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    <recommendedItem id="20100101_19_376"
                     title="Stress of Prostate Cancer Diagnosis May Be Deadly (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/HematologyOncology/ProstateCancer/tb/18268?impressionId=1265779877604"
                     
      Men have a slightly, but statistically significant, increased risk of dying from cardiovascular disease in the year after learning they have prostate cancer, researchers found.&lt;br&gt;
&lt;br&gt;The risk was greatest in the first month after diagnosis (standardized mortality ratio 2.05, 95% CI 1.89 to 2.22), Lorelei Mucci, PhD, of Brigham and Women&apos;s Hospital in Boston, and colleagues reported online in the &lt;em&gt;Journal of the National Cancer Institute&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;The study, which covered diagnoses made from 1979 through 2004, also found an overall increased risk of suicide in the year following a prostate cancer diagnosis (SMR 1.4, 95% CI 1.2 to 1.6), although the association was not significant after screening for prostate specific antigen (PSA) became widespread.&lt;br&gt;
&lt;br&gt;The findings&lt;em&gt;&lt;/em&gt; are &quot;one additional piece in weighing the pros and cons of PSA screening,&quot; Mucci said in an interview.&lt;br&gt;
&lt;br&gt;She also said that, &quot;not only do [clinicians] need to be treating the cancer, but they need to be thinking about the social support and other support that men may need to deal with this stressful event.&quot;&lt;p&gt;&lt;/p&gt;
&lt;p&gt;A previous study by Mucci&apos;s group that looked at a Swedish population found similarly increased risks of suicide and cardiovascular death following a prostate cancer diagnosis.&lt;/p&gt;
&lt;p&gt;Because PSA testing is more extensive in the U.S., increasing the number of early-stage and indolent cancers detected, the researchers wanted to see whether the results would carry over.&lt;/p&gt;
&lt;p&gt;Using the Surveillance, Epidemiology, and End Results (SEER) Program, they looked at data from 342,497 men who were diagnosed with prostate cancer from 1979 through 2004.&lt;/p&gt;
&lt;p&gt;The number of diagnoses steadily increased throughout the study period  --  from 6,106 in 1979 to 17,688 in 2004.&lt;/p&gt;
&lt;p&gt;But the percentage of cancers that were metastatic dropped from 18.2% in the pre-PSA period (1979 to 1986) to 5% in the period of widespread testing (1993 to 2004).&lt;/p&gt;
&lt;p&gt;During the study, 148 men committed suicide within one year of learning their diagnosis, higher than the 105.2 that would be expected in the general U.S. male population.&lt;/p&gt;
&lt;p&gt;The elevated risk was only evident prior to 1993, when PSA testing became more widely used. The authors suggested that this was likely because of the potentially lower degree of stress associated with the diagnosis of indolent prostate cancer.&lt;/p&gt;
&lt;p&gt;&quot;So that&apos;s reassuring,&quot; Mucci said.&lt;/p&gt;
&lt;p&gt;However, another 6,845 men died of cardiovascular disease, which was also higher than the expected 6,282.9.&lt;/p&gt;
&lt;p&gt;Contrary to the findings regarding suicide, the risk of cardiovascular death in the first month after hearing a diagnosis was significantly increased throughout the study period.&lt;/p&gt;
&lt;p&gt;Prostate cancer patients who were not married at the time of diagnosis had higher relative risks of both suicide and cardiovascular death than married patients.The authors suggested that this may be because &quot;having someone close to confide in might alleviate the psychological stress experienced from receiving a cancer diagnosis.&quot;&lt;/p&gt;
&lt;p&gt;They also observed a clear trend between higher relative risks for suicide and cardiovascular death among patients diagnosed with a metastatic tumor, which clearly would be more stressful than diagnosis of a clinically localized tumor.&lt;/p&gt;
&lt;p&gt;&quot;This finding might further explain the decreasing excess risks that have been observed in the PSA era, in which the proportion of advanced tumors was small (i.e., 18.2% metastatic tumors in the pre-PSA era and 5.0% in the PSA era),&quot; they wrote.&lt;/p&gt;
