tbuckley/cabot-search huggingface dataset:
Proteomic profiling of phosphatidylinositol 3-kinase (PI3K) altered metastatic colorectal cancer (mCRC) after protein kinase B (Akt) inhibition: Insulin like growth factor 1 receptor (IGF1R) mediates adaptive resistance.
Authors: Maliha Nusrat, Jisu Oh, Zhi-Qin Jiang, A. Dasari, David R. Fogelman, Bryan K. Kee, David Menter, Kanwal Pratap Singh Raghav, Van Karlyle Morris, Ji Wu, Funda Meric-Bernstam, Jeffrey Morris, Michael J. Overman, Scott Kopetz
Journal: Journal of Clinical Oncology (2018)

3549 Background: We have reported earlier that Akt inhibition is clinically ineffective as monotherapy in PI3K altered (PIK3CA mutant or PTEN loss) mCRC patients (pts). The reasons for this are unknown yet vital for developing effective treatments. We hypothesized that mCRC evades Akt inhibition via adaptive signaling activation. Methods: KRASwt BRAFwt PI3K altered mCRC pts were treated with single agent oral Akt inhibitor, MK2206 (200 mg/week), on a CTEP-sponsored clinical trial (n = 18). Metastases were biopsied at baseline and on day 15. Pt derived xenografts (PDXs) were established for a co-clinical trial with either MK2206 or carrier (30% Captisol) for 3 weeks. Signaling pathways were profiled by reverse phase protein array (RPPA) on tumors from pts and PDXs, as well as on 2 CRC cell lines (KM12L4 and SW480) treated with MK2206. Protein levels from treated and untreated samples were compared by paired or student’s t-test, or ANOVA as applicable. Results: Out of 18 pts, 16 progressed and 2 had stable disease. Similarly, all treated PDXs progressed after a brief response. RPPA data was available for 15 paired biopsies, 9 treated PDXs and 10 control PDXs. MK2206 adequately inhibited pharmacodynamic (PD) markers (including pAkt T308 and pAkt S473) in PDXs, with a similar but nonsignificant trend in pAkt in pts’ biopsies. In cell lines, IGF1R rose after 24 hours and was maintained up to 7 days (P < 0.01). Similarly, treated PDXs had increased IGF1R, insulin receptor beta (INSRB) and HER3 levels (P < 0.001 for all) with a nonsignificant rise in platelet-derived growth factor receptor (PDGFR). In pts’ biopsies, IGF1R, PDGFR and STAT3 increased after two weeks of MK2206 treatment (P < 0.05 for all). MK2206 did not affect MAPK signaling. Conclusions: Akt inhibition with MK2206 in mCRC induces adaptive upregulation of receptor tyrosine kinases, namely IGF1R but also HER3 and PDGFR, resulting in reactivation of the Akt pathway. Combined analysis of cell lines, PDXs and pts' samples allows in-depth interrogation of adaptive resistance and identifies rational combination therapies worthy of further investigation.
Phase Ib venetoclax combined with bortezomib and dexamethasone in relapsed/refractory multiple myeloma.
