tbuckley/cabot-search huggingface dataset:
TCT-858 Residual inflammatory status in patients with stable coronary artery disease undergoing percutaneous coronary intervention
Authors: Deborah Kalkman, Melissa Aquino, Usman Baber, None Paul Guedeney, Sabato Sorrentino, Birgit Vogel, Bimmer Claessen, Gennaro Giustino, None Joseph Sweeny, Jason Kovacic, Pooja Vijay, Nitin Barman, Annapoorna Kini, Samin Sharma, George Dangas, Roxana Mehran
Journal: Journal of the American College of Cardiology (2018)
Voice of cancer patients: Analysis of use and efficacy of yoga and meditation in cancer patient.
Authors: Sangeeta Aggarwal, Rahul Sharma, Alok Aggarwal, Rishi Sharma
Journal: Journal of Clinical Oncology (2018)

e18801 Background: There is growing interest in complimentary& Alternative modalities to improve quality of life in cancer patients during and after the treatment. In this study, we analyzed patients’ experiences and their use and efficacy of Yoga and meditation. Methods: Many patients share their experiences as freely shared and unsolicited messages in online forums. We collected 15.7 million unique messages from 37 unrestricted cancer forums that provide clinically relevant information. We built custom ontologies for Yoga, meditation and cancer related side effects such as pain, insomnia, neuropathy, fatigue, anxiety and depression. We then used our automated system VoCP, which uses Artificial Intelligence-based techniques (e.g., deep learning, topic modeling, information retrieval, and natural language processing) to extract relevant information from these messages. Results: We found 44,800 messages from 15,784 distinct members/users discussing yoga and meditation. Most of them are inquiring and providing information about yoga/meditation. 799 members reported their use for managing symptoms and side-effects from cancer therapies and for general well-being. Type of cancers included: breast cancer (605); Lymphoma (48); Colorectal cancer (48); head & neck cancer (10); cervical cancer (10); and lung cancer (10). Use for specific reason: 621 patients for relief in effects of chemotherapy, 113 for General well-being & Quality-of-Life, 27 for muscle stiffness & range-of-motion, 19 for body-ache, 28 for anxiety, stress & Depression, 17 for bone and joint pain, 13 for lymphedema, 12 weight-issue, and 7 for fatigue. Efficacy: 189 users. Very Effective: 87, Somewhat effective: 72, Not effective: 30 Sentiment analysis: Positive: 246, Mixed: 19, Negative: 29 Conclusions: Cancer patients are increasingly finding non-pharmacological interventions such as Yoga and meditation useful to alleviate stress and side effects associated with their treatment. The VoCP interactive system reliably provides meaningful insights from patient’s point of view to their treatment, their concerns, and suggestions for supportive therapy. It also gives insight into unmet needs where more resources and research should be focused.
NOS2 polymorphisms in the prediction of benefit from FOLFIRI plus bevacizumab in mCRC patients enrolled in TRIBE trial.
Authors: Marta Schirripa, Wu Zhang, Dongyun Yang, Shu Cao, Satoshi Okazaki, Fotios Loupakis, Martin D. Berger, Yan Ning, Afsaneh Barzi, Yuji Miyamoto, Mitsukuni Suenaga, Roel Gopez, Jordan David West, Diana L. Hanna, Sara Lonardi, Francesca Bergamo, Chiara Cremolini, Alfredo Falcone, Heinz-Josef Lenz
Journal: Journal of Clinical Oncology (2016)

11597 Background: NOS2 is the inducible form of NOS. It is related to adaptive and innate immunity. In cancer development and progression both beneficial and detrimental effects have been described for NOS2 and its expression has been positively or negatively correlated with tumor progression. In the present study we evaluated the role of selected NOS2 SNPs in predicting outcome of mCRC patients. Methods: DNA was extracted from blood samples of mCRC patients treated with FOLFIRI plus bev in the TRIBE trial. 2 SNPs in the promoter region of NOS2 (rs2779248 and CCTTTrepeat (rep)) were analyzed by PCR and direct sequencing. The relation of the NOS2 SNPs with PFS and OS was evaluated through Kaplan-Meier method and log-rank test in the overall population; the correlation with response was estimated by the chi-square test. Subgroup analyses according to RAS-BRAFstatus, gender and tumor site were preplanned. Multivariable Cox regression model was used to assess the independent effect of two SNPs on PFS and OS when adjusting for the baseline demographic, clinical, and tumor characteristics that were associated with outcomes. Results: 227 patients were included in the present analyses. Main patient characteristics were the following M/F 61/39%, median age 60, range (29-75), primary tumor site right/left 27/73%, all wt/RAS mut/BRAF mut 25/68/7%. In the overall population patients carrying NOS2 CCTTT long (L) ( > 13 rep)/- variant (N = 57) showed an improved PFS compared to those carrying short (S)/S (N = 152) (median PFS 11.1 vs 9.5 months respectively, HR = 0.64 [95%CI 0.44-0.92], p = 0.010). Those results were confirmed in the multivariate analyses (HR = 0.62 [95%CI 0.41-0.93], p = 0.021).Similar findings were observed among patients with RAS mutant (multiv HR = 0.40 [95%CI 0.22-0.74], p = 0.003). Conclusions: NOS2 CCTTT rep might represent a prognostic/predictive factor of efficacy for FOLFIRI plus bevacizumab treatment. A specific interaction between NOS2 CCTTT rep and RAS mutation was observed. Since an association of high number of CCTTT rep with increased expression of NOS2 has been previously reported, we can hypothesize a possible role of NOS2 as tumor suppressor in mCRC and in particular among RAS mutant patients.
