tbuckley/cabot-search huggingface dataset:
Clinical value of Ki67 in risk-stratifying HR-positive breast cancer.
Authors: Ajaz Bulbul, Emilio Paul Araujo-Mino, Adriana Bautista, Sadaf Rashad, Masoud Khorsand-Sahbaie
Journal: Journal of Clinical Oncology (2019)

e12540 Background: Oncotype DX (ODX) is a validated clinical tool requiring efficient utilization. Ki67 protein immunohistochemistry (IHC) may represent a screening approach correlating with the Recurrence score (RS) in resource limited setting. Methods: We retrospectively studied 242 patients (Jan. 1989 – Oct. 2017) across rural practices in NM. Median time to follow-up was 8.9 (0.03, 26.8) yrs. ODX candidates evaluated included node positive (NP), negative (NN), hormone receptor (HR) positive and HER2 negative cohort. Ki67 &lt;20% (LKi-n=196) vs &gt;20% (HKi-n=46) was compared to Low/Intermediate (LODX-n=202) vs High risk ODX (HODX-n=40). Descriptive statistics, Chi-square, Kaplan Meier survival and Cox proportional hazard models were used. Results: Median age was 64 ± 13.2. Stage I (54.1%), II (42.6 %), and III (3.3%); Grade 1 (24.2%), 2 (46.7%), 3 (24.9%). LKi in (196/242) 81%, HKi in (46/242) 19%. LODX in (202/242) 83.4%, HODX in 40/242 (16.5%). LKi was associated with stage I (87%), II (78%) vs. Stage III (25%) (p=0.015). LKi was associated with lower grades 1 (100%), 2 (92%) vs grade 3 (40%) (p=&lt;0.001). LKi was associated with LODX (190/242) 94% and HKi with HODX (34/40) 85% (p &lt;0.001). ODX recategorized 3% (6/196) LKi into HODX and 26% (12/46) HKi to LODX. LKi vs HKi 10-year FFP was 0.97 + 0.01 vs 0.73 + 0.08 HR 8.31 (3.12, 22.14)(p=&lt;0.01) and 10-year OS was 0.87 + 0.03 vs 0.78 + 0.08 HR 1.77 (0.84, 3.78) (p=0.13), respectively. Ten-year OS in LKi was 0.98 + 0.02 vs 0.97 + 0.02 HR 0.42 (0.04, 3.62) (p= 0.43) with (n=46) or without (n=121) adjuvant chemotherapy respectively. Conclusions: LKi is predictive of excellent outcomes. It may have a role in risk stratification when access to ODX is limited. Lack of standardization of Ki67 reiterates the value of ODX. Prospective data are needed to confirm these findings.
CA224-060: A randomized, open label, phase II trial of relatlimab (anti-LAG-3) and nivolumab with chemotherapy versus nivolumab with chemotherapy as first-line treatment in patients with gastric or gastroesophageal junction adenocarcinoma.
Authors: Kynan Feeney, Ronan Kelly, Lara Rachel Lipton, Joseph Chao, Mirelis Acosta-Rivera, Dennis Earle, Ming Lei, Georgia Kollia, Niall C. Tebbutt
Journal: Journal of Clinical Oncology (2019)

TPS4143 Background: Blockade of the immune checkpoint receptor programmed death-1 (PD-1) has shown clinical benefit in multiple tumor types. Nivolumab (anti–PD-1) has demonstrated a survival advantage versus (vs) placebo in patients (pts) with advanced gastric cancer (GC) or gastroesophageal junction cancer (GEJC) (Kang YK et al. Lancet 2017;390:2461–71). Lymphocyte activation gene 3 (LAG-3) is an immune checkpoint molecule that negatively regulates effector T-cell function and is a marker of T-cell exhaustion. Preliminary data in melanoma suggest that combining nivolumab with relatlimab (anti–LAG-3) could improve efficacy without substantially increasing toxicity vs nivolumab especially, but not exclusively, in LAG-3-expressing pts (Ascierto PA et al. Ann Oncol 2017;28(S5):LBA18). Furthermore, LAG-3 expression was as high as 33% in an analysis of solid tumors including GC (Edwards R et al. J Immunother Cancer 2017;5(S3):P510). Study CA224-060 will assess the clinical efficacy and safety of relatlimab and nivolumab with chemotherapy for first-line treatment of GC or GEJC. Methods: This is a randomized, open-label, multicenter, phase 2 study of relatlimab and nivolumab with oxaliplatin-based chemotherapy vs nivolumab with oxaliplatin-based chemotherapy. Approximately 250 adult pts with untreated, locally advanced, unresectable or metastatic GC or GEJC will be enrolled. To be randomized, pts must have tumor tissue for analysis of biomarkers, LAG-3 status, and PD-L1 combined positive score. Key exclusion criteria include HER2-positive status, untreated CNS metastases, or significant cardiovascular disease. The primary endpoint is objective response rate (ORR) using RECIST v.1.1 by blinded independent central review in LAG-3-expressing pts. Other endpoints include investigator-assessed ORR, ORR in LAG-3-negative pts, duration of response, overall survival, progression-free survival, and safety and tolerability. Efficacy signals in biomarker subgroups will be explored. Currently, 26 sites are activated with 15 randomized pts. Clinical trial information: NCT03662659.
