Relevant bibliographies by topics / Mesothelioma, immune-checkpoint inhibitors, tumor mutational burden

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Academic literature on the topic 'Mesothelioma, immune-checkpoint inhibitors, tumor mutational burden'

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Published: 14 March 2023

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Journal articles on the topic "Mesothelioma, immune-checkpoint inhibitors, tumor mutational burden"

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Minchom, Anna, Wei Yuan, Mateus Crespo, Bora Gurel, Ines Figueiredo, Andrew Wotherspoon, Susana Miranda, et al. "Molecular and immunological features of a prolonged exceptional responder with malignant pleural mesothelioma treated initially and rechallenged with pembrolizumab." Journal for ImmunoTherapy of Cancer 8, no. 1 (March 2020): e000713. http://dx.doi.org/10.1136/jitc-2020-000713.

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BackgroundThis case represents an exceptional response to pembrolizumab in a patient with epithelioid mesothelioma with a further response on rechallenge.Case presentationA 77-year-old woman with advanced epithelioid mesothelioma extensively pretreated with chemotherapy demonstrated a prolonged response of 45 months to 52 cycles of pembrolizumab. On rechallenge with pembrolizumab, further disease stability was achieved. Serial biopsies and analysis by immunohistochemistry and immunofluorescence demonstrated marked immune infiltration and documented the emergency of markers of immune exhaustion. Whole exome sequencing demonstrated a reduction in tumor mutational burden consistent with subclone elimination by immune checkpoint inhibitor (CPI) therapy. The relapse biopsy had missense mutation in BTN2A1.ConclusionThis case supports rechallenge of programme death receptor 1 inhibitor in cases of previous CPI sensitivity and gives molecular insights.
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Mahadevan, Daruka, Li Ma, Kai Treuner, Jenna Wong, and Catherine Schnabel. "330 Integration of molecular cancer classification and next-generation sequencing to identify metastatic patients eligible for immune checkpoint inhibitors." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (November 2021): A356. http://dx.doi.org/10.1136/jitc-2021-sitc2021.330.

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BackgroundImmune checkpoint inhibitors (ICIs) have improved patient outcomes and are a new standard of care for treating a variety of cancers. Eligibility for ICIs is established through determination of tumor type and use of predictive biomarkers. PD-L1, microsatellite instability (MSI), and tumor mutation burden (TMB) are FDA-approved predictive biomarkers for ICI therapies. However, the validity of these biomarkers remains controversial, as studies have shown a failure to predict ICI response in many cancer types.1 2 The 92-gene assay (CancerTYPE ID) is a validated gene expression classifier of 50 tumor types and subtypes for metastatic patients with ambiguous diagnoses. CancerTYPE ID provides critical cancer type identification to guide ICI treatment eligibility and selection. In the current study, analyses integrating tumor type with multimodal biomarker testing for PD-L1 and TMB were evaluated to identify patients for ICI eligibility.MethodsMOSAIC (Molecular Synergy to Advance Individualized Cancer Care) is an IRB-approved, de-identified database of CancerTYPE ID results from 2572 patients with tumor-specific multimodal biomarker testing by next-generation sequencing for TMB and immunohistochemistry for PD-L1. The Cochran-Mantel-Haenszel test was used to evaluate the relationship between PD-L1 and TMB across tumor types.ResultsTumor type was determined in 2377 of 2572 cases (92.4%), comprising 27 different tumor types including 14 tumor types with FDA-approved ICI therapies. Among the top 20 tumor types, PD-L1 was present in a larger proportion of tumors (weighted mean=78.9%, range=58.3%–100%) versus TMB (20.9%, 0%–72.7%) (figure 1). Varying expression levels of PD-L1 and TMB were noted across tumor types (Figure 1), and no relationship between PD-L1 and TMB (P=0.15) was observed. Prevalence of high TMB in melanoma (42.9%) and lung adenocarcinoma (38.9%), which are more likely to respond to ICI treatment, are consistent with published data; however, prevalence of high TMB in mesothelioma (20.0%), sarcoma (23.6%) and prostatic adenocarcinoma (33.3%), which are not likely to respond to ICI treatment, are higher than previously reported.3Abstract 330 Figure 1Prevalence of PD-L1 expression and high TMB in the 27 identified tumor typesConclusionsTumor type classification and cellular context are critical for ICI eligibility. CancerTYPE ID successfully differentiated 14 ICI-eligible tumor types from 13 non-ICI-eligible tumor types. Further, since there is no relationship between PD-L1 and TMB for different tumor types, accurate tumor type identification is necessary to select the most appropriate biomarker. This highlights the clinical utility of CancerTYPE ID combined with multimodal biomarker testing to guide ICI treatment and predict response based on tumor type identification, which may improve outcomes in patients with metastatic cancer.ReferencesMcGrail DJ, Pilié PG, Rashid NU, et al. High tumor mutation burden fails to predict immune checkpoint blockade response across all cancer types. Ann Oncol 2021;32(5):661–672.Gjoerup O, Brown CA, Ross JS, et al. Identification and utilization of biomarkers to predict response to immune checkpoint inhibitors. AAPS J 2020;22(6):132.Yarchoan M, Albacker LA, Hopkins AC, et al. PD-L1 expression and tumor mutational burden are independent biomarkers in most cancers. JCI Insight 2019;4(6):e126908.
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Sokol, Ethan, Natalie Danziger, Dean Pavlick, Julia Andrea Elvin, Jo-Anne Vergilio, Jonathan Keith Killian, Douglas I. Lin, et al. "Clinically aggressive malignancies associated with STK11 germline mutations (STK11GCa): A comprehensive genomic profiling (CGP) study." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): 3558. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.3558.

