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J.W. Neal



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    O03 - NSCLC - Targeted Therapies I (ID 113)

    • Event: WCLC 2013
    • Type: Oral Abstract Session
    • Track: Medical Oncology
    • Presentations: 1
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      O03.06 - First-In-Human Evaluation of CO-1686, an Irreversible, Highly, Selective Tyrosine Kinase Inhibitor of Mutations of EGFR (Activating and T790M) (ID 1354)

      11:25 - 11:35  |  Author(s): J.W. Neal

      • Abstract
      • Presentation
      • Slides

      Background
      Efficacy of existing EGFR tyrosine kinase inhibitors (TKIs) in NSCLC is limited by emergence of the T790M mutation in approximately 60% of patients, and significant skin rash and diarrhea, caused by wild-type (WT)-EGFR inhibition. CO-1686 is an oral, covalent TKI that targets common activating EGFR mutations and T790M, while sparing WT-EGFR. Animal models suggest greatest efficacy when plasma concentrations exceed 200ng/ml for >16hrs/day.

      Methods
      This is an ongoing first-in-human dose finding study (3+3) of oral CO-1686 administered continuously in 21-day cycles. To be eligible, patients must have EGFR-mutant NSCLC and prior therapy with an EGFR TKI. All patients must undergo tumor tissue biopsy within 28 days before study drug dosing for central EGFR genotyping. Endpoints include safety, pharmacokinetics (PK), and efficacy.

      Results
      As of 12 June 2013, 45 patients have been treated with CO-1686. 31/42 (74%) were T790M+; data for three patients is pending. The median age is 58 years, 82% are female, 75% are white, and 73% ECOG 1. The median number of previous therapies was 4 (range: 1- 6), with a median of 1 (range: 1- 4) previous EGFR TKI therapies. Dosing started at 150mg QD and escalated to 900mg QD, 900mg BID and 400mg TID, with a maximum tolerated dose not yet reached. Treatment-related AEs (all grades) occurring in > 5% patients were: fatigue (19%), diarrhea (15%), nausea (14%), anemia (10%), arthralgia (7%), muscle spasms (10%), myalgia (7%), headache (7%). The majority of events were mild or moderate. Unlike other EGFR inhibitors, rash and diarrhea were not commonly seen. This AE profile is consistent with the expected lack of wild type EGFR inhibition with CO-1686. The PFS for T790M+ patients with CO-1686 plasma concentrations > 200ng/mL for > 16 hours was 194 days compared with 72.5 days for those that achieved these concentrations for < 16 hours (Figure 1). At the highest evaluated dose, 900mg BID, four T790M+ patients were evaluable for response; 3 of the 4 achieved PRs, one achieved SD. One patient at a lower dose cohort also achieved a PR. Further safety and efficacy data will be presented at the meeting. Figure 1

      Conclusion
      CO-1686 has demonstrated good tolerability and efficacy against proven T790M+ EGFR mutant NSCLC with a strong suggestion of a dose-response relationship. Additional evaluation of the optimal dose and formulation of CO-1686 are underway to further explore its potential for improved activity and better tolerability over other existing EGFR TKIs.

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    O18 - Cancer Control and Epidemiology II (ID 133)

    • Event: WCLC 2013
    • Type: Oral Abstract Session
    • Track: Prevention & Epidemiology
    • Presentations: 1
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      O18.06 - Vietnamese non-small cell lung cancer patients in California: molecular profiles and clinical characteristics (ID 1079)

      11:25 - 11:35  |  Author(s): J.W. Neal

      • Abstract
      • Presentation
      • Slides

      Background
      Lung cancer is the leading cause of cancer-related deaths worldwide with 1.3 million deaths per year. Discoveries of oncogenic mutations in non-small cell lung cancer (NSCLC) over the past decade have led to targeted therapies against epidermal growth factor receptor (EGFR) activating mutations, anaplastic lymphoma kinase (ALK) gene rearrangement, and repressor of silencing 1 (ROS1) gene rearrangement. The frequencies of these mutations and gene rearrangements have been elucidated in the Western and East Asian populations. However, the frequencies of these oncogenic alterations remain unknown in Vietnam, where lung cancer is one of the leading causes of cancer mortalities but molecular testing is not routinely performed due to limited resources. In this project, we aimed to analyze the Vietnamese patients treated at Stanford, California, with a future plan to compare with another cohort inside Vietnam.

