Saint Francis Cancer Treatment Center

Grand Island, NE, United States

Saint Francis Cancer Treatment Center

Grand Island, NE, United States
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Robert N.J.,Virginia Cancer Specialists | Saleh M.N.,Georgia Cancer Specialists | Paul D.,Rocky Mountain Cancer Center | Generali D.,Senologia e Breast Unit | And 12 more authors.
Clinical Breast Cancer | Year: 2011

Introduction: A multicenter, open-label phase III study was conducted to test whether sunitinib plus paclitaxel prolongs progression-free survival (PFS) compared with bevacizumab plus paclitaxel as first-line treatment for patients with HER2- advanced breast cancer. Patients and Methods: Patients with HER2- advanced breast cancer who were disease free for ≥ 12 months after adjuvant taxane treatment were randomized (1:1; planned enrollment 740 patients) to receive intravenous (I.V.) paclitaxel 90 mg/m2 every week for 3 weeks in 4-week cycles plus either sunitinib 25 to 37.5 mg every day or bevacizumab 10 mg/kg I.V. every 2 weeks. Results: The trial was terminated early because of futility in reaching the primary endpoint as determined by the independent data monitoring committee during an interim futility analysis. At data cutoff, 242 patients had been randomized to sunitinib-paclitaxel and 243 patients to bevacizumab-paclitaxel. Median PFS was shorter with sunitinib-paclitaxel (7.4 vs. 9.2 months; hazard ratio [HR] 1.63 [95% confidence interval (CI), 1.18-2.25]; 1-sided P =.999). At a median follow-up of 8.1 months, with 79% of sunitinib-paclitaxel and 87% of bevacizumab-paclitaxel patients alive, overall survival analysis favored bevacizumab-paclitaxel (HR 1.82 [95% CI, 1.16-2.86]; 1-sided P =.996). The objective response rate was 32% in both arms, but median duration of response was shorter with sunitinib-paclitaxel (6.3 vs. 14.8 months). Bevacizumabpaclitaxel was better tolerated than sunitinib-paclitaxel. This was primarily due to a high frequency of grade 3/4, treatment-related neutropenia with sunitinib-paclitaxel (52%) precluding delivery of the prescribed doses of both drugs. Conclusion: The sunitinib-paclitaxel regimen evaluated in this study was clinically inferior to the bevacizumabpaclitaxel regimen and is not a recommended treatment option for patients with advanced breast cancer. © 2011 Elsevier Inc. All rights reserved.


Copur M.S.,Saint Francis Cancer Treatment Center | Obermiller A.,Saint Francis Cancer Treatment Center
Clinical Colorectal Cancer | Year: 2011

Vascular endothelial growth factor (VEGF) signaling is considered to be one of the key factors involved in tumor-associated angiogenesis. Inhibition of angiogenesis has significantly improved anticancer therapy making it one of the cornerstones of treatment for various solid tumors. Several antiangiogenesis inhibitory compounds (eg, bevacizumab, sunitinib, sorafenib) are now widely used in the treatment of patients with colorectal, nonsmall-cell lung, advanced renal cell, hepatocellular, and breast cancer. One of the most commonly observed side effects of inhibition of VEGF signaling is hypertension, which is dose-dependent and varies in incidence among the different angiogenesis inhibitor drugs. Poorly controlled hypertension not only can lead to cardiovascular events, renal disease, and stroke, but may also necessitate discontinuation of anticancer therapy, thereby potentially limiting overall clinical benefit. In contrast, hypertension induced by VEGF inhibitors has been shown to represent an important pharmacodynamic biomarker of oncologic response. For the practicing oncologist, knowledge and optimal management of this toxicity is essential. Because of the lack of controlled studies on this topic, no clear recommendations are available. In this article, we review the available preclinical and clinical data on the pathogenesis and management of hypertension resulting from anti-VEGF inhibitor therapy and propose a treatment algorithm that our group has now implemented for daily clinical practice. © 2011 Elsevier Inc. All rights reserved.


Clark D.,Saint Francis Cancer Treatment Center | Gauchan D.,Saint Francis Cancer Treatment Center | Ramaekers R.,Saint Francis Cancer Treatment Center | Norvell M.,Saint Francis Cancer Treatment Center | Copur M.S.,Saint Francis Cancer Treatment Center
Oncology Research | Year: 2015

Radiation recall syndrome is an acute inflammatory reaction developing at anatomical sites of previously irradiated tissue, weeks to months after the completion of radiation therapy. The distribution pattern of inflammation typically involves, and remains limited to, the boundaries of prior radiation treatment fields. Several classical chemotherapy drugs have been reported to have the potential for causing radiation recall syndrome. With the increasing availability and expanding use of novel biologic and targeted therapy anticancer drugs, isolated reports of radiation recall syndrome secondary to this class of agents are starting to appear in the literature. We describe a case of everolimus-induced radiation recall pneumonitis in a patient with metastatic renal cell cancer. Copyright © 2015 Cognizant Comm. Corp.


