The foodborne pathogen C. jejuni is a significant challenge for the global health care system. It is crucial to investigate C. jejuni posttranscriptional regulation by small RNAs (sRNAs) in order to understand how it adapts to different stress conditions.

Introduction Appropriate dosing of therapeutic anticoagulation during periods of thrombocytopenia remains uncertain for patients undergoing hematopoietic stem cell transplants (HSCT). There is a paucity of literature on treatment outcomes for HSCT patients treated with non-prophylactic, but reduced doses of therapeutic anticoagulation during thrombocytopenia. The primary objective was to determine the incidence of major bleeding events during thrombocytopenia when reduced-dose enoxaparin was administered. Methods This is a retrospective review of patients with a venous thromboembolic event (VTE) who underwent HSCT and received reduced-dose enoxaparin during thrombocytopenia at the Massachusetts General Hospital (MGH) from April 1, 2016 to August 31, 2018. Incidence of recurrent VTE and bleeding events for up to one month were investigated. Rates of recurrent VTE and enoxaparin dose adjustments (0.5 mg/kg twice daily vs 1 mg/kg daily) were also reviewed. Results Out of 172 patients reviewed, 27 patients met inclusion criteria. There were no recurrent VTEs within one month of initial enoxaparin dose reduction. There was one major bleeding episode that occurred while a patient was on full-dose enoxaparin; believed to be related to cyclophosphamide cardiopulmonary toxicity and resulted in death. There were six non-major bleeding episodes, only one of which was clinically significant and resulted in the discontinuation of enoxaparin. Conclusion Our evaluation of therapeutic enoxaparin dose reductions for thrombocytopenia in the HSCT patient population found this practice to be effective in reducing the recurrence of VTE with no major bleeding adverse events. However, the rate of non-significant minor bleeds should be monitored while on reduced-dose enoxaparin.

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14539 Background: More than 300 different mutations have been described in von Hippel-Lindau (VHL) families and nearly 100 in sporadic RCC. In familial cases, there is an excess of mutations in exon 3 and exon 1, whereas mutations are evenly distributed in sporadic cases. Recent evidence suggests the importance of genotype/phenotype correlations with different VHL gene mutations contributing to a tumor’s unique biological behavior. We performed a pilot study to compare the incidence and type of VHL mutation in IL-2 complete responders (CR) and non-responders (NR). Methods: Genomic DNA was extracted from 20 frozen clear cell tumour samples (10 CR and 10 NR) using Qiamp DNA mini kits (Qiagen). Four amplimers covering the entire coding sequence and three exon/intron junctions of the VHL gene were synthesized by PCR. PCR products were subsequently purified and were sequenced using Big Dye Primer Cycle Sequencing kit (Perkin-Elmer Applied Biosystems) and an automated DNA sequencer (Perkin-Elmer Applied Biosystems). Point mutation detection was performed on DNA sequencing gels from colored peak chromatograms. Mutation bearing sequences were confirmed by a second round of PCR and sequencing. Results: In the CR patients, only 2 out of 10 samples (20%) had evidence of a VHL mutation. These VHL mutations included a false sense mutations in exon 2, comprised of a C to T transition at position 646 in the cDNA, creating a stop codon, and a frameshift mutation in exon 1 introducing in one allele an abnormal stop codon at the beginning of exon 3 potentially leading to a shorter protein product. In the 10 non-responder samples, there was also a 2 out of 10 (20%) incidence of VHL mutations. These mutations included a complex 12 nucleotide deletion in the third exon in the a domain of the protein, and a G deletion in the first exon introducing a premature stop codon. Conclusions: In this small pilot study of metastatic RCC patients, there were relatively few VHL gene mutations, and VHL mutations did not appear to correlate with response to IL-2 therapy. This study, however, does not assess inactivation of VHL genes due to hypermethylation. An expanded genetic profile to evaluate IL-2 responders versus non-responders using 500k SNP Chips is underway. No significant financial relationships to disclose.