      Methods
      We collected molecular and clinical variables of NSCLC patients of Vietnamese origin, based on patients' self-reported ethnicity, language, or country of origin, treated at Stanford from 2009 to 2012. Comparison of the molecular and clinical characteristics of never smokers versus smokers was performed with Pearson's chi-squared test for nominal variables and Student's t test for continuous variables. Survival analyses were done using the Kaplan-Meier method and Cox proportional hazards modeling.

      Results
      Forty-six patients of Vietnamese origin were seen at the Stanford thoracic oncology clinic from 2009 to 2012, including 22 men and 24 women with a mean age of 58 years. Twenty-seven (58.7%) were never-smokers. Forty-two (91.3%) of the tumors were adenocarcinoma. Ten patients (21.7%) presented at stage I, none at stage II, 8 patients (17.4%) at stage III, 28 patients (60.9%) at stage IV. Fifteen patients out of 28 tested for EGFR (53.6%) had an activating mutation; 14 of these 15 patients were never-smokers. Five patients out of 16 tested for ALK (31.3%) had ALK gene rearrangement. No ROS1 gene rearrangement out of 3 patients tested was found. Only one patient, a former smoker, out of 23 tested (4.4%) was found to have a KRAS mutation. Eighteen out of 27 never-smokers (66.7%) and 3 out of 19 smokers (15.8%) had a targetable driver mutation (EGFR, ALK, or ROS1). For all stages, the median overall survival (OS) for never-smokers was 22.3 months (95% confidence interval (CI); 11.9 months, 24.3 months) compared to 12.9 months (95% CI; 5.8 months, 20.0 months) for smokers. For only stage IV, the median OS for never-smokers was 21.2 months (95% CI; 13.0 months, 24.3 months) compared to 11.6 months (95% CI; 1.4 months, 30.9 months) for smokers.

      Conclusion
      Approximately two-thirds of never-smoker patients of Vietnamese origin had NSCLC with a targetable driver mutation. OS differ markedly by smoking status. The high percentage of Vietnamese patients in California with driver mutations warrants further studies to evaluate the frequencies of NSCLC driver mutations inside Vietnam, strongly suggesting that nationwide implementation of routine molecular testing will have a positive impact on clinical management of Vietnamese patients with NSCLC.

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    P1.24 - Poster Session 1 - Clinical Care (ID 146)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Supportive Care
    • Presentations: 1
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      P1.24-048 - Stage 1 results of a 2-stage phase II trial of single agent amrubicin in patients with previously treated thymic malignancies (ID 3175)

      09:30 - 09:30  |  Author(s): J.W. Neal

      • Abstract

      Background
      There are limited treatment options for patient with advanced thymic malignancies and the utility of many of the available chemotherapies is restricted by cumulative toxicity such as neuropathy (taxanes) and cardiomyopathy (anthracyclines). We designed this study to look at single agent amrubicin, a third generation anthracycline and topoisomerase II inhibitor with minimal cardiac toxicity, in patients with advanced thymic malignancies.

      Methods
      Eligible patients have confirmed thymic malignancy (thymoma (T) or thymic carcinoma (TC)) with progression or relapse after at least 1 prior chemotherapeutic regimen, and adequate organ function including left ventricular ejection fraction (LVEF) of >50%. The initial treatment plan consisted of amrubicin at 40 mg/m[2] IV days 1-3 repeated in 3-week cycles. The study is a Simon 2-stage design based on a null hypothesis of a true response rate <5%, with 90% power to detect a 20% true response rate and a plan to accrue 12 evaluable patients in stage 1, then if at least 1 response is seen, to add 25 additional evaluable patients in stage 2 for a total of 39 patients.

      Results
      Enrollment was initiated in July 2011. Here, we report on the first 12 patients, all enrolled at Stanford University over a 19-month period. Of the first 12 patients enrolled, 11 were dosed. All were pre-treated (5 with prior anthracycline). There were 5 women and 7 men; age range of 30-67 years old; 6 were of Asian ethnicity, 5 were non-Hispanic White and 1 was Hispanic. After enrollment of the first 8 patients, of whom 3 were hospitalized with febrile neutropenia (FN) (38%), the study was amended to a starting dose of 35 mg/m[2] days 1-3 repeated in 3-week cycles. Other than FN in the 3 patients mentioned above, G4 thrombocytopenia in 1 patient, and treatment-related G3 fatigue in 2 patients, other toxicities were generally mild and well tolerated. No significant changes in LVEF have been noted on serial echocardiograms. Of the 11 treated patients, there were 3 partial responses (2 T and 1 TC), 7 with stable disease for at least 4 cycles, and 1 with progressive disease (PD) after 2 cycles (TC). Of the 11 treated patients, only 1 patient, with PD after C2, has stopped before completing 6 cycles, and 5 to date have tolerated >10 cycles (with others still on treatment who may receive >10 cycles), with 15 cycles as the highest number to date.

