Sharkey L C, Rosol T J, Gröne A, Ward H, Steinmeyer C
Department of Veterinary Biosciences, College of Veterinary Medicine, Ohio State University, Columbus 43210, USA.
J Vet Intern Med. 1996 Nov-Dec;10(6):405-8. doi: 10.1111/j.1939-1676.1996.tb02088.x.
A dog with a pulmonary papillary carcinoma and a cat with a dermal tubular adenocarcinoma had profound paraneoplastic neutrophilic leukocytosis with no clinically detectable inflammatory foci. To investigate the mechanism of the leukocytosis, oligonucleotide primers were designed from the cDNA sequences of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) of dogs. Reverse transcription polymerase chain reaction was performed on tumor tissues, and specific amplification of G-CSF and GM-CSF was obtained with the tumor RNA in the dog. The tumor RNA in the cat demonstrated specific amplification of G-CSF but not GM-CSF. These findings are consistent with the production of G-CSF and/or GM-CSF by neoplasms as a mechanism for paraneoplastic leukocytosis in small animals.
一只患有肺乳头状癌的狗和一只患有皮肤管状腺癌的猫出现了严重的副肿瘤性中性粒细胞增多症,且无临床可检测到的炎症病灶。为了研究白细胞增多的机制,根据狗的粒细胞集落刺激因子(G-CSF)和粒细胞-巨噬细胞集落刺激因子(GM-CSF)的cDNA序列设计了寡核苷酸引物。对肿瘤组织进行逆转录聚合酶链反应,在狗的肿瘤RNA中获得了G-CSF和GM-CSF的特异性扩增。猫的肿瘤RNA显示出G-CSF的特异性扩增,但未显示GM-CSF的扩增。这些发现与肿瘤产生G-CSF和/或GM-CSF作为小动物副肿瘤性白细胞增多症的机制一致。