Histopathological staging of atrophic lesions of gastric mucosa.

Objective: To study the histopathological staging of atrophic lesions of the gastric mucosa. Methods: Histology and immunohistochemistry were used to closely examine 2144 specimens of atrophic gastric mucosa that were taken from endoscopic biopsies. Results: When the gastric mucosa epithelium is affected by infection, chemical stimulation, immune factors, genetic factors, and other factors, it may cause an atrophy of gastric mucosa epithelium and a decrease in the number of glands, intestinal metaplasia, hyperplasia of smooth muscle fibers, and atrophy of stem cells in the proliferative zone. In this study, we characterized the above lesions as atrophic lesions of the gastric mucosa. Based on the morphological and histological characteristics of the lesion, as well as the law of cell proliferation and transformation during its occurrence and development, we propose five stages. We also noted the onset age, gender correlation, and histopathological characteristics of each stage of gastric mucosal atrophies. Conclusion: Understanding the pathological staging of gastric mucosal atrophy is essential for treating patients correctly and keeping track of changes in malignant cells. It is also very important in preventing the initiation of gastric cancer or from getting worse.

Histopathological staging and differential diagnosis of marginal zone lymphoma of gastric mucosa-associated lymphoid tissue.

The purpose of this study was to explore the histopathological staging and differential diagnosis of marginal zone lymphoma in gastric mucosa-associated lymphoid tissue (MALT lymphoma). We performed detailed histomorphology and immunohistochemistry investigations as well as genetic testing on endoscopic biopsy and endoscopic mucosal resection specimens from 18 patients with gastric MALT lymphoma. We found that gastric MALT lymphoma typically begins as a small, isolated area outside the lymphoid follicular mantle zone or proliferates in a multifocal, patchy manner, gradually spreads to the interfollicular zone, forming diffuse proliferation, invades the gastric mucosal glands, and infiltrates or proliferates into the center of peripheral reactive lymphoid follicles. Abnormally proliferating lymphocytes invade the surrounding lymphoid follicles, resulting in damage, atrophy, and disappearance of their normal follicles as well as of the gastric mucosa glands, forming diffuse proliferation. Redifferentiation and proliferation lead to the transformation of lymphocytes; that is, MALT transitions into highly invasive lymphoma. Based on our findings in this study, we propose the following five stages in the process of development and progression of gastric MALT lymphoma: the stage of cell proliferation outside the lymphoid follicular mantle zone; the stage of heterogeneous proliferative lymphoepithelial lesion; the stage of reactive lymphoid follicular implantation; the stage of lymphoid follicular clonal proliferation; and the stage of MALT transforming into highly invasive lymphoma. We examined the differential diagnosis of histopathological features at each stage. The clinicopathological staging of gastric MALT lymphoma can help clinicians provide accurate treatment and track malignant cell transformation, thus playing a significant role in controlling its development and progression.

Histopathological features of glandular atrophy of the lamina propria of the gastric mucosa during its occurrence and development.

OBJECTIVE: To explore the histopathological features of glandular atrophy of the lamina propria of gastric mucosa during its occurrence and development. METHOD: We performed detailed histological observation and immunohistochemical examination on the endoscopic biopsy and ESD endoscopic resection specimens of 896 patients with glandular atrophy of the lamina propria of gastric mucosa. The EnVision two-step method was used for immunohistochemical staining, and the slices were incubated with primary antibody CK7, CK20, villin, CDX2, MUC5AC, MUC6, p53 and ki-67. Hematoxylin staining was performed and observed under the microscope and statistically analyzed. RESULTS: In the initial stage of glandular atrophy of the lamina propria, the proliferation area of the deep gastric pits, and the isthmus and neck of the gastric glands are characterized by roughly normal structure of the glandular structure, increased mesenchyme, and widened space between glands. Subsequently, the gland becomes smaller in volume and less in number, especially at the base, in the gastric glandular part of the gastric unit. The disease at this stage has higher incidence, and occurs more often in the elderly who account for 64.0% (573/896) of our study group. The disease in this stage may exhibit some lesions that are physiologic (age-related degeneration) while others are pathological. Therefore, this condition is called simple glandular atrophy of the lamina propria of the gastric mucosa. When the gastric mucosal epithelium is subjected to infection or repeated infections, chemical stimuli, immune factors, and genetic factors, it can lead to the proliferation and transformation of stem cells in the proliferation area of the deep gastric pits, and the isthmus and neck of the gastric glands, forming single ducts, multiple ducts, or a proliferation of patchy cells. Then, atypical hyperplasia (intraepithelial neoplasia) presents, finally leading to gastric adenocarcinoma. CONCLUSION: Understanding the histopathological characteristics of glandular atrophy of the lamina propria of gastric mucosa is of great significance in controlling the occurrence and development of gastric cancer.

