Malignant transformation and subsequent leptomeningeal carcinomatosis of a gastric polyp in a dog.

Progressive carcinogenesis of a gastric polyp with transformation to gastric adenocarcinoma and subsequent development of leptomeningeal carcinomatosis is described in an adult male Scottish terrier. Presenting clinical signs consisted of vomiting with intermittent hematemesis. Surgical biopsies over the course of 14 months documented the progression from gastric polyp to minimally invasive gastric carcinoma to invasive gastric adenocarcinoma, a pathogenesis not previously documented in veterinary oncology. The patient ultimately developed neurologic pathology and was euthanized, and necropsy evaluation identified widespread carcinomatosis with accompanying leptomeningeal metastasis. As in humans, gastric polyps in dogs rarely have malignant potential.

G-protein-coupled estrogen receptor prevents nuclear factor-kappa B promoter activation by Helicobacter pylori cytotoxin-associated gene A in gastric cancer cells.

Helicobacter pylori is a well-known pathogen that causes chronic gastritis, leading to the development of gastric cancer. This bacterium has also been detected in dogs, and symptoms similar to those in humans have been reported. The cytotoxin-associated gene A (CagA) is involved in pathogenesis through aberrant activation of host signal transduction, including the nuclear factor-kappa B (NF-κB) pathway. We have previously shown the anti-inflammatory effect of the G-protein-coupled estrogen receptor (GPER) via inhibiting of NF-κB activation in several cells. Therefore, here, we investigated the effect of GPER on CagA-mediated NF-κB promoter activity and showed that CagA overexpression in gastric cancer cells activated the NF-κB reporter and induced interleukin 8 (il-8) expression, both of which were inhibited by the GPER agonist.

Computed tomography of suppurative and neoplastic diseases involving the canine omenta and omental bursa.

The greater and lesser omenta are fused peritoneal folds that largely delimit the omental bursa (lesser peritoneal cavity). The omental bursa is a potential space within the abdominal cavity that communicates with the greater peritoneal cavity via the omental (epiploic) foramen: it is subdivided into the omental vestibule, caudal omental recess, and splenic recess. Aims of this retrospective case series study were to describe the frequencies of CT findings of dogs with confirmed inflammatory or neoplastic disease of the omenta, omental bursa, or both. The sample included seven adult, medium-to-large breed dogs. All had fluid in the greater peritoneal cavity and 5/7 (71%) dogs also had fluid in the omental bursa. Primary suppurative inflammatory disease was present in three dogs, each dog had a large abscess with central gas in either the omental vestibule (two dogs) or caudal omental recess (one dog). Both abscesses in the omental vestibule arose from the papillary process of the caudate liver lobe and were surgically removed without complication. Neoplasia was present in four dogs and either arose from omentum (hemangiosarcoma, carcinoma) or infiltrated the omentum from an adjacent organ (splenic leiomyosarcoma, gastric adenocarcinoma). Neoplasms created mass-like tumors, infiltrative tumors, or both and had variable distribution (focal, multifocal, or locally extensive). All dogs with neoplasia were euthanized. CT signs of inflammatory and neoplastic disease overlapped, but the presence of gas might prioritize abscessation. CT signs helped decide feasibility of surgery based on extent of local invasion, especially involvement of structures passing through the porta hepatis.

Contrast-enhanced CT features of pyloric lesions in 17 dogs: Case series.

