tbuckley/cabot-search huggingface dataset:
Clinical significance of HFE gene mutations in patients with refractory anemia with ring sideroblasts (RARS).
Authors: Rama Nanah, Mrinal Patnaik, Naseema Gangat, Darci Zblewski, Rong He, Phuong L. Nguyen, Michelle A. Elliott, William J. Hogan, Mark Robert Litzow, Aref Al-Kali
Journal: Journal of Clinical Oncology (2017)

e18556 Background: RARS is a subtype of myelodysplastic syndromes (MDS) defined by &lt; 5% blasts and ≥15% ring sideroblasts (WHO 2008). Hereditary hemochromatosis is a disorder characterized by dysregulations in iron absorption, largely associated with C282Y and H63D mutations of the HFE gene. Iron levels are elevated in both disorders and pathophysiologic correlations were suggested. HFE gene mutations were previously found higher in MDS compared to controls (50% vs 36%) ( Nearman et al, Am J Hematol 2007). Methods: A total of 168 RARS patients’ data from 1994 to 2015 at Mayo Clinic were reviewed after appropriate IRB approval was obtained. All cases had their bone marrow slides reviewed at our center. We searched patients’ records retrospectively to Identify those tested for HFE gene (C282Y, H62D, S65C) mutations, done inside or outside our institution. Survival estimates were calculated using Kaplan-Meier curves. Results: Out of the 168 RARS patients, only 17 (10%) were tested for HFE gene mutations. Out of the 17 tested, 11 (65%) were found to have mutations; 2 of which (18%) had homozygous H63D mutation, 1 patient (9%) had double heterozygous H63D and C282Y mutations, 5 (45%) had only one H36D heterozygous mutation vs 3 patients (27%) with only one C282Y heterozygous mutation. Only one patient was tested for the additional S65C mutation and it was not detected. H63D mutation was present in a total of 8 patients (73%) vs C282Y mutation which was present in 4 patients (36%). Bone marrow iron stores were increased in all 17 tested patients, except one who had decreased stores, this patient had one heterozygous C282Y mutation. Median overall survival (mOS) was 117 months in the HFE mutated patients vs 75 months in the non-mutated (p = 0.6). Conclusions: Our study found the HFE gene, when tested, to be mutated in higher frequencies among patients with RARS compared to that reported in the general population (65% vs 36%), with H63D mutation in almost three quarters of all mutated patients. Although it did not reach statistical significance, the longer survival observed among HFE mutated patients compared to the wild-type raises the question whether testing for HFE gene mutations among patients with MDS-RARS should be further explored.
Effects of hydrogen gas on exhausted CD8<sup>+</sup> T cells (PD-1-positive, terminally differentiated CD8<sup>+</sup> T cells).
Authors: Junji Akagi, Hideo Baba
Journal: Journal of Clinical Oncology (2017)

e23071 Background: CD8 + T cells progress from an early-differentiated (early-CD8 + T cells) to a terminally differentiated state (terminal-CD8 + T cells). PD-1 expression is rapidly upregulated in antigen-activated T cells, and rapidly downregulated when the antigen is cleared. In the presence of persistent antigen stimulation, such as that in cancer patients, PD-1 expression is not downregulated and terminal-CD8 + T cells become exhausted. Methods: Using flow cytometry, we investigated PD-1 expression in CD8 + T cells in the peripheral blood of 37 patients with stage IV cancer, before and after they received hydrogen gas treatment. We analyzed associations between treatment and progression-free survival (PFS) using Cox and Kaplan-Meier survival analyses. Results: Treatment lead to partial response (PR) in 12 patients and stable disease (SD) in 14 patients, with response rates of 32.4% and 37.8%, respectively (with an overall clinical response rate of 70.3%), and reduced the number of PD-1-positive, terminal-CD8 + T cells in 9 of 12 patients with PR (75%) and in 8 of 14 patients with SD (57%). However, in 8 of 11 patients with progressive disease (PD) (72.7%), these cell counts increased. Multivariate analyses demonstrated that higher PD-1-positive, terminal-CD8 + T cell counts were associated with shorter PFS periods, both before (hazard ratio [HR] = 3.23; 95% confidence interval [CI], 1.475–7.070; p = 0.003) and after (HR = 2.75; 95% CI, 1.273–5.951; p = 0.01) treatment, although the hazard ratio was decreased by treatment. Additional analysis showed that patients with higher PD-1-positive, terminal-CD8 + T cell counts had shorter survival rates than those with lower counts, both before and after treatment (log rank test, p = 0.001 and p = 0.005, respectively). The 20-month survival rates for patients with higher PD-1-positive, terminal-CD8 + T cell counts improved from 0% to 36.7% after treatment. Conclusions: These results suggest that PD-1-positive, terminal-CD8 + T cell counts are highly associated with PFS duration in patients with stage IV carcinomas, and hydrogen gas treatment contributes to clinical outcomes by reducing PD-1-positive, terminal-CD8 + T cell counts.
