An 11-year-old spayed female dog was presented for a large mass on the left proximal pelvic limb. The mass appeared three months prior to presentation in the location of a previous corticosteroid injection, Kenalog (0.05 mg/kg triamcinolone,. No vaccinations or injections had been previously given in this area. The mass spanned from the left stifle to the coxofemoral joint and was firm, circular, non-moveable, and diffusely mixed within the musculature of the thigh. A left external complete hemipelvectomy was performed. Histopathology was consistent with a Grade III fibromyxosarcoma. The dog died naturally at home five months after surgery. This is the first account of association of a corticosteroid injection with formation of a fibromyxosarcoma in a dog. Keywords: Injection Site Sarcoma; FibromyxosarcomaAn 11 year old, 7.7 kg, spayed female Wire Fox Terrier was presented for evaluation of a 3-month history of a very large mass on the left pelvic limb. The dog had a history of suspected skin allergies that began when she was 9 years old. No testing or skin biopsies were performed to confirm this, but she appeared to respond to empirical treatment for atopic dermatitis. She was treated with subcutaneous Kenalog (0.05 mg/kg triamcinolone) injections in the dorsal cervical region every four weeks for the past two years. Three months prior to surgical evaluation, a 0.05 mg/kg Kenalog injection was given subcutaneously in the left pelvic limb. Two days after the injection, a small firm mass appeared in the region of the injection site. The dog had no previous history of having an injection or vaccination in the left pelvic limb. She was presented to her regular veterinarian for evaluation of the mass, which had grown rapidly in the two weeks post-injection and was referred to another hospital. Fine needle aspiration was performed and showed a large amount of blood and some spindle shaped/mesenchymal cells. Because this sample was inconclusive, surgical biopsy was recommended for definitive diagnosis. At the time of incisional biopsy, the mass was softball size. Three view thoracic radiographs were within normal limits and there was no evidence of metastasis. Histopathology revealed a mass composed of plump haphazardly arranged spindle to stellate-shaped cells. The cells had moderate nuclear size, greater than 20 mitotic figures seen in 10 high power fields, and adipose tissue infiltrates. Radical resection of the mass and referral to a veterinary surgeon was recommended. Due to financial constraints, the owner opted not to follow through with consultation and surgical removal at that time.The dog was presented to us for further evaluation and treatment 8 weeks after incisional biopsy. On presentation, the dog was bright, alert, and responsive with normal heart and respiratory rates. No peripheral lymphadenopathy was palpated. The dog had a non-weight bearing lameness of the left hind limb. Over the left lateral femur, there was a 10 cm x14 cm x13 cm, firm, circular, non-moveable mass that was diffusely mixed...
Previously we reported that mithramycin represses multiple pathways critical for stem cell signaling and pluripotency in lung cancer cells. This phenomenon coincided with decreased side population fraction and dramatic dose-dependent growth arrest of lung cancer cells in vitro and in vivo. In the present study, microarray, quantitative reverse transcriptase polymerase chain reaction and immunoblot experiments were performed to further examine the effects of mithramycin on stem cell gene expression in lung cancer cells. This analysis revealed that mithramycin significantly inhibited expression of musashi-2 (MSI2), which encodes a RNA binding protein that mediates self-renewal and pluripotency in normal stem cells and has been implicated in mediating aggressive phenotype of a variety of human malignancies. MSI2 expression levels were significantly increased in non-small cell lung cancer lines and were even more dramatically elevated in small-cell lung cancer lines relative to cultured normal human respiratory epithelial cells (small airway epithelial cells / normal human bronchial epithelia / human bronchial epithelial cells; P , 0.001). MSI2 expression levels in primary lung cancers were significantly higher than those detected in adjacent paired normal lung parenchyma (P , 0.0003). Consistent with its putative role as a pluripotency factor, MSI2 messenger RNA as well as protein levels were significantly increased in induced pluripotent stem cells derived from normal human small airway epithelial cells, as well as side population fractions of lung cancer cells. Transient knockdown of MSI2 significantly inhibited proliferation of lung cancer cells; this phenomenon coincided with downregulation of octamer-binding transcription factor 4 (Oct4), Nanog, and MYC. To date, we have been unable to stably knock-down MSI2 in lung cancer cells in vitro or in vivo, suggesting a strong selection pressure to maintain expression of this pluripotency factor during pulmonary carcinogenesis. Under conditions potentially achievable in clinical settings, mithramycin significantly inhibited MSI2 expression in lung cancer cells in vitro and in vivo in a time-and dose-dependent manner. Collectively, these finding suggest MSI2 is a potential master regulator of stem cell gene expression and pluripotency in lung cancer cells, and a novel target for lung cancer therapy. Rationale: The effects of hookah smoke on respiratory epithelia have not been well characterized.Objectives: To characterize and compare the effects of hookah tobacco smoke and conventional cigarette smoke on the epigenome and transcriptome of human respiratory epithelia.Methods: Normal human small airway epithelial cells and cyclindependent kinase 4/human telomerase reverse transcriptaseimmortalized human bronchial epithelial cells were cultured for 5 days in normal media in the presence or absence of water pipe condensates or cigarette smoke condensates under relevant exposure conditions. CyQUANT assay (Thermo Fisher Scientific), RNA sequencing, quantitative reverse tran...
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