Effect modifiers in a randomized phase III trial of low-dose tamoxifen in breast preinvasive disease.
Authors: Andrea De Censi, Matteo Puntoni, Aliana Guerrieri-Gonzaga, Silvia Caviglia, Franca Avino, Laura Cortesi, Antonio Ponti, Maria Grazia Paquola, Fabio Falcini, Marcella Gulisano, Maria Digennaro, Anna Cariello, Katia Cagossi, Harriet Ann Johansson, Graziella Pinotti, Matteo Lazzeroni, Tania Buttiron Webber, Davide Corradengo, Luca Boni, Bernardo Bonanni
Journal: Journal of Clinical Oncology (2019)

1500 Background: Low-dose tamoxifen (babytam) at 5 mg/day for 3 years decreases local or contralateral recurrence by 52% in women with hormone sensitive breast pre-invasive neoplasia after surgery (DeCensi et al JCO 2019). Here we report the results of exploratory analyses to assess whether the benefit of babytam varies among subgroups of patients defined by individual characteristics. Methods: Post-hoc subgroup analyses were performed according to a mixed approach based on the test for interaction and biological plausibility. Incidence of invasive breast cancer or DCIS was the primary endpoint. HRs were estimated using Cox proportional-hazards modeling. Results: Age at menopause, smoking status and Ki-67 exhibited a significant interaction with treatment. Specifically, the effect of babytam was greater in women aged &gt; 50y (n = 293, HR = 0.27, 95%CI: 0.10-0.73) than in women aged ≤50y (n = 207, HR = 0.86, 0.35-2.07), p-interaction = .09. Never smokers (n = 307) had a greater benefit than former (n = 68) or current smokers (n = 97): HR = 0.28, 0.11-0.70 vs HR = 0.57, 0.09-3.45 vs HR = 1.51, 0.41-5.64, respectively (p = .05). Tumors with Ki-67 above the median level of 10% (n = 133) had a greater effect (HR = 0.27, 0.09-0.81) than Ki-67 ≤10% (n = 145, HR = 1.58, 0.45-5.60, p = .04). Weaker statistical interactions (p &gt; .1) were also found for waist circumference and hot flashes (HF) at baseline. Women with waist circumference ≥89 cm (metabolic syndrome, n = 208) had a greater effect (HR = 0.22, 0.07-0.78) than women &lt; 89 cm (n = 228, HR = 0.61, 0.25-1.46). Compared with placebo and no HF, babytam effect was stronger in women with HF (HR = 0.13, 0.02-0.96) than in women on babytam and no HF (HR = 0.50, 0.24-1.03) or placebo and HF (HR = 0.72, 0.31-1.69, log-rank p-trend = .004). Additional subgroups according to obesity, family history of breast or ovarian cancer, alcohol use, extent of surgery, radiotherapy for DCIS, ER and HER2 expression, positive margins and treatment compliance showed no significant heterogeneity of treatment. Conclusions: Exploratory analyses showed a trend to a higher effect of babytam in women aged 50 or older, never smokers, women with hot flashes or abdominal obesity and tumors with Ki-67 above 10%. Our results provide insight into the efficacy of babytam towards a personalized preventive approach. Clinical trial information: NCT01357772.
Development of a baseline prognostic cytokine signature that correlates with nivolumab (NIVO) clearance (CL): Translational pharmacokinetic/pharmacodynamic (PK/PD) analysis in patients with renal cell carcinoma (RCC).