Up-regulation of <i>BAALC/MN1/MLLT11/EVI1</i> gene cluster in relation to <i>MYC</i> / BCL2 protein co-expression and poor overall survival in acute myeloid leukemia (AML).
Authors: Mohammad Omer Mansoor, Fahad Farooq, Ariz Akhter, Mohammad Kashif Mughal
Journal: Journal of Clinical Oncology (2016)

7045 Background: Molecular heterogeneity is the basis of dismal prognosis in AML. Current clinical risk evaluation by karyotyping and a few genetic mutations appear insufficient to provide defined directions for novel targeted therapies. Complex molecular technologies require transition into widely available laboratory platforms, like immunohistochemistry, for better integration into routine clinical / laboratory practices. MYC and BCL2 protein co-expression is associated with aggressive clinical behaviour in diffuse large B-cell lymphoma; however, this proteomic signature is not studied in AML patients, as risk stratification tool. Methods: In a defined subset (MYC+/BCL+ or MYC-/BCL-) of AML patients (n = 20), we utilized diagnostic bone marrow biopsy material to examine expression signature of several genes (n = 12) of established prognostic value in AML (TP53; RB1; NRAS; EVL1; MN1; ERG; MLLT11; PRAME; BAALC; FLT3; WT1; SOCS2; GUSB; TBP). Digital RNA quantification was determined, utilizing nCounter , Nanostring plate form. Transcript levels were correlated with MYC/BCL2 protein expression pattern; karyotype (favourable, intermediate and unfavourable risk group) and overall survival (OS), irrespective (+/-) of therapy or cause of death. Results: Unsupervised K-means++ clustering defined two distinct groups with high and low transcript levels of BAALC/MN1/MLLT11/EVI1/SOCS2 genes (> 2.0 fold difference; P < 0.001). Higher mRNA signature correlated with higher prevalence of MYC/BCL2 co-expression (P < 0.05) and poor OS (log rank test, P < 0.036) but remains unrelated to conventional cytogenetic risk groups (fisher exact test, P < 0.084). Conclusions: This pilot study present limited but useful data, to stipulate direction to refine the prognostication scheme of AML patients outside conventional cytogenetic risk groups. It also presents some biologic rationale to the use of novel agents targeting MYC and or BCL2 genes in combinational chemotherapy for AML patients.
Natural history of t(11;14) multiple myeloma (MM).
Authors: Arjun Lakshman, Muhamad Alhaj Moustafa, S.Vincent Rajkumar, Angela Dispenzieri, Morie A. Gertz, Francis Buadi, Martha Lacy, David Dingli, Suzanne R. Hayman, Wilson I. Gonsalves, Prashant Kapoor, Nelson Leung, Yi Lin, Ronald S. Go, Taxiarchis Kourelis, John Anthony Lust, Stephen Russell, Steven R. Zeldenrust, Robert A. Kyle, Shaji Kumar
Journal: Journal of Clinical Oncology (2017)

8014 Background: t(11;14) is a standard risk cytogenetic marker in MM. Methods: We reviewed 366 patients with MM who had t(11;14) by FISH and 732 age and period-matched controls without t(11;14), seen at our institution from 2004 to 2014 and outcomes were analyzed using time to first progression or death (PFS1) and overall survival (OS). Results: For the t(11;14) group at diagnosis, the median age was 63.7 yr (range, 22.1-95.4) with 64.5% of patients being male. Eighty nine (24.3%) patients were above 70 yr of age at diagnosis. 33.8%, 40.3% and 25.9% patients belonged to ISS 1, II and III stages respectively. 