Pyloric outflow obstructions can be caused by several types of lesions. When a thickened gastric wall and pyloric mass are detected, malignant neoplasia must be differentiated from chronic hypertrophic pyloric gastropathy. CT can characterize gastric tumors. However, based on the authors' review of the literature, there is limited information about the CT findings of pyloric lesions. The purpose of this retrospective case series study was to assess the CT findings of canine pyloric lesions. The following CT parameters were recorded: anatomical area, involved area, lesion shape, growth patterns of wall thickening lesions, enhancement pattern of the lesion in the early and delayed phases, lymphomegaly, and pulmonary metastasis. Seventeen dogs were included in this study and had the following final diagnoses: hyperplasia (five dogs), adenoma (five dogs), adenocarcinoma (three dogs), gastrointestinal stromal tumor (GIST; two dogs), polyposis (one dog), and pyogenic granuloma (one dog). Hyperplasia, adenoma, and polyposis formed mass lesions that involved the mucosal layer. Lymphomegaly was detected in two Jack Russell terriers with hyperplasia; however, the causes were unknown because we did not perform biopsies. All adenocarcinomas formed wall-thickened lesion that involved the outer layer, with lymphomegaly. All GISTs formed mass lesion that involved the outer layer. The pyogenic granulomas formed symmetric wall-thickened lesion that involved the mucosal and outer layers. CT facilitated the characterization of canine pyloric lesions using contrast enhancement, based on the involved area and lesion shape. However, polyposis may require caution in diagnosis based on CT findings alone.

Gastric neuroendocrine carcinoma (carcinoid) in a ferret (Mustela putorius furo).

A well-differentiated neuroendocrine carcinoma of the stomach (gastric carcinoid) with transcoelomic and lymph node metastasis was confirmed on post-mortem examination of a 3-year-old, spayed female, domestic ferret (Mustela putorius furo). The animal was initially presented with a history of persistent vomiting which progressed to weight loss, a palpable abdominal mass, and melena. The ferret received palliative treatment and was euthanized 9 mo after initial presentation. The clinical, ultrasonographical, cytological, gross pathological, histopathological, and immunohistochemical findings are described. Gastric neuroendocrine carcinomas are rarely reported in animals; this is the first description in a ferret. Key clinical message: Veterinary practitioners and diagnosticians should include neuroendocrine carcinoma as a differential diagnosis when encountering gastric neoplasms in ferrets and be aware of the potential for aggressive behavior and widely spread metastasis.

Carcinome neuroendocrine gastrique (carcinoïde) chez un furet ( Mustela putorius furo ). Un carcinome neuroendocrinien bien différencié de l'estomac (carcinoïde gastrique) avec des métastases transcoelomiques et ganglionnaires a été confirmé lors de l'autopsie d'une femelle furet domestique (Mustela putorius furo) stérilisée de 3 ans. L'animal a été initialement présenté avec des antécédents de vomissements persistants qui ont évolué vers une perte de poids, une masse abdominale palpable et un méléna. Le furet a reçu un traitement palliatif et a été euthanasié 9 mois après la présentation initiale. Les résultats cliniques, échographiques, cytologiques, de pathologie macroscopique, histopathologiques et immunohistochimiques sont décrits. Les carcinomes neuroendocriniens gastriques sont rarement rapportés chez les animaux; c'est la première description chez un furet.Message clinique clé:Les praticiens vétérinaires et les diagnosticiens doivent inclure le carcinome neuroendocrinien comme diagnostic différentiel lorsqu'ils rencontrent des néoplasmes gastriques chez les furets et être conscients du potentiel de comportement agressif et de métastases largement disséminées.(Traduit par Dr Serge Messier).

Vimentin and Ki-67 immunolabeling in canine gastric carcinomas and their prognostic value.

This study evaluated the expression of vimentin and Ki-67 proliferative index (PI) by immunohistochemistry in 30 canine gastric carcinomas (GCs) and a possible association with clinical and pathological features and patient's survival time. Vimentin immunoreactivity was assessed in neoplastic cells (in primary lesions, emboli, and metastases) and tumor-associated stroma (TAS) of canine GCs. Ki-67 PI was quantified in the neoplastic epithelial component. Vimentin immunolabeling in neoplastic cells was found in 30% of the primary lesions, in 82% of the neoplastic emboli, and in 50% of the metastases; in TAS, it was observed in all cases. A mean of 16% of the TAS was immunolabeled for vimentin. High vimentin immunolabeling in the TAS (>16%) was detected in 40% of cases. The average value of Ki-67 PI was 50%, and 80% of the lesions had Ki-67 PI above 20%. Vimentin immunolabeling in neoplastic cells was more frequent in less-differentiated carcinomas (diffuse [29%] and indeterminate types [75%]) than well-differentiated carcinomas (intestinal type [0%], P = .049). No significant differences were observed in vimentin immunolabeling in the TAS or Ki-67 PI according to histological diagnosis, depth of invasion, presence of neoplastic emboli or metastases. However, vimentin immunolabeling in the TAS was positively correlated with Ki-67 PI (r = .394, P = .031). Furthermore, a moderate negative correlation was observed between Ki-67 PI and survival time (r = -0.540). Our results suggest that vimentin and Ki-67 PI have potential for providing prognostic information in cases of canine GCs.