      Conclusion
      Amrubicin, at 35 mg/m[2] IV days 1-3 on a 3-week cycle, shows promise as a single agent in pre-treated patients with thymoma and thymic carcinoma with a 27% RR in the first 11 treated patients. This exceeded the threshold for proceeding to step 2 and the study will now continue to a total of 39 patients and has expanded to other sites including Indiana University.

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    P2.15 - Poster Session 2 - Thymoma (ID 191)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Thymoma & Other Thoracic Malignancies
    • Presentations: 1
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      P2.15-003 - Gli1, Notch1 and CTNNB1 Expression by Automated Quantitative Immunofluorescence (AQUA) in a Thymic Malignancy Tissue Microarray (TMA) (ID 778)

      09:30 - 09:30  |  Author(s): J.W. Neal

      • Abstract

      Background
      Thymoma is a rare malignancy, with a paucity of data on its biology and on the role of targeted therapeutics. Wnt, notch and sonic hedgehog pathway interactions between thymocytes and thymic stroma are important to both thymus and T-cell development. AQUAnalysis[®] is a digital image analysis software that continuously measures multiplexed protein expression and has the potential to overcome limitations of small sample sizes and tissue heterogeneity in the tumor microenvironment. We analyzed a thymoma TMA for gli1, notch1 and CTNNB1 (β-Catenin) expression by AQUA[®] as surrogate markers of activity of the sonic hedgehog, notch and wnt pathways, respectively. We hypothesized this preclinical screen may provide rationale for attacking these pathways with targeted therapeutics in thymoma.

      Methods
      A TMA was constructed from 68 patients with thymic malignancies and 8 benign thymic controls at Stanford University School of Medicine (Stanford, CA). Gli1, notch1 and CTNNB1 expression were assayed using quantitative fluorescent immunohistochemistry at the Tom Baker Cancer Center (Alberta, Canada). The TMA was stained with anti-gli1 rabbit mAb (monoclonal antibody), clone EPR4523 (Epitomics, Burlingame, CA, USA); anti-Notch1 rabbit mAb, clone EP1238Y (Epitomics, Burlingame, CA, USA); and anti-beta-catenin mouse mAb, clone β-Catenin-1 (Dako Mississauga, ON, Canada) using a Dako autostainer. To isolate expression of these stem-cell pathway proteins separately in the tumor and the lymphocytes, the TMA was also stained with anti-pan-cytokeratin guinea pig mAb (Acris, San Diego, CA, USA); anti-vimentin rat mAb, clone 280618 (R&D Systems, Minneapolis, MN, USA); and anti-CD45 rabbit mAb, clone EP322Y (Epitomics, Burlingame, CA, USA). Automated image acquisition was performed using an Aperio Scanscope FL (Aperio Inc., Vista, CA, USA). Images were then analyzed using the AQUAnalysis® program, version 2.3.4.1. A tumor-specific mask and a tumor cytoplasmic mask were generated to distinguish thymoma cells from surrounding stromal tissue by thresholding the pan-cytokeratin images to identify pan-cytokeratin positive cells as tumor cells and define the tumor cytoplasm. Statistical analysis was performed using SAS Enterprise Guide v5.0 (Cary, NC). Two-tailed t-tests were used to compare the differences between thymic tumor and benign control tissue. ANOVA and Dunnett’s t-test was used to compare differences in gli1, notch1, and CTNNB1 expression by WHO histology.

      Results
      Demographics for 68 patients: M:F (53%/47%), Mean age at diagnosis: 55 years, WHO Histology: A (10%), B (57%), AB (24%), C (4%), unclassified (4%), Pathologic Masaoka Stage: I (46%), IIa (18%), IIb (4%), III (18%), IVa (9%) IVb (6%). No difference in gli1 (mean 201 vs. 211, p=0.31), CTNNB1 (mean 396 vs. 418, p=0.66) or notch1 expression (mean 317 vs. 325, p=0.82) was noted between thymic tumors and controls. In a subset analysis, we found no significant differences by WHO histology compared to controls.