13% patients had elevated LDH. Monosomy 17 or del 17p were identified in 10.6% patients. The median follow up period was 56.9 months (m) (95% CI: 54.6-62.2) and 209 (57.1%) patients were alive at last follow-up. Among patients receiving proteasome inhibitor (PI)-based, immunomodulator (IMiD)-based, PI+IMiD based or other agent based induction therapy, 71.2%, 70.3%, 90.4% and 37.5% patients respectively attained ≥PR as best response to induction (p &lt; 0.01). During their course, 223 (60.9%) patients underwent stem cell transplant. Median PFS1 and OS were 23.1 (CI: 20.8-27.9) and 78.6 (CI: 66.7-105.9) m respectively. Among the controls, high risk cytogenetics (HRC) was present in 142 (19.4%), and the median OS was 83.8 m (CI: 70.8-97.0) being comparable to t(11;14) group (p = 0.8). For all 1098 patients, using a Cox-proportional hazards model with age &gt; 70 years, induction therapy (novel agent-based vs others), cytogenetics [HRC vs t(11;14) without HRC vs no HRC or t(11;14)], and ISS stage III vs II/I as predictors, age &gt; 70 years [HR-2.2 (CI: 1.8-2.8) and p &lt; 0.01], ISS III vs ISS II/I [HR-1.4 (CI: 1.1-1.8) and p &lt; 0.01] and HRC [HR of 2.1 (CI: 1.6-2.8) vs no HRC or t(11;14) (p &lt; 0.01) and 1.9 (CI = 1.4-2.6) for t(11;14) without HRC (p &lt; 0.01)were associated with reduced OS. The risk for reduced OS did not differ between t(11;14) without HRC, and those without t(11;14) or HRC [HR-1.1 (CI: 0.9-1.4), p = 0.4]. Conclusions: Our study characterizes the outcomes of a large cohort of MM patients with t(11;14) at diagnosis. Advanced age, HRC and advanced stage at diagnosis were associated with worse OS in our cohort. t(11;14) MM without HRC does not differ in outcome compared to non-t(11;14) MM without HRC.
Camrelizumab (SHR-1210) alone or in combination with gemcitabine plus cisplatin for nasopharyngeal carcinoma: results from two single-arm, phase 1 trials
Authors: Wenfeng Fang, Yunpeng Yang, Yuxiang Ma, Shaodong Hong, Lizhu Lin, Xiaohui He, Jianping Xiong, Ping Li, Hongyun Zhao, Yan Huang, Yang Zhang, Likun Chen, Ningning Zhou, Yuanyuan Zhao, Xue Hou, Qing Yang, Li Zhang
Journal: The Lancet Oncology (2018)
Prospective analysis of CEA, circulating DNA (cDNA) and circulating tumor cells (CTC) kinetics in patients (pts) treated for a metastatic colorectal cancer (mCRC).
Authors: David Sefrioui, Nasrin Sarafan-Vasseur, Emmanuel Toure, Julien Delacour, Frederic Ziegler, Caroline Thill, Alice Gangloff, France Blanchard, Ludivine Beaussire, Karine Bouhier Leporrier, Marie-Pierre Galais, Anne Perdrix, Florian Clatot, Fabrice Jardin, Jean-Christophe Sabourin, Thierry Frébourg, Pierre Michel, Frédéric Di Fiore
Journal: Journal of Clinical Oncology (2016)

3560 Background: CEA, cDNA and CTC have been reported as useful markers in mCRC pts treated with chemotherapy (CT)-based regimen. We previously reported that CEA kinetic (threshold 0.05) was associated with outcome [J Clin Oncol 2008;26:3681-6]. We designed a prospective muticentric trial for CEA kinetic validation and to evaluate cDNA and CTC kinetics. Methods: mCRCpts, PS 0-2, with CEA ≥ 5µg/L, who started a CT were included. Plasma were taken from baseline (T0) to the fourth cycle for CEA and at T0 and 6 weeks (W6) for cDNA and CTC kinetics. Cell-free DNA (cfDNA) was quantified by fluorimetric method, circulating tumour DNA (ctDNA) by Digital PCR, and CTC (CTC+ vs CTC-) by ScreenCellâ method. Primary endpoint was control disease (CD) (response/stable vs progressive disease (PD)) (RECIST 1.1) according to CEA kinetic. Secondary endpoints were progression-free survival (PFS) and overall survival (OS) according to T0 median CEA, cfDNA, ctDNA, CTC +/- and kinetics. Results: A total of 200 mCRC pts were included with a median follow-up of 12 months (m) (range 1-41). CtDNA was detected in 90% from the 95 RAS/BRAF mutated tumours. Mean CEA, cfDNA and ctDNA significantly decreased from T0 to W6 (respectively 436 vs 244, p < 0.0001; 98 vs 35, p = 0.01; 20.3 vs 5.2, p < 0.0001). A total of 54.7% were CTC+ at T0 versus 60% at W6 (NS). CEA kinetic (≤ 0.05 threshold) was associated with CD (90 vs 