tbuckley/cabot-search huggingface dataset:
Contents Vol. 74, 2005
Authors: Andreas Michalsen, Paul Grossman, Nils Lehmann, Nicola T.M. Knoblauch, Anna Paul, Susanne Moebus, Thomas Budde, Gustav J. Dobos, Scott B. Patten, Corrado Barbui, Paul M.G. Emmelkamp, Emanuele Caroppo, Urs Hepp, Hanspeter Moergeli, Stefan Büchi, Lutz Wittmann, Ulrich Schnyder, Gopinath Ranjith, Jan Knapen, Peter van de Vliet, Herman van Coppenolle, Ans David, Joseph Peuskens, Guido Pieters, Koen Knapen, Marius Nickel, Cerstin Nickel, Karin Tritt, Claas Lahmann, Peter Leiberich, Moritz Muehlbacher, Christoph Egger, Wolfhardt Rother, Thomas Loew, Anselmo Ruffatti, Lina Minervini, Maria Romano, Nicoletta Sonino, Sanna K. Pallaskorpi, Erkki T. Isometsä, Markus M. Henriksson, Kirsi H. Suominen, Jouko K. Lönnqvist, Paolo Cassano, Claudio N. Soares, Cristina Cusin, Alessandra Mascarini, Lee S. Cohen, Maurizio Fava, Angelo Picardi, Alessandro Toni, Richard Balon
Journal: Psychotherapy and Psychosomatics (2005)
Predictors of accrual success for cooperative group trials: The Cancer and Leukemia Group B (Alliance) experience.
Authors: David Hirsch Gordon, Qianying Liu, Ben Kleinman, Theodore Karrison, Michael Kelly, Gini F. Fleming
Journal: Journal of Clinical Oncology (2013)

TPS6645 Background: Clinical trials that fail to meet accrual waste patient, physician, and institution resources. We explored factors that predict for poor accrual to cooperative group trials in order to improve trial design and target resources to support or increase accrual when needed. Methods: Twenty trial characteristics were collected for Cancer and Leukemia Group B (CALGB) trials that closed between 06/01/02 and 06/01/12. We evaluated accrual in two ways: (1) logistic regression applied to accrual success/failure as a binary outcome; (2) treated the ratio of actual to expected accrual rate as a continuous response and applied linear regression to the square root of the ratio. Results: 110 trials (phase III=27, phase I/II=83) were examined. 89 (80.9 %) met the accrual goal, 21 (19.1%) did not. For trials that met their accrual goal, time to accrual ranged from 0.5 to 8.8 years and was non-normally distributed, with 57% accruing within 3 years and 83% accruing within 5 years. Phase III trials took longer to accrue (univariate p&lt;0.001) but were not less likely to meet accrual goal (p=0.30). Provision of study drug was an important predictor of success in both analyses performed (borderline significant in success/failure analysis); having at least one agent provided by the study was significantly associated with better accrual. Factors not found to affect accrual included: Time from concept approval by CALGB to study activation, research-only biopsies, and estimated rarity of disease being studied. Conclusion: Provision of drug as a predictor of accrual success has not been previously reported, and will need to be confirmed. This factor is likely a surrogate for physician and patient eagerness to have access to a drug not otherwise available.
Phase I study of the safety and efficacy of INC280 in patients with advanced MET-dependent solid tumors.