Equine Gastric Squamous Cell Carcinoma in a Friesian Stallion.

A 7-year-old Friesian stallion with a history of oesophageal stenosis, weight loss, inappetence, and recurrent hyperthermia was referred for gastroscopy. The stomach mucosa surrounding the oesophageal opening showed a large, necrotic, and ulcerated mass. On post-mortem examination, a very large, cauliflower-like neoplasm was seen, affecting non-glandular gastric mucosa. Nodular lesions were observed, scattered on the omentum, the spleen, and the liver. Microscopic findings allowed the diagnosis of gastric squamous cell carcinoma with abdominal metastasis. Biomolecular investigations demonstrated the presence of EcPV-2 genes in neoplastic lesions, thus supporting the role of EcPV-2 in the ethiology of equine gastric cancer.

Alimentary Tract Neoplasia in Captive Bearded Dragons (Pogona spp).

There are multiple reports of gastric neuroendocrine carcinoma in bearded dragons (Pogona spp), but other types of alimentary neoplasia are rarely reported. In a retrospective study, we identified 51 cases of neoplasia, including gastric (n = 26), oral (n = 18), intestinal (n = 13), oesophageal (n = 3) and cloacal (n = 2) neoplasms. Round cell neoplasia was diagnosed in the alimentary tract in 14 cases, all of which had extra-alimentary involvement, most commonly in the liver, lung, spleen and kidney, and was considered to be the cause of death or euthanasia in all cases. Oral neoplasms included sarcoma, adenomatous polyp, round cell neoplasia, fibromatous epulis of periodontal ligament origin and myxoma. Apart from disseminated round cell neoplasia, all the oral neoplasms, including sarcomas, were not associated with death or euthanasia and had a good to excellent prognosis. Oesophageal neoplasms included round cell neoplasia. Gastric neoplasms included neuroendocrine carcinoma, round cell neoplasia, adenocarcinoma and sarcoma. Intestinal neoplasms included round cell neoplasia, sarcoma, adenocarcinoma and metastatic sarcoma. All oesophageal, gastric and intestinal neoplasms were associated with death or euthanasia and had a poor to grave prognosis. Cloacal neoplasms included round cell tumours and squamous cell carcinoma, and all were primary alimentary tumours except for the round cell tumours and one metastatic sarcoma. Round cell neoplasia and gastric neuroendocrine carcinoma were the most common diagnoses. Sarcomas and polyps were common in the oral cavity and rare to absent elsewhere. Adenocarcinoma was rare and only identified in the stomach and intestines.

Gastrointestinal stromal tumors with Kit gene mutation in 4 guinea pigs (Cavia porcellus).

Gastrointestinal stromal tumors (GISTs) have been rarely reported in guinea pigs. We aimed to characterize the clinical and pathological features of GISTs in 4 guinea pigs and investigate the presence of mutations in exon 11 of the KIT proto-oncogene receptor tyrosine kinase (Kit) gene. Two subjects were male and 2 were female; 2 were 6 years old, 1 was 7 years old, and 1 was of an unknown age. Three cases had primary gastric tumors, whereas 1 had a primary small intestinal tumor. All cases had tumors that extended from the submucosa to the serosa with extraluminal growth. A gastric tumor had gastric, pancreatic, and cecal metastases. Histologically, the tumors were sharply demarcated and composed of spindle cells arranged in bundles, intermixed with small amounts of collagenous stroma. The tumor cells had mild atypia with few mitotic figures (0-5/50 high power fields, 7.95 mm2) and were immunolabeled for KIT and Discovered-on-GIST 1 (DOG1). All cases had mutations in exon 11 of the Kit gene. These findings indicate that GISTs in guinea pigs are similar to those in humans and dogs. GISTs in guinea pigs are potentially malignant submucosal tumors with KIT- and DOG1-immunolabeling, exon 11 KIT mutations, and the possibility of metastasis.