52%, p < 0.0001), PFS (8 vs 3 m; Hazard ratio (HR) 0.5, p < 0.0001) and OS (16 vs 12.5m, HR 0.62, p = 0.021). Median (low vs high) cfDNA and ctDNA at T0 were associated with PFS (7.8 vs 5.6m, HR 1.7, p = 0.0009 and 7.5 vs 5m, HR 2.1, p = 0.001, respectively) and OS (18.7 vs 13m, HR 2, p < 0.0001 and 19 vs 12m, HR 2.3, p = 0.0007, respectively). Among tested threshold, a decrease of ctDNA from T0 to w6 (factor > 2.6) was associated with CD (80 vs 20%, p < 0.0001) with a trend for PFS (p = 0.11). CEA kinetic > 0.05 (adjusted Odds Ratio (ORa) = 22.2), ctDNA kinetic ≤ 2.6 (ORa = 15.1) and median cfDNA (ORa = 0.10) were independent factor of PD. Conclusions: This prospective study confirmed that CEA kinetic is clinically relevant for CT monitoring in mCRC. Our results also highlight that cfDNA and ctDNA are both associated with outcome.
Management of transaminase elevations in patients receiving idelalisib.
Authors: William G. Wierda, Steven Coutre, Ian Flinn, Ajay K. Gopal, Susan Mary O'Brien, Gilles A. Salles, Andrew David Zelenetz, Terry Newcomb, Christopher C Waldapfel, Wei Ye, Paolo Ghia
Journal: Journal of Clinical Oncology (2016)

7532 Background: Transaminase elevation associated with idelalisib (IDELA) typically occurs early during treatment (median onset, 8 wk) and is often asymptomatic. Currently recommended management of grade [G] ≥3 (>5–20X upper limit of normal) ALT/AST elevation involves dose interruption with reinitiation upon resolution to G ≤1. This post hoc analysis evaluated outcomes after treatment-emergent G ≥3 ALT/AST elevation in IDELA clinical trials. Methods: An integrated safety analysis was conducted of 9 studies and 1073 patients (pts) with previously treated CLL (n=538), untreated CLL or SLL (n=105), and other previously treated B-cell malignancies (iNHL, MCL, DLBCL, AML, MM, Hodgkin lymphoma; n=430) who received IDELA alone (50–350 mg BID) or as combination therapy (100–150 mg BID). Clinical laboratory values were assessed for G ≥3 ALT/AST elevation, resolution to G ≤1, and event recurrence at any time on study. Results: Of all 1073 pts evaluated, 51% experienced any-grade ALT/AST elevation, with a median time to onset of 5.6 wk. The incidence of G ≥3 ALT/AST elevation was 14% with a median time to onset of 1st event of 5.6 wk and a median time to resolution of 3.3 wk. Outcomes for pts with G ≥3 ALT/AST elevation (table) were comparable whether IDELA was used alone or in combination. Conclusions: Of patients with G ≥3 ALT/AST elevation managed with IDELA dose interruption and subsequent rechallenge, 70% had no event recurrence. Most (95%) events that did recur resolved during the analysis period. These data support dose interruption at G3 with rechallenge at the treating physician’s discretion. Evaluations of pt characteristics associated with development of any-grade or G ≥3 ALT/AST elevation and G ≥3 ALT/AST recurrence, and of G ≥3 ALT/AST management based on (including but not limited to) early (≤3 mo) vs late onset and recurrence, resolution grade, steroid use, and repeated rechallenge, as well as related outcomes, are ongoing. Clinical trial information: NCT01539512, NCT01539291, NCT01659021, NCT01393106, NCT01282424, NCT01203930, NCT01090414, NCT010880.n (%) IDELA Combination (n=588) IDELA Alone (n=485) Total (N=1073) Pts with any G ≥3 ALT/AST 77 (13) 68 (14) 145 (14) Resolved to G ≤1 69/77 (90) 64/68 (94) 133/145 (92) Rechallenged 63/77 (82) 47/68 (70) 110/145 (76) Recurrence of G ≥3 ALT/AST 19/63 (30) 15/47 (32) 34/110 (31) Recurrence resolved to G ≤1 18/19 (95) 14/15 (93) 32/34 (94)
Results of long-term follow-up for patients with advanced gastrointestinal stromal tumor underwent palliative surgery after tyrosine kinase inhibitors therapy.
