Frequent loss of Brm expression in gastric cancer correlates with histologic features and differentiation state

The mammalian SWI/SNF chromatin remodeling complex, an essential epigenetic regulator, contains either a single Brm or BRG1 molecule as its catalytic subunit. We observed frequent loss of Brm expression but not of BRG1 in human gastric cancer cell lines. Treatment with histone deacetylase inhibitor rescued Brm expression, indicating epigenetic regulation of this gene, and an RNA interference-based colony formation assay revealed antioncogenic properties of Brm. Brm immunostaining of 89 primary gastric cancers showed an obvious reduction in 60 cases (67%) and a severe decrease in 37 cases (42%). Loss of Brm is frequent in the major gastric cancer types (well- or moderately-differentiated tubular adenocarcinoma and poorly-differentiated adenocarcinoma) and positively correlates with the undifferentiated state. Among the minor gastric cancer types, Brm expression persists in signet-ring cell carcinoma and mucinous adenocarcinoma, but a marked decrease is observed in papillary adenocarcinoma. Intestinal metaplasia never shows decreased expression, indicating that Brm is a valid marker of gastric oncogenesis. In contrast, BRG1 is retained in most cases; a concomitant loss of BRG1 and Brm is rare in gastric cancer, contrary to other malignancies. We further show that Brm is required for villin expression, a definitive marker of intestinal metaplasia and differentiation. Via regulating such genes important for gut differentiation, Brm should play significant roles in determining the histologic features of gastric malignancy.     

Decreased expression of galectin-3 is associated with metastatic potential of liver fluke-associated cholangiocarcinoma

Galectin-3, a beta-galactoside-binding lectin, is a multifunctional protein implicated in a variety of biological functions, including tumour cell adhesion, proliferation, differentiation, cancer progression and metastasis. The present study was performed to clarify the impact of galectin-3 expression on patients with liver fluke-associated cholangiocarcinoma. Galectin-3 expression was examined immunohistochemically in 53 patients with intrahepatic cholangiocarcinoma, who had undergone surgery without pre-operative therapy. All bile duct epithelium expressed galectin-3 with different intensities, according to the different histological subtypes. The poorly-differentiated type expressed galectin-3 less intensely than the papillary, well- to moderately-differentiated types (P=0.012). We observed the association of low galectin-3 expression with lymphatic invasion (P=0.002). Suppression of galectin-3 expression in two human cholangiocarcinoma cell lines using siRNA targeted to galectin-3 significantly increased cell migration and invasion without alterations in cell proliferation. Regulation of galectin-3 expression may therefore be an alternative therapeutic approach to control metastasis of cholangiocarcinoma.     

Prognostic value of histological variants of adenosquamous carcinoma of the corpus uteri

A relationship between histologically-established degree of tumor differentiation and survival was studied in 72 cases of adenosquamous cancer of the uterus (33 well-differentiated and 39 poorly-differentiated adenosquamous carcinoma). The distribution of 5-year survival rates was as follows: well-differentiated endometrial adenocarcinoma-94.6, well-differentiated adenosquamous carcinoma-88.3 and moderately-differentiated carcinoma of the endometrium-75.4 per cent. Five-year survival rate in poorly-differentiated adenosquamous cancer group (44.9%) did not differ significantly from that of poorly-differentiated adenocarcinoma (39.7%). Histoarchitectonical peculiarities of well- and poorly-differentiated adenosquamous cancer have prognostic value and should be taken into account in morphological diagnostics of endometrial cancer.     

Immunohistochemical detection of cluster 1 small cell lung cancer antigen and chromogranin A in lung carcinomas.

