共查询到20条相似文献，搜索用时 218 毫秒
1.
2.
3.
4.
5.
犬肥大细胞瘤(Canine mast cell tumor, MCT)是起源于真皮组织肥大细胞的恶性肿瘤,最常见于躯干、四肢和头颈部。犬肥大细胞瘤的临床表现多样,其表面可能脱毛、溃疡、红斑、色素过度沉着。一例患犬通过临床症状检查、血常规、血液生化、C-反应蛋白(C-reactive protein, CRP)、X射线以及病理组织学观察,最终确诊为犬的多发性肥大细胞瘤。对该犬实施了肿瘤及周围健康组织切除手术,并建议术后进行化疗,为后续提高犬多发性肥大细胞瘤治疗和诊断水平提供参考。 相似文献
6.
7.
8.
为了解当前犬肿瘤疾病的临床诊断及治疗现状，本文记录了一例患病泰迪犬的临床症状、治疗过程及预后情况，并对患病犬进行临床综合诊断、实验室诊断、影像学检查和手术摘除疗法。通过对切除肿瘤进行病理组织学观察，进一步研判了肿瘤类型。经综合诊断，该泰迪犬患肥大细胞瘤（恶性肿瘤），已向乳腺周围和口腔局部扩散，目前正在使用长春新碱化疗药物维持，需定期复诊。 相似文献
9.
10.
犬肥大细胞瘤的病理学观察 总被引：1，自引：0，他引：1
<正>肥大细胞的肿瘤性增生称之为肥大细胞瘤(Mast Cell Tumors),犬肥大细胞瘤占犬全部皮肤肿瘤的16%21%[1],是犬最为常见的皮肤肿瘤。犬发生肥大细胞瘤的病因目前还未知,可能同慢性炎症或使用皮肤刺激剂有关。作者就本实验室接诊的两例犬皮肤肥大细胞瘤报告如下。1材料与方法病料分别来自本市2所动物医院送检病例,病例1为可卡犬,雄性,8岁,头顶部、左耳道口下方皮肤肿物增生较快,直径1 cm;病例2为京巴犬,雌性,12岁,腹部皮下肿物。兽医切除肿物(附带 相似文献
11.
OBJECTIVE: To evaluate molecular abnormalities in the c-kit gene of canine mast cell tumors (MCT) with different grades of cellular differentiation. SAMPLE POPULATION: 31 normal tissue specimens from dogs and 45 canine MCT classified according to grade of cell differentiation. PROCEDURES: Genomic DNA extractions were made from canine MCT and normal tissues. Parts of exon 11, intron 11, and exon 12 of the c-kit gene were amplified by use of polymerase chain reaction. These regions were cloned, sequenced, and compared with GenBank sequences of the National Center for Biotechnology International. A statistical analysis was used to compare sequences from canine MCT and normal tissues. RESULTS: A significantly higher percentage of homozygous intron 11 deletion was found in canine MCT (49%) than in normal tissues (13%). This percentage was also higher in moderately and poorly differentiated MCT, compared with well-differentiated MCT Although no mutations were detected in any of the specimens, a polymorphism at amino acid position 606 of the canine c-kit sequence was found in all the studied sequences. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated a relationship between intron 11 deletion and MCT and the grade of MCT differentiation. We suggest that intron 11 deletion may be implicated in the pathogenesis of MCT and could be used as a marker for diagnosis and prognosis of canine MCT. 相似文献
12.