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3558 Background: Germline mutations in the STK11 ( LKB1) mTOR pathway gene are associated with Peutz-Jehger’s Syndrome and a variety of malignancies of variable clinical aggressiveness. Recent evidence also links STK11 inactivation with failure to benefit from anti-cancer immune checkpoint inhibitor (IO) therapy in NSCLC. Methods: Using hybrid capture based CGP on extracted tumor DNA and a published “somatic-germline-zygosity” SGZ data analysis algorithm on 212,470 samples of clinically advanced malignancies, we identified 103 (0.05%) STK11GCa inactivating base substitutions or indels. Tumor mutational burden (TMB) was determined on up to 1.1 Mbp of sequenced DNA and microsatellite instability (MSI) was determined on 114 loci. PD-L1 expression was determined by IHC (Dako 22C3). Results: 57 (55%) STK11GCa cases were NSCLC, 7 (7%) STK11GCa cases each were CRC, breast, pancreatic and unknown primary carcinomas, and 3 (3%) were gynecologic cancers. Amongst all samples included in this analysis, STK11 germline alterations were found in 0.15% NSCLC, 0.03% CRC, 0.03% breast, 0.08% pancreas, 0.06% unknown primary carcinoma and 0.03% of gynecologic cancers. Additional malignancies harboring STK11GCa included melanoma, gastroesophageal, HNSCC, bladder, HCC, lymphoma and mesothelioma. In STK11GCa, the median patient age at sequencing was 61 years (range 2 to > 89 years); gender distribution was 52% female and 48% male. STK11GCa cases had a median of 6.5 genomic alterations (GA)/tumor and KEAP1, another IO resistance gene, was co-altered in 10%. Currently untargetable GA were detected in TP53 (50%), KRAS (38% with 9% in potentially targetable G12C), CDKN2A (32%), CDKN2B (22%), SMARCA4 (19%), MYC (11%), and APC (10%). Potentially targetable GA, which have also been linked in some studies to IO efficacy, included GA in BRAF (10%), EGFR (9%) and PBRM1 (4%). No targetable gene rearrangements or fusions were identified. No MSI High cases were identified. The median TMB was 5 mut/Mb with 23 % >10 mut/Mb and 4% >20 mut/Mb. 15% of 20 evaluated STK11GCA cases were PD-L1 high (>50% tumor cell staining). Conclusions: STK11GCa include a wide variety of primary tumors with a paucity of co-occurring targetable GA. Although these tumors have significant PD-L1 staining and a subset harbor other markers of potential IO efficacy, the inactivated STK11 in these tumors may contribute to IO resistance and lack of responsiveness to immunotherapies.
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Lujambio, Amaia. "The more (mutations), the better." Science Translational Medicine 11, no. 477 (January 30, 2019): eaaw5320. http://dx.doi.org/10.1126/scitranslmed.aaw5320.