Eighteen small cell lung cancers (SCLCs), 108 non-SCLCs (67 adenocarcinomas, 29 squamous cell carcinomas and 12 large cell carcinomas) were immunohistochemically examined for expressions of cluster 1 SCLC antigen/N-CAM and chromogranin A with monoclonal antibodies NCC-Lu-243 and anti-chromogranin A. The cell membranes of all the SCLCs and three of the 67 adenocarcinomas (4.5%) were stained for cluster 1 SCLC antigen/N-CAM. Eight of the 18 SCLCs (44.4%), and three of the 67 adenocarcinomas (4.5%) were stained for chromogranin A, but no squamous cell carcinoma or large cell carcinoma was stained for both antigens. Two of the three adenocarcinomas which expressed cluster 1 SCLC antigen/N-CAM had been suspected of being either SCLC or poorly-differentiated adenocarcinoma cytologically, and were resected after chemotherapy and radiotherapy. Histologically, they were poorly-differentiated adenocarcinoma with rosette-like tubules. The remaining one was moderately-differentiated papillary adenocarcinoma resembling bronchial surface epithelial cells without mucin (BSE type adenocarcinoma). The three adenocarcinomas which expressed chromogranin A were well- to moderately-differentiated BSE type adenocarcinomas, and stained tumor cells were distributed sparsely as neuroendocrine cells in the normal bronchial mucosa. One of them also expressed cluster 1 SCLC antigen/N-CAM. In the present study, we demonstrated the usefulness of NCC-Lu-243 in the immunohistochemical detection of adenocarcinomas with neuroendocrine features.     

Nuclear accumulation of p53 protein in gastric cancer strongly correlates with enlargement of nuclear area of cancer cells

The nuclear area (NA) of cancer cells have been reported to be a useful prognostic indicator in various tumors. However, this image analysis of cancer nucleus has only rarely been applied to gastric adenocarcinoma. Moreover, it remains to be shown what types of biological factors influence this nuclear feature. In this study, we analyzed the area of cancer nuclei in tumors from 97 patients with advanced gastric cancer (t3, n0, stage II) by using hematoxylin and eosin stained slides with a computer-assisted image-analysis system. The morphometric data were compared with clinicopathological and biological status of the tumors. The mean NA of 50 tumors with venous invasion (50 microm2) was significantly larger than that of 47 tumors without venous invasion (38 microm2, p<0.0001). There was a significant correlation between the NAs of cancer cells and the p53 labeling indices of tumors (p=0.0012) and Ki-67 labeling indices of tumors (p=0.0324). However, no significant correlation was detected between the NAs of cancer cells and other factors, such as, tumor size, DNA ploidy pattern, expression of vascular endothelial growth factor (VEGF), or microvessel density of tumors. The five-year survival rate of 49 patients with large nuclear area (NA > or =41 microm2, 63%) was significantly lower than that of 48 patients with small nuclear area (NA <41 microm2, 78%, p=0.043). Data from computerized morphometry are objective and can be obtained rapidly by conventional microscopic analysis. The NA of cancer cells in advanced gastric cancer appears to predict the ability to invade the microvessels in the gastric wall. This nuclear morphological feature strongly correlated with p53 accumulation in the nuclei of gastric adenocarcinoma.     

Clinical importance of correlations between p53 immunoreactivity and clinicopathological parameters in lung carcinoma

Many studies have revealed the frequency of p53 abnormalities in lung cancer. However, clinico-pathological studies of p53 abnormalities have yielded conflicting results. We examined the p53 immunoreactivity and studied the correlations of p53 status and clinicopathological parameters in 76 primary lung cancers. By using DO-7 antibody, different degrees of p53 immunoreactivity was detected in 8 of 30 small cell lung cancer (SCLC, 26.6%) and 22 of 46 non-small cell lung cancer (NSCLC, 47.8%), 6 of 19 adenocarcinoma, 16 of 27 epidermoid carcinoma cases. In the whole group, no correlation was detected between the p53 status and the histological types of tumor, local tumor invasion, nodal status, and distant metastasis and patient characteristics, such as age, gender or smoking habit. P53 status was also found to have no effect on survival. However, in the NSCLC group, there was a significantly higher p53 immunoreactivity in well- and moderately-differentiated tumors (p<0.05). Patients with p53 immunoreactivity had a poor therapeutic response in the whole group. We concluded that, although p53 immunreactivity may be found in NSCLC, this does not correlate with clinicopathological parameters except therapeutic response. In SCLC p53 immunreactivity can be negligible.     