Authors: Haibo Qiu, Zhongguo Zhou, Xingyu Feng, Xiaowei Sun, Yingbo Chen, Yuanxiang Guan, Dazhi Xu, Yuanfang Li, Wei Li, Youqing Zhan, Rui-hua Xu, Zhiwei Zhou
Journal: Journal of Clinical Oncology (2016)

e22515 Background: Tyrosine kinase inhibitors (TKIs) have dramatic efficacy in the majority of patients with advanced gastrointestinal stromal tumors (GIST), while most of the patients developed resistant eventually, surgical debulking may prolong survival in patients with metastatic disease. Methods: We evaluated safety and clinical outcomes in a single institution series of advanced GIST patients from January 2002 to December 2008, Patients were categorized into two groups based on whether underwent surgical resection (Surgery Group vs Non-surgery Group). Results: 156 patients had been recruited in this study, including 87 patients underwent surgical resection and 69 patients kept on TKIs treatment. Preoperative agents were either imatinib (125 patients; 80.1%) or Sunitnib (31patients, 19.9%). There was no difference in the clinicalpathological features between two groups, 4 patients had surgical complications. Median follow-up was 23.7 months, the overall survival (OS) and Progression-Free Survival (PFS) of the patients in surgical group were longer than the non-surgical group, PFS: 46.1months vs 33.8 months (p < 0.01), OS: 54.8 months vs 40.4 months, the 2 years progression-free disease rate was 89.7% vs 85.5% (P < 0.01), respectively. In the subgroup analysis for the patients received surgery, 3 years progression-free survival was 93.3%, 46.9%, and 24% for patients with partial response, stable disease, progression to TKIs therapy (P < 0.01). Median PFS was 56.0 months in patients who were affected only by liver metastases, 64.0 months in those with peritoneal disease and 29.6 months in those with both liver and peritoneal metastases. Median PFS of patients underwent R0/R1 resection was 62.7 months compared with 29.4 months of the patients with R2 resection (P < 0.01). Conclusions: Patients with advanced GISTs have prolonged overall survival after debulking procedures. Surgery for patients with metastatic GIST who have responsive disease after TKIs treatment should be considered.
Ensartinib (X-396), a second-generation ALK TKI, in Chinese ALK-positive non-small cell lung cancer: A phase I, dose-escalation study.
Authors: Wenfeng Fang, Yuxiang Ma, Jianjin Huang, Yang Zhang, Benyan Zou, Hongyun Zhao, Yunpeng Yang, Yan Huang, Jing Zhao, Lieming Ding, Fenlai Tan, Li Zhang
Journal: Journal of Clinical Oncology (2018)

e21122 Background: Ensartinib (X-396) is a novel, selective, oral ALK inhibitor with 10-fold higher potency than crizotinib, which is effective and well tolerated in US ALK+ NSCLC patients at 225 mg QD as recommended phase 2 dose (RP2D). Here we present a phase 1 dose-escalation study of ensartinib in Chinese ALK+ NSCLC patients. Methods: Patients with advanced NSCLC and ALK+ were eligible. Starting dose was 150 mg once daily given continuously in 28-day cycle using a conventional 3+3 dose escalation design. At the RP2D, additional patients were enrolled in an expansion cohort. Results: 22 patients were enrolled and treated in this study ( 11 patients for dose escalation and 11 patients for dose expansion)Most patients with lung adenocarcinoma progressed on prior systemic treatment (including crizotinib and ceritinib). All patients experienced at least one treatment-related adverse event, in which 8 had grade 3 or higher events with skin rash (27.3%) as the most common one. DLT was seen in the 250 mg dose cohort including 2 grade 3 rash. At present, in 14 evaluable patients, partial response (measured at cycle 1) and stable disease were achieved in 9 (64.3%) and 3 (21.4%) patients, respectively. The key PK parameters are summarized in table 1. Updated curative effect and PK data will be presented at the 2018 ASCO annual meeting. Conclusions: Ensartinib