Budget impact model (BIM) to evaluate treatment costs associated with variable utilization rates of cabazitaxel in metastatic castration-resistant prostate cancer (mCRPC).
Authors: Edward Joseph Drea, Shelby Corman, Alex R Cockerham, Miraj Patel, Louis Hudspeth, Andrew Kenneth Yu
Journal: Journal of Clinical Oncology (2017)

e18321 Background: Cabazitaxel (CBZ) is a microtubule inhibitor indicated in combination with prednisone for treatment of patients with mCRPC previously treated with a docetaxel (DOC)-containing regimen. Recently published results of the PROSELICA trial may provide the basis for changing utilization rates of CBZ. Methods: A BIM was developed to project the overall costs of varying utilization rates of post-DOC treatment modalities for the management of mCRPC. Treatment costs of two dosage schema for CBZ were compared to abiraterone acetate, enzalutamide, and radium-223. Prevalence of mCRPC was estimated using US Census and population modeling data. Medication costs were derived from published benchmarks; dosing/monitoring information from prescribing information; and duration of therapy from published trials. Rates and costs of Grade 3 / 4 adverse events (AEs) per published trials were also incorporated. Results: In a hypothetical 1 million member US health plan, 100 pts are estimated to receive 2 nd line (2L) treatment for mCRPC. Reported utilization rates for 2L agents calculate to a PMPM of $0.623. Following publication of the PROSELICA study, modeling a potential increase in CBZ 20 mg/m 2 utilization from 0% to 7% and modeling a 12% to 16% utilization rate change for CBZ 25 mg/m 2 , costs are projected to decrease by -$0.022 PMPM or $265,033 over a one year period. Although AE costs of management calculate higher for the CBZ doses, lower monitoring and drug acquisition costs contribute to account for these findings (Table 1). Conclusions: Increasing utilization rates of CBZ in 2L mCRPC can result in a slight cost decrease due to variation in CBZ dosing and AE rates, and lower monitoring and acquisition costs. [Table: see text]
Impact of age and comorbidity on treatment of non-small cell lung cancer (NSCLC) recurrence (AFT-03).