      Conclusion
      AQUA® was used to help overcome limitations of analyzing protein expression in histologically heterogeneous thymic tumors with small sample sizes. We found no clinically or statistically significant increased expression of gli1, notch1, and CTNNB1 in thymoma compared to benign thymic tissue. Thus, this study provides no evidence for upregulation of the sonic hedgehog, notch or wnt pathways in thymic tumors.

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    P3.01 - Poster Session 3 - Cancer Biology (ID 147)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Biology
    • Presentations: 1
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      P3.01-007 - Energy metabolism in lung adenocarcinoma (ID 2557)

      09:30 - 09:30  |  Author(s): J.W. Neal

      • Abstract

      Background
      Cancer cells have defects in regulatory circuits governing proliferation and homeostasis. Consequently, cell metabolism is altered to meet the demand for accelerated, deregulated growth. Metabolic perturbations arising from malignant transformation have not been well characterized in human lung cancers in situ. The most well known metabolic derangement(s) in tumors is that of enhanced glycolysis and a decrease in mitochondrial oxidative phosphorylation. We wanted to characterize this phenomenon more accurately in human lung adenocarcinomas by metabolomic profiling.

      Methods
      We performed metabolomic analysis of matched pairs of solid, non-small cell lung adenocarcinomas and normal lung tissue from 25 surgically resected patients. Metabolites were extracted by a methanol-chloroform-water technique. The resulting extracts were divided into multiple fractions. Ultrahigh performance liquid chromatography/ mass spectrometry coupled with tandem mass spectrometry and gas chromatography/ mass spectrometry experiments were conducted. Agilent MassHunter Qualitative software was utilized. The Molecular Feature Extractor was utilized to find features in raw data files. Extracted peaks were retention time aligned using Mass Profiler Professional and unique features detected by least squares analysis. The Agilent version of the Metlin database was utilized to identify metabolites. Matched pairs t-test identified biochemicals significantly altered between tumor and normal specimens. The false discovery rate method assessed for significance; p-value ≤ 0.05 and q-value < 0.10.

      Results
      Based on known library standards to identify biochemicals, our global metabolomic profiling found 204 overexpressed and 42 underexpressed metabolites in tumors relative to normal lung (p< 0.05). We observed altered metabolite levels in lung tumors that mapped to not one, but two glucose utilization pathways. Glucose-6-P (2.7-fold), fructose-6-P (2.6-fold), fructose-1,6-bisP (6.9-fold), lactate (2.7-fold), and NAD[+] (1.4-fold) were significantly upregulated in tumors consistent with an aerobic glycolysis (i.e. Warburg) biosignature, the major source of ATP. Concurrently, pentose phosphate pathway (PPP) metabolites were upregulated in tumors: ribulose-5-P (2.6-fold), ribulose (3.6-fold), ribitol (4.6-fold), ribose (4-fold), and sedoheptulose-7-P (3-fold). Our data reveals evidence of multiple active pathways to explain glucose utilization in lung adenocarcinomas. The PPP is important to protect against oxidative stress as it serves to generate NADPH, and is a key anabolic pathway of nucleotide synthesis by generating the ribose-5-P backbone for proliferating cells. Observing both pathways simultaneously in lung adenocarcinomas suggests they are coupled to give tumors a growth advantage over normal tissue. Consistent with this, we observed an overall increasing nucleotide biosynthesis signature in tumors: multiple metabolites (range 2 to 17-fold) in purine and pyrimidine pathways were significantly elevated.

      Conclusion
      Metabolomic analysis identified a unique glucose energetic biosignature in lung tumors that is more complex that just a single process/ pathway. Our results suggest a specific strategy to target lung adenocarcinomas by exploiting their high glucose uptake.

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    P3.06 - Poster Session 3 - Prognostic and Predictive Biomarkers (ID 178)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Biology
    • Presentations: 1
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      P3.06-003 - Correlative Analysis of Circulating Biomarkers from a Phase 1b/2 trial of Cabozantinib (C) with or without Erlotinib (E) in Patients (Pts) with Advanced or Metastatic Non-Small Cell Lung Cancer (NSCLC) (ID 266)

      09:30 - 09:30  |  Author(s): J.W. Neal

      • Abstract

      Background
      Cabozantinib (C) is a potent ATP-competitive inhibitor of MET and vascular endothelial growth factor receptor 2 (VEGFR2) along with KIT, RET, AXL, TIE2, and FLT3. Hepatocyte growth factor (HGF), the ligand of MET, and VEGF act synergistically to promote angiogenesis. There are currently no widely accepted prognostic or predictive biomarkers for anti-angiogenic agents.

