The report, led by Freya Townsend of Wear Referrals Veterinary Hospital in Stockton-on-Tees, United Kingdom, describes three dogs in which metastatic mast cell tumours produced polyostotic vertebral lesions, meaning tumour deposits scattered across multiple vertebrae rather than a single site of bone destruction. According to the authors, only one previous report in the veterinary literature has documented polyostotic mast cell tumour metastasis affecting the vertebrae. That scarcity is precisely what makes the new series noteworthy: it suggests that mast cell tumours deserve a place on the differential diagnosis list for extradural and polyostotic vertebral disease, a consideration that could influence biopsy decisions, staging protocols and prognostic conversations with owners.

The first case involved an eight-year-old neutered male small crossbreed presented originally for a small, raised mass on the upper lip. Histopathology classified it as a grade II tumour under the traditional Patnaik system and low grade under the more prognostically stringent Kiupel system, with a low mitotic count of one mitosis per ten high-power fields. The mass was excised completely, albeit with a narrow deep margin. Seven months later, the right mandibular lymph node was enlarged and biopsy confirmed metastatic mast cell disease. Fine needle aspirates of the opposite lymph node, liver and spleen were reassuringly negative at that stage, and the dog was started on lomustine chemotherapy. When a subcutaneous nodule later appeared at the surgical site and cytology again confirmed metastasis, treatment was switched to toceranib phosphate before referral to a specialist oncology service.

At the referral hospital, computed tomography revealed enlargement of the right mandibular and bilateral medial retropharyngeal lymph nodes, and surgical removal of these nodes confirmed overt metastatic mast cell infiltration, graded HN3 under the Weishaar classification system for nodal mast cell metastasis. The dog then received vinblastine chemotherapy combined with prednisolone, followed by a five-day course of radiotherapy totalling 20 Gy to the surgical site. One week after radiotherapy ended, the dog became reluctant to exercise. Neurological examination revealed pain on palpation of the thoracolumbar region, and within another week the dog had developed a hunched spine and ambulatory paraparesis, with absent postural reactions in the pelvic limbs. Blood work showed elevated C-reactive protein alongside neutropenia, leukopenia and reduced platelets, consistent with both inflammatory disease and chemotherapy side effects.

The second case was a fifteen-year-old neutered female springer spaniel whose story began with removal of a two-centimetre subcutaneous mass from the right caudal mammary gland. That tumour carried a high mitotic count exceeding ten mitoses per ten high-power fields, and the regional lymph node was already invaded by sheets of hyperchromatic, intermediately differentiated mast cells, classified HN2. The mass tested negative for a c-KIT mutation. Seven months after surgery, a new groin mass and imaging findings of enlarged abdominal lymph nodes and liver nodules confirmed widespread metastasis, and vinblastine with prednisolone was initiated. Two months into chemotherapy, the dog developed ambulatory paraparesis that progressed to non-ambulatory paraparesis by the time of specialist assessment, with pain suspected on palpation of the cervical spine and neurological signs localising to the mid-thoracic spinal cord segments.

The third patient, a thirteen-year-old neutered male Nova Scotia Duck Tolling Retriever, had a long history of mast cell tumours, including a recurrent low-grade shoulder mass and, more recently, a twenty-millimetre high-grade Kiupel tumour on the mid back with narrow surgical margins. Abdominal ultrasound had already shown nodular changes in the liver and spleen. The dog completed a twelve-week course of vinblastine and prednisolone but skipped restaging, and seven months later returned with a one-week history of non-ambulatory paraparesis, a large thoracic wall mass in the armpit region, and pain on palpation of the cranial thoracic spine. Neurological deficits again localised to the T3-L3 spinal cord segments, while reduced withdrawal reflex in the right forelimb was attributed to the large mass itself.

Magnetic resonance imaging of the vertebral column in all three dogs revealed the series’ defining finding: multiple lesions across many vertebrae, ranging from well-defined nodules to ill-defined patches, accompanied by similar lesions in the iliac bones of all three dogs and, in some, the ribs, sternebrae and scapula. Technically, every vertebral lesion appeared mildly hyperintense to isointense relative to the spinal cord on both T2-weighted and T1-weighted sequences, hyperintense on short tau inversion recovery sequences, and showed moderate homogeneous enhancement after gadolinium contrast. Vertebral shape was preserved, but cortical osteolysis was present in all cases, and several lesions breached the cortical margins to invade the extradural space and perivertebral soft tissues, compressing the spinal cord from moderately to severely. All three dogs were humanely euthanised following imaging, at the request of their caregivers.

