Prioritizing targeted therapies in an evidence-based manner, integrating biological context and functional precision medicine.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e14065-e14065
Author(s):  
Simina Boca ◽  
Krithika Bhuvaneshwar ◽  
Virneliz Fernandez-Vega ◽  
Jayaram Kancherla ◽  
Shruti Rao ◽  
...  
Keyword(s):  
Precision Medicine ◽  
Targeted Therapies ◽  
Evidence Based ◽  
Tumor Type ◽  
Molecular Alterations ◽  
Her2 Breast Cancer ◽  
Evidence Level ◽  
Molecular Profiles ◽  
Tumor Types ◽  
Biological Context

e14065 Background: It is becoming increasingly common for cancer patients to undergo molecular profiling of their tumors in order to see whether there are any actionable DNA, gene expression, or protein expression signatures. For example, individuals with ER+ or HER2+ breast cancer or KRAS wild type (non-mutated) colorectal cancer are prescribed specific targeted therapies. When an individual’s molecular alterations do not match any currently-approved recommendations for their tumor type, their clinician may consider prescribing a therapy approved in a different tumor type. Unfortunately, tumors often eventually become resistant to the therapies they are exposed to, leading to a narrowing of options after each therapy line. Methods: We previously developed CDGnet, an evidence-based approach and web-based tool for prioritizing targeted therapies based on tumor molecular profiles based on known pathways which provide biological context. CDGnet considers approved therapies with biomarkers among the alterations for the individual’s tumor type and other tumor types as the first and second evidence level categories respectively. These are followed by therapies that target or have as biomarkers genes or proteins downstream of altered oncogenes, considering curated pathways for the individual’s tumor type and other tumor types as the third and fourth evidence level categories respectively. We are currently expanding CDGnet in order to include data from high-throughput screening (HTS) experiments of NCI oncologic drugs performed on patient-derived organoids. The concept of “functional precision medicine” consists of using functional drug efficacy determination directly on individual patients, in this case by considering drugs with low half maximal effective concentrations (EC50) which are tested on tissues derived from the actual patients. Results: We will present extensions to CDGnet that allow users to upload both the molecular profiles and the HTS data to see whether any drugs are predicted by both approaches or whether specific combinations appear promising for further testing. Preliminary results on a set of glioblastoma samples will be presented. Conclusions: We hope that extending CDGnet to also include HTS data will eventually allow a truly multi-factorial personalized oncology approach, whereby both molecular alterations at the DNA, RNA, and protein levels and patient-derived organoids will be considered in deciding on treatment plans for individuals.

Incorporating HER2/HER3 targeted therapies across solid tumors: Assessing the impact of digital education on clinician practice patterns.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 11036-11036
Author(s):  
Tariqa Ackbarali ◽  
Wendy Turell ◽  
Elizabeth L. del Nido ◽  
Adam Brufsky ◽  
Stephen V. Liu
Keyword(s):  
Breast Cancer ◽  
Gastric Cancer ◽  
Clinical Practice ◽  
Patient Experience ◽  
Targeted Therapies ◽  
Her2 Breast Cancer ◽  
Treatment Plans ◽  
Tumor Types ◽  
Behavioral Impact

