Connections of a telencephalic vocal-control nucleus, the lateral magnocellular nucleus of the anterior neostriatum (lMAN), were studied in adult male zebra finches. Anterograde transport of horseradish peroxidase (alone or conjugated to wheat germ agglutinin) revealed that neurons in lMAN project to another forebrain song-control nucleus, the robust nucleus of the archistriatum (RA). RA is known to project onto the hypoglossal motor neurons that innervate the vocal organ. Retrograde transport of HRP from lMAN labeled a large thalamic nucleus, the medial portion of the dorsolateral nucleus of the thalamus (DLM). DLM in turn receives input from another nucleus of the song-control system, area X of the parolfactory lobe. We confirmed results of previous studies showing that area X receives a projection from the ventral area of Tsai (AVT) in the midbrain. In addition, we replicated results of previous experiments with canaries showing that the song-control nucleus HVc (caudal nucleus of the ventral hyperstriatum) receives input from three sources: the medial magnocellular nucleus of the anterior neostriatum (mMAN), the interfacial nucleus (NIf), and the uvae-form nucleus (Uva) of the thalamus. HVc neurons project to area X and to RA. In summary, there is a path from AVT in the midbrain, to area X, to DLM, and then to lMAN; HVc projects to X and hence indirectly to lMAN. We do not yet know the afferent connections of AVT. Thus, lMAN receives indirect input from a variety of other sources, including other regions known to be involved with vocal control.

Key Points Responses and survival with venetoclax for “real-world” AML patients were promising but inferior to those treated in a clinical trial. Compared with induction, response rates are as high as would be predicted and venetoclax patients had a lower than expected early death rate.

Background: The time-limited combination of venetoclax and obinutuzumab (VenG) was established by the German CLL Study Group in the CLL14 trial for the upfront management of newly diagnosed chronic lymphocytic leukemia (CLL), showing a superior progression free survival benefit. The incidence of grade 3-4 neutropenia was reported in the range of 52.8%-57.7%. However, patients who develop neutropenia with this combination have yet to be formally characterized in the literature as it has impact on the clinical practice setting.Aim: To determine the incidence of grade 3 and 4 neutropenia and identify risk factors for neutropenia among CLL patients treated with the VenG regimen.Methods: We conducted a retrospective, single-center study of all adult patients with a diagnosis of CLL treated with VenG at the University of Colorado Hospital.Demographic information, laboratory data, clinical data, and medication prescriptions were collected from the patients' electronic medical record.Results: A total of 14 patients (73%) developed neutropenia during the course of therapy. The mean time to neutropenia from the start of treatment was 42 days (range 1-131). Our cohort harbored more high risk disease features and more comorbidities (CIRS score of 12). Four patients (28.6%) in the neutropenic group developed infectious complications during therapy and 6 (31%) patients were unable to be dose escalated to the final FDA approved dose of 400 mg.Conclusion: Our study cohort had higher incidence of grade 3 and 4 neutropenia occurring in 73% of patients. This could be attributed to a higher rate of comorbidities, high risk features, concomitant interacting medications, and prior chemotherapy. Further studies are warranted to determine if growth factor support is efficacious to achieve dose escalation with this therapy.

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The risk of developing venous thromboembolism (VTE) is four to seven times higher in patients with cancer than in those without. At JADPRO Live 2022, presenters discussed risk factors and assessing patients for VTE, as well as how to protect patients against VTE in both the inpatient and outpatient clinic settings. They reviewed selecting an appropriate anticoagulation treatment, including the choice of agent and duration of treatment for the patient with cancer, and finally the steps needed to assess and treat patients experiencing therapeutic anticoagulation failure.