&lt;p&gt;&lt;strong&gt;&lt;/strong&gt;&lt;/p&gt;
&lt;p&gt;Risk of cardiovascular death was magnified for patients with metastatic tumors (SMR 3.22, 95% CI 2.68 to 3.84) compared with those with local or regional tumors (SMR 1.57, 95% CI 1.42 to 1.74)(&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;Prostate cancer patients who were not married at the time of diagnosis had higher relative risks of both suicide and cardiovascular death than married patients.&lt;/p&gt;
&lt;p&gt;The authors acknowledged some limitations of the study, including the lack of a cancer-free group as reference and the lack of information on physical or mental health status, other prevalent disorders or comorbid illness at diagnosis, and prostate cancer treatment.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study received funding from the Swedish Council for Working Life and Social Research.&lt;/p&gt;&lt;p&gt;The authors reported no conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_364"
                     title="ADT for Prostate Cancer Raises Heart Risks"
                     score="0.009"
                     href="http://www.medpagetoday.com/Urology/ProstateCancer/tb/18250?impressionId=1265779877604"
                     
      &lt;p&gt;Androgen deprivation therapy (ADT) for prostate cancer can exacerbate cardiac risk factors and may increase the risk of heart attack and cardiac death, according to an advisory supported by four medical organizations.&lt;/p&gt;
&lt;p&gt;However, the groups did not offer specific guidelines for clinicians on when to employ ADT therapy or avoid it.&lt;/p&gt;
&lt;p&gt;Clinical trials have shown that ADT increases body weight, decreases lean mass and increases fat mass, reduces insulin sensitivity, and triggers or worsens dyslipidemia.&lt;/p&gt;
&lt;p&gt;Several studies have demonstrated a significant increase in cardiovascular death in prostate cancer patients treated with hormonal therapy or bilateral orchiectomy, although some studies have shown no association between ADT and increased cardiovascular risk, according to a report that will appear in the Feb. 16 issue of &lt;em&gt;Circulation: Journal of the American Heart Association&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Some evidence also suggests ADT may predispose men to metabolic syndrome.&lt;/p&gt;
&lt;p&gt;&quot;Based on current data, it was appropriate to conclude that there may be a relationship between ADT therapy in patients with prostate cancer and future cardiovascular risk,&quot; Glenn N. Levine, MD, of Baylor College of Medicine in Houston and chair of the advisory writing committee, said in a statement.&lt;/p&gt;
&lt;p&gt;The writing committee comprised representatives of the American Heart Association, American Urological Association, and American Cancer Society. Additionally, the American Society for Radiation Oncology endorsed the advisory.&lt;/p&gt;
&lt;p&gt;The authors&apos; review of literature showed that ADT increased cardiovascular risk in 1% to 6% of various studies&apos; patient populations. With that in mind, &quot;the decision about whether to initiate ADT should be based on weighing the benefits of therapy with this potential modest risk,&quot; Levine said.&lt;/p&gt;
&lt;p&gt;The decision to initiate ADT should remain with the physician who has responsibility for treating a patient with prostate cancer, the authors wrote. That includes patients with known cardiac disease.&lt;/p&gt;
&lt;p&gt;&quot;It is the consensus of the writing group that there is no clear indication for patients for whom ADT is believed to be beneficial to be referred to internists, endocrinologists, or cardiologists for evaluation before initiation of ADT,&quot; the authors said.&lt;/p&gt;
&lt;p&gt;&quot;The decision as to whether or not to initiate ADT in patients with cardiac disease, in whom the benefits of therapy would be weighed against any possible risks, is most appropriately made by the physician treating the patient for prostate cancer.&quot;&lt;/p&gt;