      Methods
      This is a retrospective correlative biomarker study from the phase 1b/2 trial of C+/-E in stage IIIB-IV NSCLC. All pts had to fail prior therapy with E. Both drugs are oral and dosed daily. C dosing is in the free-base equivalent weight. In phase I, there was a 2 week lead in with E and the cohorts included: 1A (60 mg C+150 mg E), 2A (60 mg C+100 mg E), 3A (100 mg C+100 mg E), 4A (100 mg C+50 mg E), and 2B (40 mg C+150 mg E). In phase II, both drugs started simultaneously: Arm A (100 mg C) and Arm B (100 mg C+50 mg E). Pts were included in the study if a pre-E+C and post-C > day 29 plasma sample was available. The Milliplex 13-plex and Luminex 51-plex assays were used. For this preliminary analysis, select markers previously implicated in angiogenesis (bFGF, VEGF, sVEGFR1-3, IL-6, IL-8, IL-12, IL-17, PDGF-BB, ICAM-1, VCAM-1) and those of interest (ligands of KIT and MET- SCF and HGF, respectively) were analyzed. Log transformed mean fluorescence intensity (MFI) values and Wilcoxon Rank paired sum tests were used to detect changes from day 1-29. A change from baseline was noted to be significant if at least 15% (median) with α<0.05 (2-sided) and a trend if 10-15% (median) with α<0.08 (2-sided).

      Results
      73 pts included: 52 phase I and 21 phase II; median age 60 years; 23M/50F; 56.2% nonsmoker; 91.8% adenocarcinomas. The pts with samples from both time points were divided into two groups due to limited sample size and included: Group R (complete/partial response and stable disease> 6 months; n=22) and Group NR (stable disease< 6 months and progressive disease; n=51). The only marker that changed in a single direction in all subjects within a group was sVEGFR2 in group R. Overall, significant decreases were noted in sVEGFR1-3, IL-6, PDGF-BB, and trended in IL12p70 and IL-17. By subgroups: Group R had significant decreases in bFGF, VEGF, sVEGFR1-3, IL-6, IL-8, IL-12(p40+p70), IL-17, PDGF-BB, SCF, and trended in HGF (median 10.1% ↓, p=0.0275); and Group NR had significant decreases in sVEGFR2-3, IL-6, PDGF-BB, and trended in sVEGFR-1, IL-6, and IL-17.

      Conclusion
      Both groups R+NR had a decrease in sVEGFR-2, suggesting that this is a marker of treatment with C rather than a marker of response. However, overall group R had larger dynamic decreases of immune markers than group NR. HGF, which is targeted downstream by C and plays a role in angiogenesis and E resistance, had a trend to decrease in group R but not group NR. This study is retrospective with a small sample size, imbalanced numbers per response subgroup, and is exploratory in nature.

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    P3.11 - Poster Session 3 - NSCLC Novel Therapies (ID 211)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Medical Oncology
    • Presentations: 1
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      P3.11-006 - Erlotinib (E) and Dovitinib (TKI258) (D) in Patients (pts) with Metastatic Non-Small Cell Lung Cancer (NSCLC): A Significant Pharmacokinetic (PK) Interaction (ID 878)

      09:30 - 09:30  |  Author(s): J.W. Neal

      • Abstract

      Background
      Dovitinib (TKI 258) is an oral antiangiogenic agent that targets PDGFR, KIT, FLT3, VEGF, RET, and FGFR. Dovitinib induces CYP1A1/A2, CYP2C19, CYP2C9, and it inhibits CYP3A4. Dovitinib is metabolized mainly by FMO, CYP3A4, and CYP1A1/A2. Erlotinib is metabolized mostly by CYP3A4 (70%) but also by CYP3A5, CYP1A1, and CYP1A2.

      Methods
      This is a phase I 3+3 trial of E+D in patients with EGFR wild-type or mutated metastatic NSCLC who could have previously received E. Four cohorts were planned with E given daily and D given 5 days on/2 days off, starting after a 2-week lead-in of E alone. Only two cohorts enrolled due to dose limiting toxicity (DLT): cohort 1 [150 mg E +300 mg D] and cohort -1 [150 mg E+200 mg D]. Plasma concentrations of E and its metabolite OSI-420 were measured on day 14+/-4 (E alone; pre-dose, 2, 4, 6, 8, and 24 hours) and day 29 +/- 4 (D+E, at same time points). Pharmacokinetic (PK) samples were analyzed by a validated liquid chromatography-tandem mass spectrometry assay. PK parameters for E and OSI-420 were estimated from the plasma concentration data via noncompartmental analysis. Paired-t tests on log transformed PK parameters were used to detect a statistical difference (α < 0.05, 2-sided) between E alone versus E+D treatment days.