11036 Background: Improved understanding of the interactions between HER2 and HER3, the heterogeneity of HER-expressing disease, and mechanisms of resistance to anti-HER2 therapy has led to increasing number of treatment options to address clinical needs. Tumor types of interest, impacted by HER2/HER3 expression and pathophysiology were breast cancer, non-small cell lung cancer (NSCLC), gastric cancer, and colorectal cancer (CRC). Increasing competency in these areas is deemed critical to clinician’s ability to individualize treatment plans and improve patient outcomes. Methods: A 2-hour CME activity was broadcast live-online in September 2020 and remains on-demand through September 2021 at OMedLive.com. The educational initiative was divided into one hour addressing HER2 and HER3, testing guidelines, resistance mechanisms and emerging data elucidating recent and ongoing clinical trials across NSCLC, gastric cancer, and CRC. The second hour focused on individualizing metastatic HER2+ breast cancer, HER2-low breast cancer as an emerging subtype, and management of side effects. Knowledge and competence questions were administered pre-, immediate post-, and 2 mos. post-activity. Behavioral impact questions were also asked at follow-up. Data from these questions were analyzed to determine engagement and clinical impact. Results: To date, 448 clinicians participated in the activity. Across the seven CME test questions, improvements in knowledge and competence were observed in the clinical applications of HER2-directed agents and HER3 antibody drug conjugates (ADCs), first-line standard of care for HER2+ breast cancer, and adverse event management for HER2 ADCs. At 2-mos. follow-up, 67% reported improved behavioral impact on both clinical practice and patient experience and outcomes. Clinicians provided specific write-in examples of these changes, noting improved patient-reported outcomes, improved treatment adherence, improved competence developing treatment plans, and increased understanding of HER2/HER3 pathophysiology. Updated and expanded results will be shared. Conclusions: The activity was successful in improving clinician understanding of the relationship between HER2/HER3, pathophysiology across tumor types, and applications of emerging targeted therapies. Open-ended responses to behavioral impact questions illustrated clear improvements in clinician-reported patient experience and outcomes, clinical practice management, and knowledge of emerging HER2/HER3 therapies and their uses across multiple solid tumors.

Molecular profiling using the 92-gene assay for tumor classification of brain metastases.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e13583-e13583
Author(s):  
Andrew Jacob Brenner ◽  
Raul Collazo ◽  
Catherine A. Schnabel ◽  
F Anthony Greco
Keyword(s):  
Brain Metastases ◽  
Targeted Therapies ◽  
Primary Tumor ◽  
Tumor Type ◽  
Federal Drug Administration ◽  
Gene Assay ◽  
Clinical Series ◽  
The Us ◽  
Tumor Types

e13583 Background: Nearly 200,000 patients are diagnosed with brain metastases in the US annually. Advances in targeted therapies make definitive diagnosis of the primary tumor type important but can be challenging in many patients. The 92-gene assay is a validated gene expression classifier of 50 tumor types/subtypes for patients with uncertain diagnoses. Results from a clinical series of brain biopsies and potential impact on treatment were evaluated. Methods: An IRB-approved, de-identified database of clinical and molecular information from biopsies (N = 24,486) submitted for testing with the 92-gene assay (CancerTYPE ID, Biotheranostics, Inc.) as part of routine care were reviewed. Descriptive analysis included patient demographics and molecular diagnoses. Results: Analysis included 464 brain biopsies. A molecular diagnosis was provided in 433 (93.3%) tested ( < 5% assay failure rate) with 24 different tumor types. Six primary tumor types made up the majority (67.4%) with almost one-third of the molecular predictions being Lung (31.2%), followed by Neuroendocrine (NET) (9.9%), Sarcoma (7.9%), Skin (6.4%), Gastroesophageal (6.2%), and Urinary bladder (5.8%). All of these 6 tumor types, for which activity in the CNS has been documented, have immune checkpoint inhibitors or other targeted therapies approved in selected cases by the US Federal Drug Administration (FDA) (Table). Conclusions: Molecular classification of brain metastases can identify distinct tumor types for which there are FDA approved targeted medications. Improving diagnostic precision with the 92-gene assay helps identify a subset of therapy-responsive metastatic brain tumors, thus improving therapy and possibly providing better outcomes and survival. [Table: see text]

MyPathway HER2 basket study: Pertuzumab (P) + trastuzumab (H) treatment of a large, tissue-agnostic cohort of patients with HER2-positive advanced solid tumors.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 3004-3004
Author(s):  
Funda Meric-Bernstam ◽  
John Hainsworth ◽  
Ron Bose ◽  
Howard A. Burris III ◽  
Claire Frances Friedman ◽  
...  
Keyword(s):  
Solid Tumors ◽  
Targeted Therapies ◽  
Objective Response ◽  
Tumor Type ◽  
Loading Dose ◽  
Advanced Solid Tumors ◽  
Wild Type ◽  
Her2 Positive ◽  
Molecular Alterations ◽  
Kras Status