Immunohistochemical detection of CD133 expression in colorectal cancer: a clinicopathological study

CD133 has been reported to be a cancer-initiating cell marker in colorectal carcinoma. The objective of this study was to evaluate the frequency of CD133 expression in colorectal cancer, the distribution of CD133-positive cancer cells, and their relationship to clinicopathological features, including survival. An immunohistochemical examination of CD133 expression and a clinicopathological analysis were performed in the 189 consecutive colorectal cancer patients. CD133 expression was seen at the luminal surface of cancer glands mainly with cribriform features. Expression was detected in only 29 of the 189 tumors (15.3%). Of these, 21 tumors (11.1%) showed CD133 overexpression. All 21 tumors with CD133 overexpression were diagnosed as well- or moderately-differentiated adenocarcinoma. There was no difference in the distribution of CD133 expressing cells between the invasive area and surface area. Although there was no difference in recurrence-free survival between patients with CD133 overexpression and without, the patients with CD133 overexpression had significantly poorer overall survival ( P =  0.03). CD133 overexpression is a risk factor for poorer overall survival in patients with well- and moderately-differentiated adenocarcinoma. Expression of this cancer-initiating cell marker may vary with the histological type of the cancer, and further investigation of the relationship between its expression and clinicopathological features may be necessary. ( Cancer Sci 2008; 99: 1578–1583)     

Reduced Fhit expression is associated with mismatch repair deficiency in human advanced colorectal carcinoma

The Fragile Histidine Triad gene, encompassing the FRA3B fragile site at chromosome 3p14.2, is a candidate tumour suppressor gene involved in multiple tumour types including colorectal carcinomas. Recently, it has been reported that the Fragile Histidine Triad gene may be a target of damage in a fraction of mismatch deficient tumours. To explore this hypothesis, we analysed both Fragile histidine triad and mismatch repair protein (Msh2 and Mlh1) expression using immumohistochemical methods in 52 advanced colorectal carcinomas (19 well-, 17 moderately-, and 16 poorly-differentiated). In addition, we examined whether the Fragile histidine triad and mismatch repair protein expression correlated with p53 expression and clinicopathological findings. Significant loss or reduction of Fragile histidine triad expression was noted in 18 of the 52 (34.6%) advanced colorectal carcinomas: 2 (10.5%) well-differentiated, 3 (17.6%) moderately-differentiated, 13 (81.3%) poorly-differentiated carcinomas, the frequency being significantly higher in the latter than that in the former two (P<0.0001). Loss of mismatch repair protein (mainly, Mlh1) expression was detected in 21 of the 52 (40.4%) colorectal carcinomas. Moreover, reduced Fragile histidine triad expression was significantly associated with absence of mismatch repair protein expression in the advanced colorectal carcinomas (P<0.0001). However, the Fragile histidine triad and mismatch repair protein expression was not significantly associated with p53 expression. These results suggested that reduced Fragile histidine triad expression might be correlated with mismatch repair expression, but not with p53 expression.     

