Background This report describes a case of solitary tracheal lymphoma in a 14-year-old alpaca mare. Case presentation The alpaca was referred for dyspnea and inspiratory noise. The clinical examination included complete blood cell count, blood chemistry, endoscopy, ultrasound, radiographs, and computed tomography (CT). A solitary tracheal intraluminal and juxtatracheal lymphoma was diagnosed by fine needle aspiration (FNA). The owner requested euthanasia due to the uncertain prognosis. At postmortem examination, the presence of solitary lymphoma without involvement of other organs was confirmed. Immunohistochemical analysis confirmed a B-cell origin. Conclusions Although multicentric lymphoma is the most commonly described neoplasia affecting South American camelids (SAC), solitary forms of the disease may occur.

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BRCA1 and BRCA2 both function in DNA double-strand break repair by homologous recombination (HR). Due to their HR-defect, BRCA1/2-deficient cancers are sensitive to poly(ADP-ribose) polymerase inhibitors (PARPi) but they eventually acquire resistance. Preclinical studies yielded several PARPi resistance mechanisms that do not involve BRCA1/2 reactivation, but their relevance in the clinic remains elusive. To investigate which BRCA1/2-independent mechanisms drive spontaneous resistance in vivo, we combined molecular profiling with functional analysis of the HR status of matched PARPi-naive and PARPi-resistant mouse mammary tumors harboring large intragenic deletions that prevent functional restoration of BRCA1/2. We observed restoration of HR in 64% of PARPi-resistant BRCA1-deficient tumors but none in the PARPi-resistant BRCA2-deficient tumors. Moreover, we found that 53BP1 loss is the prevalent resistance mechanism in HR-proficient BRCA1-deficient tumors, whereas resistance in BRCA2-deficient tumors is mainly induced by the loss of PARG. Our combined multi-omics analysis catalogued additional genes and pathways potentially involved in modulating PARPi response.

Case summary A 7-month-old domestic shorthair cat was presented for evaluation of stunted growth, recurrent hypoglycaemia during the first months of its life and altered mentation. Complete blood count and biochemistry were unremarkable, except for mildly elevated serum creatinine concentration (despite low muscle mass) and concurrent isosthenuria. Hyposomatotropism was diagnosed based on persistent low circulating insulin-like growth factor 1 concentrations and a lack of response of circulating growth hormone (GH) concentration after the administration of GH-releasing hormone. Other endocrinopathies such as hypothyroidism and hypoadrenocorticism were excluded. MRI of the brain revealed a fluid-filled empty sella tursica, consistent with a pituitary cyst and atrophy/hypoplasia of the pituitary. Echocardiography was unremarkable at the time of diagnosis of hyposomatotropism. Three months later, ovariohysterectomy revealed immature ovaries, raising the suspicion of luteinising and follicle-stimulating hormone deficiency. At 1 year of age, the cat developed congestive heart failure secondarily to dilated cardiomyopathy (DCM) with severely reduced left ventricular systolic function and died a few days later. Pathology showed atrophy of the adenohypophysis, epithelial delineation of the pituitary cysts, mild cardiomegaly, multifocal fibrosis of the left ventricle and a mild, multifocal, chronic epicarditis. Relevance and novel information GH deficiency is a very rare endocrinopathy in cats. This is the first case to describe the development of DCM with concurrent hyposomatotropism, which has previously been reported in human medicine. Other notable abnormalities that could be related to GH deficiency are juvenile self-limiting hypoglycaemia, behavioural changes and possible nephropathy.