Gastric Plasmacytoma with Immunoglobulin Lambda Light Chain Deposition in a Dog.

A 12-year-old castrated male Jack Russell Terrier presented with intermittent vomiting. Abdominal ultrasonographic examination detected a thickened stomach wall with a mass measuring approximately 1.5 cm in diameter. Computed tomography revealed a solitary mass measuring approximately 2.1 cm in diameter between the submucosa and muscle layers in the greater curvature the pyloric region of the stomach, and a swelling in the hepatic lymph node. The gastric mass was composed of round neoplastic cells arranged in a diffuse pattern. The neoplastic cells had a round nucleus and a pale abundant cytoplasm. Multinucleated giant cells were often found. Hyalinized eosinophilic material, which did not stain with Congo red and had no affinity for thioflavin T, was also observed. Neoplastic cells were immunopositive for MUM1, CD79a and Ig lambda light chain but negative for CD3, CD20, BLA36, IgG and Ig kappa light chain. Stromal eosinophilic material was positive for Ig lambda light chain. The neoplasm was therefore diagnosed as a gastric plasmacytoma with non-amyloid Ig lambda light chain deposition.

Safety of alternate-day treatment with TS-1TM (tegafur/gimeracil/oteracil) in tumor-bearing dogs: a pilot study.

Tegafur is a prodrug of fluoropyrimidine 5-fluorouracil (5-FU), while TS-1TM is an oral fixed-dose combination of three active drugs, tegafur, gimeracil, and oteracil. This pilot study evaluated the safety of tegafur/gimeracil/oteracil in the treatment of cancers in dogs. Tegafur/gimeracil/oteracil was administered orally at a mean dose of 1.1 mg/kg twice daily on alternate days, Monday-Wednesday-Friday, every week to 11 dogs with tumors. Partial response and stable disease were observed in one dog each, whereas six exhibited progressive disease. Three dogs were not assessed. Adverse events, the most serious being grade 2, were noted in seven dogs. Adverse events were acceptable, and the drug was effective in some dogs. Therefore, tegafur/gimeracil/oteracil may be useful for treating malignant solid tumors in canines.

Comparison of the clinical, ultrasound, and CT findings in 13 dogs with gastric neoplasia.

Diagnosis of gastric tumors in dogs is difficult and is often obtained by biopsy following identification of a mass through ultrasound (US) or endoscopy. In human medicine, modalities such as CT and endoscopy are standard of care in the diagnosis and staging of gastric tumors. Although one veterinary study has described CT findings of gastric tumors in dogs using iatrogenic gas dilation, there are no veterinary studies that have directly compared the usefulness of US versus CT in the diagnosis and staging of these tumors. This retrospective, descriptive study evaluated US and CT images from 13 dogs. Gastric tumor diagnoses included leiomyoma (n = 4), adenocarcinoma (n = 3), leiomyosarcoma (n = 3), gastrointestinal stromal tumor (n = 2), and lymphoma (n = 1). Computed tomography was successful in identification of 92% of gastric tumors, while US identified only 69%. Computed tomography identified more locations of lymphadenopathy and correctly identified the location of gastric tumors more frequently than US when compared to the surgical, endoscopic, or necropsy reports. Most features seen on US and CT overlapped between the different tumor types. Lymphoma had a lower mean attenuation in CT than the other gastric tumors and was the only gastric tumor to not have complete loss of the gastric wall layering on US. As expected, adenocarcinoma appeared as gastric wall thickening with regional lymphadenopathy. Findings supported using CT as an ancillary diagnostic test for characterizing and staging gastric tumors in dogs and assisting in the selection of surgical candidates.

Endoscopic Endocautery Polypectomy for the Treatment of Duodenal and Gastric Polyps in a Cat.

