7 research outputs found

    Risk factors for developing inflammatory breast cancer: an epidemiological study of a single patient population

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    Inflammatory breast cancer (IBC) is a rare and aggressive form of breast cancer, with a particularly poor prognosis. Identification of epidemiologic risk factors for IBC might shed light on causes of the disease, and guide screening and perhaps treatment. Previous studies have suggested that race, geographic location, body mass index (BMI), menopausal status, age at menarche, parity, duration of lactation, and exposure to mouse mammary tumor virus may be key risk factors in the development of IBC. This retrospective epidemiologic study examines the risk factors for IBC in predominantly Caucasian patients treated at the Dana Farber Cancer Institute (DFCI) in Boston, MA. The risk factors that were examined in this study include the following: BMI, family history of having breast cancer, comorbidities, duration of symptoms associated with IBC prior to diagnosis, season of diagnosis, and molecular subtypes of breast cancer. Additionally, the descriptive statistics for the mean age of diagnosis, race, menopausal status, genetic predisposition, and the presence of metastases in distant organs were also determined. This study showed that there is some evidence of a hereditary component and seasonal variation to the disease. Furthermore, this study reiterates the association of high body mass index (BMI) and IBC. The data collected from the DFCI IBC patient population suggest that modifiable lifestyle factors, perhaps due to a lack of awareness of the disease, might be crucial in the development of IBC. Further research is needed to explore the unique risk factors in developing IBC elucidated in this study in order to better understand and prevent such an aggressive disease

    Distance to Treatment with Radical Cystectomy in a Rural State: Long Car Rides, Equivalent Outcomes

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    PURPOSE: Radical Cystectomy (RC) is a complex surgery with better outcomes reported when performed at high volume centers. This may lead to patients traveling farther for care. We examined the impact of travel distance on clinical outcomes. METHODS: 220 patients undergoing RC from 2015-2021 were retrospectively reviewed. Distance traveled to the treatment center by patient zip codes was classified as 12.5 mi with low-grade complications were more likely to be managed at an OSH (57.5%, p = 0.01). There was no difference in time to initiation of neoadjuvant chemotherapy (p=0.99) or time to RC following NAC (p=0.23) by distance traveled. For 49 MIBC patients proceeding directly to surgery without NAC, time from diagnosis to RC was increased if traveling \u3e12.5 mi (p=0.04). CONCLUSIONS: Increased travel distance did not impact early postoperative outcomes. Distance traveled may impact access to care, such as time to surgery or location of readmission to the treatment center post-operatively

    Lenalidomide Enhances Immune Checkpoint Blockade-Induced Immune Response in Multiple Myeloma

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    International audiencePurpose: PD-1/PD-L1 signaling promotes tumor growth while inhibiting effector cell-mediated antitumor immune responses. Here, we assessed the impact of single and dual blockade of PD-1/ PD-L1, alone or in combination with lenalidomide, on accessory and immune cell function as well as multiple myeloma cell growth in the bone marrow (BM) milieu. Experimental Design: Surface expression of PD-1 on immune effector cells, and PD-L1 expression on CD138 Ăľ multiple mye-loma cells and myeloid-derived suppressor cells (MDSC) were determined in BM from newly diagnosed (ND) multiple myelo-ma and relapsed/refractory (RR) multiple myeloma versus healthy donor (HD). We defined the impact of single and dual blockade of PD-1/PD-L1, alone and with lenalidomide, on auto-logous anti-multiple myeloma immune response and tumor cell growth. Results: Both ND and RR patient multiple myeloma cells have increased PD-L1 mRNA and surface expression compared with HD. There is also a significant increase in PD-1 expression on effector cells in multiple myeloma. Importantly, PD-1/PD-L1 blockade abrogates BM stromal cell (BMSC)-induced multiple myeloma growth, and combined blockade of PD-1/PD-L1 with lenalidomide further inhibits BMSC-induced tumor growth. These effects are associated with induction of intracellular expression of IFNg and granzyme B in effector cells. Importantly, PD-L1 expression in multiple myeloma is higher on MDSC than on antigen-presenting cells, and PD-1/PD-L1 blockade inhibits MDSC-mediated multiple myeloma growth. Finally, lenalido-mide with PD-1/PD-L1 blockade inhibits MDSC-mediated immune suppression. Conclusions: Our data therefore demonstrate that checkpoint signaling plays an important role in providing the tumor-promoting , immune-suppressive microenvironment in multiple myeloma, and that PD-1/PD-L1 blockade induces anti-multiple myeloma immune response that can be enhanced by lenalido-mide, providing the framework for clinical evaluation of combination therapy
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