Authors: Melisa L. Wong, Timothy L. McMurry, George J. Stukenborg, Amanda B. Francescatti, Jessica R. Schumacher, Louise C. Walter, Benjamin D. Kozower
Journal: Journal of Clinical Oncology (2016)

10037 Background: Older adults with NSCLC with no comorbidities are at risk of under treatment after initial diagnosis while those with severe comorbidities are at risk of over treatment. However, national data on how age and comorbidity impact treatment of recurrent NSCLC are limited. Methods: Through a special study mechanism of the National Cancer Database, we randomly selected 9668 patients with surgically resected stage I-III NSCLC in 2006-07 from 1147 cancer facilities. Registrars reabstracted detailed preoperative comorbidity, recurrence, and treatment information to supplement existing data. Patients were stratified by recurrence status and predictors of active treatment vs supportive care only were analyzed using multiple logistic regression. Results: Median age at diagnosis was 67 (IQR 60-74). The most common comorbidities were COPD (40%) and CAD (21%). After 5-year median follow up, 62% had no recurrence, 11% had locoregional, and 27% had distant recurrence. Among those with locoregional recurrence, 79% received treatment (28% chemo, 25% chemo/radiation, 16% radiation, 10% surgery); 21% received supportive care only. Older patients (adjusted OR 0.73 per decade, p = .0008) and those with substance abuse (aOR 0.41, p = .008) were less likely to receive treatment. Women and patients with symptomatic or ipsilateral lung recurrence (vs lymph node) were also less likely to receive treatment (all p < .02). Among those with distant recurrence, 77% received treatment (30% radiation, 23% chemo, 13% chemo/radiation, 11% surgery); 23% received supportive care only. Older patients were less likely to receive treatment (aOR 0.75, p = .0001) while those without any comorbidities were more likely to receive treatment (aOR 1.65, p = .018). Metastatic site also predicted treatment: contralateral lung or liver metastases decreased the odds of treatment while brain or bone metastases increased the odds (all p < .05). Conclusions: Older patients, independent of comorbidity, were less likely to receive treatment for both locoregional and distant NSCLC recurrence. In contrast, the impact of comorbidity was stronger for distant recurrence, highlighting the importance of avoiding over treatment in the palliative setting.
Efficiency of anlotinib hydrochloride as 3<sup>rd</sup> line treatment in patients (pts) from a randomized, double-blind, placebo-controlled phase III trial, an exploratory subgroup analysis of ALTER0303 trial for the previous therapy strategy effect.
Authors: Qiming Wang, Baohui Han, Kai Li, Li Zhang, Jianhua Shi, Zhehai Wang, Ying Cheng, Jianxing He, Yuankai Shi, Weiqiang Chen, Xiuwen Wang, Yi Luo, Kejun Nan, Faguang Jin, Baolan Li
Journal: Journal of Clinical Oncology (2018)

e21182 Background: ALTER 0303 trial (NCT02388919) has demonstrated that anlotinib could significantly prolonged OS (primary point) and PFS in refractory advanced NSCLC pts as 3rd line treatment. Methods: All eligible adult IIIB/IV NSCLC pts were stratified by EGFR type and previous therapeutic strategies. The impacts on the efficacy of anlotinib were analyzed by OS and PFS. Results: According to different EGFR mutation status, data for the impact of previous therapeutic strategies on anlotinib treatment have shown in the following table Conclusions: The subgroup analysis indicated that in the 3rd line treatment pts could benefit from anlotinib regardless of the previous therapeutic strategies. Clinical trial information: NCT02388919. EGFR type WT M+ M+ Pem/Pla 57 vs 135 Doc/Pla 66 vs 125 Pac/Pla 40 vs 68 Vin/Pla 23 vs 53 Gem/Pla 59 vs 116 Pem/Pla 37 vs 74 Doc/Pla 34 vs 63 Pac/Pla 14 vs 27 Vin/Pla 13 vs 21 Gem/Pla 18 vs 40 Gefitinib 20 vs 49 Erlotinib 12 vs 22 Icotinib 11 vs 26 1st line 11 vs 16 2nd line 31 vs 75 mOS Placebo 7.17 6.30 7.13 6.13 7.17 6.27 6.23 6.93 4.03 4.98 4.23 9.73 4.03 3.53 7.03 Anlotinib 8.60 9.83 7.93 9.10 8.37 10.60 11.10 15.13 NE 11.10 10.60 15.83 9.43 11.10 10.70 P 0.201 0.061 0.287 0.043 0.644 0.030 0.107 0.174 0.010 0.062 0.008 0.347 0.246 0.019 0.170 HR 0.79 (0.55, 