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Hsiehchen, David, Magdalena Espinoza, Cristina Valero, Chul Ahn, and Luc G. T. Morris. "Impact of tumor mutational burden on checkpoint inhibitor drug eligibility and outcomes across racial groups." Journal for ImmunoTherapy of Cancer 9, no. 11 (November 2021): e003683. http://dx.doi.org/10.1136/jitc-2021-003683.

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The FDA approval of immune checkpoint inhibitors for cancers with tumor mutation burden (TMB) of at least 10 mut/Mb is postulated to reduce healthcare disparities by broadly expanding treatment eligibility. In a cohort of 39,400 patients with available genomic and race data, black and Asian patients were less likely to have TMB-high cancers in multiple types of malignancies based on the currently approved cut-off. Decreasing TMB thresholds preferentially increased the eligibility of minority patients for immune checkpoint inhibitors while retaining predictive value of treatment benefit in a cohort of immune checkpoint inhibitor treated patients. This study highlights differing distributions of TMB-high cancers between racial groups and provides guidance in developing more rational eligibility criteria for immune checkpoint inhibitors.
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An, Ho Jung, Hong Jae Chon, and Chan Kim. "Peripheral Blood-Based Biomarkers for Immune Checkpoint Inhibitors." International Journal of Molecular Sciences 22, no. 17 (August 30, 2021): 9414. http://dx.doi.org/10.3390/ijms22179414.

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As cancer immunotherapy using immune checkpoint inhibitors (ICIs) is rapidly evolving in clinical practice, it is necessary to identify biomarkers that will allow the selection of cancer patients who will benefit most or least from ICIs and to longitudinally monitor patients’ immune responses during treatment. Various peripheral blood-based immune biomarkers are being identified with recent advances in high-throughput multiplexed analytical technologies. The identification of these biomarkers, which can be easily detected in blood samples using non-invasive and repeatable methods, will contribute to overcoming the limitations of previously used tissue-based biomarkers. Here, we discuss the potential of circulating immune cells, soluble immune and inflammatory molecules, circulating tumor cells and DNA, exosomes, and the blood-based tumor mutational burden, as biomarkers for the prediction of immune responses and clinical benefit from ICI treatment in patients with advanced cancer.
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Giordano, Frank A., Marlon R. Veldwijk, Carsten Herskind, and Frederik Wenz. "Radiotherapy, tumor mutational burden, and immune checkpoint inhibitors: time to do the math." Strahlentherapie und Onkologie 194, no. 10 (July 20, 2018): 873–75. http://dx.doi.org/10.1007/s00066-018-1341-z.

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Duchemann, Boris, Jordi Remon, Marie Naigeon, Laura Mezquita, Roberto Ferrara, Lydie Cassard, Jean Mehdi Jouniaux, et al. "Integrating Circulating Biomarkers in the Immune Checkpoint Inhibitor Treatment in Lung Cancer." Cancers 12, no. 12 (December 3, 2020): 3625. http://dx.doi.org/10.3390/cancers12123625.