Ohmori K Kawarai S Yasuda N Tanaka A Matsuda H Nishimura R Sasaki N Tsujimoto H Masuda K 《Veterinary immunology and immunopathology》2008,126(1-2):43-53
Gain-of-function mutations in the proto-oncogene c-kit have been considered the molecular mechanism of neoplastic proliferation of mast cells. However, the importance of c-kit gene mutations is not well evaluated in canine mast cell tumors (MCTs). In the present study, we established and characterized a mast cell line, HRMC, derived from a dog with MCT. We also examined c-kit mutations in HRMC cells and assessed an inhibitory effect of a tyrosine kinase inhibitor, STI571, on HRMC cells. HRMC cells had cytoplasmic metachromatic granules, chymase and tryptase, and expressed both KIT and FcepsilonRI on the cell surface. HRMC cells contained histamine and released beta-hexosaminidase through FcepsilonRI cross-linking and calcium ionophore stimulation. Nucleotide sequence analysis demonstrated no mutations in an open reading frame of c-kit cDNA and genomic DNA of the juxtamembrane domain of c-kit in HRMC cells. STI571 did not show any inhibitory effects on the proliferation of HRMC cells. These findings clearly demonstrated the existence of c-kit mutations-independent neoplastic canine mast cell proliferation. The growth factor-independent mast cell line established in this study might be valuable to explore novel mechanisms of c-kit mutations-independent neoplastic proliferation of mast cells in dogs. 相似文献
13.
Yamada O Kobayashi M Sugisaki O Ishii N Ito K Kuroki S Sasaki Y Isotani M Ono K Washizu T Bonkobara M 《Veterinary immunology and immunopathology》2011,142(1-2):101-106
Target therapy using the tyrosine kinase inhibitor imatinib is one of the new therapeutic approaches for canine mast cell tumors (MCTs). In the present report, we demonstrate a clinical response to imatinib in a dog with MCT carrying a c-kit c.1523A>T mutation. Moreover, the effect of this mutation on the phosphorylation status of KIT and the inhibitory potency of imatinib on the phosphorylation of the mutant KIT were examined in vitro. A dog with a MCT tumor mass on the right forelimb sole with lymph node metastasis and mastocytemia was treated with imatinib. The MCT mass markedly shrank and mastocytemia became undetectable with 2 weeks of treatment. The lymph node enlarged by metastasis became normal in size with 5 weeks of treatment. From the sequencing analysis of c-kit in tumor cells, a substitution mutation c.1523A>T that alters the amino acid composition (p.Asn508Ile) within the extracellular domain of KIT was identified. The mutant KIT expressed on 293 cells showed ligand-independent phosphorylation and imatinib suppressed this phosphorylation in a dose-dependent manner. From these findings, imatinib was considered to elicit a clinical response in a canine case of MCT via inhibition of the constitutively activated KIT caused by a c-kit c.1523A>T mutation. 相似文献
14.
Isotani M Ishida N Tominaga M Tamura K Yagihara H Ochi S Kato R Kobayashi T Fujita M Fujino Y Setoguchi A Ono K Washizu T Bonkobara M 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2008,22(4):985-988
BACKGROUND: Imatinib mesylate is a small molecule targeted at dysregulated protein-tyrosine kinase. Mutation of c-kit exon 11, which induces constitutive phosphorylation of KIT, is one of the mechanisms for the development or progression of mast cell tumor (MCT) in dogs. The purpose of this study was to examine the therapeutic potential of imatinib mesylate in canine MCT. HYPOTHESIS: Imatinib mesylate has activity against MCT in dogs, and response to treatment can be correlated to presence of mutation within exon 11 of c-kit. ANIMALS: Twenty-one dogs with MCT with gross tumor burden and median tumor size of 7.2 cm (range, 1.0-25.3 cm) before treatment. METHODS: Tumors were analyzed for mutation of c-kit exon 11. Imatinib mesylate was administered PO to the dogs at a dose of 10 mg/kg daily for 1-9 weeks. RESULTS: Ten of 21 dogs (48%) had some beneficial response to imatinib mesylate treatment within 14 days of treatment initiation. All 5 dogs with a demonstrable c-kit mutation in exon 11 responded to the drug (1 complete remission, 4 partial remission). CONCLUSIONS AND CLINICAL IMPORTANCE: Imatinib mesylate has clinical activity against MCT in dogs. Response could not be predicted based on presence of absence of a mutation in exon 11 of c-kit. 相似文献
15.