Authors: Philippe Moreau, Asher Alban Akmal Chanan-Khan, Andrew Warwick Roberts, Amit Agarwal, Thierry Facon, Shaji Kumar, Cyrille Touzeau, Susan Diehl, Jaclyn Cordero, Jeremy A Ross, Wijith Munasinghe, Ming Zhu, Ahmed H. Salem, Joel Leverson, Paulo Cesar Maciag, Maria E. Verdugo, Simon J Harrison
Journal: Journal of Clinical Oncology (2016)

8011 Background: BCL-2 and MCL-1 promote multiple myeloma (MM) cell survival. Bortezomib (B) inhibits MCL-1 activity, and venetoclax (VEN), an oral, selective BCL-2 inhibitor, enhances its efficacy in MM xenograft models. Methods: In this phase 1b study of VEN with B and dexamethasone (D) in relapsed/refractory (RR) MM, pts received daily VEN, per assigned dose escalation (DE) cohorts (50–1200 mg), combined with B (1.3 mg/m2SC) and D (20 mg PO) for 11 cycles, and VEN alone thereafter. Results: 45 pts were enrolled as of 9/17/15. Median age was 65; 29/16 M/F; 24 ISS stage II/III. The median (range) number of prior lines of therapy was 4 (1–13). 38 pts received prior B (19 refractory), 36 had lenalidomide (26 refractory), and 32 had prior SCT. AEs occurring in ≥ 30% of pts were constipation (40%), diarrhea (38%), thrombocytopenia (33%), insomnia (29%). Grade 3/4 AEs in ≥ 10%: thrombocytopenia (22%), anemia (16%). SAEs in ≥ 2 pts were pneumonia (n = 3), cardiac failure, embolism, pyrexia, respiratory failure, sepsis, thrombocytopenia (n = 2 each). One DLT was observed, and MTD was not reached. 30 pts discontinued (DC): 24 related to PD (3 died), 2 due to AE, 4 withdrew consent. Dose-normalized PK for VEN with BD was similar to VEN monotherapy. 41/45 pts were evaluable for efficacy (Table). Preliminary results also indicate that pts with 1–3 prior lines of therapy (N = 18) had higher ORR (83.3%) vs. pts with 4–6 (N = 13, 38.5% ORR) or ≥ 7 prior lines of therapy (N = 10, 10% ORR). Conclusions: VEN with BD has an acceptable safety profile and evidence of anti-tumor activity in RR MM; response rates were highest in pts naïve or sensitive to prior B, or with 1–3 prior therapies. Currently, DE is complete and safety expansion ongoing at 800 mg. Clinical trial information: NCT01794507.Best response by prior B status, n (%) B Naïve (n = 6) B Sensitive (n = 17) B Refractory (n = 18) All (n = 41) ORR 6 (100) 12 (71) 3 (17) 21 (51) ≥ VGPR 5 (83) 6 (35) 0 11 (27) sCR 1 (17) 1 (6) 0 2 (5) CR 1 (17) 1 (6) 0 2 (5) VGPR 3 (50) 4 (24) 0 7 (17) PR 1 (17) 6 (35) 3 (17) 10 (24) MR 0 0 2 (11) 2 (5) SD 0 2 (12) 4 (22) 6 (15) PD 0 3 (18) 8 (44) 11 (27) DC before assessment 0 0 1 (6) 1 (2) Median (range) time on study*, months 9.8 (0.6–16.5) 5.5 (0.5–18.3) 1.3 (0.3–13.5) 4.9 (0.3–18.3) *All pts (n = 45): 1st dose to cut-off (active pts) or last dose (DC pts)
Immuno-oncology biomarker study in a large cohort of LC-SCRUM-Japan: Assessment of PD-L1 expression and tumor mutation burden in non-small cell lung cancer patients treated with immune checkpoint inhibitors.
Authors: Kiyotaka Yoh, Shingo Matsumoto, Kazumi Nishino, Naoki Furuya, Shingo Miyamoto, Satoshi Oizumi, Shigeki Hashimoto, Shunichi Sugawara, Masahiro Kodani, Norio Okamoto, Satoshi Hara, Yuichiro Hayashi, Noriko Motoi, Genichiro Ishii, Koichi Goto
Journal: Journal of Clinical Oncology (2018)

9070 Background: PD-L1 high expression and high tumor mutation burden (TMB) are reported to be correlated with high sensitivity to immune checkpoint inhibitor (ICI) in non-small cell lung cancer (NSCLC). This immuno-oncology biomarker study is ongoing as part of nationwide genomic screening by LC-SCRUM-Japan. Planned accrual is 1000 patients. Methods: Lung cancer patients enrolled in LC-SCRUM-Japan were primarily screened with targeted next-generation sequencing with Oncomine™ Comprehensive Assay (OCA) and monitored clinical course and survival every 6 months. To explore new biomarkers for ICI in the treatment of NSCLC, further analyses of 4 immunohistochemistry (IHC) assays for PD-L1 expression (22C3, 28-8, SP263 and SP142) and whole-exome sequencing (WES) to determine TMB level were conducted in 1000 and 400 patients, respectively. Results: Among 1635 patients with lung cancer enrolled in LC-SCRUM-Japan between Feb 2017 and Jan 2018, 621 NSCLC patients were enrolled in this immuno-oncology biomarker study. The results of PD-L1 IHC with 420 patients, OCA with 380 patients, WES with 50 patients, were analyzed at data cutoff point of Jan 4, 2018. Median TMB level by WES was 72 (2 to 515) and median TMB level by OCA was 7.6 mutation/Mb (0 to 30.8). There was no significant association between each PD-L1 expression and TMB by WES. TMB by OCA had a weak correlation with TMB by WES (R2= 0.31). Seventy-seven patients treated with ICI were evaluable for clinical response. Among 6 responders to ICI, TMB level by WES was various (19, 26, 26, 109, 144, and 249). Of these, 2 had both high TMB by WES (≥ median 72) and PD-L1 high expression; 2 had TMB low/PD-L1 high; 1 had TMB high/PD-L1 low: 1 had TMB low/PD-L1 low but high TMB by OCA (15.4 mutation/Mb). Conclusions: High TMB level appears to produce high sensitivity to ICI in patients with NSCLC, independent of PD-L1 high expression. Based on WES analyses in a large cohort, the findings to explore a precise predictive immuno-oncology biomarker to maximize the therapeutic benefits will be reported at the meeting.