&lt;p&gt;However, the potential adverse metabolic effects warrant periodic evaluation by a patient&apos;s primary care physician, they added.&lt;/p&gt;
&lt;p&gt;Noting a lack of clinical guidance for follow-up of patients treated with ADT, the advisory authors concluded that at least an annual assessment of blood glucose and lipids seems reasonable. They also called for prospective assessment of cardiovascular risk factors before and after ADT is begun in future clinical trials.&lt;/p&gt;

    </recommendedItem>
    <recommendedItem id="20100101_19_336"
                     title="In Prostate CA, Sexual Decline After Radiation Has Limit (CME/CE)"
                     score="0.006"
                     href="http://www.medpagetoday.com/HematologyOncology/ProstateCancer/tb/18214?impressionId=1265779877604"
                     
      &lt;p&gt;Sexual function declines in the first two years after external beam radiation therapy for prostate cancer but stabilizes thereafter, according to data from a prospective cohort study.&lt;/p&gt;
&lt;p&gt;All parameters of sexual function declined significantly (&lt;em&gt;P&lt;/em&gt;&lt;0.05) in the first two years after external-beam radiation therapy (EBRT), Richard Valicenti, MD, of the University of California Davis, and colleagues found.&lt;/p&gt;
&lt;p&gt;But for years two through six of follow-up, none of the evaluated parameters of sexual function changed significantly.&lt;/p&gt;
&lt;p&gt;Pretreatment sexual function was the strongest predictor of sexual function at any time after EBRT, the investigators reported in the January issue of the &lt;em&gt;International Journal of Radiation Oncology*Biology*Physics&lt;/em&gt;&lt;em&gt;&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Their findings debunk the perception that sexual function declines continually after radiation therapy for prostate cancer.&lt;/p&gt;
&lt;p&gt;&quot;The results of this study allow patients and their partners to have a fuller understanding of the long-term sexual side effects of EBRT, and what they can expect after treatment should aid in deciding on a treatment course,&quot; Valicenti said in a statement.&lt;/p&gt;
&lt;p&gt;Reported rates of impotency after EBRT for prostate cancer have ranged from 8% to 85%, a variation the authors attributed to the different instruments used to assess sexual function. Moreover, many studies included men who received androgen deprivation therapy in addition to EBRT, possibly masking the contributions of radiation therapy to changes in sexual function.&lt;/p&gt;
&lt;p&gt;Several recent studies have suggested that rates of sexual dysfunction increase with follow-up. However, few studies included pretreatment assessment of sexual function or conducted serial assessments of sexual function after EBRT, the authors wrote.&lt;/p&gt;
&lt;p&gt;To shed more light on the question, the investigators prospectively followed 143 men who completed a sexual function questionnaire prior to EBRT for prostate cancer and at each follow-up visit. The questionnaire assessed four domains of sexual function: sexual drive, erectile function, ejaculatory function, and overall satisfaction.&lt;/p&gt;
&lt;p&gt;The mean age of the patients was 69, median Gleason score was 6, and median total radiation dose was 73.8 Gy (range of 66.6 to 79.2 Gy).&lt;/p&gt;
&lt;p&gt;During a median four-years of follow-up, the study participants completed a total of 1,187 questionnaires. Some patients were followed for as long as eight years after EBRT.&lt;/p&gt;
&lt;p&gt;Baseline scores for sexual drive and erectile function were significantly associated with patient age (&lt;em&gt;P&lt;/em&gt;=0.003 and &lt;em&gt;P&lt;/em&gt;=0.004, respectively). Ejaculatory function was significantly associated with age, race, and marital status (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05).&lt;/p&gt;
&lt;p&gt;Scores on all four domains of sexual function, as well as the total score, declined significantly in the first two years after EBRT (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05) compared with baseline values.&lt;/p&gt;