Endoscopic polypectomy is commonly performed in human medicine, with large-scale studies reported. However, few reports have described its use in veterinary medicine and, specifically, the procedure in the case of duodenal polyps in cats has not been reported. A 7 kg 14-year-old cat presented with recurrent vomiting for several months. Gastroduodenoscopy revealed a pedunculated polyp at the pyloric antrum and another in the duodenum, with its head protruding into the pylorus. Endoscopic polypectomy was performed using an electrosurgical snare with no recurrence of clinical signs after six months. Duodenal polypectomy in cats may be difficult because of space limitation but it can be safe, minimally invasive, and successful, thus avoiding more invasive surgical techniques. Endoscopic polypectomy may be a viable alternative to surgery in cats with gastric and duodenal polyps.

Gastric mucosal pathology in Belgian Shepherd dogs with and without clinical signs of gastric disease.

BACKGROUND: Gastric carcinoma (GC) is uncommon in dogs, except in predisposed breeds such as Belgian Shepherd dogs (BSD) of the Tervuren and Groenendael varieties. When GC is diagnosed in dogs it is often late in the disease, resulting in a poorer prognosis. The aim of this prospective clinical study was to investigate possible associations of gastric mucosal pathologies with clinical signs, laboratory test results and GC in BSD. An online survey gathered epidemiological data to generate potential risk factors for vomiting as the predominant gastric clinical sign, and supported patient recruitment for endoscopy. Canine Chronic Enteropathy Clinical Activity Index (CCECAI) score and signs of gastroesophageal reflux (GER) were used to allocate BSD older than five years to either Group A, with signs of gastric disease, or Group B, without signs. Findings in the clinical history, laboratory tests and gastric histopathology of endoscopic biopsies were statistically analysed in search of associations. RESULTS: The online survey included 232 responses. Logistic regression analysis recognized an association of vomiting with gagging, poor appetite and change in attitude. Recruitment for endoscopy included 16 BSD in Group A (mean age 9.1 ± 1.8 years, mean CCECAI = 3.1 ± 2.2 and signs of GER); and 11 in Group B (mean age 9.8 ± 1.4 years, CCECAI = 0, no signs of GER). Seven (25.9%) of the 27 BSD (Group A 4/16, Group B 3/11) had leukopenia. Serum C-reactive protein tended to be increased with more advanced GC (P = 0.063). Frequency of GC, mucosal atrophy, mucous metaplasia, or glandular dysplasia did not differ between groups. GC was frequently diagnosed (6/27), even without clinical signs (2/11). The odds ratio for vomiting (OR = 9.9; P = 0.016) was increased only when glandular dysplasia was present. GC was associated with mucous metaplasia (P = 0.024) and glandular dysplasia (P = 0.006), but not with mucosal atrophy (P = 1). CONCLUSIONS: GC can develop as an occult disease, associated with metaplasia and dysplasia of the gastric mucosa. Suggestive clinical signs, notably vomiting, should warrant timely endoscopy in BSD. Extensive endoscopic screening of asymptomatic dogs remains, however, unrealistic. Therefore, biomarkers of mucosal pathology preceding clinical illness are needed to support an indication for endoscopy and enable early diagnosis of GC.

Hypertrophic gastropathy associated with gastric sarcoma in a dog.

A 14-y-old spayed female Labrador Retriever was presented with an 8-mo history of chronic vomiting. Abdominal ultrasound and gastrointestinal endoscopy revealed a mass protruding into the gastric lumen, with cytologic features suggestive of sarcoma. A partial gastrectomy was performed; the gastric body and antrum were thickened, with a cerebriform appearance of the mucosal surface. Histologic examination revealed a submucosal neoplastic proliferation of fusiform cells variably arranged in irregular bundles and scattered whorls. Fusiform cells strongly reacted to antibodies against vimentin, S100, and neuron-specific enolase; glial fibrillary acidic protein was moderately and multifocally expressed. Pancytokeratin, KIT, α-smooth muscle actin, and desmin were nonreactive. Histologic and immunohistochemical findings suggested a diagnosis of gastric sarcoma with features referable to a non-GIST (gastrointestinal stromal tumor), non-smooth muscle NIMT (non-angiogenic, non-lymphogenic intestinal mesenchymal tumor). The overlying gastric mucosa was thickened by elongated and dilated gastric glands, predominantly lined by intensely periodic acid-Schiff-stained mucous cells. This altered mucosal architecture was suggestive of Ménétrier-like disease. Although this disease has been hypothesized to predispose to gastric adenocarcinoma in dogs, an association with gastric sarcoma has not been documented previously in the veterinary literature, to our knowledge.