Authors: Rui Wang, Xiao Shao, Junying Zheng, Yuko Ishii, Irene Pak, Amit Roy, Akintunde Bello, Richard Lee, Joshua Zhang, Megan Wind-Rotolo, Yan Feng
Journal: Journal of Clinical Oncology (2019)

2544 Background: CL of checkpoint inhibitors has been identified as a predictive covariate of overall survival (OS) in several tumors. Determination of CL requires post-treatment samples, which negates its utility as a baseline prognostic biomarker. This study aims to identify a baseline composite cytokine signature that correlates with NIVO CL in patients with RCC using translational PK/PD analysis. Methods: Peripheral serum PK (NIVO CL) and serum biomarkers to assess PD (Myriad Rules-Based Medicine customized inflammatory cytokine panel) were analyzed from 985 patients with RCC enrolled in 3 clinical trials. CheckMate (CM) 009 (NCT01358721) and CM 025 (NCT01668784) of NIVO (n = 481) were used for model development (training dataset). CM 010 (NCT01354431) of NIVO and a cohort treated with everolimus in CM 025 were included in model application (test dataset; n = 504). PK/PD analyses were conducted using a machine learning algorithm with performance assessed by receiver operating characteristic (ROC) curve and accuracy by confusion matrix. Results: The model selected the top-10 baseline inflammatory cytokines to form a composite cytokine signature, which predicted NIVO CL (high vs low) that was significantly associated with OS (p &lt; 0.001) across all 3 studies (training and test datasets). The same cytokine features were associated with OS of everolimus (p &lt; 0.01), suggesting the potential prognostic nature of the composite signature. The PK/PD analysis provided a robust description of the association between selected cytokines and CL (ROC = 0.71). Identified cytokines (eg, serum C-reactive protein known to reflect immune cell modulation) have been shown individually to be associated with RCC prognosis. A multivariable approach resulting in tumor-specific composite signatures may provide more accurate prognostic value. Conclusions: The baseline composite cytokine signature could serve as a clinically useful biomarker for patients with RCC, pending further evaluation, as it may provide improved prognostic accuracy for long-term clinical outcome compared to individual cytokines.
Sex-specific mortality trends in adolescents and young adults with cancer from 2007 to 2016.
Authors: Allison Close, Brittani Seynnaeve, Kimberly Miller, Louis Rapkin
Journal: Journal of Clinical Oncology (2019)

1570 Background: Adolescents and young adults (AYA) aged 15-39 years make up approximately 70,000 new oncology cases in the USA. Historically, mortality from cancer has smaller incremental improvements in AYA patients when compared to children and older adults, and not much is known about current sex-specific trends. We assessed overall and sex specific AYA mortality for the last 10 years (2007-2016). Methods: Trends in age-adjusted mortality rates per 100,000 (1972-2016) were obtained from the CDC’s National Center for Health Statistics (NCHS). Average annual percent changes (AAPCs) in relative survival were analyzed using NCI’s JPSurv webtool and mortality AAPCs were quantified using Joinpoint regression analysis. Results: Overall declines in mortality are similar in AYA men and women from 1972-2016, with 54% and 51% decline, respectively. In the most recent 10 years of data (2007 to 2016), combined sex AYA mortality AAPC’s declined by about 0.8% per year, slightly slower than declines in children &lt;15 years (1.3% per year) and adults ages &gt;40 years (1.5% per year). Among AYA males there have been 10 year AAPC mortality declines in leukemia (-1.8%), Hodgkin lymphoma (HL) (-5.1%), Non-Hodgkin lymphoma (NHL) (-4.1%) and melanoma of the skin (-3.4%). For AYA females, 10 year AAPC mortality declines occurred in leukemia (-1.9%), ovarian (-1.5%), HL (-10%), NHL (-4.9%) and melanoma (-2.8%). These declines have been offset by stable or increasing mortality rates for several common AYA cancers, including colorectal cancer (CRC) (1.1%) and bone and joint cancer (0.6%) in AYA males. AYA females have experienced mortality increases for CRC (0.6%), bone and joint cancer (0.5%) and uterine corpus cancer (2.8%). Conclusions: In general, mortality rates for both AYA men and women have declined over the past 10 years due to decreased mortality in hematologic malignancies and melanoma. Despite overall improvement, tumor categories in both AYA males and female such as CRC, bone and joint cancer, and uterine corpus cancers show increasing mortality. These diseases require specific investigations by both pediatric and adult researchers.
Tracking plasma KRAS mutations (mu) in lung adenocarcinoma (LUAC) patients (p) and branching evolution.
