) higher compared with the similar grouping from NJ (grouping Btwo) (52% v 22%), although mean age in both groups was non significantly different. This deviation betwixt the two countries may be due to environmental factors that predispose to the carcinogenic phenotype of GIM in Japanese patients. The difference may also exist a result of the chronicity of gastritis and GIM due to H pylori infection which has a higher incidence and early conquering in Japanese patients compared with those in NJ. This hypothesis is supported by the fact that even within the same population of Japanese patients, mAb Das-1 reactivity was significantly (p<0.001) higher in H pylori positive compared with H pylori negative patients (68% v 25%). The per centum of positivity of GIM to mAb Das-1 in the H pylori negative group from Japan was in a similar range as that observed in a population from NJ11 and from Boston.20 Unfortunately, the H pylori status of NJ patients was unknown just could be expected to be much lower than in the Japanese population. H pylori status was too bachelor for all of the 35 GIM with cancer patients from Japan (group Aone) just not from NJ (group Atwo). 30 of 35 (86%) patients in group A1 were positive for H pylori . Reactivity to mAb Das-1 against this group (Aone) was significantly higher than in the subgroup Bane (GIM without carcinoma patients from Japan) (94% 5 52%; p<0.01). Similarly, immunoreactivity with mAb Das-ane in GIM from NJ patients, with and without carcinoma (Aii v B2), was significantly dissimilar (92% v 22%; p<0.0001). These data suggest that chronic H pylori infection clearly predisposes to the colonic phenotype of GIM although at that place may be additional factors for gastric carcinogenesis. However, irrespective of geographical location and aetiologic factors, colonic metaplasia is strongly associated with gastric carcinoma. Geographic differences in the incidence and distribution of GIM have likewise been reported, although the phenotype of GIM in these particular patients is unknown.21
In a recent written report by Glickman et al, the apply of mAb Das-1 was studied in determining the cellular phenotype of Barrett's oesophagus and GIM from various gastric locations in patients without a history of gastric carcinoma.twenty All cases in their written report of a consummate-type of GIM from the gastric antrum were negative for mAb Das-one, stressing the fact that there is a lack of incomplete or colonic phenotype in non-cancer patients. Furthermore, in this report from Boston, the frequency of mAb Das-1 reactivity in GIM from the antrum was comparable with our grouping B patients from NJ (thirteen% v 22%). In our previous reports,10, xi mAb Das-1 showed a remarkable sensitivity and specificity in detecting Barrett's oesophagus, and has helped differentiate Barrett's oesophagus from GIM of the gastric cardia.20 The 95% reactivity of mAb Das-1 with specialised columnar epithelium in Barrett's oesophagus past the states10 and by others,20 that has been strongly associated with adenocarcinoma of the oesophagus,22 tin exist compared with the 93% reactivity in the GIM from gastric carcinoma patients, suggesting a precancerous phase that is detected by mAb Das-1. This is farther supported by the fact that the cancer areas from the same 56/lx (93%) patients with gastric carcinoma also reacted with the antibody. Indeed, staining in the cancer cells was, in full general, more intense and lengthened. These data, in addition to earlier reports,six, 23 strongly propose that a metaplastic process of colonic phenotype is involved in the histogenesis of most of the gastric carcinoma. That mAb Das-i recognises an epitope associated with precancerous states of epithelial tissue is also supported past its reactivity against chronic cystitis profunda that leads to bladder carcinoma24 and to adenomatous polyps of the modest intestine, particularly associated with familial polyposis and with small intestinal carcinoma.25 The smaller percentage (approximately 10%) of gastric carcinomas that did not react with mAb Das-one may have a different cellular phenotype. Indeed, 2/iv non-reactive cancers were histologically of the diffuse-type. In our earlier study, for example, each of the 13 squamous cell carcinomas of the oesophagus did not react with mAb Das-one,10 and similarly, carcinoma of the prostate did non react with mAb Das-one 26, whereas carcinoma of the float did react.24
In conclusion, staining a parallel alkane section of GIM with mAb Das-one, in addition to the standard H&E and AB/PAS/HID stains, can be useful in differentiating the colonic cellular phenotype of IM that is more highly associated with gastric carcinoma. Its reactivity is conspicuously evident in GIM associated with gastric carcinoma, and is significantly (p<0.0001) higher than GIM from non-cancer patients, although ecology hazard factors such as H pylori status and perhaps nutrition may increase positivity amid Japanese and other Asian countries. Some of the mAb Das-1 positive GIM from not-cancer patients (group B) may develop gastric carcinoma later a certain length of time, although this can only exist proved past a long term longitudinal report. Yet, mAb Das-1 may identify the "at risk" grouping of patients with histological GIM, and thus may help to institute toll effective surveillance.
Acknowledgments
This piece of work was presented in part at the almanac meetings of the American Gastroenterological Association 2000 and 2001. KKD is the recipient of the Intel Science Talent Search Award for office of this work. This piece of work was supported in part by enquiry grants NIDDK, RO1 DK47673, and RO1 DK63618 from the National Institutes of Health, Bethesda, Medico, Usa.
Abbreviations
-
AB, alcian blueish
-
GIM, gastric intestinal metaplasia
-
HID, high fe diamine
-
PAS, periodic acid-Schiff
-
mAb, monoclonal antibody
-
H&E, haematoxylin-eosin
-
NJ, New Jersey
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1773674/
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