Partial Gastrectomy at the Time of Splenectomy in Two Dogs With Splenic Neoplasia and Gastric Involvement.

Splenic malignancies are reported in 30%-76% of dogs presenting with splenic masses, and splenectomy is the cornerstone in their management. However, long term prognosis is guarded due to the high rates of distant metastases reported both for HSA and nonangiogenic nonlymphomatous sarcomas. Metastases from splenic tumors usually occur to regional lymph nodes, liver, omentum, and lungs. These case series aim to describe 2 cases of splenic neoplasia with gastric involvement and report the surgical technique and outcomes associated with the condition. Two mixed-breed dogs were referred for a splenic mass and underwent explorative celiotomy. In both cases, the splenic mass was firmly attached to the gastric wall, and splenectomy with concurrent partial gastrectomy was thus performed. In case 1, liver lobectomy due to a hepatic mass was also performed. In case 2, the regional nodes were also excised due to lymphoadenomegaly. Both dogs recovered uneventfully from surgery and were discharged from the hospital at 72 and 96 hours. Histopathological examination was costent with splenic undifferentiated sarcoma and hepatic adenocarcinoma in one dog. The other dog had a diagnosis of malignant fibrous histiocytoma with nodal metastases. Neoplastic invasion of the stomach was histologically confirmed in both dogs. Adjuvant chemotherapy was refused, and both dogs were euthanized due to tumor progression at 71 and 58 days, respectively. According to our results, splenectomy with concurrent gastrectomy is feasible in dogs with splenic tumours involving the gastric wall. However, long term prognosis is poor, as previously reported for metastatic splenic sarcomas.

Epitheliotropic T-cell lymphoma in 2 half-sibling bontebok.

We diagnosed epitheliotropic T-cell lymphoma of the forestomachs in 2 aged, half-sibling, zoo-managed bontebok (Damaliscus pygargus pygargus). One bontebok also had mesenteric lymph node and cutaneous involvement. Both animals had a history of chronic abdominal distension and diminished body condition that resulted in euthanasia. At autopsy, both animals had marked ruminal distension with diffusely blunted ruminal papillae and reticular crests. In case 1, there was an increased amount and particle length of the ruminoreticular fibrous material with scant fluid, and a 2-cm diameter focus of cutaneous crusting adjacent to a mammary teat. In case 2, the rumen and reticulum were fluid-distended with decreased fibrous material. Histologically in case 1, the rumen, reticulum, omasum, and skin had intraepithelial nests and sheets of neoplastic small lymphocytes; in case 2, the rumen and reticulum had a similar neoplastic cell population. Immunohistochemically, neoplastic lymphocytes were immunoreactive for CD3 and negative for CD20, confirming the diagnosis of epitheliotropic T-cell lymphoma.

Risk and characteristics of gastric carcinoma in the chow chow dog.

Gastric carcinoma is not commonly reported in dogs. There is an increased risk, however, in certain breeds such as the Belgian Tervuren. Review of the Veterinary Medical Database (VMDB) established an increase in risk for gastric carcinoma in the chow chow breed. In 106 chow chow dogs signs commenced, on average, 3 weeks before definitive diagnosis. The most common clinical signs were vomiting, loss of appetite, diarrhea, and melena. Most affected dogs were euthanized, without treatment, within 2 weeks of diagnosis. Two dogs which were treated aggressively (surgery and chemotherapy) survived a considerably longer time (12 and 36 months). Histologically, these chow chow dogs comprised a similar histologic type as familial gastric carcinoma in humans; diffuse-type carcinoma that was enriched in the signet ring and mucinous variants. Understanding the pathogenesis of diffuse gastric carcinoma in the chow chow dog may provide insight into the biology of this aggressive cancer in humans.