Authors: Yung-Jue Bang, Wu-Chou Su, Do-Hyun Nam, Wan-Teck Lim, Todd Michael Bauer, Irene Brana, Ronnie Tung-Ping Poon, David S. Hong, Chia-Chi Lin, Bin Peng, Yingxi Zhang, Sylvia Zhao, Arun Kumar, Mikhail Akimov, Brigette Ma
Journal: Journal of Clinical Oncology (2014)

2520^ Background: Aberrations in the MET receptor tyrosine kinase pathway occur in various human malignancies (via MET amplification, mutation, or overexpression) driving cell proliferation, survival and metastasis. INC280 is a highly selective, oral small molecule MET inhibitor with preclinical activity in human tumor models. This dose escalation study evaluated INC280 in patients (pts) with MET dependent advanced solid tumors. Methods: In this Phase (Ph) I study, the primary objective was to determine the MTD or recommended Ph II dose (RP2D), safety and tolerability of INC280; secondary objectives included preliminary antitumor activity and PK. Eligible pts (aged ≥18 years, ECOG PS ≤2) had tumors that were refractory to current therapy or for which no effective therapy exists, and confirmed MET dysregulation (by FISH or IHC). An adaptive Bayesian logistic regression model guided dose escalation in establishing the MTD/RP2D. Results: As of December 2, 2013, 33 pts were enrolled in the dose-escalation part of the study (79% male, median age 57 years, 61% PS 0). The most common tumors were hepatocellular carcinoma (HCC; 45%) and colon cancer (21%). Pts were treated in 6 dose cohorts of 100–600 mg BID. DLTs occurred at 200 mg BID, 250 mg BID and 450 mg BID (1 pt each). DLTs were Gr 3 fatigue (2 pts), and Gr 3 serum bilirubin increased. The most frequent drug-related AEs (any grade [Gr]) were decreased appetite (33%), nausea (30%), vomiting (27%), and fatigue (27%). The most common drug-related Gr 3/4 AEs were fatigue (9%), and decreased appetite (6%). INC280 plasma concentration generally increased with dose; mean steady state AUClast and Cmax following 600 mg BID were 6630 ng/mL and 29800 ng*h/mL, respectively, with a median Tmaxof 1.9 h and a mean apparent terminal half-life 3.1 h. Stable disease was reported in 8/33 (24%) heavily pretreated pts. Paired biopsy data showed near-complete phospho-MET shutdown in a colorectal cancer pt at 450 mg BID. Conclusions: Oral INC280 BID is well tolerated, and the RP2D is 600 mg BID. Dose expansion is ongoing in pts with NSCLC, HCC, and other tumors. These results suggest INC280 should be further evaluated, and Ph II studies in various solid tumors are ongoing. Clinical trial information: NCT01324479.
Differential impact of cisplatin dose intensity on human papillomavirus (HPV)-related (+) and HPV-unrelated (−) locoregionally advanced head and neck squamous cell carcinoma (LAHNSCC).
Authors: Anna Spreafico, Shao Hui Huang, Wei Xu, Roberta Granata, Chen-Shin Liu, John N. Waldron, Eric Chen, Jolie Ringash, Andrew Bayley, Kelvin K. Chan, Andrew J. Hope, Albiruni R. A. Razak, Bayardo Perez-Ordonez, Ilan Weinreb, Paolo Bossi, Ester Orlandi, Lisa F. Licitra, Brian O'Sullivan, Lillian L. Siu, Joon-Hyung J. Kim
Journal: Journal of Clinical Oncology (2015)

6020 Background: Definitive radiotherapy with concurrent cisplatin (CDDP) is a standard treatment for patients (pts) with LAHNSCC. We evaluated the impact of CDDP dose intensity (mg/m2) on overall survival (OS) of HPV+ and HPV- LAHNSCC pts. Methods: Princess Margaret Cancer Centre (PM) and Istituto Nazionale dei Tumori (INT) LAHNSCC cohorts treated from 2000 to 2012 were reviewed. Kaplan-Meier method was used to estimate the 5-year (yr) OS in HPV+ vs HPV− pts. HPV status was determined by p16 staining or in situ hybridization HPV DNA for all oropharyngeal (OPC), unknown primary (UNK), and ≤ 10 pack-year (PY) smoking laryngo-hypopharyngeal cancer (LHC). Untested p16, >10 PY LHC pts were assumed HPV−. Multivariable analysis (MVA) with Cox regression identified OS predictors for HPV+ and HPV− pts. Results: A total of 659 pts (584 PM; 75 INT) were evaluated. Pts characteristics included: median age 58 (range: 27-81); primary site: OPC 73%, LHC 24%, UNK 3%; non-smokers 27%; stage: T4 25%, N2c-N3 60%; HPV+ 404 (61%), HPV− 255 (39%) pts. Median CDDP dose was 200 mg/m2 for both HPV+ and HPV− cohorts. Median follow-up was 4.3 yrs. Five year OS was inferior for HPV− CDDP ≤ 200 vs > 200 mg/m2 (44 vs 62%, p < 0.01), while no difference was detected in HPV+ CDDP ≤ 200 vs > 200 mg/m2 (83 vs 87%, p = 0.30), confirmed by MVA (Table). In N3 or T4 HPV+ pts, a trend on OS in CDDP >200 mg/m2(HR = 0.62, 95% CI: 0.30-1.31) was observed. Conclusions: In this large multicenter cohort study, CDDP dose intensity ≤ 200 mg/m2had a detrimental impact on OS in HPV− LAHNSCC pts. The impact of CDDP dose intensity on HPV+ pts was not significant. These results warrant prospective validation. MVA for OS in HPV+ and HPV– pts. HR (95% CI) & p value CDDP (mg/m2) > 200 vs ≤ 200 Age 1 yr increment Smoking 10 PY increment T HPV+: T4 vs T0-3 HPV–: T3-4 vs T1-2 N HPV+: N2c-3 vs N0-2b HPV–: N2b-3 vs N0-2a Disease Site Non-OPC vs OPC HPV+ 0.8 (0.4-1.4) p = 0.46 0.98 (0.95-1.01) p = 0.25 1.2 (1.02-1.3) p = 0.03 2.5 (1.3-4.5) p < 0.01 2.4 (1.3-4.4) p < 0.01 NA HPV– 0.5 (0.3-0.8) p < 0.01 1.00 (0.98-1.02) p = 0.93 1.1 (0.98-1.2) p = 0.12 1.4 (0.9-2.1) p = 0.13 2.4 (1.5-3.9) p < 0.01 1.2 (0.8-1.8) p = 0.38
