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Candidal vertebral osteomyelitis represents an extremely rare invasive mycosis and can be difficult to treat due to poor drug penetration into bony tissue. We report on a case of vertebral osteomyelitis caused by Candida krusei in a patient who had neutropenia as a result of chemotherapy for acute myelogenous leukaemia. The patient received prophylactic liposomal amphotericin B during chemotherapy but became febrile and experienced severe lumbar pain. Magnetic resonance imaging revealed vertebral osteochondrosis. C. krusei was recovered from blood cultures and voriconazole monotherapy was initiated but proved unsuccessful. The patient was then started on caspofungin monotherapy, which was discontinued after Candida krusei was no longer recoverable from blood cultures. However, as lumbar pain increased and spinal biopsy confirmed the presence of Candida krusei, caspofungin therapy was resumed. Oral posaconazole was added to the regimen when the patient did not improve after 30 days of caspofungin therapy. Combined antimycotic therapy resulted in a successful outcome. [ABSTRACT FROM AUTHOR]

Objective: By implementing a focused must-have vaccination strategy (Easy Vaccination in Oncology [EVO]), we aimed to increase rates for high-impact vaccinations (Streptococcus pneumoniae, influenza, herpes zoster and hepatitis B) in the at-risk population of oncological patients., Methods: In this German multicentre interventional non-randomised controlled two-arm open trial with repeated cross-sectional data collection, we evaluated the EVO strategy as an easy to implement approach. Vaccination rates were assessed in the outpatient setting and re-assessed after 3 months. A generalised linear mixed model (GLMM) was used to assess the primary endpoint (Streptococcus pneumoniae vaccination rates according to recommendations), taking clustering within clinics into account., Results: Vaccination rates substantially increased in the intervention group; Streptococcus pneumoniae +21.5% (+16.7% according to recommendations), influenza +12.2%, herpes zoster +13.3% (+13.6% age group 50+), and hepatitis B +11%. Vaccination rates in the control group tended to decrease or increase only moderately (-5.8% [-3.8%], +7.4%, +2.1% [1.4%], and -1.7%, respectively). GLMM showed significant effect of the intervention (OR 7.50, 95% CI 2.18-25.80, p = 0.001)., Conclusion: This easy-to-implement and resource-saving approach has the potential to increase vaccination rates in oncological patients and to have a considerable impact protecting oncological patients from preventable infectious diseases., Clinical Trial Registration: The study was registered at the German Resister for Clinical Studies (DRKS) under DRKS00020118., (© 2022 John Wiley & Sons Ltd.)

Familial gastrointestinal stromal tumor (GIST) syndrome is a rare autosomal dominant genetic disorder. We report on a kindred in which 3 family members carry a germline mutation (c.1727T>C, p.L576P) in exon 11 of the KIT gene. This mutation was not reported so far in familial GISTs. Apart from multiple GISTs in 2 of the mutation carriers, all of them had multiple hyperpigmented skin macules and a history of achalasia-like stenosis of the esophagus in early childhood. In the index patient >100 tumors and a diffuse Cajal cell hyperplasia of the small bowel occurred. Sequencing of DNA extracted from tumor tissue of one of his GISTs revealed the KIT mutation in exon 11 (c.1727T>C). By array comparative genomic hybridization whole chromosomal gains 3, 5, 7, 9, 12, 15, and 18 were detected. In addition, we could identify a gain on chromosome 4, spanning the KIT gene. Together with the family described here, 24 unrelated cases with proven germline mutations in KIT have been reported. In these families the diagnosis was established from the age of 30 years onwards. Because in 1 patient reported here the GIST was a coincidental finding at the age of 15 years, the tumors might occur at a very young age and remain unnoticed until they-either due to increasing size, ulceration, or malignant progression-become symptomatic. Therefore, we propose to start screening patients with known KIT mutations from a younger age.

Introduction: Most cancer vaccination trials have been performed in human leukocyte antigen (HLA)-A2 positive populations. Some studies have used HLA-A2 negative patients as control group. However, HLA-type and HLA-expression can interact with tumor biology and possibly affect prognosis. HLA-A2 negative patients might constitute an inadequate control group., Materials and Methods: Patients with colorectal cancer were serologically analyzed for HLA-A2 expression. Patients were evaluated for tumor stage, grading, tumor location. Overall survival (OAS) of HLA-A2 positive and HLA-A2 negative patients was compared., Results: One hundred forty-four patients were evaluable (50% HLA-A2+). Median age was 62 years. UICC stage III or IV: 45.8%. Gender, location, and UICC stage were equally distributed between HLA-A2 subgroups. HLA-A2 positive patients more frequently had grade 3 histology (27.8% vs 13.9%) and chemotherapy (62.9% vs 45.6%). At a median follow-up of 75.8 months, median OAS for the entire study population was 123.3 months, 5-year OAS was 77.5%. No statistically significant difference in OAS was observed between HLA-A2 positive and negative patients (116.5 vs 157 months, 5-year-OAS 74.1+/-11.6% vs 81+/-11.6%, p=0.46). Expectedly, patients with UICC stage I and II disease lived significantly longer than patients with stage III and IV (5-year OAS 94.3% vs 53.4%; p<0.001). A significantly superior OAS was also found for women, independent of stage or HLA status., Conclusion: HLA-A2 positive patients exhibit poorer tumor differentiation. This might account for a non-significant difference in OAS. The use of HLA-A2 negative patients as control cohort in CRC vaccinations would rather underestimate potential treatment-related survival effects. Therefore, we suggest they constitute a valid auxiliary control group.

We report the establishment and characterization, including HLA-typing, immunophenotypic and molecular cytogenetic analysis, of a novel EBV-negative cell line (BLUE-1) derived from adult relapsed sporadic Burkitt lymphoma. BLUE-1 carries the pathognomonic t(8;14)(q24;q32) effecting MYC/IgHJ fusion and a novel t(6;20)(q15;q11.2) originally present in the patient, analysis of which may facilitate identification of gene target(s) of recurrent 6q rearrangements in B-cell neoplasia. Our findings are discussed in light of the current understanding of endemic and sporadic Burkitt lymphoma. BLUE-1 grows well in culture and should be a useful lymphoma research tool.

The amount of CD34+ cells is important to predict the quality of stem cell transplants and ensure safe engraftment after high-dose chemotherapy. Further, daily controls of the patients' peripheral blood CD34+ cell counts are performed to optimize peripheral blood stem cell collection, especially in patients with low CD34+ cell numbers. Therefore, the use of reliable reference samples is mandatory for quality assurance, both in terms of patient safety and reproducibility of results from different laboratories. We report our first experience with CD-Chex CD34, containing stabilized placental cord blood cells in preservative medium with defined concentrations of CD34+ cells. Analysis was performed according to standard operating procedures. Three lots were tested sequentially on a day per day use. The expected CD34+ values were 28.6-, 36.7- and 28.1 microl(-1), respectively, and the mean measured values were 27.4 +/- 2.75 microl(-1) (n = 25, range 21 - 33 microl(-1), coefficient of variation [CV] 10.0%), 29.9 +/- 2.39 microl(-1) (n = 17, range 26 - 35 microl(-1), CV 8.0%), and 27.2 +/- 2.24 micro1(-1) (n = 18, range 24 - 34 microl(-1), CV 8.2%). Serial dilution (1:2 to 1:10) with normal peripheral blood or PBS w/o Ca++/Mg++ gave adequate results. We conclude that the control samples used in this setting are reliable and thus helpful to increase the accuracy in the analysis of CD34+ cells.