Authors: Jillian Bracht, Niki Karachaliou, Richard B. Lanman, Daniel Dix, Iris Faull, Rebecca Nagy, Noemí López, Ramon Palmero, Santiago Viteri Ramirez, Margarita Majem, Alvaro Taus, Enric Carcereny Costa, Javier Garde, Francois Riva, Andrea Malfettone, Miguel Sampayo, Ana Drozdowskyj, Enriqueta Felip, Rafael Rosell
Journal: Journal of Clinical Oncology (2019)

9055 Background: KRAS m in LUAC p are recalcitrant to therapy. In mice models and p, STK11 m confer poor prognosis. Patients with KRAS, or KRAS with TP53 m, benefit from immunotherapy (IO). We used a cell free DNA (cfDNA) sequencing platform to sub-group 53 LUAC p with KRAS m from the Spanish Lung Liquid versus Invasive biopsy Program (SLLIP, NCT03248089), according to the coexistence of TP53 and STK11 m. We evaluated the treatment outcome in the KRAS subgroups and we explored the mutational evolution at 2 weeks (w), and at the end of the study (EOS). Methods: SLLIP was a multi-center observational study in patients with treatment-naïve metastatic LUAC. Genotyping, with a clinically validated cfDNA assay (Guardant360) was performed at 3 time points: before start of treatment, at 2 w, and upon progression or at 12 months (mo). Oncoprints were constructed based on mutation status and variant allele frequency (VAF). Results: 53 p with KRAS alterations were included. 36 male; median age 59; 46 current/ex-smokers; 64% received 1 st line platinum-based chemotherapy (CT), 4% platinum-based CT+IO, 8% platinum-based CT plus bevacizumab, and 24% other or no therapy. 13 p had only KRAS m (K-only group), 25 p had KRAS + TP53 m (KP group), and 15 p had KRAS + STK11 with or without TP53 m (KS group). Median progression-free survival was 3.5 mo for all 53 p, 4.8 mo for the K-only group, 4.4 mo for the KP group, and only 2.6 mo for the KS group (p = 0.05 for KS versus K-only). The average VAF for K-only, KP, and KS groups at EOS were 6.4%, 9.7%, and 46%, respectively. When looking at p with cfDNA analysis at the three time points, the following were observed: In the K-only group, 25% lost KRAS m at 2 w and 50% at EOS. 50% and 75% gained TP53 m, at 2 w and EOS, respectively. None gained STK11 at the 2 time points. In the KP group, 40% lost KRAS m at 2 w but all had KRAS m at EOS. 20% and 10% lost TP53 m, at 2 w and EOS, respectively. 10% gained STK11 m at the 2 time points. In the KS group, 33% lost KRAS m at the 2 time points. All and 33% lost STK11 m at 2 w and EOS, respectively. 66% gained TP53 at the 2 time points. Conclusions: Subgroups of KRAS m traced in cfDNA confirm dismal prognosis to 1 st line therapies. These findings prompt us to tailor IO for K-only or KP subgroups. For p with STK11 m, restoration of the STK11 function is warranted. Clinical trial information: NCT03248089.
Comparative genomic profiling from tumor tissue and circulating tumor DNA (ctDNA) in 111 patients (Pts) with metastatic clear cell renal cell carcinoma.