Trastuzumab-HER/2 binding induced inhibition of cell growth and HER/2 tyrosine kinase activity
Authors: S. Welt, T. Shay, C. Lanning, K. Horton, D. Kostyal
Journal: Journal of Clinical Oncology (2007)

21146 Background: Cell lines containing the HER/2 amplicon are sensitive to Trastuzumab (T) mediated inhibition of cell growth. T blockade of cell growth signaling pathways have been hypothesized to occur by two mechanisms, inhibition of homo and hetro-dimerization of HER/2 with members of the EGFr family and inhibition of HER/2 phosphorylation. Methods: BT 474 and SK-BR3 breast cancer cell lines containing the HER/2 amplicon were cultured under condition demonstrating inhibitory effects of T by MTT and 3 H-Thymidine incorporation (0.25–50 micrograms/ml for up to 9 days). RNA extracts from treated and un-treated cells were analyzed and compared using two immunoassays for phosphorylated HER/2. Various growth conditions were assessed for T inhibition of phosphorylation including, serum free media, fetal calf serum, human pre and post menopausal serum, breast cancer patient's serum and normal male serum. Results: Breast cancer cell lines BT 474 and SK-BR3 both demonstrated cell growth inhibition when cultured with T over a wide range of concentrations down to 0.25 microgram/ml. The inhibitory effects on SK-BR3 were low but statistically significant in both MTT and 3 H-Thymidine incorporation assays. Examining this same concentration range of T on these cell lines demonstrated no appreciable reduction of phosphorylation by western blot analysis at various time points after exposure to T. Two different immune assays for HER/2 phosphorylation were analyzed. Further examination of replacement of fetal calf serum by human female pre and post menopausal serum samples or similar samples from breast cancer patients did not result in reduction of the phosphorylation signal. Conclusions: In this in vitro model T does not mediate effects through HER/2 tyrosine kinase inhibition under conditions that simulate clinical conditions. Whether inhibition of phosphorylation will be apparent at later time points is unknown. These finding may explain the activity of lapatinib, a HER/2 tyrosine kinase inhibitor, on T resistant breast cancer. No significant financial relationships to disclose.
Activation of the BMP-BMPR pathway conferred resistance to EGFR-TKIs in lung squamous cell carcinomas patients with EGFR mutations.
Authors: Jie Wang, Zhijie Wang, Zhenxiang Li, Zhirong Shen, Shuai Fu, Zhentao Liu, Liang Cheng, Hua Bai, Jianchun Duan, Jun Zhao, Shuhang Wang, Minglei Zhuo
Journal: Journal of Clinical Oncology (2015)

e19077 Background: The criterion for defining clinical subtype of lung cancer is gradually transiting from histopathology to genetic variations in driver genes. Targeting these driver mutations such as sensitizing EGFR mutations has dramatically improved the prognosis of advanced non-small lung cancer (NSCLC), however the therapeutic benefit of this regimen on NSCLC seemed to be different between lung adenocarcinomas and squamous cell carcinomas (SqCC). Methods: Two cohorts of SqCC patients with or without EGFR mutations and cell lines are used for this study. The methods included gene aberrance detection, IHC, ICC, cell viability test, western-blot analysis, soft agar foci formation, RNA sequencing analysis, protein chip and subcutaneous in vivo experiments. Results: Report here that lung SqCC harboring EGFR mutations show resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) was correlated with the activation of BMP-BMPR-Smad1/5-p70S6K. The combinational treatment of these tumor cells with EGFR-TKI together with the inhibitors specific to BMPR or downstream mTOR effectively reversed the resistance to EGFR-TKI. Moreover, blocking the whole pathway of PI3K-AKT-mTOR with PI3K/mTOR dual inhibitor BEZ235 also showed efficacy toward this subtype of lung SqCC in animal models. Conclusions: This study details the scientific basis for a feasible clinical solution for squamous cell carcinomas with EGFR mutations.
