Partial cytogenetic response with toceranib and prednisone treatment in a young dog with chronic monocytic leukemia

Pérez, Mayrim L.; Culver, Sarah; Owen, Jennifer L.; Dunbar, Mark D.; Kow, Kelvin; Breen, Matthew; Milner, Rowan J.

doi:10.1097/cad.0000000000000018

Cited by 13 publications

(8 citation statements)

References 20 publications

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“…RB1 deletions in chronic lymphocytic leukaemia and BCR-ABL fusion in chronic myeloid leukaemia (CML) were among the first cytogenetic aberrations detected in canine cancers that mirror the corresponding human cancers [107]. The BCR-ABL tyrosine kinase translocation (the so-called 'Raleigh chromosome' in dogs and 'Philadelphia chromosome' in humans) has since been demonstrated to be present in additional subtypes [108,109] and proven useful for monitoring cytogenetic remission in CMLs [110]. Another canine study included acute lymphoblastic leukaemia (ALL)/acute undifferentiated leukaemia (AUL) (N ¼ 11) and chronic lymphocytic leukaemia (CLL) (N ¼ 12) and demonstrated increased c-KIT expression in the ALL/AUL samples [111], offering the possibility of using tyrosine kinase inhibitors as a treatment option in canine leukaemia, an approach similar to that used for human leukaemia with tyrosine kinase-affected pathways.…”

Section: (Ii) Leukaemiamentioning

confidence: 99%

Comparative oncology: what dogs and other species can teach us about humans with cancer

Schiffman

Breen

2015

Phil. Trans. R. Soc. B

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One contribution of 18 to a theme issue 'Cancer across life: Peto's paradox and the promise of comparative oncology'. Over 1.66 million humans (approx. 500/100 000 population rate) and over 4.2 million dogs (approx. 5300/100 000 population rate) are diagnosed with cancer annually in the USA. The interdisciplinary field of comparative oncology offers a unique and strong opportunity to learn more about universal cancer risk and development through epidemiology, genetic and genomic investigations. Working across species, researchers from human and veterinary medicine can combine scientific findings to understand more quickly the origins of cancer and translate these findings to novel therapies to benefit both human and animals. This review begins with the genetic origins of canines and their advantage in cancer research. We next focus on recent findings in comparative oncology related to inherited, or genetic, risk for tumour development. We then detail the somatic, or genomic, changes within tumours and the similarities between species. The shared cancers between humans and dogs that we discuss include sarcoma (osteosarcoma, soft tissue sarcoma, histiocytic sarcoma, hemangiosarcoma), haematological malignancies (lymphoma, leukaemia), bladder cancer, intracranial neoplasms (meningioma, glioma) and melanoma. Tumour risk in other animal species is also briefly discussed. As the field of genomics advances, we predict that comparative oncology will continue to benefit both humans and the animals that live among us.

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Section: (Ii) Leukaemiamentioning

confidence: 99%

Comparative oncology: what dogs and other species can teach us about humans with cancer

Schiffman

Breen

2015

Phil. Trans. R. Soc. B

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305

315

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“…The BCR-ABL translocation has also been detected in three dogs with chronic monocytic leukaemia (Cruz Cardona et al, 2011;Culver et al, 2013;Pérez et al, 2013) and in one dog with acute myeloblastic leukaemia (Figueiredo et al, 2012) by FISH analysis. Although the nucleotide sequence of DNA fusion junctions for BCR-ABL translocations has not yet been analysed, these findings suggest the presence of BCR-ABL in a certain subset of leukaemia in dogs, which would make imatinib a potential therapeutic approach for these canine tumours, similar to humans.…”

Section: Bcr-abl In Canine Leukaemiamentioning

confidence: 93%

Dysregulation of tyrosine kinases and use of imatinib in small animal practice

Bonkobara

2015

The Veterinary Journal

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Imatinib inhibits the activity of several tyrosine kinases, including BCR-ABL, KIT and platelet-derived growth factor receptor (PDGFR). Dysregulation of KIT is found in mast cell tumours (MCTs) and KIT is mutated in approximately 30% and 70% of canine and feline MCTs, respectively. KIT mutations have also been reported in canine and feline gastrointestinal stromal tumours (GISTs), canine acute myeloid leukaemia and canine melanoma. In addition, BCR-ABL and PDGFR mutations have been found in canine leukaemia and haemangiosarcoma, respectively. Imatinib has anti-tumour activity with tolerable toxicity towards a certain subset of MCTs in dogs and cats. Favourable clinical responses are likely to be associated with the presence of KIT mutation. Anti-tumour activity of imatinib has also been demonstrated in canine GISTs with a KIT mutation and in feline hypereosinophilic syndrome; however, to date only one of each of these cases has been reported. In conclusion, analysis of KIT mutations appears to provide valuable data for individual treatment with imatinib in dogs and cats.

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“…BCR-ABL1 translocations have been documented in canine CML (Breen and Modiano 2008), chronic monocytic leukemia (CMoL) (Cruz et al 2011;Pérez et al 2013), chronic myelomonocytic leukemia (CMML) , and AML (Figueiredo et al 2012). Deletion of RB1, the most prevalent copy number change in human CLL, has also been identified in a subset of canine B-CLLs (Breen and Modiano 2008).…”

Section: Introductionmentioning

confidence: 96%

Genome-wide assessment of recurrent genomic imbalances in canine leukemia identifies evolutionarily conserved regions for subtype differentiation

et al. 2015

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Leukemia in dogs is a heterogeneous disease with survival ranging from days to years, depending on the subtype. Strides have been made in both human and canine leukemia to improve classification and understanding of pathogenesis through immunophenotyping, yet classification and choosing appropriate therapy remains challenging. In this study, we assessed 123 cases of canine leukemia (28 ALLs, 24 AMLs, 25 B-CLLs, and 46 T-CLLs) using high-resolution oligonucleotide array comparative genomic hybridization (oaCGH) to detect DNA copy number alterations (CNAs). For the first time, such data were used to identify recurrent CNAs and inclusive genes that may be potential drivers of subtype-specific pathogenesis. We performed predictive modeling to identify CNAs that could reliably differentiate acute subtypes (ALL vs. AML) and chronic subtypes (B-CLL vs. T-CLL) and used this model to differentiate cases with up to 83.3 and 95.8 % precision, respectively, based on CNAs at only one to three genomic regions. In addition, CGH datasets for canine and human leukemia were compared to reveal evolutionarily conserved copy number changes between species, including the shared gain of HSA 21q in ALL and ∼25 Mb of shared gain of HSA 12 and loss of HSA 13q14 in CLL. These findings support the use of canine leukemia as a relevant in vivo model for human leukemia and justify the need to further explore the conserved genomic regions of interest for their clinical impact.

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Partial cytogenetic response with toceranib and prednisone treatment in a young dog with chronic monocytic leukemia

Cited by 13 publications

References 20 publications

Comparative oncology: what dogs and other species can teach us about humans with cancer

Comparative oncology: what dogs and other species can teach us about humans with cancer

Dysregulation of tyrosine kinases and use of imatinib in small animal practice

Genome-wide assessment of recurrent genomic imbalances in canine leukemia identifies evolutionarily conserved regions for subtype differentiation

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