细胞骨架蛋白4.1N与E-cadherin、β-catenin在胃癌中的表达及其临床意义

目的 探讨胃癌组织、癌旁胃组织中细胞骨架蛋白4.1N与E-cadherin、β-catenin在胃癌转移 扩散中的作用及三者间的相互关系。方法 收集52例胃癌标本（腺癌）、30例距癌组织边缘10 cm以 上的癌旁胃组织标本作为对照。应用免疫组织化学Elivision法检测这些组织中的细胞骨架蛋白4.1N与 E-cadherin、β-catenin的蛋白表达情况。结果 胃癌组织中细胞骨架蛋白4.1N、E-cadherin及β-catenin 蛋白表达明显低于对照组（P<0.05）;低分化胃癌组织中细胞骨架蛋白4.1N与E-cadherin、β-catenin的 蛋白表达较高-中分化胃癌组织表达显著降低（P<0.05）;细胞骨架蛋白4.1N与E-cadherin、β-catenin 的蛋白在无淋巴结转移的胃癌组与有淋巴结转移的胃癌组间比较差异有统计学意义（P<0.05）;细胞 骨架蛋白4.1N与E-cadherin、β-catenin的蛋白在胃癌组织中的IOD值随着TNM分期的增高而降低,组间 比较差异具有统计学意义（P<0.05）,细胞骨架蛋白4.1N与E-cadherin、β-catenin的蛋白的表达与胃癌 患者的年龄、性别无关（P>0.05）;细胞骨架蛋白4.1N与E-cadherin（r=0.381,P<0.05）、E-cadherin 与β-catenin（r=0.571,P<0.05）、细胞骨架蛋白4.1N与β-catenin（r=0.602,P<0.05）之间均呈正相关 关系。结论 细胞骨架蛋白4.1N与E-cadherin、β-catenin在胃癌中的表达呈正相关,三者在胃癌发生发 展中可能具有重要的协同作用。     

非小细胞肺癌组织中P27表达及定位与磷酸化AKT的关系

背景与目的:抑癌基因的失活在肿瘤的发生发展中有重要作用。p27的失活包括P27表达的减少或丢失及P27的胞浆错定位。AKT是一种丝氨酸/苏氨酸激酶,活化状态的AKT[磷酸化AKT(phosphorylatedAKT),p-AKT]能够调节细胞周期中的多个效应分子,其中包括对P27表达及定位的调节。本研究旨在探讨P27在非小细胞肺癌中(NSCLC)中的表达、定位及与p-AKT之间的相关性。方法:应用免疫组化的方法,分别检测NSCLC组织80例、非肿瘤性肺组织标本35例中P27蛋白的核、浆表达及磷酸化AKT的表达,并对它们与临床病理因素的相关性进行分析。结果:在NSCLC组织中,P27蛋白总阳性率为72.5%,其中胞核阳性率为46.3%;在非肿瘤性肺组织中P27总阳性率及胞核阳性率均为94.3%,两组对比P27总阳性率及胞核阳性率差异均有显著性意义(P<0.01)。80例NSCLC中有21例呈现单纯胞浆阳性;而在非肿瘤性肺组织中未见单纯胞浆阳性表达,两组对比差异有显著性意义(P<0.01)。P27的胞核表达在无淋巴结转移组和病理高、中分化组明显高于淋巴结转移组、低分化组的表达,组间比较差别具有显著性意义(P<0.05);P27的胞核表达与患者年龄、性别、肿瘤类型、TNM分期无关(P>0.05)。P27的胞浆表达与临床病理特征无关(P>0.05)。p-AKT蛋白在NSCLC中阳性表达率为78.8%,在非肿瘤性肺组织中呈阴性表达,两组之间差异有显著性意义(P<0.05);p-AKT在腺癌高、中分化组的表达(95.0%)高于低分化组的表达(50.0%)(P<0.01)。在NSCLC中,p-AKT的表达与P27胞浆表达呈正相关(r=0.437,P<0.01);p-AKT的表达与P27胞核表达无相关关系(r=0.175,P>0.05)。结论:NSCLCP27胞核表达的减少或丢失可能与肺癌的恶性发展有关;NSCLC中P27单纯性胞浆表达可能是肺癌细胞表达的特征之一;磷酸化AKT可能参与了对P27胞浆定位的调节,但与P27胞核表达无明显相关关系。     

Differential expression of peroxisome proliferator-activated receptor in histologically different human gastric cancer tissues