Real-life 2-year therapeutic strategies in the management of 2003 metastatic non-small-cell lung cancers (NSCLCs) in French general hospital.
Authors: Didier Debieuvre, Francois Goupil, Bertrand Lemaire, Dominique Herman, Lionel Falchero, Patrick-Aldo Renault, Antoine Levy, Patrick Dumont, Nadine Paillot, Philippe Masson, Jean-Renaud Barriere, Yannick Duval, Bernard Asselain, Francois Blanchon, Francis Martin, Michel Grivaux
Journal: Journal of Clinical Oncology (2015)

e19110 Background: In the last few years, new drugs and strategies have emerged in the management of lung cancer (LC). ESCAP-2011-CPHG, promoted by the French College of General Hospital Respiratory Physicians, is an ancillary study of KBP-2010-CPHG, a prospective multicenter epidemiological study aiming to describe the characteristics and survival of patients with LC diagnosed in 2010 and managed in French general hospital chest departments. The aim of the study is to describe therapeutic strategies in LC during the first 2-year after diagnosis. Methods: For each patient, a standardized form was completed following each change in treatment strategy, up to 2 years after diagnosis. Results: 53 of the 104 centers (7051 patients) participating in KBP-2010-CPHG agreed to participate in ESCAP-2011-CPHG, which corresponded to 3943 patients, including 2003 patients with metastatic NSCLC. There was no significant difference in baseline characteristics between KBP-2010-CPHG and ESCAP-2011-CPHG patients. In patients with metastatic NSCLC, the 1st therapeutic strategies were chemotherapy alone (56%) and palliative chemotherapy plus incidental radiotherapy (35%); 4% of patients died without any implemented therapeutic strategy. 29% of patients with chemotherapy alone died without undergoing any other strategy, 70% had a 2nd strategy (72% chemotherapy alone). 35% of patients with radiochemotherapy died without undergoing any other strategy, 64% had a 2nd strategy (73%chemotherapy alone). The most frequent chemotherapy during strategy 1 was platinum salts doublet with pemetrexed (39%), followed by platinum salts doublet with paclitaxel (15%). Chemotherapy during strategy 2 was 2nd line chemotherapy (67%) or maintenance therapy (25%). EGFR-TKi (34%) and docetaxel (26%) alone were the most frequently prescribed drugs for 2nd line chemotherapy, and pemetrexed (44%) and EGFR-TKi (26%) alone for maintenance therapy. Conclusions: These findings are preliminary and need to be further analyzed per type of patient or histology.
Use of early 18f-fluorodeoxyglucose-positron emission tomography to predict clinical outcome of patients with advanced non-small cell lung cancer on gefitinib treatment versus carboplatin plus paclitaxel.
