BCG treatment of periocular sarcoid

Lavach, J D; Sullins, K. E.; Roberts, Steven M.; Severin, G A; Wheeler, Clayton E.; Lueker, David C.

doi:10.1111/j.2042-3306.1985.tb02552.x

Cited by 62 publications

(43 citation statements)

References 12 publications

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“…Sarcoids are the most common skin tumors in horses [1–3], with prevalence rates ranging from 12.9 to 67% of all equine tumors [4, 5]. They appear as benign fibroblastic skin tumors, and are characterized by rare regression, invasiveness and high recurrence following surgery [6–8].…”

Section: Introductionmentioning

confidence: 99%

Expression of vascular endothelial growth factor (VEGF) in equine sarcoid

et al. 2018

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BackgroundSarcoids are the mostcommon skin tumors in horses, characterized by rare regression, invasiveness and high recurrence following surgical intervention and Delta Papillomaviruses are widely recognized as the causative agents of the disease. In order to gain new insights into equine sarcoid development, we have evaluated, in 25 equine sarcoids, by immunohistochemistry and western blotting analysis, the expression levels of VEGF, Ki67 and bcl-2. Moreover, we have measured microvessel density and specific vessel parameters.ResultsAll sarcoid samples showed a strong and finely granular cytoplasmatic staining for VEGF in the majority (90%) of keratinocytes, sarcoid fibroblasts and endothelial cells. Numerous small blood vessels, immunostained with Von Willebrand factor, often appeared irregular in shape and without a distinct lumen, with mean values of microvessel area and perimeter lower than normal. Moreover, in all sarcoid samples, Ki67 immunoreactivity was moderately positive in 5–10% of dermal sarcoid fibroblasts, while Bcl2 immunoreactivity was detected in 52% of the sarcoid samples, with a weak staining in 20–50% of dermal sarcoid fibroblasts. Biochemical analysis was consistent with immunohistochemical results.ConclusionsThis study has provided evidence that in equine sarcoid: VEGF was strongly expressed; the increased number of vessels was not associated with their complete maturation, probably leading to a hypoxic condition, which could increase VEGF synthesis; the levels of sarcoid fibroblasts proliferation were very low. Concluding, VEGF may have a role in equine sarcoid development, not only through the increase of angiogenesis, but also through the control of sarcoid fibroblast activity.

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Section: Introductionmentioning

confidence: 99%

Expression of vascular endothelial growth factor (VEGF) in equine sarcoid

et al. 2018

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“…Equine sarcoids are the most common skin tumours in equids worldwide (Jackson, 1936;Pascoe & Summers, 1981;Ragland et al, 1970) with reported prevalence rates ranging from 12.9 to 67 % of all equine tumours (Lavach et al, 1985). Six clinical types of sarcoid are recognized including occult, verrucouse, nodular, fibroblastic, mixed and malignant types (Knottenbelt, 2005).…”

Section: Introductionmentioning

confidence: 99%

Different contribution of bovine papillomavirus type 1 oncoproteins to the transformation of equine fibroblasts