Copur M.S.,Saint Francis Cancer Treatment Center | Ramaekers R.,Sloan Kettering Cancer Center | Gonen M.,Sloan Kettering Cancer Center | Gulzow M.,Sloan Kettering Cancer Center | And 10 more authors.
Journal of Oncology Practice | Year: 2016

Purpose: Although 85% of patients with cancer are diagnosed and treated in the community setting, only 3% are enrolled onto clinical trials. Lack of adequate time, infrastructure, resources, incentives, and reimbursement adversely affect clinical trial participation. In July 2007, Saint Francis Cancer Treatment Center (SFCTC) in Grand-Island, Nebraska, was selected as one of the initial 16 sites for the National Cancer Institute Community Cancer Centers Program (NCCCP). Methods: Clinical trial and related activities data at SFCTC 5 years before and 5 years during the NCCCP were gathered and compared. Data included information on patients in clinical trials, number and type of trials, ratio of underserved patients, staffing, collection and storage of tissue samples, availability of new cancer services, and organizational infrastructure and linkage to National Cancer Institute-designated cancer centers. Results: The number and percentage of patients enrolled onto clinical trials increased from 89 (3.2%) to 640 (23%; P <.001). All enrollees were rural Nebraskans, with 70% age >65 years. Available treatment and non-treatment (eg, prevention, biospecimen, cancer control) trials increased from eight and three per year to 28 and 12 per year (P5.012), respectively. Staffing increased from 1.2 to 3.9 full-time equivalents (P=.012). A genetic counselor, smoking cessation counselor, and outreach project coordinator and two nurse navigators were hired. The number of tissue samples collected and/or stored increased from 26 (19%) to 320 (52%; P< .001). Conclusion: NCCCP participation had a direct and positive impact on all activities, with enhanced access to expanded types of trials and cancer care services. Our data demonstrate the feasibility of successful implementation of an expanded spectrum of clinical trials and programs in a rural community. Copyright © 2015 by American Society of Clinical Oncology.


Jamison C.,University of Nebraska Medical Center | Nelson D.,Saint Francis Cancer Treatment Center | Eren M.,Saint Francis Cancer Treatment Center | Gauchan D.,Saint Francis Cancer Treatment Center | And 3 more authors.
Oncology Research | Year: 2016

Efficacy and safety of dasatinib in chronic phase (CP) chronic myelogenous leukemia (CML) patients has been well established. Initially approved dose and schedule of 70 mg twice daily has been changed to 100 mg once daily after demonstration of the same efficacy with less toxicity. Some patients require significant dose reductions to enable continued treatment with dasatinib. Even at a dose of 80 mg once daily, several patients may require further dose reductions due to substantial toxicity while maintaining good control of their disease. We report two CP-CML patients achieving and maintaining major molecular responses while on very low doses of dasatinib, ultimately achieving undetectable levels of BCR-ABL fusion transcript in their peripheral blood. Observations of several CP-CML cases responding remarkably well to dasatinib despite very low dose and frequent dose interruptions challenge our current understanding and the accuracy of the data regarding the optimum dose and schedule of this drug. In selected intolerant patients, low-dose dasatinib therapy may be a safe and effective alternative treatment option before a treatment discontinuation or change considered. Copyright © 2016 Cognizant, LLC.


Saif M.W.,Columbia University | Kaley K.,Yale University | Chu E.,Yale University | Copur M.S.,Saint Francis Cancer Treatment Center
Clinical Colorectal Cancer | Year: 2010