Randomized, placebo-controlled, phase III study of aprepitant in preventing chemotherapy-induced nausea and vomiting in children: Analysis by age group.
Authors: Hyoung Jin Kang, Susan Loftus, Cara DiCristina, Stuart Green, Ruji Yao, Christian M. Zwaan
Journal: Journal of Clinical Oncology (2016)

10579 Background: Aprepitant, an oral neurokinin-1 inhibitor, was superior to placebo in preventing chemotherapy-induced nausea and vomiting (CINV) in pediatric patients in a randomized, double-blind, placebo-controlled phase 3 study (NCT01362530). This prespecified analysis explores efficacy and safety of aprepitant by age group. Methods: Patients aged 6 months (mo) to 17 years (y) scheduled to receive moderately, highly, or very highly emetogenic chemotherapy (MEC, HEC, and VHEC, respectively) were randomly assigned 1:1 to receive an oral aprepitant regimen (patients aged 12-17 y: day [D]1: 125 mg, D2-3: 80 mg; patients aged <12 y: D1: 3.0 mg/kg, D2-3: 2.0 mg/kg) with ondansetron (D1) or ondansetron (D1) with matching placebo. Dexamethasone (dex) use was allowed. Primary end point was the proportion of patients with complete response (CR) (no vomiting, no retching, and no use of rescue medication) in the delayed phase (25-120 hours after chemotherapy initiation). For this analysis, patients were stratified by prespecified age groups and further by use of dexamethasone and use of VHEC. Results: In total, 302 patients were analyzed. Age groups were 6 mo to <2 y (n = 35), 2 to <6 y (n = 88), 6 to <12 y (n = 84), and 12 to 17 y (n = 95). Better control based on CR was observed in the aprepitant arm irrespective of age group (Table). Rates of adverse events were similar across age groups. Conclusions: Aprepitant appears safe and efficacious in preventing CINV in pediatric patients across age subgroups. Clinical trial information: NCT01362530.Age Group Stratified Group Aprepitant Regimen n/N (%) Control Regimen n/N (%) 6 mo–<2 y Total 9/19 (47) 4/16 (25) Dex 3/6 (50) 1/4 (25) No dex 6/13 (46) 3/12 (25) VHEC 6/13 (46) 0/11 (0) No VHEC 3/6 (50) 4/5 (80) 2–<6 y Total 25/45 (56) 16/43 (37) Dex 4/11 (36) 4/10 (40) No dex 21/34 (62) 12/33 (36) VHEC 11/25 (44) 10/26 (39) No VHEC 14/20 (70) 6/17 (35) 6–<12 y Total 19/41 (46) 14/43 (33) Dex 3/12 (25) 3/13 (23) No dex 16/29 (55) 11/30 (37) VHEC 10/26 (39) 7/27 (26) No VHEC 9/15 (60) 7/16 (44) 12–17 y Total 24/47 (51) 5/48 (10) Dex 6/15 (40) 1/15 (7) No dex 18/32 (56) 4/33 (12) VHEC 15/35 (43) 3/37 (8) No VHEC 9/12 (75) 2/11 (18)
Discover <i>BCL6</i> translocations partner gene in diffuse large b-cell lymphoma by target-captured next generation sequencing.