3004 Background: HER2 ( ERBB2) amplification and/or overexpression is observed in 2–3% of solid tumors, and is often associated with more aggressive disease. Thus far, HER2-targeted therapies are FDA-approved only for breast, gastric, and gastroesophageal cancers. MyPathway (NCT02091141) is a non-randomized, phase 2a multi-basket study assessing the activity of FDA-approved targeted therapies in non-indicated advanced solid tumors with relevant molecular alterations. We report results from the MyPathway HER2 basket, comprising a large, tissue-agnostic cohort of patients (pts) with HER2-altered tumors treated with P + H. Methods: Pts in this analysis were aged ≥18 years and had HER2-amplified and/or overexpressed tumors. Pts received P (840-mg IV loading dose, then 420-mg every 3 weeks [q3w]) + H (8-mg/kg IV loading dose, then 6-mg/kg q3w). The primary efficacy endpoint was investigator-assessed objective response rate (ORR). Other endpoints included disease control rate (DCR, defined by objective response or stable disease >4 mos) and duration of response (DOR). Subgroup analyses were completed by tumor type and KRAS status. Results: Pts were fully enrolled from April 14, 2014 to June 15, 2020. By January 22, 2021, 260 pts were efficacy-evaluable. Confirmed ORR (cORR) was 23.1% (60/260, including 5 complete responses; 95% confidence interval [CI] 18.1–28.7), DCR was 44.2% (115/260, 95% CI 38.1–50.5), and median DOR was 7.9 mos (95% CI 6.2–9.3). In 199 pts with wild-type KRAS tumors, cORR was 25.6% (51/199, 95% CI 19.7–32.3), DCR was 48.7% (97/199, 95% CI 41.6–55.9), and median DOR was 8.3 mos (95% CI 6.2–10.8). In comparison, in 26 pts with KRAS-mutated tumors, cORR was 3.8% (1/26, responder had colorectal cancer; 95% CI 0.1–19.6), DCR was 3.8% (1/26, 95% CI 0.1–19.6), and DOR was 2.7 mos. KRAS status was unknown in 35/260 pts (cORR 22.9% [8/35, 95% CI 10.4–40.1]; median DOR 6.7 mos [95% CI 2.5–12.7]). Clinical outcomes by tumor type are shown in the Table. Conclusions: P+H was active in a wide variety of KRAS wild-type HER2-amplified/overexpressed tumor types, but had limited activity in KRAS-mutated tumors. Clinical trial information: NCT02091141. [Table: see text]

scholarly journals Genetic Mutations and Epigenetic Modifications: Driving Cancer and Informing Precision Medicine

2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Krysta Mila Coyle ◽  
Jeanette E. Boudreau ◽  
Paola Marcato
Keyword(s):  
Cancer Treatment ◽  
Precision Medicine ◽  
Cancer Progression ◽  
Targeted Therapies ◽  
Acquired Resistance ◽  
Therapeutic Success ◽  
Cancer Subtypes ◽  
Molecular Alterations ◽  
Molecular Features ◽  
History Of

Cancer treatment is undergoing a significant revolution from “one-size-fits-all” cytotoxic therapies to tailored approaches that precisely target molecular alterations. Precision strategies for drug development and patient stratification, based on the molecular features of tumors, are the next logical step in a long history of approaches to cancer therapy. In this review, we discuss the history of cancer treatment from generic natural extracts and radical surgical procedures to site-specific and combinatorial treatment regimens, which have incrementally improved patient outcomes. We discuss the related contributions of genetics and epigenetics to cancer progression and the response to targeted therapies and identify challenges and opportunities for the success of precision medicine. The identification of patients who will benefit from targeted therapies is more complex than simply identifying patients whose tumors harbour the targeted aberration, and intratumoral heterogeneity makes it difficult to determine if a precision therapy is successful during treatment. This heterogeneity enables tumors to develop resistance to targeted approaches; therefore, the rational combination of therapeutic agents will limit the threat of acquired resistance to therapeutic success. By incorporating the view of malignant transformation modulated by networks of genetic and epigenetic interactions, molecular strategies will enable precision medicine for effective treatment across cancer subtypes.