Introduction: Cetuximab therapy has been effectively combined with cytotoxic chemotherapy in the first-, second-, and third-line treatment settings. In general, treatment with cetuximab is well tolerated, though it has been associated with the development of hypersensitivity reactions (HSRs). In the case of severe HSRs, further therapy with cetuximab is not possible. In contrast with cetuximab, HSRs have been rarely observed with panitumumab therapy. Currently, panitumumab is indicated for patients with metastatic colorectal cancer (mCRC) with progressive refractory disease, and there is recent evidence documenting its clinical efficacy with cytotoxic chemotherapy in the first-line and second-line settings. However, the safety and efficacy of panitumumab after progression with cetuximab has not been well documented. Patients and Methods: We present a retrospective review of our experience in treating 15 patients with mCRC who tolerated panitumumab with clinical benefit after failure on cetuximab therapy from November 2006 through September 2008 at the Yale Cancer Center in New Haven, CT and at the Saint Francis Cancer Treatment Center in Grand Island, NE. KRAS status was retrospectively assessed in patients with readily available tumor tissue. Results: All 15 patients were treated with a standard dose of panitumumab 6 mg/kg intravenously every 2 weeks. No patient received premedication therapy. Of the 15 patients treated, 4 received only 2 doses of panitumumab but stopped further therapy because of deterioration in performance status. Of the 11 evaluable patients, we noted minor radiographic responses (Response Evaluation Criteria in Solid Tumors) in 3 patients and stable disease (SD) in 3 other patients after 8 weeks of therapy. Five patients had evidence for progressive disease, and further therapy was stopped. The median duration of SD was 4 months (range, 2-8 months). Among the 11 evaluable patients, 1 patient achieved > 50% reduction in carcinoembryonic antigen (CEA; 112 to 49 U/L), 3 patients had a 25% reduction (59 to 43 U/L, 84 to 61 U/L, and 67 to 42 U/L), and 1 patient had minor reduction in CEA (98 to 83 U/L). All patients tolerated panitumumab well with no occurrence of hypersensitivity reactions. Grade 3/4 toxicities were skin rash in 5 patients and asthenia in 1 patient. The other adverse events observed included grade 1-2 skin rash in 2 patients, grade 2 paronychia in 4 patients, grade 2 hypomagnesemia in 2 patients, and fatigue in 3 patients. One patient had wild-type KRAS, and this individual experienced a minor response to antibody therapy with > 50% reduction in CEA. A second patient was found to have mutant KRAS and, in terms of clinical response, this patient experienced SD for 6 months. The third patient evaluated had mutant KRAS, and this individual was unable to tolerate more than 2 doses and was therefore not evaluable for response. Conclusion: Panitumumab may represent an alternative treatment strategy for patients with refractory mCRC who have experienced failure with standard therapy including cetuximab-based regimens. Our relatively small clinical experience suggests that cetuximab and panitumumab may exert their antitumor activity through different mechanisms; however, further work is required to investigate this potentially interesting issue.


PubMed | Saint Francis Cancer Treatment Center
Type: Journal Article | Journal: Clinical colorectal cancer | Year: 2011

Vascular endothelial growth factor (VEGF) signaling is considered to be one of the key factors involved in tumor-associated angiogenesis. Inhibition of angiogenesis has significantly improved anticancer therapy making it one of the cornerstones of treatment for various solid tumors. Several antiangiogenesis inhibitory compounds (eg, bevacizumab, sunitinib, sorafenib) are now widely used in the treatment of patients with colorectal, non-small-cell lung, advanced renal cell, hepatocellular, and breast cancer. One of the most commonly observed side effects of inhibition of VEGF signaling is hypertension, which is dose-dependent and varies in incidence among the different angiogenesis inhibitor drugs. Poorly controlled hypertension not only can lead to cardiovascular events, renal disease, and stroke, but may also necessitate discontinuation of anticancer therapy, thereby potentially limiting overall clinical benefit. In contrast, hypertension induced by VEGF inhibitors has been shown to represent an important pharmacodynamic biomarker of oncologic response. For the practicing oncologist, knowledge and optimal management of this toxicity is essential. Because of the lack of controlled studies on this topic, no clear recommendations are available. In this article, we review the available preclinical and clinical data on the pathogenesis and management of hypertension resulting from anti-VEGF inhibitor therapy and propose a treatment algorithm that our group has now implemented for daily clinical practice.


PubMed | Saint Francis Cancer Treatment Center
Type: Case Reports | Journal: Oncology research | Year: 2015

Radiation recall syndrome is an acute inflammatory reaction developing at anatomical sites of previously irradiated tissue, weeks to months after the completion of radiation therapy. The distribution pattern of inflammation typically involves, and remains limited to, the boundaries of prior radiation treatment fields. Several classical chemotherapy drugs have been reported to have the potential for causing radiation recall syndrome. With the increasing availability and expanding use of novel biologic and targeted therapy anticancer drugs, isolated reports of radiation recall syndrome secondary to this class of agents are starting to appear in the literature. We describe a case of everolimus-induced radiation recall pneumonitis in a patient with metastatic renal cell cancer.

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