Authors: Hui Zhou, Xinhua Du, Youhong Tang, Jianqiu Wu, Wei Liu, Yuting Yi, Lian Dai, Zhou Ouyang, Mingyang Deng, Yan-Fang Guan, Xin Yi, Ling Yang, Xuefeng Xia
Journal: Journal of Clinical Oncology (2018)

e19527 Background: BCL6 translocations (3q27) are the most common chromosomal abnormalities in diffuse large B-cell lymphoma (DLBCL), with numerous immunoglobulin (Ig) and non-Ig genes as partners. Contrary to Ig/BCL6 fusions typical by high BCL6 gene expression, in non-Ig/BCL6 fusions were observed unexpectedly low BCL6 mRNA levels. From the clinical point of view, the survival rate of DLBCL patients with non-Ig partners is inferior to those with Ig/BCL6 fusions. Consequently, the BCL6 translocation pattern is a potential prognostic indicator. Methods: A total of 21 DLBCL patients were enrolled in the study. Target-captured next generation sequencing was performed on circulating tumor DNA or tumor tissue genomic DNA, which enables simultaneously assess somatic single-nucleotide variants, insertions/deletions and copy-number alterations across 612 genes, and detects rearrangements across 35 genes. Results: In total, we identified 251 genetic alterations with a median of 10 (1-33) mutations per patient. PCLO (33.3%), TP53 (23.8%) and PRDM1 (23.8%) were commonly mutated in DLBCL. The manifest frequent mutations in TP53, CD79B (14.3%), CREBBP (14.3%), ATM (9.5%) and MYD88 (9.5%) for which there currently exist potential targeted therapies. 47.6% (10/21) of patients exhibit gene rearrangements, including BCL6, BCL2, ALK and MLL. 33.3% (7/21) of patients acquired BCL6 translocations. Three patients (42.9%) were Ig/BCL6 fusions, the partner gene of non-Ig/BCL6 fusions patients was EIF4A2, IKZF1, HIST1H4I, respectively (Table 1). Conclusions: Target-captured next-generation sequencing can be used to discover the BCL6 gene breakpoints and partner gene in DLBCL. Table 1 The breakpoints of the BCL6 gene translocation No. Gene1 Breakpoint 1 Gene2 Breakpoint 2 #03 BCL6 3:187459697 IgH 14:106325612; 14:106325561; 14:106325171 #08 BCL6 3:187462592 IKZF1 7:50350549 #09 BCL6 3:187462705 IgH 14:106326064 #11 BCL6 3:187462751 EIF4A2 3:186501730 #12 BCL6 3:187462678; 3:187462685 HIST1H4I 6:27107174; 6:27107163 #18 BCL6 3:187462109; 3:187462161 EIF4A2 3:186502930; 3:186502945 #19 BCL6 3:187462687 IgK 2:89544822
Prognostic factors and combined histologies in 205 resected small cell lung cancer (SCLC) patients.
Authors: Xiao-Liang Zhao, Justine N McCutcheon, Bhaskar Kallakury, Joeffrey J Chahine, Mark Raffeld, Drew Pratt, Yu-Long Chen, Bin Zhang, Hua Zhang, Yu-Wen Zhang, Chang-li Wang, Giuseppe Giaccone
Journal: Journal of Clinical Oncology (2017)

e20009 Background: SCLC accounts for 15%-20% of all lung cancer, 2%-5% of them are combined SCLC. The objectives of this study were to evaluate the prognostic factors in a large series of resected SCLC patients, and to perform genetic analysis of combined forms. Methods: 205 SCLC cases were resected at Tianjin Cancer Hospital between 1/2005 and 12/2015. We analyzed: gender, age, type of resection, cigarette index (CI), tumor markers (CEA, SCC, NSE, Cyfra21-1), R resection type, number of resected lymph nodes (LNs), ratio of metastatic LNs, and pathological stage. All combined SCLC cases were identified by H&amp;E staining and confirmed by immunohistochemistry. The different components were microdissected using an automated dissection system (MillisectTM, Roche Diagnostics) and DNA was extracted and subjected to targeted exome sequencing. Results: The median follow-up time was 24 (2-121) months. Median survival time of all the patients was 24 months; 5-year survival rates were 51.4% overall, and 69.5%, 66.5%, 34.4%, and 0% for pathological stage I, II, III, and IV, respectively. Multivariate analysis indicated age, CI, complete resection, number of resected LNs and the ratio of metastatic LNs as independent prognostic factors. Twelve cases of combined SCLC were identified out of 170 with adequate histological material: 6/12 were combined with squamous cell carcinoma. 1-, 3-, 5-year survival rates were 73.3%, 0% and 0%. There were no significant differences between combined SCLC and pure SCLC with respect to gender, age, pathological stage, LN status and tumor markers. Three cases were successfully sequenced. Around 50% gene mutations were present in both components (10/24; 14/27; 4/5 respectively). TP53 mutations were present in all three cases. One case displayed amplification of 2 genes in both components. Interestingly, there were also gene mutations and amplifications that are unique to one of the components. Conclusions: In this large resected SCLC series we identified CI, complete resection, resected number of LNs and ratio of metastatic LNs to be prognostic. Combined SCLC had worse survival than pure SCLC. The histologically different components had a significant number of common as well as unique genetic alterations.