Use of next-generation sequencing (NGS) to identify actionable genomic alterations (GA) in diverse solid tumor types: The Foundation Medicine (FMI) experience with 2,200+ clinical samples.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 11020-11020 ◽  
Author(s):  
Vincent A. Miller ◽  
Jeffrey S. Ross ◽  
Kai Wang ◽  
Siraj M. Ali ◽  
Geoff Otto ◽  
...  
Keyword(s):  
Targeted Therapies ◽  
Drug Targets ◽  
Treatment Options ◽  
Additional Treatment ◽  
Clinical Samples ◽  
Tumor Type ◽  
Kinase Gene ◽  
Hybridization Capture ◽  
Small Indels ◽  
Tumor Types

11020 Background: ST oncology has been transformed by the linkage of GA with targeted therapeutics. Unfortunately, most STs still have no target detected by clinically available assays. More comprehensive testing platforms are needed to determine GA in ST and thus broaden treatment options. We developed a ST NGS diagnostic assay, optimized for routine clinical FFPE specimens including core and fine needle biopsies and malignant effusions, and analyzed > 2,200 patients’ tumors in a CLIA-certified lab (Foundation Medicine). Methods: Hybridization capture of 3,320 exons from 182 cancer-related genes and 37 introns of 14 genes commonly rearranged in cancer was applied to ≥ 50ng of DNA extracted from 2,200+ consecutive FFPE tumor specimens and sequenced to high unique coverage. GA (base substitutions, small indels, rearrangements, copy number alterations) were categorized as “actionable” if directly linked to a clinically available targeted treatment option or a mechanism-driven clinical trial. Results: 2,112/2,221 (95%) of specimens (most common 1° sites: lung 18%, breast 14%, colon 7%, other 34%) were successfully profiled (mean coverage 1134X). Alterations were reported in 155/182 (85%) of genes. Seventy-six percent of cases harbored ≥1 actionable GA, mean 1.6 (range 0-16); sixty-two percent harbored at least one actionable GA not assayed by available tumor-type specific tests or hotspot panels. This approach has led to novel insights into advanced cancer including: 13 novel, potentially druggable kinase gene fusions; alterations in known drug targets (e.g. ALK, EGFR, ERRB2, KIT, MET, PDGFR α and β, RAF1 and RET) in novel tumor types and new mechanisms of resistance to approved targeted therapies. Several patients demonstrated dramatic responses to treatment with targeted therapies directed against these alterations. Conclusions: Comprehensive NGS genomic profiling was successful in profiling >2,200 unselected clinical cases, identified actionable alterations in 76% of cases and provided additional treatment options for 62% of patients targeting alterations in genes not assayed by available hotspot panels.

scholarly journals OTHR-16. MOLECULAR PROFILING USING THE 92-GENE ASSAY FOR TUMOR CLASSIFICATION OF BRAIN METASTASES

2019 ◽  
Vol 1 (Supplement_1) ◽  
pp. i21-i21
Author(s):  
Andrew Brenner ◽  
Raul Collazo ◽  
Catherine Schnabel ◽  
Anthony Greco
Keyword(s):  
Brain Metastases ◽  
Targeted Therapies ◽  
Primary Tumor ◽  
Tumor Type ◽  
Federal Drug Administration ◽  
Gene Assay ◽  
Clinical Series ◽  
The Us ◽  
Tumor Types

Abstract BACKGROUND: Nearly 200,000 patients are diagnosed with brain metastases in the US annually. Advances in targeted therapies make definitive diagnosis of the primary tumor type important but can be challenging in many patients. The 92-gene assay is a validated gene expression classifier of 50 tumor types for patients with uncertain tissue of origin diagnoses. Results from a clinical series of brain biopsies and potential impact on treatment were evaluated. METHODS: An IRB approved, de-identified database of clinical and molecular information from biopsies (N = 24,486) submitted for testing with the 92-gene assay (CancerTYPE ID, Biotheranostics, Inc.) as part of routine care were reviewed. Descriptive analysis included patient demographics and molecular diagnoses. RESULTS: Analysis included 464 brain biopsies. A molecular diagnosis was provided in 433 (93.3%) tested (&lt; 5% assay failure rate) with 24 different tumor types. Six primary tumor types made up the majority (67.4%) with almost one-third of the molecular predictions being Lung (31.2%), followed by Neuroendocrine (NET) (9.9%), Sarcoma (7.9%), Skin (6.4%), Gastroesophageal (6.2%), and Urinary bladder (5.8%). All of these 6 tumor types, for which activity in the CNS has been documented, have immune checkpoint inhibitors or other targeted therapies approved in selected cases by the US Federal Drug Administration (FDA). CONCLUSIONS: Molecular classification of brain metastases can identify distinct tumor types for which there are FDA approved targeted medications. Improving diagnostic precision with the 92-gene assay helps identify a subset of therapy-responsive metastatic brain tumors, thus improving therapy and possibly providing better outcomes and survival.

scholarly journals Tissue-agnostic drug approvals: how does this apply to patients with breast cancer?