Gastric cancer cell lines express peroxisome proliferator-activated receptor gamma (PPARgamma), and treatment with PPARgamma ligands suppresses growth of subgroup of these cell lines. However, expression and subcellular distribution of PPARgamma in human gastric cancer tissues is still unknown. Therefore, expression and subcellular localization of PPARgamma were examined among different histological types of gastric cancer tissues. Immunohistochemical staining for PPARgamma was performed using biopsy specimens of human gastric cancer of various histological types, gastric adenomas, and intestinal metaplasia. All samples of intestinal metaplasia and most samples of gastric tumors, except for signet ring cell carcinoma, expressed PPARgamma in the epithelial cells. Most samples of signet ring cell cancer lacked PPARgamma expression. All samples of intestinal metaplasia expressed PPARgamma only in the cytosol. For adenoma, 90% was positive for PPARgamma in cytosol, and 40% was positive in nuclei, for well-differentiated adenocarcinoma, 80% was positive in cytosol, and 20% was positive in nuclei. For moderately differentiated adenocarcinomas, 70% was positive for cytosol, and 80% was positive for nuclei; for poorly differentiated adenocarcinoma, 30% was positive in cytosol, and 70% was positive in nuclei. The frequency of samples with positive cytosolic staining decreased as the differentiation stage turned from intestinal metaplasia to adenoma, well-, moderately-, and poorly-differentiated cancers. Simultaneously, there was a tendency toward an increased frequency of samples with positive nuclear PPARgamma staining as the differentiation stage transformed from intestinal metaplasia to poorly-differentiated cancer. There was a striking difference in subcellular localization according to the differentiation levels of gastric dysplastic cells. The findings also supported an intestinal metaplasia-adenoma-well-differentiated gastric cancer sequence, and signet ring cell cancer was suggested to be of a different lineage from other types of gastric cancers.     

血管内皮生长因子和抑癌基因p53在胃癌中的表达及其临床意义

目的 :研究血管内皮生长因子 (vascularendothelialgrowthfactor,VEGF)和抑癌基因p53表达的的相关性 ,与胃癌临床病理学指标的关系及其联合表达对胃癌患者预后的影响。方法 :应用免疫组化法同时检测 1 0 8例胃癌组织VEGF和P53蛋白表达水平。结果 :本组病例VEGF蛋白表达阳性率为 53 .7% ,P53蛋白表达阳性率为 57.4 % ,且两者呈正相关 (P <0 .0 1 )。VEGF蛋白表达水平与浆膜浸润、淋巴结转移和TNM分期有关 (P <0 .0 1 )。P53蛋白表达水平与患者年龄、肿瘤部位、脉管侵犯、浆膜浸润、淋巴结转移和TNM分期有关 (P <0 .0 5)。并且两者的表达和胃癌患者的预后呈负相关 (P <0 .0 1 )。结论 :VEGF和P53蛋白的表达呈正相关和胃癌的生物学特性有关 ,可作为估计胃癌预后的重要因素     

早期胃癌临床病理特点及免疫表型分析

目的探讨早期胃癌的临床病理特点及免疫组织化学特点。方法由胃镜活检标本病理组织学观察,再经手术切除证实的47例早期胃癌,采用免疫组化S-P法对p21、p53、PTEN、APC等9种相关基因蛋白进行了检测。结果早期胃癌肉眼形态：Ⅰ型隆起型占4.3%（2/47）;Ⅱ型平坦型占72.3%（34/47）;Ⅲ型凹陷型占23.4%（11/47）。组织病理学类型：乳头状腺癌14.9%（7/47）,管状腺癌27.7%（13/47）,黏液腺癌10.6%（5/47）,低分化腺癌17.2%（8/47）,印戒细胞癌25.3%（12/47）和未分化癌4.3%（2/47）。早期胃癌根据厚度和大小分为6种,其中小黏膜癌10.6%（5/47）,浅表黏膜癌34.0%（16/47）,小黏膜下层癌40.4%（19/47）,浅表黏膜下层癌14.9%（7/47）,穿透型Pen A型癌4.3%（2/47）,穿透型Pen B型癌10.6%（5/47）。免疫表型：胃癌相关糖类抗原CA50、CA19-9、CA242阳性表达均在70%以上;胃癌相关抑癌基因蛋白p16、p53、APC、PTEN阳性表达分别为42.6%、48.9%、51.1%和53.2%;肿瘤抑制因子p21阳性表达40.4%;凋亡抑制基因Survivin 59.6%;细胞增殖指数Ki-67〈40%。随访结果：47例患者随访3～108个月,健康状况良好。结论早期胃癌预后好,组织病理学诊断须联合免疫表型,以提高早期诊断率,降低误诊率。     