Risques et caractéristiques d'un carcinome gastrique chez le chien de race chow-chow. Le carcinome gastrique n'est par rapporté fréquemment chez les chiens. Il y a toutefois une augmentation du risque chez certaines espèces telle que le Tervuren belge. Une revue de la base de données Veterinary Medical Database (VMDB) a établi une augmentation dans le risque pour le carcinome gastrique chez la race chow chow. Chez 106 chiens chow chow les signes débutèrent, en moyenne, 3 semaines avant le diagnostic définitif. Les signes cliniques les plus fréquents étaient vomissement, perte d'appétit, diarrhée et méléna. La plupart des chiens affectés furent euthanasiés, sans traitement, à l'intérieur de 2 semaines du diagnostic. Deux chiens furent traités de manière agressive (chirurgie et chimiothérapie) ont survécu beaucoup plus longtemps (12 et 36 mois). Histologiquement, ces chiens chow chow comprennent un type histologique similaire aux carcinomes gastrique familiaux chez les humains; le carcinome de type-diffus qui s'est développé dans les variants de cellules en bague à chatons et mucineux. Comprendre la pathogénie du carcinome gastrique diffus chez le chien chow chow pourrait fournir des informations sur la biologie de ce cancer agressif chez l'humain.(Traduit par Dr Serge Messier).

Tn and Sialyl-Tn antigens in canine gastric tissues.

Malignant transformation is often associated with abnormal protein glycosylation expressed, amongst others, by the accumulation of simple mucin-type carbohydrates namely Tn and Sialyl-Tn (STn) antigens. These are usually limited in normal tissues and their increased expression has been associated with cancer progression and poor prognosis. This study aims to evaluate the role of Tn and STn antigens in the neoplastic transformation of the canine gastric mucosa and to correlate their putative immunoexpression alterations with some pathological features. Tn and STn antigens expression were immunohistochemically evaluated in canine normal gastric mucosa (n = 3), gastric polyps (n = 9) and gastric carcinomas (n = 25), neoplastic emboli (n = 12) and metastases (n = 8). In normal gastric mucosa, Tn antigen was detected in the gastric epithelial cells, while STn antigen was absent. Similarly, all gastric polyps expressed Tn antigen, but none displayed STn antigen immunostaining. In carcinomas, Tn antigen was expressed in 96% of the cases and STn antigen in 68% of the neoplasms. STn antigen was significantly higher in carcinomas compared with normal mucosa (P < .05). No correlation was found between each antigen and the different subtypes of tumours according to WHO classification, tumour differentiation, lymph vascular invasion or metastasis. All neoplastic emboli expressed both antigens, and the expression score was similar or higher than that displayed by the neoplastic cells of the primary tumour. The high prevalence of STn antigen in gastric carcinomas compared with normal mucosa highlights the cancer-associated nature of this antigen. Our results link STn antigen expression to neoplastic transformation and suggest that it may be a useful marker of gastric cancer progression in dogs.

A Subset of Equine Gastric Squamous Cell Carcinomas Is Associated With Equus Caballus Papillomavirus-2 Infection.

Squamous cell carcinoma (SCC) is the most common neoplasm of the equine stomach. However, the mechanisms underlying malignant transformation are unknown. As Equus caballus papillomavirus-2 (EcPV-2) is a likely cause of some genital SCCs, we hypothesized that EcPV-2 is associated with a subset of equine gastric SCCs. To this aim, we performed polymerase chain reaction (PCR) and in situ hybridization (ISH) for EcPV-2 E6/ E7 oncogenes on 11 gastric SCCs and on gastric samples from 15 control horses with no SCC. PCR for EcPV-2 was positive in 7/11 (64%) gastric SCCs; non-SCC gastric samples were all negative. Intense hybridization signals for EcPV-2 E6/E7 nucleic acid were detected by ISH within tumor cells in 5/11 (45%) gastric SCCs, including distant metastases. No hybridization signals were detected within any of the non-SCC gastric cases. This study provides support for a potential association between EcPV-2 infection and a subset of equine gastric SCC.