Objective:To evaluate association of sociodemographic, anthropometric, and epidemiological factors with result of mammogram in women undergoing breast cancer screening.Methods:This is a cross-sectional study with data obtained through interviews, anthropometric measurements, and mammography of 600 women aged 40 to 69 years at the Preventive Medicine Department of Hospital de Câncer de Barretos, Brazil, in 2014. The results of these examinations in the BI-RADS categories 1 and 2 were grouped and classified in this study as normal mammogram outcome, and those of BI-RADS categories 3, 4A, 4B, 4C, and 5 were grouped and classified as altered mammogram outcome. The statistical analysis included the Student's t-test to compare means, as well as odds ratios (OR), with their corresponding 95% confidence intervals (95%CI), to verify an association by means of the multivariate analysis.Results:Of 600 women evaluated, 45% belonged to the age group of 40–49 years-old and 60.2% were classified as BI-RADS category 2. The multivariate analysis showed that women with blood hypertension (OR: 2.64; 95%CI: 1.07–6.49; p<0.05) were more likely to present changes in the mammography, while physical activity was associated with lower chances (OR: 0.30; 95%CI: 0.11–0.81; p<0.05).Conclusion:Hypertensive women undergoing screening mammography are more likely to present mammographic changes, whereas women practicing physical activity have lower chances (70%) of presenting changes in the breast compared with sedentary individuals.

2376 Poster Board II-353 Background: Patients with relapsed or refractory CLL/SLL and patients with mantle cell lymphoma (McL) have a poor prognosis. Overall response rate (ORR) to salvage therapy for refractory patients is approximately 10-30%, and survival benefit with current treatment approaches is limited. Phase II studies of single agent lenalidomide in patients with relapsed or refractory CLL revealed an ORR of 32-58% (7-17% CR), depending on treatment dose, scheduled used and duration of treatment with lenalidomide. In patients with refractory or relapsed McL, lenalidomide treatment resulted in an ORR of 53% (CR 20%, PR 33%), and a 14-month median duration of response (Habermann et al 2009). Recent in vitro studies have shown that lenalidomide enhances the rituximab-induced killing of NHL cell lines and B-CLL cells via ADCC by restoring the defective T-cell and NK-cell mediated ability to form immune synapses to exert tumor cell cytotoxicity. Methods: Patients with relapsed or refractory CLL/SLL or McL received oral lenalidomide via dose escalation as follows, 2.5 mg on days 1-7, 5mg on day 8-14 and 10mg on day 15-21 followed by 7 days of rest in 28-day cycle; for cycle 2 and beyond 20mg was given on day 1-21 on a 28 day cycle. Rituximab was dosed at 375mg/m2 IV weekly for 4 weeks starting on day 15 of cycle 1. Treatment was continued until disease progression or toxicity. All patients were given allopurinol 300mg orally twice per day starting 3 days prior to first dose of lenalidomide. CT scans, and bone marrow biopsies were done every 2 months to assess for response. Primary objectives were overall response rate (CR+PR) and safety and tolerability of the combination regimen. Results: 17 patients were enrolled on study (13 patients with CLL/SLL and 4 patients with McL). Median number of prior chemotherapies was 3 (range 1-5). Median age was 64 years (range 42-80). Among patients with CLL, the most common cytogenetic abnormalities were trisomy 12 (isolated n=3, associated with other abnormalities n=4), del11q (isolated n=1, with others n=3), isolated del13q (n=1), complex cytogenetics with 3 or more abnormalities (n=4 including 1 patient with del 17p). Responses were assessed every 2 months after initiation of therapy. Response rate for 13 evaluable patients (10 with CLL and 3 with McL) relative to months on treatment with lenalidomide are summarized in the table. Although all responses were PR, the rate of PR improved with continued therapy suggesting increased responses with a longer duration of treatment with lenalidomide. Currently, 7 patients are still receiving active treatment on study, all with CLL (3 achieved a PR and 4 have SD). Of the 4 patients with McL enrolled on study, 1 achieved a PR after 2 months of therapy; 1 achieved SD after 2 months of therapy with a sustained SD after 6 months; 1 patient achieved SD after 2 months, but progressed after 6 months on treatment. The regimen was well tolerated. Most common (>5%) toxicities include neutropenia (35% grade 3, 6% grade 4), fatigue (17% grade 1-2, 6% grade 3), tumor flare (12% grade 2, 12% grade 3), acute renal insufficiency (6% grade 1, 12% grade 3), rituximab related infusion reactions (6% grade 2, 6% grade 3), flu-like symptoms (6% grade 2, 6% grade 3), venous thromboembolic disease (6% grade 2, 6% grade 3), infections (11% including 1 patient with fatal endocarditis), and hypercalcemia (11% grade 4). Correlative studies are ongoing. Conclusions: The combination of lenalidomide with Rituximab is a promising combination regimen in CLL patients with very poor prognosis who have undergone multiple lines of therapy. This treatment combination appears tolerable with observed events consistent with the use of these two agents in other studies. Further investigation is warranted, possibly in the front line setting and in combination with other agents. Disclosures: Lancet: Celgene: Research Funding.