Clinicopathological features and differential diagnosis of gastric pleomorphic giant cell carcinoma.

The aim of this study was to investigate the clinicopathological features and differential diagnosis of gastric pleomorphic giant cell carcinoma. Histopathology, immunohistochemistry, and human epidermal growth factor receptor 2 (HER2) gene testing were conducted for seven cases of gastric pleomorphic giant cell carcinoma. In histomorphological terms, all seven cases involved pleomorphic giant cell carcinoma, accounting for more than 10% of the entire tumor, with pleomorphic spindle cells and giant cells mixed with various histomorphological structures of adenocarcinoma with high, intermediate, and low differentiation. There was large heterogeneity in the HER2 protein expression and HER2 gene amplification in the gastric pleomorphic giant cell carcinoma, and both levels of HER2 were focal in three cases, accounting for 42.9% (3/7). The mismatch repair gene proteins MLH1, MSH2, PMS2, and MSH6 were positive. Routine immunohistochemical markers, i.e., pan-cytokeratin, epithelial membrane antigen, villin, caudal-type homeobox 2, E-cadherin, and p53, were positive in the gastric pleomorphic giant cell carcinoma, while vimentin, calponin, smooth muscle actin, nestin, S-100, cluster of differentiation (CD) 99, desmin, and CD34 were focally expressed in both the spindle and the giant cells, with Ki-67-positive cells accounting for 70-80%. Gastric pleomorphic giant cell carcinoma presents multiple histomorphological features and is easily confused with various tumors. Clarifying the histopathological features of this type of tumor is important for differential diagnosis and precise treatment.

The significance of the microlymphangiogenesis, microangiogenesis, and combined detection of programmed cell death-1 protein (PD-1)/ki67 in gastric cancer tissues.

PURPOSE: To investigate the relationship between the microlymphangiogenesis, microangiogenesis, and combined detection of the programmed cell death-1 protein (PD-1)/ki67 in patients with gastric cancer as well as the disease prognosis. METHODS: Immunohistochemistry was used to detect the microlymphatic density (MLD) and microvessel density (MVD) in the central and peripheral zones in 92 cases of gastric cancer, along with the number of PD-1- and ki67-positive tumor cells. RESULTS: The central zone of the gastric cancer tissue contained fewer atretic cord-like lymphatic vessels than the peripheral zone, while the peripheral zone contained an increased number of lymphatic vessels compared with the central zone. In most cases, the lumen was also dilated. Compared with the MLD in the peripheral zone, the MLD in central zone was significantly decreased. Compared with the number of PD-1-positive cells in the peripheral zone, the number of PD-1-positive cells in the central zone was significantly decreased, and compared with the number of ki67-positive cells in the peripheral zone. The differences in the microlymphangiogenesis, microangiogenesis, and the number of PD-1- and ki67-positive cells among the different histological types were not statistically significant. The microlymphangiogenesis, microangiogenesis, and PD-1- and ki67-positive cells were significantly decreased in the gastric cancer tissues from the patients in stages T1 and T2 compared with the gastric cancer tissues from the patients in stages T3 and T4. CONCLUSIONS: The detection of the MLD and MVD as well as the positive expression of PD-1 and ki67 in gastric cancer tissue are important reference indicators for judging the prognosis of gastric cancer.

Computer analysis of abnormal proliferation and transformation cells in gastric mucosa and its clinical significance.

