Splanchnic vein thrombosis occurred in 1.8% patients of AP. The use of AC was reasonably safe with no fatal bleeding complications. However, there was no significant difference in the recanalization rates in those with and without AC.

BackgroundDoxorubicin has been shown to inhibit proliferation of cancer cells through proteolytic activation of CREB3L1 (cAMP response element binding protein 3-like 1), a transcription factor synthesized as a membrane-bound precursor. Upon doxorubicin treatment, CREB3L1 is cleaved so that the N-terminal domain of the protein can reach the nucleus where it activates transcription of genes that inhibit cell proliferation. These results suggest that the level of CREB3L1 in cancer cells may determine their sensitivity to doxorubicin.MethodsMice transplanted with 6 lines of renal cell carcinoma (RCC) were injected with doxorubicin to observe the effect of the chemotherapy on tumor growth. Immunohistochemistry and bioinformatics analyses were performed to compare CREB3L1 levels in types of cancer known to respond to doxorubicin versus those resistant to doxorubicin.ResultsHigher levels of CREB3L1 protein are correlated with increased doxorubicin sensitivity of xenograft RCC tumors (p = 0.017 by Pearson analysis). From patient tumor biopsies we analyzed, CREB3L1 was expressed in 19% of RCC, which is generally resistant to doxorubicin, but in 70% of diffuse large B-cell lymphoma that is sensitive to doxorubicin. Doxorubicin is used as the standard treatment for cancers that express the highest levels of CREB3L1 such as osteosarcoma and malignant fibrous histiocytoma but is not generally used to treat those that express the lowest levels of CREB3L1 such as RCC.ConclusionIdentification of CREB3L1 as the biomarker for doxorubicin sensitivity may markedly improve the doxorubicin response rate by applying doxorubicin only to patients with cancers expressing CREB3L1.

Introduction: Long-term data regarding kidney transplantation (KTx) patients with monoclonal gammopathy of undetermined significance (MGUS) are scarce. We evaluated the long-term outcomes of these patients in a single-center retrospective study from the Mayo Clinic, Rochester, Minn., USA. Methods: Patients who had an MGUS before transplant or developed one after KTx were selected. Monoclonal protein was screened as part of the KTx evaluation by serum protein electrophoresis. Screening for posttransplant lymphoproliferative disorder (PTLD) or MGUS after transplant was not required by protocol. Patients with multiple myeloma, dysproteinemia-related kidney disease or no pretransplant serum protein electrophoresis were excluded. Results: Between 1963 and 2006, 3,518 patients underwent KTx. MGUS was identified in 42 patients, with 23 before transplant and 19 after transplant. Median follow-up for these patients was 8.5 years (range 0.3–37). Four (17.4%) pretransplant MGUS patients developed a hematologic malignancy: 2 smoldering multiple myeloma and 2 PTLD – an Epstein-Barr virus-positive diffuse large cell lymphoma and a Hodgkin lymphoma. None of the 19 patients who developed an MGUS after transplant progressed to multiple myeloma, but 2 (10.5%) developed Epstein-Barr virus-negative T cell lymphoproliferative disorders at 16 and 26 years after transplant. Median survival was 26.1 and 28.0 years for the pretransplant and posttransplant MGUS groups, respectively. Conclusion: Progression from true MGUS to multiple myeloma is rare after KTx. KTx appears safe in true MGUS patients if the monoclonal gammopathy was not the cause of the kidney disease. None of the patients progressed to multiple myeloma, but 2 developed smoldering multiple myeloma and several developed PTLD. Further studies are needed to explain the relationship between MGUS and PTLD.

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