4413 BACKGROUND In concert with emerging effectiveness data, we are learning that the side effect profile of lenalidomide (L) in CLL may be different from that observed with other malignancies, such as multiple myeloma (MM) or myelodysplastic syndrome (MDS). In particular, at lower doses than typically used for MM or MDS, a unique tumor flare response (TFR) has been observed for which the mechanism is still unclear, but may be related to a “cytokine release” phenomenon. CASE REPORT Here we would like to describe 3 cases of hypercalcemia that occurred in 3 of 17 patients with fludarabine refractory CLL treated at the Moffitt Cancer Center: 2 patients who were on a clinical trial of lenalidomide plus rituximab (LR), and 1 patient who was treated with L outside of a clinical trial setting. Case 1 Pt #1 was initiated on (LR) on 12/2007 for CLL with bulky LAN, elevated wbc (110K), and 90% bone marrow (BM) involvement. By day 6, his calcium peaked at 11.78 and was accompanied by a drop in wbc to 15K. He had no other evidence of TFR, and was specifically without complaints of back pain or tender/progressive LAN. He was treated with IV fluids and steroids which promptly corrected his calcium, after which L was resumed. His course has been complicated by neutropenia requiring G-CSF. Although LAN remains stable, he has had an excellent BM response, with only 40% CLL seen on reevaluation in 06/2009. Case 2 Pt #2 was initiated on LR on 8/2008 for CLL with bulky LAN, mildly elevated wbc (20.5K) and 60% BM involvement. By day 4 his calcium peaked at 16.94, at which time he presented to our urgent care center with weakness, sweats, back pain, nausea and vomiting. No tender or progressive LAN was appreciated. He was treated with IV fluids, pamidronate, calcitonin and steroids which normalized his calcium. An attempt was made to restart L, which again produced hypercalcemia after 4 days. No further attempts were made to resume this medication. A workup performed during the first episode of hypercalcemia was notable for a slight elevation in the PTHrp (8.5). Case 3 Pt #3 was initiated on L alone on 6/2008 for CLL with bulky LAN, elevated wbc (283.6K), and 95% BM involvement. By day 4, his calcium peaked to 14.64, and was associated with a TFR, including a rise in wbc (306K), LDH (1285), and enlarging/painful LAN. The hypercalcemia was treated with IV fluids, zoledronate, and steroids. Bendamustine was immediately initiated for the treatment of CLL with dramatic improvement on lymph nodes and WBC counts. Following 1 cycle of bendamustine, L was resumed, with stabilization of his disease. Workup in these patients was unremarkable, with normal VitD/PTH levels, and only a mild elevation of PTHrp in Pt#2 (see table), in whom hypercalcemia had reoccurred upon rechallenge with L. Pt#1 and #3 were successfully retreated without recurrent hypercalcemia, though, Pt#3 received prior cytoreductive therapy with bendamustine. CONCLUSION Hypercalcemia is a rare complication of advanced B-cell malignancies seen with lymphokine/cytokine mediated bone disruption. Increased production of l,25-(OH) 2D by lymphocytes may also lead to hypercalcemia, and in CLL it is mainly associated with Ritcher's transformation or presence of osteolytic lesions. Here we report on 3 cases of hypercalcemia, which were identified during L treatment in CLL, and which had not been observed in other studies of L. We hypothesize that the hypercalcemia could be a direct reflection of increased cytokine levels, including IL-6, TNFα, and, MIP-1α, which are known to influence osteoclastogenesis. Interestingly, IL-6 is known to act synergistically with PTHrp in experimental models to drive hypercalcemia, which may be relevant for the patient who developed recurrent hypercalcemia on rechallenge with L. Levels of cytokines at different time points are now under investigation and are anticipated for presentation at the meeting. These events indicate that serum chemistries of patients initiating treatment with lenalidomide should be closely monitored during the first weeks of treatment. Disclosures: Off Label Use: Lenalidomide is an immune modulator drug currently being studied for efficacy in conjunction with Rituxan in chronic lymphocytic leukemia. This abstract summarizes a unique side effect, hypercalcemia, seen among a small cohort of patients on this study.. Lancet:Celgene: Research Funding. Pinilla:Novartis: Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Bristol-Myers Squibb: Research Funding; exelixis: Research Funding.