Post-mortem histopathology cemented the diagnosis. In the first two dogs, neoplastic round cells filled the intertrabecular spaces of affected vertebrae, effacing normal haematopoietic tissue and, in the first case, extending into adjacent skeletal muscle and the extradural space, with mitotic counts of 49 and 5 per ten high-power fields respectively. Immunohistochemistry proved decisive: the neoplastic cells stained positive for CD117, a marker of mast cells, with c-KIT staining patterns II and III, while negative CD3 and negative CD20 or CD79A staining excluded both T-cell and B-cell lymphoma. In the third dog, the vertebral body itself showed only inflammatory change, but the extradural mass at T5 displayed a neoplastic round cell population with a mitotic count of 30 per ten high-power fields and confirmatory CD117 positivity. Splenic and hepatic metastasis was confirmed in the first two dogs, underscoring that none of the three had isolated spinal disease.

The imaging signature carries practical weight. In a retrospective study of sixty dogs with vertebral column tumours, preservation of vertebral shape, homogeneous contrast enhancement and lesions centred on bone were features associated with round cell neoplasms, a group that includes mast cell tumours, lymphoma, multiple myeloma, plasma cell tumours and histiocytic sarcoma. The signal intensities reported here, iso- to mildly hyperintense on T1 and T2 weighting, resemble those described for vertebral multiple myeloma and lymphoma, meaning mast cell metastasis can mimic its more familiar round cell cousins. Notably, the authors highlight that their T1 and T2 findings differ from the only prior polyostotic case, in which lesions were T1 hypointense and T2 hyperintense, adding to the recognised variability of mast cell tumour metastases.

What distinguishes this series from earlier reports is the pattern of bone involvement. Previous descriptions of mast cell tumours invading bone have mostly involved local infiltration or lysis near the primary tumour, such as a subcutaneous tumour invading the stifle joint and adjacent tibial plateau, or a disseminated tumour eroding the sphenoid bone and causing blindness. Most reported spinal mast cell tumours have been extradural masses compressing the cord without touching the vertebrae at all. By contrast, the three dogs described here developed distant metastatic deposits as multiple focal lesions in separate vertebrae, a haematogenous spread pattern more reminiscent of carcinoma or multiple myeloma than of the typical mast cell tumour. The authors conclude that metastasis should be actively considered in any dog with a previously diagnosed mast cell tumour that develops spinal pain, and that mast cell disease belongs among the differentials for polyostotic, extradural vertebral lesions, a message that may prompt earlier biopsy and more complete staging in similar patients.

Subject of Research: Metastatic mast cell tumours causing polyostotic vertebral lesions in dogs

Article Title: Metastatic mast cell tumours causing polyostotic vertebral lesions in three dogs

Article References: Metastatic mast cell tumours causing polyostotic vertebral lesions in three dogs. (n.d.). https://doi.org/10.1186/s44356-025-00050-3

Image Credits: AI Generated

DOI: 10.1186/s44356-025-00050-3

Keywords: canine, mast cell tumour, metastasis, vertebral lesions, MRI, histopathology, veterinary oncology, spinal tumour, polyostotic, CD117, round cell tumour, paraparesis

Meningioma, a tumor arising from the meninges—the protective membranes enveloping the brain and spinal cord—is the most frequently diagnosed intracranial neoplasm in dogs, accounting for roughly half of all canine primary brain tumors. In humans, meningiomas represent approximately 40 percent of primary brain tumors. Despite this shared prominence, diagnostic criteria for canine meningioma have remained poorly codified, and until now no study had subjected a large cohort of canine cases to standardized review by a panel of multiple pathologists working alongside physician neuropathologists.

The CBTC board, which brought together veterinary pathologists and human neuropathologists from institutions across the United States and Europe, undertook a comprehensive evaluation of 190 cases of canine meningioma. Tumors were collected from the diagnostic archives of ten veterinary schools, including Auburn, Colorado State, Cornell, Mississippi State, Ohio State, Texas A&M, UC Davis, Illinois, Penn, and Virginia Tech. Samples came exclusively from treatment-naïve patients, prioritized when collected within the previous five years and accompanied by clinical follow-up data such as tumor location, therapy, progression, and cause of death. Histology slides were cut at four micrometers, stained with hematoxylin and eosin, and digitally scanned at 40X resolution, allowing every reviewer to examine identical digital images.

To enable direct comparison with human medicine, the board applied the 2016 World Health Organization classification and grading guidelines for human meningioma to each canine tumor. Reviewers assessed histologic subtype, mitotic count within a fixed region of 2.37 square millimeters, invasion into surrounding nervous tissue, geographic coagulative necrosis, and the atypical features used in human grading: sheeting architecture, small-cell formation, hypercellularity, and macronucleoli. The process began with a virtual meeting in October 2020 to familiarize the physician neuropathologists with canine histology, followed by additional consensus sessions to resolve difficult diagnostic calls before a final independent assessment of all cases by October 2021.

The results demonstrated that canine meningiomas mirror the morphologic diversity of the human disease. The overwhelming majority of tumors—140 of 190, or roughly 74 percent—were classified as meningothelial, with transitional, microcystic, psammomatous, rhabdoid, fibrous, metaplastic, clear cell, and chordoid subtypes making up the remainder. Most cases, 109 tumors or 57 percent, were assigned grade 2 under the human WHO scheme, while 79 were grade 1 and only two reached grade 3. Roughly 60 percent of tumors with assessable adjacent brain or spinal cord tissue showed invasion into the nervous system, and features such as necrosis, sheeting, and hypercellularity were commonly observed, closely paralleling the histologic picture of atypical human meningioma.