To investigate the image computer analysis of abnormally proliferating transformed cells of gastric mucosa and its clinical significance. The pathological pictures of gastric adenomatous polyp cells, abnormally proliferating altered cells, and tubular adenocarcinoma cells in the stomach mucosa were assessed by image computer method on a total of 96 gastroscopic biopsy and ESD resection specimens. The data of cytoplasmic area, nuclear area, nuclear-cytoplasmic ratio, nuclear factor and N-heterotypic index of gastric adenomatous polyps, abnormal proliferative transformation and gastric intramucosal tubular adenocarcinoma were collected, and the mean, standard deviation and variance were calculated respectively. Standard Error, Maximum, Minimum Parameters and Statistical Structure. There were substantial discrepancies between gastric mucosal gastric adenomatous polyp cells and gastric mucosal abnormally proliferating transformed cells, according to the five data in the abnormal cells in the stomach mucosal proliferation area (p < 0.01); There was no significant difference between cells (p > 0.05). Computer analysis of cell images can provide quantitative values for the pathological diagnosis of gastric adenomatous polyp cells, abnormally proliferating transformed cells and tubular adenocarcinoma cells in the gastric mucosa, especially the degree of atypical proliferation. The monitoring of abnormally proliferated and transformed cells in gastric mucosa is of great significance for clinicians to accurately treat and track cell transformation, and to control the occurrence and development of gastric adenocarcinoma.

Histopathological Features of Helicobacter pylori Infection in Gastric Mucosa.

Objective: To investigate the histopathological characteristics of Helicobacter pylori (Hp) infection in the gastric mucosa in the process from occurrence to intraepithelial neoplasia. Methods: Specimens obtained from the endoscopic biopsy and endoscopic submucosal dissection of 2457 cases of gastric Hp infection were observed and assessed in detail using histology and immunohistochemistry techniques. The condition was divided according to the histopathological characteristics of gastric mucosal damage caused by Hp infection. The histopathological characteristics and immunophenotype of each stage were subsequently elucidated. Results: Helicobacter pylori is initially implanted in the mucus layer covered by the epithelium on the surface of the gastric mucosa. It then selectively adheres to the cytoplasm of the surface mucus cells, which makes the oval and spherical particles containing mucus that is wrapped by the bounded membrane in the cytoplasm on the nucleus of the surface mucus cells disappear, while the cytoplasm undergoes spiderweb-like vacuolar degeneration. This leads to the proliferation and transformation of the surface mucous cells before developing into intraepithelial neoplasia. In the process of histomorphology, mucosal ulcers, mucosal lymphoid tissue proliferation, gland atrophy, intestinal epithelial metaplasia, mucosa-associated lymphoid tissue lymphoma, and adenocarcinoma may occur. In this study, the condition was divided into five stages according to the histopathological characteristics of gastric mucosal damage caused by Hp infection, as well as the degree of gastric mucosal damage and involvement depth as follows: the mucus infection stage, the surface epithelial cell infection stage, the lamina propria lesion stage, the mucosal atrophy stage, and the intraepithelial neoplasia stage. Conclusion: Understanding the histopathological characteristics of gastric Hp infection in terms of its occurrence and development into intraepithelial neoplasia is conducive to the precise treatment and tracking of malignant cell transformation, and is of great significance in controlling the occurrence and development of gastric cancer.

Clinicopathological characteristics of signet-ring cell carcinoma derived from gastric fovelar epithelium.

OBJECTIVE: We aimed to investigate the immunophenotype, differential diagnosis, and clinicopathological characteristics of signet-ring cell carcinoma (SRCC) derived from gastric foveolar epithelium. METHODS: Clinical characteristics, endoscopic findings, histopathological features, and follow-up data of seven cases of SRCC derived from gastric foveolar epithelium with small intramucosal lesions were analyzed. RESULTS: Seven patients with a mean age of 38.3 years were diagnosed with SRCC derived from gastric foveolar epithelium and small intramucosal lesions, all of them were negative for CDH-1 germline mutation. The glands proliferated and expanded, and then morphologically transformed into signet-ring cells and formed clonal hyperplastic SRCC, which expanded laterally along the gastric foveolar cells to a length of 3-6 mm. Periodic acid Schiff staining was positive, while CK7 and MUC6 were negative, in all cases. Ki-67-positive cells ranged 37%-60%. During a follow-up period of 6-30 months, no patients experienced tumor recurrence or metastasis. CONCLUSIONS: SRCC derived from gastric foveolar epithelium is originated from the proliferative region of the bottom of the gastric pit and gland neck. It is easily missed diagnosed or misdiagnosed as it grows laterally along the gastric foveolar cells. Biological behavior, genetics, and etiology of such SRCC, as well as the clinicopathological characteristics, need to be further studied.