Yuan

Gault

Campo

et al. 2010

Journal of General Virology

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Equine sarcoids represent the most common skin tumours in equids worldwide, characterized by localized invasion, rare regression and high recurrence following surgical intervention. Bovine papillomavirus type 1 (BPV-1) and less commonly BPV-2 are now widely recognized as the causative agents of the disease. Fibroblasts isolated from sarcoids are highly invasive. Invasion is associated with a high level of viral gene expression and matrix metalloproteinase upregulation. However, it remains unclear to what extent BPV-1 proteins are involved in the transformation of equine cells. To address this question, the individual viral genes E5, E6 and E7 were overexpressed in normal equine fibroblasts (EqPalF cells) and in the immortal but not fully transformed sarcoid-derived EqS02a cell line. The proliferation and invasiveness of these cell lines were assessed. E5 and E6 were found to be responsible for the enhanced cell proliferation and induction of increased invasion in EqS02a cells, whilst E7 appeared to enhance cell anchorage independence. Knockdown of BPV-1 oncogene expression by small interfering RNA reversed the transformed phenotype of sarcoid fibroblasts. Together, these observations strongly suggest that BPV-1 proteins play indispensable roles in the transformation of equine fibroblasts. These data also suggest that BPV-1 proteins are potential drug targets for equine sarcoid therapy. INTRODUCTIONEquine sarcoids are the most common skin tumours in equids worldwide (Jackson, 1936;Pascoe & Summers, 1981;Ragland et al., 1970) with reported prevalence rates ranging from 12.9 to 67 % of all equine tumours (Lavach et al., 1985). Six clinical types of sarcoid are recognized including occult, verrucouse, nodular, fibroblastic, mixed and malignant types (Knottenbelt, 2005). Equine sarcoids rarely regress, are notoriously difficult to treat and are associated with a high recurrence rate following surgical intervention (Knottenbelt, 2005;Martens et al., 2001a;Tarwid et al., 1985). The high recurrence may be associated with the invasiveness of sarcoid fibroblasts (Yuan et al., 2010a), which allows cells to infiltrate into tumoursurrounding healthy tissues. Bovine papillomavirus (BPV) DNA has also been detected in apparently healthy skin away from the tumour site (Carr et al., 2001), and tumour recurrence is most frequent when surgical margins are positive for BPV DNA (Martens et al., 2001a). After excision of primary tumours, disseminated tumour cells may be able to invade the surgical margins under the chemoattractant stimulation of the chemokines and growth factors produced during wound healing. Thus, prevention of sarcoid cell invasion in combination with surgical excision may reduce the risk of tumour recurrence.BPV type 1 (BPV-1) and less commonly BPV-2 are now widely recognized as the causative agents of equine sarcoids. This is based on the fact that (i) BPV-1/-2 DNA is detected in the majority of sarcoid tumours (Chambers et al., 2003b; Martens et al., 2001a, b;Otten et al., 1993;Reid et al., 1994), (ii) BPV genes ...

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“…The results obtained with repeated local administration of BCG in superficial bladder cancer in humans [2, 3, 5, 13, 20-22, 26, 27] and in sarcoids in horses [16,23,28,29,33] stimulated the present study of the effect of repeated treatment of BOSCC with BCG. Moreover, in a previous study of Klein et al [17] it was suggested that the success of the therapy might be correlated with the ability of the immune system to generate long-lasting BCG-specific memory.…”

Section: Introductionmentioning

confidence: 54%

“…Repeated intralesional injections of BCG in horses with fibro-epithelial tumours (equine sarcoids) resulted in complete cure in 50%-90% of the animals [16,23,28,29,33]. There was no recurrence after repeated treatment [16].…”

Section: Introductionmentioning

confidence: 96%

Immunotherapy of bovine ocular squamous cell carcinoma by repeated intralesional injections of live bacillus Calmette-Guérin (BCG) or BCG cell walls

Rutten

Klein

Jong

et al. 1991

Cancer Immunol Immunother

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(a) recurrence of the primary tumour was not observed after repeated BCG treatment; (b) the frequency of metastases was not decreased compared to results obtained with a single treatment; (c) regression was correlated with a positive delayed-type hypersensitivity reaction to PPD (P less than 0.05) 6 months after treatment; (d) no significant differences were observed when the clinical results of treatment with live BCG and the BCG cell wall vaccine were compared.

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BCG treatment of periocular sarcoid

Cited by 62 publications

References 12 publications

Expression of vascular endothelial growth factor (VEGF) in equine sarcoid

Expression of vascular endothelial growth factor (VEGF) in equine sarcoid

Different contribution of bovine papillomavirus type 1 oncoproteins to the transformation of equine fibroblasts

Immunotherapy of bovine ocular squamous cell carcinoma by repeated intralesional injections of live bacillus Calmette-Guérin (BCG) or BCG cell walls

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