was well tolerated in Chinese ALK-positive NSCLC patients with favorable antitumor activity.RP2D was established at 225 mg QD. A phase II, single-arm study is recruiting to further confirm the efficacy of ensartinib in crizotinib-resistant ALK-positive NSCLC patients in China (NCT03215693). Table 1 PK analysis Clinical trial information: NCT02959619. T1/2 (h) Tmax (h) Cmax (ng/mL) AUC 0-t (h*ng/mL) Single dose (Mean [SD]) 150mg (n = 3) 30.2 (5.34) 5 (2.65) 111 (16.2) 1400 (169) 200mg (n = 3) 24.9 (5.39) 3 (1) 240 (103) 2760 (1250) 225mg (n = 15) 29.5 (7.59) 3.6 (1.96) 221 (79.1) 2929 (1136) 250mg (n = 2) 21.0 (2.44) 4.0 (0) 226 (24.0) 3143.3 (724) Multiple dose (Mean [SD]) 150mg (n = 3) 29.9 (6.95) 3 (1.00) 272 (76.4) 3820 (546) 200mg (n = 3) 28.0 (5.87) 2.67 (1.15) 543 (157) 8620 (3330) 225mg (n = 9) 36.4 (14.02) 3.1 (0.78) 505 (208.5) 8132 (3640)
High SPARC expression in treated sarcomas may correlate with decreased overall survival.
Authors: Matthew Lasowski, Matthew Stemm, John A. Charlson, Manpreet Bedi, Alexander C. Mackinnon
Journal: Journal of Clinical Oncology (2016)

e22529 Background: The identification of prognostic and predictive indicators is an important area of research in oncology. Secreted protein acidic and rich in cysteine (SPARC) has been assessed as a correlative marker for tumor response in several types of cancer.[i] SPARC has also been demonstrated to be a prognostic marker in soft-tissue sarcomas (STS). [ii] In this study, we utilized quantitative immunohistochemistry (qIHC) to investigate SPARC expression in a heterogeneous STS population of paired biopsy (treatment naïve) and resected (neoadjuvant treated) STS samples. Methods: Tumor specimens were obtained from 35 patients at initial diagnosis and at time of resection after neoadjuvant treatment. SPARC expression was analyzed blindly using qIHC and interpreted as either high or low expression. Expression was determined by the Region Score, with 0-1.49 for low expression and ≥ 1.5 for high SPARC expression. Overall survival (OS) was determined by retrospective review of patient records. Kaplan-Meier and log-rank analysis were performed in regard to SPARC expression levels. Results: 19 of 35 and 16 of 35 patients had tumors with low and high SPARC expression, respectively, at time of initial biopsy. At resection, 18 of 35 and 17 of 35 had low and high SPARC expression, respectively, in their post-treatment STS. The populations were evenly distributed with regard to treatment, stage, Karnofsky Performance Status, smoking status, sex, and age. Kaplan-Meier curves showed no significant difference in OS between high or low SPARC expression at time of biopsy (p = 0.5669). There was a trend toward worse OS with high SPARC expression in the post-treatment resected tumors (23 mo vs. 53 mo, respectively, p = 0.0709) Conclusions: Quantitative analysis of SPARC expression in paired biopsy and resected STS from 35 patients suggests that high SPARC expression may be associated with decreased OS. However, further studies with larger sample size are warranted in order to detect the true correlation with survival and other factors influencing outcomes. i Desai N et al. Translational Oncology. 2009;2(2):59-64. ii Sherif S Morgan et al. Clinical Sarcoma Research 2014;4:2
Prospective front-line management patterns in the Real World Metastatic Renal Cell Cancer (MaRCC) Registry.
Authors: Michael Roger Harrison, Nrupen Anjan Bhavsar, Steven Paul Wolf, Brian Addis Costello, Ulka N. Vaishampayan, Christos Kyriakopoulos, Walter Michael Stadler, Hans J. Hammers, Leonard Joseph Appleman, Che-Kai Tsao, Sumanta K. Pal, Arif Hussain, Heather S.L. Jim, Azah Borham, Daniel J. George
Journal: Journal of Clinical Oncology (2016)

e16097Background: In the past decade, 8 regimens were approved for metastatic renal cell carcinoma (mRCC) leading to a quickly changing clinical landscape. Trials addressing treatment (tx) efficacy...