The Histopathological Types and Distribution Characteristics of Gastric Mixed Tumors.

Objective: The present study aimed to investigate the histopathological types and distribution characteristics of gastric mixed tumors. Methods: Detailed histological observations, together with related immunohistochemical and genetic tests, were analyzed on 960 surgically resected samples in 6 hospitals with gastric mixed tumors from May 2017 to May 2021 in this retrospective study. Results: Epithelial-derived tumors accounted for 80.10% (769/960) of the gastric mixed tumor samples studied, and tumors of different tissue origins accounting for 10.83% (104/960), mesenchymal-derived tumors accounting for 6.25% (60/960), neuroendocrine tumors accounting for 2.40% (23/960), and lymphoma accounting for 0.42% (4/960). The histological types of gastric mixed tumors identified as most commonly were epithelial originated, followed by mixed tumors of different tissue originated, then mixed neuroendocrine, lymphoma, and mesenchymal originated in sequence. The histological number of gastric mixed tumors was ≤ 3 in 83.23% (799/960) of cases and > 4 in 16.77% (161/960) of cases. The mixed histological patterns of gastric mixed tumors were divided into three types: those with tumor cells interspersed with each other, those with incomplete fibrous tissue separation, and those without fibrous tissue separation. The gene target characteristics of gastric mixed tumors were the existence of multi-gene mutation, including human epidermalgrowth factor receptor-2 (HER2) gene amplification, key result areas (K-ras) and platelet-derived growth factor receptor alpha (PDGFRA). Conclusion: Gastric mixed tumors should be adequately sampled, each piece of tissue should be involved in the morphological proportional division of the tumor, and any independent histological component should be written into the pathological examination report.

How Does Helicobacter pylori Infection Cause Gastric Mucosal Atrophy.

Objective: To investigate the occurrence and development of gastric mucosal atrophy due to Helicobacter pylori (Hp) infection and the accompanying histomorphological features. Methods: Detailed histological observations and immunohistochemical examinations were conducted via 197 endoscopic biopsies and endoscopic submucosal dissection specimens of gastric mucosal atrophic lesions with gastric Hp infection. Detailed observation was made of columnar cells in the proliferative region of the deep gastric pit and the isthmus of the gastric gland, as well as the upper part of the glandular cervix. Results: The infection of the gastric mucosa by Hp firstly led to the proliferative disorder of stem cells in the normal proliferative region of the gastric mucosa. This caused substantial propagation of cells in the proliferative region of the deep gastric pit and the isthmus of the gastric gland, as well as the upper part of the glandular cervix, as a means to replenish the damaged surface mucus cells. However, the propagation of stem cells in the proliferative region was insufficient for downward migration, and the normal physiological process of differentiation into fundic/pyloric gland cells was disrupted, resulting in glandular atrophy of the intrinsic layer of the gastric mucosa. Persistent Hp infection and disruption of stem cell proliferation in the proliferative region subsequently resulted in extensive segmental hyperplasia of the gastric mucosa and glandular atrophy of the lamina propria. Conclusion: The occurrence, development, and histomorphological features of gastric mucosal atrophy due to gastric Hp infection provide a reliable pathological basis for precise treatment by clinicians and are of great significance for controlling the development of gastric cancer.

Research on the Histological Features and Pathological Types of Gastric Adenocarcinoma With Mucinous Differentiation.