OBJECTIVE: To evaluate splenic mast cell tumors (MCT) of cats for activating mutations in the proto-oncogene c-kit. SAMPLE POPULATION: 10 formalin-fixed, paraffin-embedded splenic MCT from cats in the pathology database of the Veterinary Medical Teaching Hospital at the University of California, Davis. PROCEDURE: Genomic DNA was isolated from tumor specimens, and the polymerase chain reaction (PCR) procedure was performed for exons 11, 12, and 17. The PCR products were analyzed by use of agarose gel electrophoresis and then directly sequenced. RESULTS: We did not identify mutations in the juxtamembrane domain (encoded by exons 11 and 12) or catalytic domain (encoded by exon 17) of c-kit in any of the splenic MCT specimens. CONCLUSIONS AND CLINICAL RELEVANCE: Although mutations in the proto-oncogene c-kit occur frequently in naturally developing MCT in dogs and aggressive mastocytosis in humans, the data reported here documented that dysregulation of Kit function through activating mutations is unlikely in splenic MCT of cats. Therapeutic strategies aimed at inhibiting Kit signaling (ie, kinase inhibitors such as imatinib [STl571]) may not be of benefit for the treatment of this disease in cats. 相似文献
16.
Zavodovskaya R Chien MB London CA 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2004,18(6):915-917
Mast cell tumor (MCT) is one of the most common tumors of dogs. Some affected dogs develop multiple cutaneous tumors in various locations over months to years. In these cases, it is not clear whether the tumors have arisen de novo, or if each tumor represents a recurrence of the previously excised original tumor (ie, distant metastasis). We used the presence of an internal tandem duplication (ITD) in c-kit to demonstrate that in 2 dogs with recurrent cutaneous MCT that had developed over 1-2 years, each recurrent MCT tumor possessed an identical ITD when compared to the original MCT, indicating that the multiple tumors were clonal in origin. This study demonstrates that similar to the situation in humans, specific somatic mutations identified in oncogenes found in canine neoplasms can be used to provide evidence of tumor clonality. 相似文献
17.
本研究旨在探讨炎症因子（白细胞介素10, IL-10）对牛瘤胃上皮细胞中挥发性脂肪酸（VFA）吸收相关蛋白基因表达的影响。试验采用随机区组设计,在瘤胃上皮细胞体外培养条件下,研究50 ng·mL-1浓度的IL-10对牛瘤胃上皮细胞中核因子（NF-κB）、假定阴离子转运蛋白1（PAT1）、阴离子交换蛋白2（AE2）、单羧酸转运蛋白1（MCT1）、单羧酸转运蛋白4（MCT4）、钠氢离子交换蛋白1（NHE1）基因表达的影响。结果表明,在中性条件下,IL-10添加显著下调了NF-κB、PAT1、MCT1、NHE1基因的表达（P<0.05）,AE2基因的表达显著性上调（P<0.05）,而对MCT4基因的表达没有显著影响。在酸性条件下,IL-10添加组的NF-κB基因表达被显著性抑制（P<0.05）,而PAT1、MCT1、MCT4基因表达显著上调（P<0.05）。pH5.5组与pH7.2组比较,pH5.5组NF-κB基因表达显著性上调（P<0.05）。结果提示,在炎症条件下,白细胞介素10作为一种抗炎因子,可以缓解瘤胃上皮细胞炎症反应从而促进VFA吸收相关蛋白基因的表达。 相似文献
18.
本试验旨在研究奶牛采食前后瘤胃中短链脂肪酸(SCFA)浓度的变化及其吸收相关蛋白表达量的差异。试验选用3头体重(720±30)kg且装有瘘管的健康荷斯坦牛(动物伦理审查编号为SXAU-EAW-2019-C002013),采食精粗比为40:60的日粮(10kg),试验预试期10d,于第11天饲喂前开始取样,采用气相色谱法检测奶牛采食前(0 h)和采食后(1、2、3、4、5、6、7、8 h)瘤胃液中SCFA浓度;并采用荧光定量PCR方法检测瘤胃上皮组织中与SCFA吸收相关的蛋白表达量。结果表明:在采食后1 h奶牛瘤胃中SCFA浓度最高(P<0.05);在采食后一段时间内(2~5h)与SCFA吸收相关蛋白表达量上调(P<0.05),AE2、MCT1基因表达量均在5 h最高,PAT1、NHE3基因表达量均在4 h最高,MCT4基因表达量在4、5、6h均较高,NHE1基因表达量在2h达到最高;AE2、MCT1、MCT4、NHE1基因表达量与SCFA浓度负相关或正相关(P<0.05),AE2、MCT1、MCT4基因表达量与瘤胃内pH正相关(P<0.05)。以上结果初步揭示,在采食后一定时间内,瘤胃中与SCFA吸收相关蛋白表达受SCFA浓度和pH的调节。 相似文献
19.