Hexachlorobenzene as a possible major contributor to the dioxin activity of human milk.
Authors: A P van Birgelen
Journal: Environmental Health Perspectives (1998)

A dioxinlike compound is a compound that binds to the aryl hydrocarbon (Ah) receptor, results in dioxinlike effects, and bioaccumulates. These are the three factors for including dioxinlike chemicals in the toxic equivalency factor (TEF) concept. Risk assessment of dioxinlike compounds is based on using these TEFs. Hexachlorobenzene (HCB) has all three features and should therefore be included in this TEF concept. Relative potency values express the potency of a specific compound in comparison to 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), the most potent dioxinlike compound, with a relative potency value of 1. For the estimation of the total dioxin activity in an environmental biological sample, the TEF value of a compound is multiplied by the concentration in the specific matrix. This results in a certain amount of toxic equivalents (TEQs) for this compound. The summation of all TEQs in a certain mixture gives the total dioxin activity of this mixture. HCB binds to the Ah receptor about 10,000 times less than TCDD. HCB is also about 10,000 times less potent than TCDD based on in vitro cytochrome P4501A induction and porphyrin accumulation. Using a relative potency value of 0.0001, HCB could add 10-60% to the total TEQ in human milk samples in most countries. In a few countries such as Spain, Slovakia, and the Czech Republic, HCB levels in human milk expressed as TEQ could contribute up to a factor of six to the total TEQ in comparison to the contribution of polychlorinated dioxins, dibenzofurans, and biphenyls together, i.e., up to a daily intake of about 1 ng TEQ/kg for a breast-fed infant. The HCB levels in human milk in these countries are about the same as in India. Biochemical, immunological, and neurological alterations have been observed in infants fed breast milk in countries with relatively low TEQ levels in human milk. Based on the above information, it is clear that HCB should be classified as a dioxinlike compound, that more studies are needed to reduce the uncertainty in the estimation of a relative potency value for HCB, and that epidemiological studies should be undertaken in infants fed breast milk in countries with high HCB exposure levels. Furthermore, measurements of HCB levels in human and environmental samples in conjunction with other dioxinlike compounds is a prerequisite to estimate the total dioxin activity in these samples.
Phase 2, multicenter study of the EZH2 inhibitor tazemetostat as monotherapy in adults with relapsed or refractory (R/R) malignant mesothelioma (MM) with BAP1 inactivation.
Authors: Marjorie Glass Zauderer, Peter Szlosarek, Sylvestre Le Moulec, Sanjay Popat, Paul Taylor, David Planchard, Arnaud Scherpereel, Thierry Jahan, Marianna Koczywas, Martin Forster, Robert B. Cameron, Tobias Peikert, Carly Campbell, Inbal Sapir, Alice McDonald, Coreen Oei, Alicia Clawson, Maria Roche, Dean A. Fennell
Journal: Journal of Clinical Oncology (2018)

8515 Background: MM often presents at an advanced stage with a median survival of ~1 year. Treatments are limited; none clearly improve survival in second-line. In 40–60% of MM patients (pts) BRCA1 associated protein 1 (BAP1) is inactive and linked to a dependency on EZH2 (enhancer of zeste-homolog 2). EZH2 regulates gene expression to prevent differentiation of stem and progenitor cells, and aberrant EZH2 activity is implicated as an oncogenic driver. Tazemetostat, a potent, selective, oral EZH2 inhibitor demonstrated clinical activity in other malignancies; here we report preliminary data in inactive BAP1 MM. Methods: This is a phase 2, multicenter, open-label, single-arm study of tazemetostat (800 mg po BID) in pts with measurable R/R MM. PK and safety were assessed in a cohort of 13 pts. Efficacy was assessed via a 2-stage Green Dahlberg