Objective: To discuss the histological features, pathological types, and prognosis of gastric adenocarcinoma with mucinous differentiation. Methods: Specimens of 189 cases of gastric adenocarcinoma with mucinous differentiation were collected for detailed histomorphology, immunohistochemistry, fluorescence in situ hybridization, and follow-up. Results: In accordance with the morphological and histological structural features of the cancer cells as well as the area ratio of the mucus, gastric adenocarcinoma with mucinous differentiation was divided into four types, namely pure mucinous carcinoma, intraductal papillary mucinous carcinoma, signet ring cell type mucinous carcinoma, and mixed cell type mucinous carcinoma. Based on the macroscopic types according to Bormann's classification, pure mucinous carcinoma was mostly Type I, intraductal papillary mucinous carcinoma was mostly Type II, signet ring cell type mucinous carcinoma was mostly Type IV, and mixed cell type mucinous carcinoma was mostly Type III. The 5-year survival rate was 69.2, 64.2, 0, and 31.5%, respectively. There was a statistical difference in the lymph node metastasis rate and survival rate of the four carcinoma types. The invasion features of pure mucinous carcinoma entailed penetrating corrosively in a push-in form, without blood vessel or lymphatic metastasis and with few lymphocytes and lymphatic nodules in the marginal area. Thus, there was little lymph node metastasis and invasion of nerves. The HER2 protein expression rate was 40.2% (76/189), the HER2 gene amplification detected by FISH technology was 16.9% (32/189). Conclusion: The independent histological type, four subtypes, and histopathological classification of gastric mucinous adenocarcinoma are important for the prognosis evaluation and precise treatment of this disease.

Histopathological classification and follow-up analysis of chronic atrophic gastritis.

BACKGROUND: The pathological diagnosis and follow-up analysis of gastric mucosal biopsy have been paid much attention, and some scholars have proposed the pathological diagnosis of 12 kinds of lesions and accompanying pathological diagnosis, which is of great significance for the treatment of precision gastric diseases, the improvement of the early diagnosis rate of gastric cancer, and the reduction of missed diagnosis rate and misdiagnosis rate. AIM: To perform a histopathological classification and follow-up analysis of chronic atrophic gastritis (CAG). METHODS: A total of 2248 CAG tissue samples were collected, and data of their clinical characteristics were also gathered. Based on these samples, the expression levels of Mucin 1 (MUC1), MUC2, MUC5AC, and MUC6 in CAG tissue were tested by immunohistochemical assay. Moreover, we followed these patients for up to four years. The difference between different stages of gastroscopic biopsy was observed. RESULTS: Through observation, it is believed that CAG should be divided into four types, simple type, hyperplasia type, intestinal metaplasia (IM) type, and intraepithelial neoplasia (IEN) type. Simple CAG accounted for 9.1% (205/2248), which was more common in elderly people over 60 years old. The main change was that the lamina propria glands were reduced in size and number. Hyperplastic CAG accounted for 29.1% (654/2248), mostly occurring between 40 and 60 years old. The main change was that the lamina propria glands were atrophy accompanied by glandular hyperplasia and slight expansion of the glands. IM CAG accounted for 50.4% (1132/2248), most of which increased with age, and were more common in those over 50 years. The atrophy of the lamina propria glands was accompanied by significant IM, and the mucus containing sialic acid or sulfate was distinguished according to the nature of the mucus. The IEN type CAG accounted for 11.4% (257/2248), which developed from the previous types, with severe gland atrophy and reduced mucus secretion, and is an important precancerous lesion. CONCLUSION: The histological typing of CAG is convenient to understand the property of lesion, determine the follow-up time, and guide the clinical treatment.

Gastric aggressive fibromatosis: report of a case and review of the literature.

OBJECTIVES: To describe a rare case of aggressive fibromatosis of the stomach and discuss the differential diagnoses. METHODS: A 47-year-old man presented with nonspecific abdominal pain. Gastroscopy revealed stomach wall swelling. An antral gastrectomy was performed. Histological examination revealed spindle-shaped cells and morphology typical of aggressive fibromatosis. We performed a literature search to identify conditions with features similar to those of aggressive fibromatosis. RESULTS: Aggressive fibromatosis does not metastasize, but it is locally invasive and has a tendency to relapse; however, our patient has not had recurrence > 1 year after surgery. Aggressive fibromatosis of the stomach may be confused with an inflammatory fibroid polyp, a gastrointestinal stromal tumor, schwannoma, leiomyoma, inflammatory myofibroblastic tumor, scirrhous carcinoma of the stomach, follicular dendritic cell sarcoma, inflammatory malignant fibrous histiocytoma, myofibroma/myofibromatosis, and solitary fibrous tumor of the stomach. CONCLUSIONS: Aggressive fibromatosis of the stomach is a rare spindle cell tumor that must be differentiated from a variety of conditions.