&lt;p&gt;Investigators grouped the patients according to baseline sexual function. Analysis of scores for patients above and below the median sexual function value showed that differences in sexual function persisted over time. Regression analysis showed that baseline score was the best predictor of later scores for all of the domains assessed (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;A separate analysis of scores from years two through six showed no significant changes in any of the domains: sexual drive, &lt;em&gt;P&lt;/em&gt;=0.067; erectile function, &lt;em&gt;P&lt;/em&gt;=0.5; ejaculatory function, &lt;em&gt;P&lt;/em&gt;=0.6; and overall satisfaction, &lt;em&gt;P&lt;/em&gt;=0.44.&lt;/p&gt;
&lt;p&gt;Baseline scores indicated that 74.1% of the study participants were sexually potent before EBRT. Among those who were potent before treatment, 74.4% remained potent at one year and 70.4% at two years after EBRT. The one- and two-year potency rates differed significantly from baseline, but the investigators found no statistically significant change in potency from years two through six.&lt;/p&gt;
&lt;p&gt;&quot;Our data have indicated that the widely held opinion that sexual function has a slow, progressive decline after EBRT might be incorrect,&quot; the authors wrote in conclusion. &quot;Most sexual function decline in men undergoing EBRT for prostate cancer occurred in the first two years after treatment and all domains of sexual function, including erectile dysfunction, then appeared to stabilize.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The authors reported no relevant disclosures.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_267"
                     title="Public-Private Divide Found in Prostate Cancer Treatment (CME/CE)"
                     score="0.001"
                     href="http://www.medpagetoday.com/HematologyOncology/ProstateCancer/tb/18118?impressionId=1265779877604"
                     
      &lt;p&gt;Treatment that men receive for prostate cancer may depend less on their condition and more on where they are treated, a new study found.&lt;/p&gt;
&lt;p&gt;Moreover, men treated by private hospitals were nearly two and a half times more likely to receive radiation therapy (OR 2.36; 95% CI 1.37 to 4.07) and more than four and a half times more likely to receive primary androgen deprivation therapy (OR 4.71; 95% CI 2.15 to 10.36) than surgery, which was the predominant treatment at county hospitals, according to findings published Jan. 25 in &lt;em&gt;Cancer&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Patients in private hospitals were also more likely to be white.&lt;/p&gt;
&lt;p&gt;&quot;This is the first study to compare prostate cancer treatments between private and public institutions, and it reveals a novel variable influencing treatment choice: healthcare venue,&quot; J. Kellogg Parsons, MD, MHS, of the University of California San Diego, and colleagues wrote.&lt;/p&gt;
&lt;p&gt;&quot;Men treated at county hospitals were significantly more likely to undergo surgery, whereas those treated by private providers were more likely to undergo radiotherapy or primary androgen deprivation, irrespective of age, race, comorbidity status, clinical tumor stage, Gleason sum, and D&apos;Amico risk stratification.&quot;&lt;/p&gt;
&lt;p&gt;&quot;A likely explanation for this imparity is that the initial provider in the county hospitals was always a urologist, whereas at the private venues the initial providers were a mix of urologists, radiation oncologists, and medical oncologists,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;In the U.S. in 2009, more than 190,000 men were diagnosed with prostate cancer and more than 27,000 men died from the disease, according to the National Cancer Institute. Although life expectancy, other illnesses, cancer severity, and patient preference may play a role in treatment choice, the common treatments for localized prostate cancer  --  surgery, radiation, and hormone therapy  --  all have pros and cons, and experts differ on which option is more effective.&lt;/p&gt;