Yet the clinical correlation told a more complicated story. Among the subset of patients with detailed progression and cause-of-death information, and again in a larger cohort restricted to live/dead status, there was no statistically significant difference in outcome between grade 1 and grade 2 canine tumors. Relative risk ratios for death at one, two, and three years after diagnosis—0.75, 0.93, and 1.02 respectively—were all statistically insignificant. This challenges the assumption that the human WHO grading framework, which strongly predicts recurrence and progression in people, can be transplanted wholesale to veterinary patients. Several features that signal higher grade in humans, notably macronucleoli and small-cell formation, appeared frequently even in grade 1 canine tumors, and medical pathologists on the board repeatedly observed that macronucleoli occur more often in canine tumors regardless of grade.

One feature did emerge as potentially meaningful: necrosis. Although many progressing tumors lacked necrosis, every case in the outcome-linked subset that did exhibit necrosis went on to show clinical progression, compared with 57 percent of cases lacking it. The authors suggest that necrosis, when present, may be a significant indicator of more aggressive behavior and a critical feature for future prognostic studies. Brain tumors were also significantly more likely than spinal tumors to show necrosis. Notably, the study echoes a shifting paradigm in human medicine, where tumors showing brain invasion without other atypical features—so-called brain-invasive, otherwise benign tumors—now benefit from additional molecular testing, suggesting that molecular characterization could likewise improve prognostication in dogs.

The review also shed light on the reproducibility of diagnosis across specialists. Interobserver agreement, measured by intraclass correlation coefficients, was generally low for most histologic features, with the highest agreement—0.44 for both—achieved for necrosis and CNS invasion, the same features that command the highest concordance in human meningioma review. Concordance exceeded 70 percent for most histologic subtypes, especially those with distinctive appearances such as clear cell and microcystic tumors, while mitotic counting proved the least reliable. Interestingly, veterinary pathologists agreed with one another significantly more often than physician neuropathologists on histologic subtype, hypercellularity, and macronucleoli, suggesting that species-specific experience is critical for diagnostic consistency.

Clinically, the cohort reflected established patterns of canine disease. The median patient age was ten years, and mixed-breed dogs, Golden Retrievers, Labrador Retrievers, Boxers, and West Highland Terriers were the most commonly represented breeds. Most tumors arose over the brain, particularly the olfactory and frontal lobes, with a smaller proportion in the cervical spinal cord. Surgery remained the mainstay of treatment, with a median survival of 437 days for dogs treated surgically, while dogs receiving surgery combined with radiation or other adjuvant therapies survived longer on average, at 28 to 55 months, consistent with previously reported ranges.

The CBTC board concluded that while canine and human meningioma share important histologic features, a revised grading framework specific to dogs is needed, distinct from the human WHO scheme. The consortium recommends that future studies include review of all slides by at least three pathologists, systematic evaluation of location, subtype, mitotic count, invasion, necrosis, and other atypical features, and enrollment limited to cases with complete clinical follow-up. The authors also call for the kind of large-scale, shared cancer databases in veterinary medicine that exist in human oncology, and note that molecular characterization, transcriptional profiling, and immune landscape studies of related canine tumor collections are already underway. If successful, these efforts could position the canine patient as a genuinely translational model—accelerating biomarker discovery and therapeutic development for both dogs and the humans who love them.

Subject of Research: Comparative pathology of canine and human meningioma and the validation of dogs as a naturally occurring model for human meningioma research

Article Title: A comparative evaluation of canine meningioma supporting the canine patient as a naturally occurring animal model for human meningioma: a report from the NCI Comparative Brain Tumor Consortium (CBTC) meningioma pathology board

Article References: Church, M. E., Rissi, D. R., Koehler, J. W., Miller, A. D., Beck, J. A., Belluco, S., Bitar, M., Chkheidze, R., Corps, K. N., Matiasek, K., Phillips, J. J., Rajan, S., Stemmer-Rachamimov, A., Yip, S., Shih, J. H., Mazcko, C., & LeBlanc, A. (2026). A comparative evaluation of canine meningioma supporting the canine patient as a naturally occurring animal model for human meningioma: a report from the NCI Comparative Brain Tumor Consortium (CBTC) meningioma pathology board. Veterinary Oncology, 3(1), Article 16. https://doi.org/10.1186/s44356-026-00068-1

Image Credits: AI Generated

DOI: 10.1186/s44356-026-00068-1

Keywords: meningioma, canine, comparative oncology, brain tumor, WHO grading, pathology, NCI Comparative Brain Tumor Consortium, veterinary oncology, CNS invasion, tumor necrosis, animal model, One Health