Methods and significance of the combined detection of HER2 gene amplification and chemosensitivity in gastric cancer.

OBJECTIVE: This study aims to investigate the significance of combined detection of HER2 gene amplification and chemosensitivity in gastric cancer. METHODS: Immunohistochemistry (IHC), fluorescence in situ hybridization (FISH) and fluorescence reverse-transcription polymerase chain reaction (RT-PCR) were used to analyze the expression of HER2 protein, HER2 gene amplification and the mRNA expression of ERCC1, TUBB3 and TYMS genes in 135 cases of gastric carcinoma. RESULTS: The expression rate of HER2 protein was 39.3% (53/135). Among these positive cases, patients with HER2 protein (3+) accounted for 9.6% (13/135), patients with HER2 protein (2+) accounted for 13.3% (18/135), and patients with HER2 protein (1+) accounted for 16.3% (22/135). The amplification rate of the HER2 gene was 35.8% (19/53). In the detection of the mRNA expression of ERCC1, TUBB3 and TYMS, 45 patients had low and moderate single gene expression, 50 patients had low and moderate double gene expression, 22 patients had low and moderate mRNA expression for ERCC1, TUBB3 and TYMS, and 18 patients had no low and moderate expression. Among the 53 patients with HER2 protein expression and 22 patients with low and moderate mRNA expression of ERCC1, TUBB3 and TYMS, 12 patients received chemotherapy and trastuzumab. Follow-up results revealed that HER2 gene status was positively correlated with the therapeutic effect of the combined treatment in patients with low mRNA expression of ERCC1, TUBB3 and TYMS. Among these patients, five patients with extensive HER2 (3+), HER2 cluster-specific amplification, and low mRNA expression of ERCC1, TUBB3 and TYMS had a total survival of up to 19.1 months. CONCLUSIONS: The detection of HER2 in gastric cancer is highly heterogeneity, and the combined detection of HER2 protein expression, HER2 gene amplification and chemosensitivity can provide important reference markers for the benefit of antitumor drugs.

Human epidermal growth factor receptor 2 expression in mixed gastric carcinoma.

AIM: To investigate human epidermal growth factor receptor 2 (HER2) amplification and protein expression in mixed gastric carcinoma. METHODS: Fluorescence in situ hybridization and immunohistochemistry were used to detect HER2 amplification and protein expression in 277 cases of mixed gastric carcinoma. Protein staining intensity was rate as 1+, 2+, or 3+. RESULTS: Of the 277 cases, 114 (41.2%) expressed HER2 protein. HER2 3+ staining was observed in 28/277 (10.1%) cases, 2+ in 37/277 (13.4%) cases, and 1+ in 49/277 (17.7%) cases. A HER2 amplification rate of 17% was detected, of which 25/28 (89.3%) were observed in the HER2 3+ staining group, 17/37 (45.9%) in 2+, and 5/49 (10.2%) in 1+. Of the 47 patients with HER2 amplification who received chemotherapy plus trastuzumab, 22 demonstrated median progression-free and overall survivals of 9.1 mo and 16.7 mo, respectively, which were significantly better than those achieved with chemotherapy alone (5.6 mo and 12.1 mo, respectively) in 19 previously treated patients (Ps < 0.05). CONCLUSION: HER2 detection in mixed gastric carcinoma displays high heterogeneity. Relatively quantitative parameters are needed for assessing the level of HER2 amplification and protein expression.

Diagnostic implications of Ki-67 expression in adipocytes and lipoblasts: an immunohistochemical study.