1.13) 0.71 (0.50, 1.02) 0.78 (0.49, 1.24) 0.56 (0.32, 0.99) 0.91 (0.63, 1.34) 0.57 (0.34, 0.95) 0.65 (0.38, 1.10) 0.54 (0.22, 1.33) 0.32 (0.13, 0.79) 0.53 (0.26, 1.05) 0.43 (0.23, 0.82) 0.62 (0.22, 1.70) 0.60 (0.25, 1.43) 0.31 (0.11, 0.87) 0.69 (0.40, 1.18) mPFS Placebo 1.40 1.63 1.80 1.00 2.67 0.73 0.73 1.37 0.98 1.07 0.87 1.12 0.73 0.83 0.87 Anlotinib 4.70 5.63 4.30 5.60 5.57 5.60 4.67 5.63 4.67 5.60 5.63 6.80 4.47 4.30 5.57 P < 0.000 < 0.000 < 0.000 < 0.000 < 0.000 < 0.000 < 0.000 < 0.000 0.030 < 0.000 < 0.000 0.003 < 0.000 0.022 < 0.000 HR 0.28 (0.19, 0.41) 0.26 (0.18, 0.38) 0.27 (0.16, 0.44) 0.20 (0.11, 0.37) 0.28 (0.19, 0.42) 0.20 (0.12, 0.32) 0.20 (0.13, 0.33) 0.25 (0.10, 0.60) 0.41 (0.18, 0.94) 0.28 (0.15, 0.53) 0.11 (0.05, 0.23) 0.31 (0.13, 0.71) 0.08 (0.02, 0.26) 0.32 (0.11, 0.91) 0.20 (0.12, 0.34)
NT5C2 germline variants alter thiopurine metabolism and are associated with acquired NT5C2 relapse mutations in childhood acute lymphoblastic leukaemia
Authors: Morten Tulstrup, Marie Grosjean, Stine Nygaard Nielsen, Kathrine Grell, Benjamin Ole Wolthers, Peder Skov Wegener, Olafur Gisli Jonsson, Bendik Lund, Arja Harila-Saari, Jonas Abrahamsson, Goda Vaitkeviciene, Kaie Pruunsild, Nina Toft, Mette Holm, Erik Hulegårdh, Sigurd Liestøl, Laimonas Griskevicius, Mari Punab, Jinhua Wang, William L. Carroll, Zeyu Zhang, Marlene D. Dalgaard, Ramneek Gupta, Jacob Nersting, Kjeld Schmiegelow
Journal: Leukemia (2018)
The adjuvant therapy for high risk GIST patients after complete resection in the clinical practice.
Authors: Toshirou Nishida, Masakazu Takagi, Masato Ozaka, Yuko Kitagawa, Yukinori Kurokawa, Yoshito Komatsu, Chikashi Ishioka, Toshihiko Doi, Haruhiko Cho, Tetsuo Kanda, Toshiro Sugiyama, Akira Sawaki, Yoshihiro Kakeji, Toshihiro Hirai, Shinji Hato, Hideo Baba, Kuniaki Shirao, Seiichi Hirota, Tatsuo Kagimura, Toru Masuzawa
Journal: Journal of Clinical Oncology (2016)

e22516 Background: Although 3-year imatinib adjuvant therapy is recommended by the guidelines, there is a lack of the data in clinical practice regarding use of adjuvant therapy and adherence. A prospective registry study for high-risk GIST in Japan examined reality of adjuvant. Methods: Between Dec. 2012 and Dec. 2015, 541 pts with histologically-confirmed high-risk GIST defined by the modified NIH classification in local site have been registered (UMIN000009531). There were 299 males and 242 females with median age of 65 yrs. In the central pathological review, H&E, immunohistochemistry, and genotyping were done. Results: Disease was located in the stomach (n = 323), small intestine (n = 164), large intestine (n = 33), or others (n = 21). PS of pts was 0 (446 pts), 1 (72 pts) and > 2 (7 pts). Median tumor size was 7.5 cm and median mitosis (local pathology) was 10/50HPF. Tumor rupture was seen in 70 pts (13%), of which 35 pts had rupture preoperatively and 30 intraoperatively. Half of ruptured GISTs (35) were small intestine. Sixty pts (11%) had received neoadjuvant therapy, and adjuvant was administered for 415 pts (77%). The % of pts receiving adjuvant therapy increased with mitosis and size, and decreased with PS although it was unrelated to location, rupture and curability (R0 vs R1). Central pathological review was done for 478 pts: KIT was positive in 459 pts (96%) and DOG1 in 460 pts (96%). Mutations were analyzed in 431 pts including 327 KIT exon 11 mutations, 32 exon 9 mutations, 12 other KIT mutations, 13 PDGFRA exon18 mutations, 1 exon 12 mutations, and 26 wild type GISTs. Although KIT immunoreactivity was consistent between central and local (concordance = 92%), 16 GISTs (3.3%), positive for KIT immunostaining in local, were diagnosed as non-GIST in the central review. They were negative or weakly positive for KIT and DOG1 in cetral and lacked mutations in KIT and PDGFRA. Of 16 pts, 12 pts had received adjuvant therapy at registration. Conclusions: The high risk GIST group in the modified NIH classification contains nearly 10% of tumor rupture in clinical practice. Adjuvant therapy was used for 3/4 of high risk GIST pts locally diagnosed. There are measurable complete discordance between local and central pathological diagnosis of GIST. Clinical trial information: UMIN000009531.