Authors: Ritesh Kotecha, Erika Gedvilaite, Samuel J. Murray, Robert J. Motzer, Dana Tsui, Martin Henner Voss
Journal: Journal of Clinical Oncology (2019)

4565 Background: Circulating tumor DNA (ctDNA) assessment is a non-invasive approach for genomic interrogation of solid tumors. As a novel tool, key benchmarks for applications in metastatic clear cell renal cell carcinoma (mccRCC) are yet to be determined. To understand the utility of ctDNA, we performed a large cohort analysis using a comparative genomics approach integrating matched primary tissue and ctDNA genomic data. Methods: Pts with prior tumor mutational profiles generated via next generation sequencing (NGS) from nephrectomy or metastatic specimens underwent single-time point plasma collection. Targeted NGS sequencing with MSK-IMPACT was performed on tumor and ctDNA with subsequent bi-directional cross genotyping using Waltz 2.0. All pts had matched germline comparison from peripheral blood; clinical data was extracted from medical record. Liberal (1-2 reads) and stringent (≥3 reads) filters were applied, with a cut-off of &lt; 30% allele frequency to remove germline mutations. Results: 111 mccRCC pts, of whom available IMDC-risk was favorable (35%), intermediate (60%), and poor-risk (5%) were included for analysis. The median time between tissue and ctDNA collection was 23 months (R: 1-177), and 96% of patients had undergone nephrectomy prior to ctDNA collection. In primary tissue sequencing, 64/111 (58%) from nephrectomy and 42/111 (42%) from metastatic sites, 569 unique alterations were identified across the whole cohort, with a median of 4 mutations/pt (R:1-23). RCC-specific alterations included VHL (88%), PBRM1 (48%), SETD2 (34%), KDM5C (17%), TP53 (14%). Across the cohort, 176 alterations were identified in ctDNA. With cross genotyping, ctDNA alterations concordant with primary tumors were detected in 20% (22/111 pts, 28 unique alterations) using stringent criteria with a median of 1 mutation/pt (R:1-2). Using liberal criteria, concordance with primary tumors was 59% (66/111 pts, 142 unique alterations) with a median of 2 mutations/pt (R: 1-8). Conclusions: This large cohort study matching oncogenomics from tumor and ctDNA highlights complexities and challenges of applying liquid biopsy in biomarker development in mccRCC.
RESIST-PC phase 2 trial: 177Lu-PSMA-617 radionuclide therapy for metastatic castrate-resistant prostate cancer.
Authors: Jeremie Calais, Wolfgang P Fendler, Matthias Eiber, MIchael Lassmann, Magnus Dahlbom, Rouzbeh Esfandiari, Jeannine Gartmann, Kathleen Nguyen, Pan Thin, Vincent Lok, Ken Herrmann, Johannes Czernin, Ebrahim Delpassand
Journal: Journal of Clinical Oncology (2019)

5028 Background: This is an investigator-initiated open-label prospective bi-centric single-arm phase 2 clinical trial (NCT03042312) of 177 Lu-PSMA-617 radionuclide therapy in patients with progressive metastatic castrate-resistant prostate cancer (mCRPC). Methods: Patients with progressive mCRPC (biochemical, radiographic or clinical) after ≥1 novel androgen axis drug (NAAD), either chemotherapy (CTX) naïve or post-CTX, with sufficient bone marrow reserve and normal kidney function were eligible. All patients underwent a screening PSMA PET/CT to confirm target expression. Patients received up to 4 cycles of 177 Lu-PSMA-617 every 8±1 weeks and were randomized into 2 treatment activities groups (6.0 or 7.4 GBq). Kidney dosimetry was performed for the first cycle. Efficacy was defined as serum PSA decline of ≥50% from baseline at 12 weeks and served as primary endpoint. Results: 64 patients (median PSA 75 ng/ml; range 0.5-2425) were included in the study. 20% were CTX naïve while 80% were post-CTX (1.9 CTX regimens on average, range 1-4). 45% completed 4 cycles of 177 Lu-PSMA-617. Androgen deprivation therapy was given concomitantly in 83%, NAAD in 23% and immunotherapy in 6%. PSA decline of ≥50% was observed in 23% of patients at 12 weeks and in 38% of patients at any time (best PSA response). The median time to best PSA response was 22 weeks (range 6-49 weeks). 16% had a PSA decline of ≥90% and 59% had any PSA decline ( &gt; 0%). Mild and transient (CTCAE grade 1-2) side effects included xerostomia (72%), nausea/vomiting (69%) and bowel movement disorders (45%). CTCAE grade 3 toxicity included nausea/vomiting (6%), anemia (8%), leukopenia (5%), kidney failure (3%), thrombocytopenia (3%), and neutropenia (3%). The mean kidney dose was 2.7 Gy for the first cycle (range 0.9-5.9) i.e. 0.4 Gy/GBq (range 0.15-0.9). There was no difference between the efficacy and toxicity for the 6.0 GBq (n = 23) and 7.4 GBq (n = 41) treatment arms. Conclusions: 177 Lu-PSMA-617 radionuclide therapy is well tolerated in patients with progressive mCRPC. PSA declined by ≥50% in 38% of patients. The best PSA response rate occurred after 3 cycles. Updated data will be provided at the time of the conference. Clinical trial information: NCT03042312.
A phase Ib/II trial of lenvatinib (len) and letrozole (let) incorporating pharmacodynamics studies in postmenopausal women with hormone receptor positive (HR+) locally advanced/metastatic breast cancer (LABC/MBC).