&lt;p&gt;Parsons and colleagues explored whether treatment location might play a role in determining what therapy a patient receives. They analyzed the records of 559 men enrolled in a state-funded public assistance program for low-income patients, known as Improving Access, Counseling and Treatment for Californians with Prostate Cancer (IMPACT), who received prostate cancer treatment between 2001 and 2006.&lt;/p&gt;
&lt;p&gt;The researchers noted that a limitation of the study was the population included in the IMPACT database -- generally patients with more severe cancer than in the general U.S. population; thus the findings may not reflect patients from other regions and socioeconomic groups.&lt;/p&gt;
&lt;p&gt;Of the participants, 315 received treatment from county hospitals and 244 received care from private facilities. No significant difference existed between the two groups in terms of age and tumor characteristics, yet the patients received varying therapies.&lt;/p&gt;
&lt;p&gt;&quot;In this economically disadvantaged cohort, prostate cancer treatments differed significantly between county hospitals and private providers,&quot; the authors wrote. &quot;These data reveal substantial variations in treatment patterns between different types of healthcare institutions that  --  given the implications for health policy and quality of care  --  merit further scrutiny.&quot;&lt;/p&gt;
&lt;p&gt;To help patients make informed decisions, develop appropriate expectations, and avoid making decisions they will regret, the authors proposed that patients with localized prostate cancer be provided access to multiple care providers so that they will be exposed to a variety of opinions and information about their disease.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The researchers did not report specific support for this analysis but the IMPACT program is supported by the state of California.&lt;/p&gt;&lt;p&gt;The reseachers reported no financial conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_260"
                     title="ASCO GI: Agent Targets IGF Receptor in Pancreatic Cancer (CME/CE)"
                     score="0"
                     href="http://www.medpagetoday.com/MeetingCoverage/ASCOGI/tb/18124?impressionId=1265779877604"
                     
      &lt;p&gt;ORLANDO  --  A majority of patients with advanced pancreatic cancer had objective responses or stable disease when treated with an inhibitor of the insulin-like growth factor (IGF) receptor, according to data from a small clinical trial reported here.&lt;/p&gt;
&lt;p&gt;A fourth of patients had partial responses that lasted beyond 11 months in some cases. Another third had disease stabilization during treatment with the monoclonal antibody MK-0646, plus chemotherapy and erlotinib (Tarceva).&lt;/p&gt;
&lt;p&gt;&quot;We observed sustained partial responses with two different regimens,&quot; Milind Javle, MD, of M.D. Anderson Cancer Center in Houston, told attendees at the Gastrointestinal Cancers Symposium.&lt;/p&gt;
&lt;p&gt;&quot;Evaluation of MK-0646 is continuing in a randomized phase II study that will include correlative studies to identify predictive markers.&quot;&lt;/p&gt;
&lt;p&gt;Activation of the IGF-1 receptor is associated with an aggressive disease course in pancreatic cancer and acquired resistance to agents that target epidermal growth factor receptor (EGFR) such as erlotinib.&lt;/p&gt;
&lt;p&gt;&lt;/p&gt;
&lt;p&gt; &lt;/p&gt;
&lt;p&gt;Preclinical studies showed that combining an IGF-1 receptor antagonist and cetuximab (Erbitux) had synergistic activity against pancreatic cell lines, Javle said.&lt;/p&gt;
&lt;p&gt;MK-0646 preferentially binds IGF-1 receptor and not the insulin receptor. The antibody inhibits stimulation of IGF-1 receptor by both IGF-1 and IGF-2, Javle continued. MK-0646 downregulates expression of IGF-1 receptor in tumor models and has demonstrated antitumor activity in xenograft models.&lt;/p&gt;
&lt;p&gt;Phase I evaluation of MK-0646 as a single agent showed the antibody was well tolerated and led to downregulation of IGF-1 receptor and other molecules associated with tumor growth. Patients occasionally developed hyperglycemia, which was controlled with oral hypoglycemic agents.&lt;/p&gt;