Authors: Masaki Kanazu, Kaoru Maruyama, Masahiko Ando, Kazuhiro Asami, Mari Ishii, Shojiro Minomo, Yoshinobu Matsuda, Tomoya Kawaguchi, Shinji Atagi, Yoko Kusunoki, Akihito Kubo, Minoru Takada
Journal: Journal of Clinical Oncology (2012)

10577 Background: Early prediction of clinical efficacy is of great value in cancer patients in avoiding unnecessary toxicities and giving them another chance for different treatments. This study aimed to assess the 18 F-fluorodeoxyglucose-positron emission tomography (FDG-PET) at 3 days on treatment as an early predictor of clinical outcome in patients with advanced non-small cell lung cancer (NSCLC) treated with gefitinib and in those treated with cytotoxic chemotherapy. Methods: This study comprised two groups: patients with stage IIIB or IV NSCLC were treated with gefitinib (250mg) once daily (gefitinib group) or with carboplatin (AUC 6, day 1) plus paclitaxel (200mg/m 2 , day 1) q21 days (CP group) according to the physicians’ choice. FDG-PET was performed before, 3 days on and 28 days on each treatment. Reduction of tumor FDG uptake was assessed by using standardized uptake value (SUV). Metabolic response was defined as reduction of FDG uptake in the tumor ≥ 25% according to the criteria of the European Organization for Research and Treatment of Cancer. Metabolic response was correlated with clinical outcomes. Results: This study included 38 patients: 19 in gefitinib group and 19 in CP group. Reduction of SUV at 3days on treatment preceded tumor shrinkage more closely in gefitinib group. Metabolic response was significantly correlated with longer progression-free survival (PFS) in gefitinib cohort (median PFS 15.8 months [95% CI 13.2-18.4] vs. 3.7 months [95% CI 0.1-8.0], p &lt; 0.001), but not in CP group (median PFS 5.7 months vs. 2.9 months, p = 0.054). Furthermore, metabolic response was significantly correlated with longer overall survival (OS) in gefitinib group (median OS 28.7 months [95%CI 23.5-33.9] vs. 9.8 months [95% CI 2.1-17.5], p = 0.009), but not in CP group (median OS 13.9 months vs. 10.5 months, p = 0.56). In multivariate analysis using Cox hazards models, metabolic response was a significant predictive factor of PFS and OS. Conclusions: Reduction of SUV levels on FDG-PET at 3 days on treatment may predict response and survival in gefitinib-treated patients with advanced NSCLC.
Long-term results of GORTEC 2000-01: A multicentric randomized phase III trial of induction chemotherapy with cisplatin plus 5-fluorouracil, with or without docetaxel, for larynx preservation.
Authors: Guillaume Janoray, Yoann Pointreau, Pascal Garaud, Sophie Chapet, Marc Alfonsi, Christian Sire, Claude Tuchais, Gilles Calais
Journal: Journal of Clinical Oncology (2015)

6002 Background: To compare the long-term efficacy and safety of induction chemotherapy with cisplatin (P) and 5-fluorouracil (F) with or without docetaxel (T) for larynx preservation. Methods: Operable patients with untreated stage-III or -IV larynx or hypopharynx invasive squamous-cell carcinoma and who required a total laryngectomy were randomly assigned to receive three cycles of induction chemotherapy with either TPF or PF, followed by radiation therapy for responders. The primary endpoint was 3-year larynx-preservation rate. Secondary endpoints included larynx dysfunction-free survival (LDFFS), overall survival, disease-free survival, locoregional control rate, cause of death, and later toxicity rates. Results: Two hundred and thirteen patients were treated with a median follow-up for surviving patients of 105 months. The 5- and 10-year larynx preservation rates were, 74.0% (95%CI, 0.64–0.82) vs. 58.1% (95%CI, 0.47–0.68) and 70.3% (95%CI, 0.58–0.8) vs. 46.5% (95%CI, 0.31–0.63, p = 0.01) in TPF versus PF arm, respectively. The 5- and 10-year LDFFS rates were 67.2% (95%CI, 0.57–0.76) vs. 46.5% (95%CI, 0.36–0.57) and 63.7% (95%CI, 0.52–0.74) vs. 37.2% (95%CI, 0.24–0.52, p = 0.001), respectively. Overall survival, disease-free survival, and locoregional control rates were not statistically improved in the TPF vs. the PF arm. Significantly fewer grade 3–4 late toxicities of the larynx occurred with the TPF regimen compared to the PF arm (9.3% vs. 17.1%, g-test, p = 0.038). Conclusions: Long-term follow-up confirms that induction chemotherapy with TPF increased larynx-preservation and larynx dysfunction-free survival. In this larynx preservation approach using induction chemotherapy, TPF should be recommended, followed by radiation therapy. Clinical trial information: NCT00169182.
Weekly ixabepilone with or without concurrent bevacizumab in the treatment of recurrent endometrial cancer.