A phase II study of MOR208 plus idelalisib in patients with relapsed or refractory chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) previously treated with a Bruton's tyrosine kinase inhibitor (MIRACLE).
Authors: Clemens-Martin Wendtner, John C. Byrd, Barbara Eichhorst, Robin Foà, Michael Hallek, Peter Hillmen, Ulrich Jäger, Wojciech Jurczak, Peter Kelemen, Kamel Laribi, Talha Munir, Philipp B Staber, Stephan Stilgenbauer, Jennifer Ann Woyach
Journal: Journal of Clinical Oncology (2016)

TPS7572 Background: Ibrutinib, a Bruton's tyrosine kinase inhibitor (BTKi), is an important treatment option for patients (pts) with CLL/SLL. Pts who progress early on ibrutinib are difficult to treat and have poor outcomes. Thus, ibrutinib-pretreated pts, including pts with ibrutinib intolerance, are in urgent need of novel therapeutic options. MOR208, an Fc-engineered, humanized, monoclonal antibody targeting the B-cell receptor CD19 (highly expressed on lymphoid malignancies) was well tolerated in a phase I study in relapsed or refractory (R/R) CLL/SLL and showed promising single-agent activity. In preclinical models, MOR208 showed synergistic activity with idelalisib (PI3Kδ inhibitor), providing a rationale for testing this combination in a clinical study. Methods: This open-label, multicenter, single-arm, phase II study has a safety run-in with a 3+7 design. Main inclusion criteria are: adult pts with CLL/SLL, R/R disease while on BTKi therapy given as single-agent or combination therapy for at least one month or intolerant to such therapy, ECOG performance status of 0–2, adequate bone marrow, hepatic and renal function. Main exclusion criteria are: BTKi treatment within 5 days prior to study drug dosing, lymphoma-specific therapy within 14 days prior to dosing, prior treatment with a CD19-targeted therapy or a PI3K inhibitor. MOR208 with idelalisib is given until disease progression, unacceptable toxicity, death or loss to follow-up, for up to a maximum of 24 cycles. MOR208 12 mg/kg is given intravenously, weekly for the first 3 cycles, and then every 2 weeks. Idelalisib is taken orally, 150 mg twice-daily. Primary endpoint is overall response rate (central review) assessed by International Workshop on CLL criteria and the Lugano criteria for SLL. Key secondary endpoints include progression-free survival, overall survival, duration of response, safety, pharmacokinetics, MOR208 immunogenicity and patient-reported outcomes. Exploratory biomarker analyses will also be performed. Enrollment and treatment are underway; 120 pts are planned. Clinical trial information: NCT02639910.
Genetically engineered T-cell therapy for HPV-associated epithelial cancers: A first in human, phase I/II clinical trial.
Authors: Stacey L. Doran, Sanja Stevanovic, Sabina Adhikary, Jared J. Gartner, Li Jia, Mei Li M. Kwong, William C Faquin, Steven Feldman, Robert Somerville, Richard Mark Sherry, James C. Yang, Steven A. Rosenberg, Christian S. Hinrichs
Journal: Journal of Clinical Oncology (2018)

3019 Background: Engineered T-cell therapy is an emerging treatment for hematological cancers. In epithelial cancers, its study has been limited. Human papillomavirus (HPV)-16+ epithelial cancers constitutively express the HPV E6 oncoprotein. We investigated treatment of metastatic HPV-16+ cancers with T cells that target E6 by an engineered T-cell receptor (E6 T cells). Methods: A phase I/II, single-center, clinical trial was conducted. Eligible subjects had a metastatic HPV-16+ cancer from any primary tumor site and had received prior platinum-based therapy. Treatment consisted of a one-time, intravenous infusion of E6 T cells. A lymphocyte-depleting conditioning regimen and systemic aldesleukin were also administered. Results: Twelve subjects were treated on this protocol. Dose-limiting toxicity was not encountered (maximum dose was 1.7 x 1011 T cells). Transduction efficiency range was 45-76%. Infused E6 T cells demonstrated engraftment at one month post-treatment in all patients (range 4-53%). Two of nine subjects in the highest dose cohort experienced tumor responses. A subject with a 6-month partial response had complete regression of one lesion and partial regression of two lesions, which were subsequently resected; the subject has no evidence of disease three years after treatment. Resected tumor from this subject demonstrated infiltration by E6 T cells that showed increased expression of the inhibitory molecule PD-1 as compared to E6 T cells in the peripheral blood (26% vs 2%). Genomic analyses were performed on the tumors of two subjects who did not respond to treatment. One subject displayed a frameshift deletion in the interferon-gamma response gene, IFNGR1. Another demonstrated loss of heterozygosity (LOH) in chromosome 6 with deletion of HLA-A*02:01, the necessary restriction element for this therapy. A subject who responded to treatment did not demonstrate genomic alterations in these pathways. Conclusions: Engineered T cells targeting E6 can induce regression of HPV+ epithelial cancers. Treatment resistance may be related to T-cell inhibition by PD-1, tumor evasion by antigen processing and presentation loss, and defects in interferon-response pathways. Clinical trial information: NCT02280811.