&lt;p&gt;Javle reported data from a phase I-II study of MK-0646 in combination with gemcitabine (Gemzar) or gemcitabine plus erlotinib. The primary objective of the first phase was to determine the maximum tolerated dose of MK-0646 in combination therapy. Investigators assessed progression-free survival (PFS) of the two combination arms in the second phase.&lt;/p&gt;
&lt;p&gt;The study included patients with stage IV pancreatic adenocarcinoma at least six months after completion of adjuvant chemotherapy.&lt;/p&gt;
&lt;p&gt;Patients were enrolled in a nonrandomized, sequential manner to two treatment arms. One arm had a regimen consisting of weekly gemcitabine plus weekly MK-0646 at either 5 mg/kg or 10 mg/kg. In the second arm, patients received gemcitabine plus daily erlotinib and one of the two doses of MK-0646.&lt;/p&gt;
&lt;p&gt;Dose-limiting hematologic toxicity was defined as grade 4 thrombocytopenia, grade 4 neutropenia lasting at least seven days, or grade 3 or higher neutropenia with fever.&lt;/p&gt;
&lt;p&gt;Dose-limiting nonhematologic toxicity was defined as any grade 3-4 adverse event except rash and controlled hyperglycemia. Delayed dosing was defined as a delay of more than 14 days necessitated by toxicity.&lt;/p&gt;
&lt;p&gt;Of 28 patients enrolled in the study, 23 (82%) required dose adjustment of gemcitabine, and seven had toxicity-associated dose adjustments of erlotinib. Five patients discontinued erlotinib because of toxicity, but no patient withdrew from the study because of toxicity.&lt;/p&gt;
&lt;p&gt;The most frequent grade 3-4 nonhematologic toxicities were hyperglycemia and fatigue (five patients each) and elevated liver enzymes and hypermagnesemia (four each). Half the patients developed grade 3-4 neutropenia and five had grade 3-4 thrombocytopenia. No cases of febrile neutropenia occurred.&lt;/p&gt;
&lt;p&gt;Maximum tolerated dose (MTD) in the first arm was not reached at the 10 mg/kg dose of MK-0646. In the erlotinib arm, MTD was reached at the 5 mg/kg dose of MK-0646.&lt;/p&gt;
&lt;p&gt;Of 24 patients evaluable for response, six (25%) had partial responses and eight (33%) had stable disease. The remaining 10 patients had progressive disease. Response duration ranged from 14 to beyond 44 weeks. Time to progression did not differ between the treatment arms.&lt;/p&gt;
&lt;p&gt;A randomized phase II study of MK-0646 has already begun, said Javle. Patients receive one of three treatment regimens: gemcitabine plus the monoclonal antibody, with or without erlotinib, or control therapy with gemcitabine and erlotinib.&lt;/p&gt;
&lt;p&gt;The activity demonstrated in the study does not constitute an antitumor signal for MK-0646, Philip A. Philip, MD, of the Karmanos Cancer Center in Detroit, said during a formal discussion of the study.&lt;/p&gt;
&lt;p&gt;&quot;Further preclinical and clinical validation of and IGF-1 receptor-based multitargeted strategy in pancreatic cancer must be undertaken,&quot; he said. &quot;Additionally, predictive biomarkers must be developed for patient selection and stratification. We need more data before we begin to design a phase III study.&quot;&lt;/p&gt;
&lt;p&gt;Hyperglycemia with MK-0646 should not come as a surprise, Philip said. The IGF-1 receptor occurring on normal cells has 84% homology with insulin receptor.&lt;/p&gt;
&lt;p&gt;&quot;There will be overlap between IGF-1 receptor and insulin receptor when targeting IGF-1 receptor,&quot; said Philip. &quot;Moreover, up to 40% of patients with pancreatic cancer have diabetes mellitus.&quot;&lt;/p&gt;
&lt;p&gt;In an ongoing intergroup trial involving a different IGF-1 receptor inhibitor, almost half the patients developed grade 1 or 2 hyperglycemia, and 14% developed grade 3 or 4, he added. However, hyperglycemia does not appear to be a dose-limiting toxicity.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by Merck.&lt;/p&gt;&lt;p&gt;One or more investigators in the study disclosed relationships with Merck.&lt;/p&gt;&lt;p&gt;Philip disclosed relationships with Bristol-Myers Squibb, ImClone, OSIP, sanofi-aventis, Genentech, Pfizer, Lilly, and Roche.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>