design in 61 pts with inactive BAP1 with a primary endpoint of 12-week disease control rate [DCR; CR or PR + SD]. Response was evaluated every 6 weeks with modified RECIST and/or RECIST 1.1. Secondary endpoints included ORR, PFS, OS, safety, population PK and response biomarkers (RNAseq, immunomodulation, exploratory prognostic indices). Results: Enrollment is complete (N = 74). Disease characteristics were typical of MM with the exception of a bias towards epithelioid histology (88%) that has a higher incidence of BAP1 inactivation. All pts had ≥1 prior systemic therapy. No pts discontinued due to AEs; however, 5 pts had dose reductions due to AEs. Fatigue (32%), decreased appetite (28%), dyspnea (28%), and nausea (27%) were the most frequently reported AEs of any grade regardless of attribution. In the efficacy portion of the study, the Stage 2 DCR criterion of ≥35% was surpassed, with 31 pts (51%) achieving disease control at 12 weeks and 15 pts (25%) sustained disease control at 24 weeks, 5 of whom are ongoing. Two of 61 patients had a confirmed partial response. Conclusions: Tazemetostat monotherapy shows promising antitumor activity, including confirmed responses and long-term disease control, with favorable safety/tolerability in pts with MM. These results support further evaluation of tazemetostat in pts with MM. Clinical trial information: NCT02860286.
Overall survival (OS) in stage II resected pancreatic cancer ( PC) using gemcitabine (Gem)/taxane adjuvant therapy (Rx): a single-institution experience.
Authors: Flavio G. Rocha, Alicia M Edwards, Margaret T Mandelson, Bruce S. Lin, Adnan Alseidi, Thomas R Biehl, Richard A. Kozarek, Scott Helton, Vincent J. Picozzi
Journal: Journal of Clinical Oncology (2016)

e15693 Background: Adjuvant rx using single-agent gem in resected PC typically has produced median / 5-year (yr) survivals of 18-22 months (mo)/ 10%, respectively. As taxanes added to gem improved OS in advanced PC, we studied this combination in the above setting. Methods: Patients (pts) with primary resected PC were identified from our institutional pancreaticobiliary database and tumor registry. Inclusion criteria were 1) no tumor recurrence prior to adjuvant rx, 2) gem/taxane given as initial adjuvant rx and 3) all adjuvant rx given at our institution. Results: 57 pts from 2010-2015 were identified per the above criteria. All pts received gem/docetaxel as adjuvant Rx. Pt characteristics were median age 65 yrs, ECOG PS 0/1 68%/30%. Path characteristics included AJCC stage I/IIA/IIB 3(5%)/15/(26%)/39 (68%), median tumor size 2.8 cm,non- poor/poor diff tumor grade 46%/54%, node positive 68%, margin positive ( < 1mm) 49%. 9/57 (16%) pts had postop week 8 Ca 19.9 > 200U/mL (range < 3-4526). With 42 mo median f/u, median DFS/OS for all pts is 30.5/52.3mo (95% CI 20.7-NR mo/ 31.0-NR mo). 5-yr actuarial OS is 49% (95% CI 29-66%, Kaplan -Meier). 2/57 pts are currently on Rx; 46/55 (84%) received ≥ 12 cycles adjuvant Rx ; 36/55 (65%) received chemoradiation (CRT) post completion adjuvant Rx. Reasons for no CRT included disease progression/death (10 pts), comorbidity/MD recommendation (6 pts), pt choice(3 pts). Both ≥ 12 cycles adjuvant Rx (HR 0.26,95% CI 0.10-0.69) and CRT ( HR 0.37, 95% CI 0.15-0.90) were associated with improved OS. 26/57 (46%) pts have recurred; 2(3%) local, 22(37%) distant , 2(3%) combined. 18/59 (32%) pts were hospitalized during adjuvant Rx; no Rx-related deaths occurred. Conclusions: 1) gem/taxane combination Rx can be successfully given as adjuvant Rx. 2) Median and 5-yr OS shown here compares favorably with use of single-agent adjuvant Rx both as published previously by our institution and with outside literature reports, particularly considering pt stage (95% stage II) and other pt path characteristics . 3) Improved OS was seen with ≥ 12 cycles adjuvant Rx and CRT.4) Further investigation into gem/taxane adjuvant Rx in resected PC is supported by these data.