20.
Grant IA Rodriguez CO Kent MS Sfilgoi G Gordon I Davis G Lord L London CA 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2008,22(2):388-393
Background: Few effective drugs are available to treat dogs with locally aggressive or metastatic mast cell disease.
Hypothesis: Vinorelbine, a semisynthetic derivative of vinblastine, is an effective drug for the treatment of canine mast cell tumors (MCT).
Animals: Twenty-four dogs with cutaneous MCT.
Methods: Dogs with at least 1 measurable, cytologically confirmed, and previously untreated cutaneous MCT received a single treatment with vinorelbine at the previously established dosage of 15 mg/m2 IV. Tumor measurements and CBC were evaluated before and 7 days after treatment. Adverse events were graded according to Veterinary Cooperative Oncology Group (VCOG) guidelines.
Statistics: Data were accrued in accordance with a Simon's 2-stage design with a noninteresting response rate of .05, a target response of .25, and α and β values of .10.
Results: Three of 24 dogs (13%) had a response to treatment, including 1 measurable complete response and 1 measurable partial response. The 3rd dog had microscopic complete response to treatment with stable measurable disease. Twenty other dogs (83%) had stable disease and 1 dog (4%) had progressive disease. Neutropenia occurred in 13 dogs (54%) (grade 1, n = 4; grade 3, n = 6; grade 4, n = 3). Gastrointestinal toxicity occurred in 11 dogs (46%) (anorexia: grade 1, n = 3; grade 2, n = 1; grade 3, n = 1; diarrhea: grade 1, n = 2; grade 3, n = 1; vomiting: grade 1, n = 5; grade 3, n = 1).
Conclusions and Clinical Importance: Vinorelbine was associated with an overall response rate of 13% and a high prevalence of neutropenia. Additional studies are indicated to determine if repeated dosing of vinorelbine or combination of vinorelbine with other drugs increases the observed biologic activity against canine MCT. 相似文献
Hypothesis: Vinorelbine, a semisynthetic derivative of vinblastine, is an effective drug for the treatment of canine mast cell tumors (MCT).
Animals: Twenty-four dogs with cutaneous MCT.
Methods: Dogs with at least 1 measurable, cytologically confirmed, and previously untreated cutaneous MCT received a single treatment with vinorelbine at the previously established dosage of 15 mg/m
Statistics: Data were accrued in accordance with a Simon's 2-stage design with a noninteresting response rate of .05, a target response of .25, and α and β values of .10.
Results: Three of 24 dogs (13%) had a response to treatment, including 1 measurable complete response and 1 measurable partial response. The 3rd dog had microscopic complete response to treatment with stable measurable disease. Twenty other dogs (83%) had stable disease and 1 dog (4%) had progressive disease. Neutropenia occurred in 13 dogs (54%) (grade 1, n = 4; grade 3, n = 6; grade 4, n = 3). Gastrointestinal toxicity occurred in 11 dogs (46%) (anorexia: grade 1, n = 3; grade 2, n = 1; grade 3, n = 1; diarrhea: grade 1, n = 2; grade 3, n = 1; vomiting: grade 1, n = 5; grade 3, n = 1).
Conclusions and Clinical Importance: Vinorelbine was associated with an overall response rate of 13% and a high prevalence of neutropenia. Additional studies are indicated to determine if repeated dosing of vinorelbine or combination of vinorelbine with other drugs increases the observed biologic activity against canine MCT. 相似文献