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Luiza N. Weis ◽  
Sara M. Tolaney ◽  
Carlos H. Barrios ◽  
Romualdo Barroso-Sousa
Keyword(s):  
Breast Cancer ◽  
Microsatellite Instability ◽  
Advanced Breast Cancer ◽  
Precision Medicine ◽  
Targeted Therapies ◽  
Clinical Characteristics ◽  
Detection Methods ◽  
Mutational Burden ◽  
Tumor Mutational Burden ◽  
Tumor Types

AbstractPrecision medicine has provided new perspectives in oncology, yielding research on the use of targeted therapies across different tumor types, regardless of their site of origin, a concept known as tissue-agnostic indication. Since 2017, the Food and Drug Administration (FDA) has approved the use of three different agents for tumor-agnostic treatment: pembrolizumab (for patients with microsatellite instability or high tumor mutational burden) and larotrectinib and entrectinib (both for use in patients harboring tumors with NTRK fusions). Importantly, the genomic alterations targeted by these agents are uncommon or rare in breast cancer, and little information exists regarding their efficacy in advanced breast cancer. In this review, we discuss the prevalence of these targets in breast cancer, their detection methods, the clinical characteristics of patients whose tumors have these alterations, and available data regarding the efficacy of these agents in breast cancer.

282 Pan-tumor analysis of the association between PD-L1 combined positive score and response to pembrolizumab monotherapy

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A308-A308
Author(s):  
Lingkang Huang ◽  
Jared Lunceford ◽  
Junshui Ma ◽  
Kenneth Emancipator
Keyword(s):  
Tumor Cells ◽  
Immune Cells ◽  
Roc Analysis ◽  
Standard Of Care ◽  
Tumor Type ◽  
Operating Characteristics ◽  
Positive Score ◽  
Combined Positive Score ◽  
Line Of Therapy ◽  
Tumor Types

BackgroundPD-L1 is expressed on both tumor and immune cells; however, the mechanism by which PD-L1 modulates the adaptive immune response on tumor versus immune cells may differ. Additionally, the prevalence of PD-L1 expression and the partitioning between tumor and immune compartments varies by tumor type. While PD-L1 expression on tumor or immune cells can be scored separately, the PD-L1 combined positive score (CPS) captures both tumor and immune cell expression in one aggregate score. We performed a retrospective, exploratory analysis of the effectiveness of CPS as an enrichment biomarker across several studies of pembrolizumab monotherapy in patients with multiple tumor types.MethodsPD-L1 expression was assessed using PD-L1 IHC 22C3 pharmDx. Expression was measured using CPS (defined as the number of PD-L1–staining cells [tumor cells, lymphocytes, macrophages] divided by the total number of tumor cells, multiplied by 100) in tumor samples from single-arm (KEYNOTE-052 [UC], KEYNOTE-059 cohort 1 [G/GEJ], KEYNOTE-086 [TNBC], KEYNOTE-158 [cervical; SCLC], KEYNOTE-180 [EC], KEYNOTE-224 [HCC], KEYNOTE-427 [RCC]) and randomized (KEYNOTE-040 [HNSCC], KEYNOTE-045 [UC], KEYNOTE-061 [G/GEJ], KEYNOTE-119 [TNBC], KEYNOTE-240 [HCC]) pembrolizumab studies. Data were pooled across tumor types for pembrolizumab and for standard-of-care (in controlled studies), and then estimates of response rate, prevalence, and receiver operating characteristics (ROC) analysis were performed over various CPS cutpoints. CPS distribution by response, tumor type, and line of therapy were also assessed.ResultsThere were 3769 treated patients with available PD-L1 CPS (pembrolizumab, n=2678; standard-of-care, n=1091). The area under the ROC curve for ORR was 0.63 (95% CI, 0.61–0.66) for pembrolizumab and 0.48 (95% CI, 0.43–0.53) for standard-of-care when a positive association was evaluated between CPS and ORR (figure 1); individual cutpoints of 1, 10, 20, and 50 were examined (table 1). Figure 2 shows a boxplot of CPS distribution for response in pembrolizumab-treated patients.Abstract 282 Table 1Response Rates and Sensitivity at Individual CPS Cutpoints for Pembrolizumab-Treated PatientsAbstract 282 Figure 1ROC analysis of PD-L1 CPS for pembrolizumab versus standard-of-care therapyAbstract 282 Figure 2Boxplot of PD-L1 CPS distribution for responders versus nonresponders in pembrolizumab-treated patients by tumor type and line of therapy in order of descending median CPSConclusionsThis retrospective, exploratory pan-tumor analysis demonstrates that CPS is an effective scoring method for measuring PD-L1 expression and can be used as a predictive biomarker to identify patients likely to respond to pembrolizumab monotherapy. CPS demonstrated enrichment of response to pembrolizumab monotherapy across most, but not all, tumor types, including some tumor types for which efficacy favors pembrolizumab regardless of PD-L1 expression, and for which a companion diagnostic is therefore not needed. In the randomized studies, CPS did not show a consistent association with ORR for standard-of-care therapy.