Aggressive angiomyxoma of the inguinal region

Aggressive angiomyxoma is a distinctive and very rare soft tissue tumor occurring almost exclusively in women. Only seven cases occurring in men have been previously reported. We herein report a case of a 74-year-old man who was admitted to our hospital presenting with a huge right inguinal mass that had grown over a 14-year period, in order to undergo surgical treatment for gastric cancer. The inguinal tumor was well-defined and demonstrated a glistening appearance on the cut surface. Histologically, the tumor was composed of bland-looking spindle and stellate cells with delicate cytoplasmic processes, which sparsely populated the fibromyxoid matrix. A prominent vascular component was also present. Immunohistochemically, the stromal cells stained consistently for vimentin and variably for muscle-specific actin, but not for alpha-smooth muscle actin, desmin, and S-100 protein. The gastric cancer was microscopically diagnosed to be papillary adenocarcinoma with serosal invasion and showing immunoreactivity for p53 protein, but not for aggressive angiomyxoma.     

The significance of ANXA7 expression and its correlation with poor cellular differentiation and enhanced metastatic potential of gastric cancer

BACKGROUND: Annexin-A7 (ANXA7) exhibits biological and genetic properties expected of a tumor suppressor gene and may play a role in cancer progression. However, the ANXA7 expression in different histological subtypes of gastric adenocarcinomas and its correlation with invasive potentials has not been elucidated. METHODS: Immunohistochemical staining of ANXA7 for 84 primary gastric adenocarcinomas was performed, and data was correlated with clinicopathological parameters of patients. RESULTS: The ANXA7 expression was well correlated with the grade of differentiation of primary tumors. Its expression was detected in 100% (8/8), 64.9% (24/37), 66.7% (2/3), 31.9% (13/31), 0% (0/3), and 0% (0/2) of well-differentiated tubular, moderately-differentiated tubular, papillary, poorly differentiated, signet-ring cell, and mucinous adenocarcinoma, respectively. According to the Lauren's classification, the ANXA7 expression was higher in intestinal type than in diffuse type tumor (71.9% vs. 6.1%, P = 0.003). The loss of expression of ANXA7 expression was significantly related to distant metastasis (P = 0.04). However, there were no significant associations between the ANXA7 expression and survival of cancer patients (P = 0.159). CONCLUSIONS: A striking correlation between ANXA7 expression and cell differentiation of gastric cancer was observed. The loss of expression of ANXA7 is associated with distant metastasis.     

Growth mode and DNA ploidy in mucosal carcinomas of the stomach

Modes of cancer growth and DNA ploidy were studied in 66 patients with mucosal carcinoma of the stomach. The modes of growth were classified into five histologic patterns; elongated tubular (three patients), expansive (18 patients), tubular and solid (14 patients), carcinoma in situ (10 patients) and infiltrative (21 patients). In every patient, all or most lesions with elongated tubular, expansive, and carcinoma in situ growths were located in the pyloric gland area of the stomach, and were less than 4 cm in diameter. Histologically, the adenocarcinomas papillary or well-, or moderately differentiated. Most lesions with an infiltrative growth were located in the intermediate pyloric and fundic glands areas, depressed in gross appearance, and composed of poorly differentiated glandular or signet ring tumor cells. The lesions with a tubular and solid growth were present in the pyloric gland or intermediate area, and were classified as well-, moderately, or poorly differentiated adenocarcinoma. All lesions with an elongated tubular, tubular and solid, and carcinoma in situ growths, and most lesions with an infiltrative growth showed a narrowly restricted DNA distribution (Type I or II), while most lesions with an expansive growth had mostly a widely scattered DNA distribution (Type III), representing a higher malignant potential.     