Authors: Dana Marie Roque, Elena Ratner, Dan-Arin Silasi, Masoud Azodi, Peter E. Schwartz, Thomas J. Rutherford, Alessandro Santin
Journal: Journal of Clinical Oncology (2012)

e15526 Background: Ixabepilone for endometrial cancer has only been evaluated in phase II studies administered at 30-40 mg/m 2 q21 days (GOG 129P, GOG 86P). The objective of this study is to describe the institutional experience using a weekly dosing strategy of ixabepilone ± bevacizumab in the treatment of paclitaxel/platinum-resistant recurrent endometrial cancer. Methods: Patients who received weekly ixabepilone (16-20 mg/m 2 on days 1, 8, 15 of a 28-day cycle) ± bevacizumab (10 mg/kg on days 1, 15 of a 28-day cycle) off-protocol were identified retrospectively. Results: Thirteen patients were included. Demographic/disease characteristics are provided in Table 1. Median time to first recurrence was 15.9 months (IQR: 9.5-21.66). Patients received a mean of 4.8 ± 1.9 cycles of ixabepilone; treatment is ongoing in 4 patients. A total of 46% of patients demonstrated either a partial response (PR, 8%) or disease stabilization (SD, 38%). PR/SD was associated with a mean decline in CA-125 of 56%. Approximately 50% of patients received concurrent bevacizumab. Of patients who did not receive concurrent bevacizumab, 83% experienced progression and 17% demonstrated SD. Median survival after ixabepilone initiation was 12.7 and 6.9 months in patients treated with and without concurrent bevacizumab, respectively (HR 0.42 [0.09-1.98]). Grade 1/2 hematologic (thrombocytopenia, 15.4%) and gastrointestinal toxicities (emesis/constipation, 7.7%) were observed infrequently. Median overall survival of this cohort was 2.88 years. Conclusions: Ixabepilone shows encouraging activity and promising durability in patients with heavily pre-treated paclitaxel/platinum-resistant recurrent endometrial cancer. Weekly dosing at 16-20mg/m 2 on days 1, 8, and 15 ± bevacizumab is well-tolerated. Additional investigation of this regimen and long-term follow-up is warranted. [Table: see text]
Number of sites of metastasis (NSM) and progression-free survival (PFS) in patients (PTS) with melanoma treated with ipilimumab (IPI).
Authors: Monique Celeste Tavares, Milton Jose De Barros E. Silva, Jose A. Rinck, Ana Claudia Machado Urvanegia, Mariana Petaccia Macedo, Clovis Pinto, Tiago Bezerra, Graziela Zibetti Dal Molin, Fábio Nasser Santos, Rosely Yamamura, Geraldine Eltz Lima, Marcello Ferretti Fanelli
Journal: Journal of Clinical Oncology (2014)

e20048 Background: Metastatic melanoma is associated with poor overall survival. IPI was recently approved to this scenario in first and more lines of treatment in many countries after two landmarks phase III studies. However, this drug benefits only few PTS and nowadays we don’t have predictive factors of response. Objective: To evaluate clinical and pathological data of PTS treated with IPI and to associate with survival data. Methods: Retrospective analysis of PTS treated with IPI during expanded access(EA) to this drug between 03/2011 and 10/2012. Results: Seventy PTS were treated during EA. Gender (M/F): 29/41, age (median): 58y, ECOG (0/1): 87.2%. Histology: 78.5% skin, 14.3% choroid, 4.3% mucosal melanoma, 2.9% others. Stage: 50.7% M1c, 34.8% M1a and 14.5% M1b. LDH was above the normal limit in 50% of PTS and 20% had brain metastasis. NSM: 81% £ 3 sites and 19% 4 or more sites. Fifty-six percent received 4 doses of IPI, (71.7% in second line). The main reason to discontinue therapy was progression of disease (PD): 48.2%. Response evaluation: 51.4% PD, 14.3% stable disease(SD), 1.4% partial response (PR) and 4.4% complete response (CR), 12.8% mixed response (MR) and 15.7% were not evaluated. In PTS with PD, 70% had weak lymphocytic infiltrate (LI) (non-brisk) and in PTS with PR or CR, 50% had strong LI (brisk). Median follow-up: 6.1months(m). The median PFS and overall survival of entire population was 3.9m and 11.5m, respectively. There was a better PFS in PTS with 3 or less sites of metastasis: 5.8m vs 2.7m (p=0.05) (figure 1) and in PTS who received 4 doses of IPI: 6.7m vs 2.0m (p=<0.01). There were no difference with respect to LDH and M1 status. Conclusions: In our study, number of sites of metastatic disease and brisk infiltrate were associated with better outcome.