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Immune checkpoint inhibitors are now a cornerstone of treatment for non-small cell lung cancer (NSCLC). Tissue-based assays, such as Programmed cell death protein 1 (PD-L1) expression or mismatch repair deficiency/microsatellite instability (MMRD/MSI) status, are approved as treatment drivers in various settings, and represent the main field of research in biomarkers for immunotherapy. Nonetheless, responses have been observed in patients with negative PD-L1 or low tumor mutational burden. Some aspects of biomarker use remain poorly understood and sub-optimal, in particular tumoral heterogeneity, time-evolving sampling, and the ability to detect patients who are unlikely to respond. Moreover, tumor biopsies offer little insight into the host’s immune status. Circulating biomarkers offer an alternative non-invasive solution to address these pitfalls. Here, we summarize current knowledge on circulating biomarkers while using liquid biopsies in patients with lung cancer who receive treatment with immune checkpoint inhibitors, in terms of their potential as being predictive of outcome as well as their role in monitoring ongoing treatment. We address host biomarkers, notably circulating immune cells and soluble systemic immune and inflammatory markers, and also review tumor markers, including blood-based tumor mutational burden, circulating tumor cells, and circulating tumor DNA. Technical requirements are discussed along with the current limitations that are associated with these promising biomarkers.
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Acosta-Medina, Aldo A., Jithma P. Abeykoon, Surendra Dasari, Antonious Z. Hazim, N. Nora Bennani, Terra Lasho, Aishwarya Ravindran, et al. "Tumor Mutational Burden in Histiocytic Neoplasms." Blood 138, Supplement 1 (November 5, 2021): 3634. http://dx.doi.org/10.1182/blood-2021-153128.

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Abstract Background Histiocytic disorders are rare hematologic neoplasms characterized by their high clinical heterogeneity. Evidence of constitutive activation of the mitogen-activated protein kinase (MAPK) pathway in a number of these disorders has led to the increasing use of BRAF- and MEK-inhibitors as a therapeutic strategy. Response to these therapies is not universal and additional effective treatment options are required. Immune checkpoint inhibitors have proven effective for a wide array of malignancies. Tumor mutational burden (TMB), the total number of somatic pathogenic variants per coding region in a tumor genome, is a clinical biomarker associated with response to immunotherapy. We have previously reported preliminary findings of low TMB in a small cohort of patients with histiocytic neoplasms (Goyal G et al. Blood 2019). In this study, our aim was to confirm the findings in a larger clinical cohort using next generation sequencing studies. Methods A retrospective review of adult patients consecutively seen at Mayo Clinic from 2017 to April 2021 and diagnosis of a histiocytic neoplasm was performed. Electronic records were queried for demographic and laboratory data of all patients who consented to undergo tumor-tissue next-generation sequencing with the Tempus-xT ® or xO ® assay (Chicago, IL), throughout the course of their evaluation. TMB was reported as the number of nonsynonymous mutations per coding area of a tumor genome. TMB across groups was compared via an independent-samples T-test or via analysis of variance and post hoc subgroup testing via Turkey's Test as required. Results Seventy-three patients were included in the study. Individual diagnoses included: Erdheim-Chester disease (ECD) in 31.5% (n=23), including 3 patients with overlap features of ECD and other histiocytoses; Rosai Dorfman disease (RDD) in 28.8% (n=21); Langerhans cell histiocytosis in 21.9% (n=16), histiocytic sarcoma (HS) in 5.5% (n=4), and other histiocytic neoplasms in 12.3% (n=10) including adult xanthogranuloma, xanthoma disseminatum, undifferentiated histiocytoses, and one case of Langerhans cell sarcoma. Median tumor percentage on analyzed samples was 30% (range 10%-90%) and was ≤20% in 29 samples. TMB was <1.0 mutations per megabase (mpMb) in 42.5% (n=31) and >5.0 mpMb in only 6 cases. Median TMB was 1.58 (range 0 - 5.26) for ECD, 1.08 (range 0 - 6.3) for LCH, 0.2 (range 0 - 5.8) for RDD, 3.19 (range 1.67 - 6.8) for HS, and 1.6 (range 0 - 7.5) for other histiocytic neoplasms (Figure 1). No clear association between increasing TMB and number of systems with histiocytic infiltration was observed (Figure 2). A significant increase in TMB was observed among the 5 cases of sarcoma as compared to the rest of the cohort (p=0.014). When not considering sarcomas, no differences were observed in TMB between patients with ECD, LCH, RDD or other histiocytoses (F=0.775; p=0.512). Conclusion In this large cohort of histiocytic disorders, TMB was low compared to that historically seen in other neoplasms though this is likely influenced by tumor purity ≤20% in 29 cases. Only 6 tumors had TMB reports with mpMb above the threshold thought to be associated with an increased likelihood of response to PD-1/PDL1-targeted therapies (>5 mpMb). Our results suggest a low likelihood of response among histiocytic disorders using immune checkpoint inhibitors. Further exploration among malignant histiocytoses (HS and Langerhans cell sarcoma) is warranted given our findings of higher TMB compared with other histiocytic neoplasms. Figure 1 Figure 1. Disclosures Bennani: Kymera: Other: Advisory Board; Vividion: Other: Advisory Board; Kyowa Kirin: Other: Advisory Board; Daichii Sankyo Inc: Other: Advisory Board; Purdue Pharma: Other: Advisory Board; Verastem: Other: Advisory Board.
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Bielska, Agata A., Walid K. Chatila, Henry Walch, Nikolaus Schultz, Zsofia K. Stadler, Jinru Shia, Diane Reidy-Lagunes, and Rona Yaeger. "Tumor Mutational Burden and Mismatch Repair Deficiency Discordance as a Mechanism of Immunotherapy Resistance." Journal of the National Comprehensive Cancer Network 19, no. 2 (February 2021): 130–33. http://dx.doi.org/10.6004/jnccn.2020.7680.