Authors: Joline Si Jing Lim, Andrea Li Ann Wong, Samuel Guan Wei Ow, Lim Siew Eng, Raghav Sundar, Gloria HJ Chan, Kritika Yadav, Valerie Heong, David Shao Peng Tan, Ross A. Soo, Cheng Ean Chee, Wei-Peng Yong, Boon C. Goh, Soo-Chin Lee
Journal: Journal of Clinical Oncology (2019)

1045 Background: Endocrine blockade (EB) is standard of care for patients (pts) with HR+ LABC/MBC. RET over-expression (RET+) occurs in up to 75% of HR+ breast cancers and is a postulated mechanism of endocrine resistance. Preclinical studies show cross talk between RET and estrogen receptor, and at least additive treatment (Tx) effect of Len+EB. Methods: We performed a phase Ib trial (3+3 dose escalation) to study safety, tolerability, pharmacodynamics and efficacy of Len+Let. Both drugs were given as continuous daily dosing with 2 weeks (wks) of Len alone, followed by Len+Let for 12 wks then surgery (LABC), or till disease progression (PD) (MBC). Serial tumor biopsies (n = 15) were done at baseline, after Len alone, 4 wks post Len+Let, and at surgery [LABC] / upon PD [MBC]. Results: 16 pts were treated (4 LABC, 12 MBC); Among MBC pts, median lines of prior Tx was 3 (range 0-10); 84.6%, 66.7%, and 58.3% had prior EB, EB+CDK4/6 inhibitor (i), and chemotherapy (CT) respectively. At dose level (DL) 1, 2/4 pts had dose-limiting toxicities (DLT). There was no DLT at DL-1, but 6/6 pts needed dose reductions (DR), with 4/6 DR within 6 wks of Len+Let (3 G3 hypertension [HTN], 1 G3 wound pain), deeming DL-1 intolerable. At DL-2, 0/6 pts had DLT; this was declared recommended phase 2 dose (RP2D). Most frequent G3 toxicities (tox) were HTN (6/16), proteinuria (2/16) and palmar-plantar erythrodysesthesia (PPE) (2/16), with no G4/5 tox. Len+Let was active with 93.8% overall disease control rate (DCR) (50.0% partial response [PR], 43.8% stable disease [SD]). Among MBCts (8/12 had prior EB+CDK4/6i), DCR ≥12 wks was 91.7%; 1 pt had sustained PR for 48 wks and 1 ongoing PR at 40 wks. 9/16 pts had RET+ tumors on immunohistochemistry at baseline, and 66.7% showed down-regulation with Tx (RECIST: 4 PR, 2 SD). Conclusions: Len+Let showed significant anti-tumor activity, even in pts who failed prior CT or EB+CDK4/6i. RP2D of 14mg Len and 2.5mg Let is tolerated with efficacy; dose expansion is currently underway. Clinical trial information: NCT02562118. [Table: see text]
Case 12-1986
Authors: Richard C. Cabot, Robert E. Scully, Eugene J. Mark, Betty U. McNeely, Warren E. Grupe, Robert B. Colvin
Journal: New England Journal of Medicine (1986)

Presentation of CaseA 15-year-old boy was admitted to the hospital because of hemoptysis.He was well until two weeks earlier, when pain and swelling developed in the left knee shortly after a fall and were accompanied by symptoms of an upper respiratory tract infection. One week later he was seen at this hospital. The temperature was 38.9°C. The pharynx was reddened; no lymphadenopathy was found, and the lungs were clear. The left knee was warm, with a small effusion; there was a full passive range of motion, with pain that was most prominent on extension; tenderness was elicited over . . .
A Randomized, Double-Blind, Phase III Study Comparing Proposed Biosimilar Rituximab (RTXM83) Versus Reference Rituximab, Both in Combination with CHOP, in the First Line Treatment of Patients with Diffuse Large B-Cell Lymphoma (DLBCL)
Authors: Myrna Candelaria, Derlis Emilio Gonzalez, Surender Kumar Beniwal, Lokanatha Dasappa, Daniel Oscar Bar, Marcia Torresan Delamain, Ashis Mukhopadhyay, David Hugo Flores, Dinesh Bhurani, Venkatraman Radhakrishnan, Alejandro Salvatierra, Ruben Dario Kowalyszyn, Oleg Lipatov, Moosa Patel, Sergio Schusterschitz, Elena Volodicheva, Luis Antonio Perez
Journal: Blood (2017)