Ki-67 expression is an important tool for distinguishing between malignant and benign tumors. It usually shows the nuclear staining. However, the cell membrane staining of MIB-1, which is one of the clones of Ki-67, in the hyalinizing trabecular adenoma of the thyroid gland and other tumors had also been reported. In our practice, we found that the 7B11 antibody could be immunoreactived with the adipose tissues inside or around tumors in the membrane. Thus, in this study, we determined if Ki-67 expression would be useful in recognizing the lipoblasts and adipocytes. The five clones of the Ki-67 antibody, namely, 7B11, K-2, SP5, MIB-1, and SP6 were selected. The adipocytes showed strong 7B11 staining in the cell membrane. The brown fat cells were strongly immunoreactive with 7B11 in the arachnoid layer of the cytoplasm. The adipocytes and brown fat cells showed positive, albeit weaker K-2 staining in the cell membrane and cytoplasm, respectively, compared to 7B11. The adipose tissues and brown fat cells were non-reactive to clones SP5, MIB-1, and SP6. All adipocytes in the lipomas, angiolipomas, uterine lipoleiomyomas, and angioleiomyolipomas showed diffusedly positive 7B11 and K-2 staining in the cell membrane, with stronger immunoreactivity to 7B11 compared with K-2. All hibernomas showed diffusedly cytoplasmic arachnoid staining of 7B11, but only focal to K-2. The lipoblasts in adipocytic tumors also showed positive 7B11 and K-2 staining; however, nearly all of the vacuolated lipoblasts showed strong 7B11 staining, only focal vacuolated lipoblasts in the adipocytic tumors were immunoreactive to K-2 positivity. All other components of the adipocytic tumors were non-reactive to 7B11, K-2, SP5, MIB-1, and SP6 in the cell membrane and cytoplasm. Our results showed that the 7B11 could well help to identify the lipoblasts, which would be useful to diagnose the malignant adipocytic tumors.

[Clinicopathologic features of gallbladder adenocarcinoma with marked stromal fibrosis--a report of 19 cases].

BACKGROUND & OBJECTIVE: Macropathologic types of gallbladder cancer are mostly polyp type, intumescent type, and cauliflower form lump. Its histological types include well or poorly differentiated adenocarcinoma, mucinous adenocarcinoma, and undifferentiated cancer. This research was to explore the clinicopathologic features of gallbladder adenocarcinoma with marked stromal fibrosis. METHODS: Pathology of 19 cases of gallbladder adenocarcinoma with marked stromal fibrosis was observed using a light microscopy and SP immunohistochemistry. Clinicopathologic features of 19 patients were analyzed. RESULTS: Most of the patients had long-term history of cholecystitis gallbladder calculus. B ultrasound showed that the gallbladder wall was irregularly thickened or presented nodosity. Observed with naked eyes, gallbladder adenocarcinoma with marked stromal fibrosis did not form cancer nodule and extrude into the gallbladder lumen, the gallbladder wall showed regional thickening, a few cases showed diffuse irregular thickening. Observed under a light microscope, the adenocarcinoma cells were mostly arranged as single layers, seldom arranged as multiple layers, and formed adenoid structures with different sizes, various shapes, and irregular arrangement; the nuclei were heterogenic with haryomitosis presented in a few cases; inflammatory cells were infiltrated in hyperplastic fibrous connective tissue of some cases. According to immune phenotyping, CK (AE1/AE3), CK (AE1), CK7 (OV-TL12/30), CK8 (C51), CK18 (Dc-10), CK19 (RCK108), and EMA (Mc-5) showed strong expression, CEA (COL-1), CK20 (Ks20. 4), and MUC-5AC (CLH2) showed moderate expression, and MUC-2 (B306. 1) showed weak expression; CK17 (E3) showed focal expression. CONCLUSIONS: The clinical manifestation, macropathologic type, histological characteristics of gallbladder adenocarcinoma with stromal fibrosis are different from other types of adenocarcinoma. Its genesis may be related to chronic cholecystitis: long-term inflammation causes regional hyperplasia and heterogeneity of the gland body, lead to focal or regional thickening of the gallbladder wall, and result in gallbladder adenocarcinoma with stromal fibrosis finally.