Molecular profile in non-small cell lung cancers (NSCLCs) occurring in elderly.
Authors: Caterina Fumagalli, Massimo Barberis, Davide Vacirca, Francesca Lombardi, Vincenzo Bagnardi, Filippo De Marinis, Lorenzo Spaggiari, Antonio Passaro, Chiara Catania, Giuseppe Viale, Elena Guerini Rocco
Journal: Journal of Clinical Oncology (2016)

10053 Background: More than 40% of NSCLCs are diagnosed in patients older than 70 years. Elderly have more comorbidities and are less tolerant to chemio-radiotherapies than younger but targeted treatments such as epidermal growth factor receptor (EGFR) or anaplastic lymphoma kinase (ALK) inhibitors could be well tolerated. Here, we sought to define the genetic profile of NSCLCs in patients older than 70 years Methods: In this single-institution study, we evaluated EGFR, KRAS mutations and ALK rearrangements in 880 pulmonary adenocarcinomas (ADK) occurring in patients older than 70 years (median 75 yrs) compared to a consecutive series of 409 patients younger than 60 years (range 18-60, median 55 yrs). Mutational status was analyzed with bi-directional Sanger sequencing and ALK rearrangement was evaluated by fluorescence in-situ hybridization (FISH). Statistical analysis was performed by Pearson's chi-square test Results: There was no difference in the prevalence of EGFR mutations between elderly and younger patients. Nevertheless, both ALK rearrangements and KRAS mutations occurred less frequently in the elderly. Moreover, statistically significant differences in KRAS codons involved and gender prevalence of KRAS mutations were found (Table) Conclusions: Though KRAS and ALK alterations are less frequent in elderly patients, no significant differences in EGFR mutations prevalence were found. Routine molecular tests driving targeted therapies should be offered to all ADK patients regardless of age. GENE N ≥ 70 yrs N ≤ 60 yrs P VALUE MUT/REARR WT MUT/REARR WT EGFR 880 140 (15.9%) 740 (84.1%) 490 91 (18.6%) 399 (81.4%) 0.21 KRAS 544 151 (27.8%) 393 (72.2 %) 274 104 (38%) 170 (62%) 0.0030* ALK 601 15 (2.5%) 586 (97.5 %) 256 15 (5.9%) 241 (94.1%) 0.014* EGFR MUT EX 18 6 (4.3%) 5 (5.5%) EX 19 83 (59.3%) 47 (51.6%) EX 20 4 (2.9%) 7 (7.7%) EX 21 41 (29.3%) 23 (25.3%) EX 20 + OTHERS (18-20; 19-20; 20-21) 6 (4.2%) 9 (9.9%) TOT 140 91 0.1700 KRAS MUT COD 12 126 (83.44 %) 95 (91.3%) COD 13 13 (8.6%) 8 (7.7%) COD 61 12 (7.9%) 1 (1%) TOT 151 104 0.041* EGFR MUT F 97 (69.3%) 56 (61.5%) M 43 (30.7%) 35 (38.5%) 0.22 KRAS MUT F 41 (27.2%) 45 (43.3%) M 110 (72.8%) 59 (56.7%) 0.0075* ALK REARR F 7 (46.7%) 12 (80%) M 8 (53.3%) 3 (20%) 0.06 F = Female M = Male MUT = Mutation REARR = Rearrangement * p < 0.05