Three advanced gastric cancer patients successfully treated by combination therapy of paclitaxel and cisplatin

We report 3 gastric cancer patients with peritoneal dissemination who were successfully treated with weekly paclitaxel and cisplatin. The patients were 2 men and 1 woman from 57 to 70 years in age. The histological types were 2 poorly-differentiated adenocarcinomas and 1 moderately-differentiated adenocarcinoma. Intravenous infusion of PTX (80 mg/m(2)) and CDDP (25 mg/m(2)) after short premedication was continued for 3 weeks followed by 1 week rest. Ascites improved only after administration of 1 course in all patients.PTX/CDDP is thought to be an effective chemotherapy showing acceptable toxicity against advanced gastric cancer with ascites.     

Caspase-8在胃腺癌组织中的表达及与临床病理特征和预后的关系

目的:探讨胃腺癌组织中Caspase-8的表达及其与患者临床病理特征、预后的关系,并进一步研究Caspase-8表达对胃癌细胞增殖的影响。方法:采用qPCR法及免疫组化法检测胃腺癌组织中Caspase-8 mRNA和蛋白的表达,并在胃腺癌细胞株中进行进一步研究。结果:胃腺癌组织中Caspase-8 mRNA和蛋白的表达均低于癌旁胃黏膜组织,Caspase-8蛋白的表达与患者的年龄、性别、脉管癌栓、淋巴结转移和浸润深度无关（P＞0.05）,而与肿瘤分化程度、临床分期有关（P＜0.05）;生存分析显示Caspase-8蛋白低表达患者生存时间短,预后不良;进一步细胞研究结果表明,抑制Caspase-8的表达可以促进胃癌细胞的增殖。结论:Caspase-8在胃腺癌中表达下调,与胃腺癌细胞的增殖相关,对预后判断可能有一定参考价值。     

Galectin-3 immunoprofile in adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma of salivary glands

Adenoid cystic carcinoma (ACC) and polymorphous low-grade adenocarcinoma (PLGA) are malignant neoplasms of salivary glands, which are similar in histologic patterns but very different in clinical behavior, treatment and prognosis. Galectin-3 is a multifunctional protein of a growing family of beta-galactoside-binding animal lectins, which is implicated in a variety of biological events such as tumor cell adhesion, proliferation, differentiation and angiogenesis. This protein was found to be implicated in cellular transformation and a correlation between its expression and cancer progression and metastasis has been described. The aim of this study was to determine the galectin-3 immunoprofile in 14 cases of ACC (2 cases of tubular subtype, 4 cases of solid subtype and 8 cases of cribriform subtype) and in 12 cases of PLGA with different histologic patterns, including lobular, tubular and cribriform aspects. Moreover, slides of normal salivary glands were included. In normal salivary glands there was strong nuclear and cytoplasmic staining for galectin-3 in ductal luminal cells. ACC showed specific staining in luminal cells mainly in the nuclei. In the tubular subtype of ACC, galectin-3 strongly stained luminal cells of the ductiform structures. The cribriform and solid subtypes showed a few positive luminal cells of small ducts present in the cribriform structures and in solid nests respectively. In the cases of PLGA, independent of the histologic architecture, all tumor cells revealed a positive cytoplasmic reaction. Galectin-3 expression seems to be related to cell differentiation more than to tumor progression and prognosis in the neoplasms studied.