      Results
      Nine patients enrolled (3 in cohort 1 and 6 in cohort (-1)). The study was suspended due to excess of DLTs. Best response was evaluable in seven patients. Two unevaluable patients on follow-up scan were on E monotherapy for ~1 month. Four patients discontinued due to grade 3 AEs (syncope (n=1), fatigue (n=1), and pulmonary embolism (n=2)). Three patients had progressive disease and 4 had stable disease (duration: 6 cycles(C), 8 C, and 1-2 C for two patients who stopped due to AE). Two patients required a dose delay in D (one for grade 2 LFT elevation, the other for grade 3 fatigue) and one required dose reduction of E to 100 mg prior to initiation of D (dose-corrected for PK analysis). Six patients had data available for PK analysis. During E alone, erlotinib exposure (average C~max~ 2308 +/- 697 ng/ml and AUC~ 0-24 ~41.0 +/- 15.6 μg*h/ml) was similar to previous reports for multiple daily doses of 150 mg. During D co-administration, the concentrations of E were reduced. C~max~ on average decreased by 83% (p= 0.022) and AUC~0-24 ~by 94% (p= 0.0039). OSI-420 exposure was also reduced during D co-administration.

      Conclusion
      Our small study demonstrates a potential significant PK interaction with decrease of E and its metabolite in the presence of D. This decrease is higher than that reported in combination studies with other CYP1A1 or CYP3A4 inducers. Dovitinib PK data is pending. Given the toxicity and the potential PK interaction, further investigation with this drug combination will be challenging.

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    P3.24 - Poster Session 3 - Supportive Care (ID 160)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Supportive Care
    • Presentations: 1
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      P3.24-049 - Palliative Care and Anti-Cancer Care Integration: Description of three models of care delivery at a tertiary medical center (ID 3182)

      09:30 - 09:30  |  Author(s): J.W. Neal

      • Abstract

      Background
      The American Society of Clinical Oncology issued a Provisional Clinical Opinion on the integration of palliative care (PC) with anti-cancer care which states, “Based upon strong evidence from a phase III RCT, patients with metastatic non-small-cell lung cancer should be offered concurrent palliative care and standard oncologic care at time of initial diagnosis.” There is both a national shortage of PC providers, as well as a lack of guidelines on the best operational ways to integrate PC into oncologic care. Here we describe different models of palliative care integration into anti-cancer care models performed at the Stanford Cancer Institute.

      Methods
      Three methods of PC integration into oncology care at Stanford Hospital and Clinics, a tertiary medical center, are being tested. These include a low resource model using a social work (SW) only intervention for advance care planning and goals of care, as well as two high resource models using an MD, advance nurse practitioner, and social worker. The first high resource model is concurrent care with joint PC and oncology visits, and the second is a traditional model of separate PC and oncology visits. Observations around successes and barriers within these various models, as well as resources needed, will be described. Data evaluated include volume, referral patterns, advance care planning, symptom assessment, and resource utilization.

      Results
      The SW only intervention was run as a pilot in thoracic oncology. Resources required for appropriate implementation included information technology (IT) for appropriate cohort identification, operations support, data management support, and team cooperation from the physician and nursing team. Process outcomes measured included % of patients seen by SW within 3 visits, documentation of advance care planning within the medical record, and co-signature of advance care planning documentation by the physician. The joint visit model utilized a high resource team (physician, nurse practitioner, and social worker) which was present concurrently with the oncology visit for advance care planning and symptom management. In addition to the resources required for the SW only intervention, this model also included a care coordinator for visit coordination. Process outcomes measured included lead time to arrange for the joint visit and documentation of advance care planning. End outcomes included discharge to hospice, hospital utilization patterns, and effective symptom management. Other outcomes included volume and number of referring providers. Our third model was a traditional clinic visit with the PC team only, not coordinated with the oncology team. Resources and outcomes were the same as for the joint visit model. A total of 529 consults were seen in the first year. 61% were seen in a traditional clinic model and 39% were seen in the concurrent model. Volume of consults have increased over time. There were 10 consults per month in January of 2012. Currently over 100 consults are seen per month.

      Conclusion
      Appropriate integration of PC into oncology care for thoracic oncology patients is still under investigation. Here we describe the strengths and weaknesses of three separate models of integration of PC with oncology care at an academic medical center.