Sarcomatoid (srcRCC) versus clear cell (ccRCC) renal cell carcinoma: A comparative comprehensive genomic profiling (CGP) study.

2021 ◽  
Vol 39 (6_suppl) ◽  
pp. 349-349
Author(s):  
Gennady Bratslavsky ◽  
Joseph M Jacob ◽  
Andrea Necchi ◽  
Philippe E. Spiess ◽  
Petros Grivas ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Clinical Course ◽  
Neuroendocrine Differentiation ◽  
Suppressor Gene ◽  
Rapid Progression ◽  
Positive Staining ◽  
Tumor Type ◽  
Tissue Samples ◽  
Comprehensive Genomic Profiling ◽  
Tumor Types

349 Background: srcRCC is a well-described histologic entity often featuring rapid progression and aggressive clinical course when compared with classic ccRCC. We queried whether CGP would uncover opportunities for targeted and immunotherapy (IO) for srcRCC patients that could individualize their treatment and entry into clinical trials. Methods: Using a hybrid capture-based CGP assay to evaluate all classes of genomic alterations (GA), 160 cases of srcRCC and 1,664 cases of ccRCC were sequenced from FFPE tissue samples. Tumor mutational burden (TMB) was determined on up to 1.1 Mbp of sequenced DNA and microsatellite instability (MSI) was determined on up to 114 loci. PD-L1 expression was determined by IHC (Dako 22C3) with low tumor cell positive staining set at 1-49% and high staining >50% expression. Results: Gender and age distributions for both tumor types were similar. srcRCC featured significantly higher GA/tumor than ccRCC (P < .0001). CGP revealed major differences with ccRCC associated more frequently with tumor suppressor gene (TSG) losses in VHL, PBRM1, TSC2 and SETD2 (all P < .0001). In contrast, srcRCC is associated with cell proliferation with increased inactivation of cell cycle regulatory genes including TP53, CDKN2A/B, MDM2 and TERT (all P < .0001). RB1 GA in srcRCC may reflect neuroendocrine differentiation occasionally found in these tumors. NF2 GA were more frequent in srcRCC (P < .0001). Conclusions: CGP reveals striking differences between srcRCC and ccRCC which may in part explain the differing histologic appearances and typical clinical course of these 2 aggressive malignancies. ccRCC is driven more by TSG loss and srcRCC is driven more by cell cycle dysregulation. Targeted therapy opportunities were uncommon for both tumor types although each featured biomarkers potentially predictive of mTOR inhibitor responses ( TSC2 in ccRCC and NF2 in srcRCC). Although the higher PBRM1 GA frequency in ccRCC may explain the IO benefit well-known for this tumor type, the srcRCC group features significantly increased TMB, CD274 amplification and PD-L1 staining which may also create IO opportunities for srcRCC patients. [Table: see text]

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