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Lynch syndrome is a heritable cancer syndrome caused by a heterozygous germline mutation in DNA mismatch repair (MMR) genes. MMR-deficient (dMMR) tumors are particularly sensitive to immune checkpoint inhibitors, an effect attributed to the higher mutation rate in these cancers. However, approximately 15% to 30% of patients with dMMR cancers do not respond to immunotherapy. This report describes 3 patients with Lynch syndrome who each had 2 primary malignancies: 1 with dMMR and a high tumor mutational burden (TMB), and 1 with dMMR but, unexpectedly, a low TMB. Two of these patients received immunotherapy for their TMB-low tumors but experienced no response. We have found that not all Lynch-associated dMMR tumors have a high TMB and propose that tumors with dMMR and TMB discordance may be resistant to immunotherapy. The possibility of dMMR/TMB discordance should be considered, particularly in less-typical Lynch cancers, in which TMB evaluation could guide the use of immune checkpoint inhibitors.
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Dissertations / Theses on the topic "Mesothelioma, immune-checkpoint inhibitors, tumor mutational burden"

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Daffinà, Maria Grazia. "PREDICTIVE BIOMARKER OF LONG TERM SURVIVAL IN MESOTHELIOMA PATIENTS TREATED WITH IMMUNE CHECKPOINT INHIBITORS." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1160848.

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Background: Targeting immune-checkpoint inhibitors (ICIs) has proven effective in a variety of tumor types. Primary and secondary resistance to treatment is emerging as a major limitation of ICIs therapy, but little data are available on efficacy of re-treatment in immune checkpoint blockade (ICB)-resistant subjects. The identification of biomarkers predictive of response to ICI and re-treatment of ICI-resistant patients are currently under investigations as promising tools in clinical practice. Aim of this study is to evaluate the efficacy, safety and clinical activity of re-treatment with tremelimumab and durvalumab in malignant mesothelioma (MM) patients who developed resistance to these agents and to investigate the role of tumour mutational burden (TMB) as a predictive biomarker of response in the phase II NIBIT-MESO-1 study. Methods: Eligible patients for re-treatment per the NIBIT-MESO-1 protocol were those who completed four dosing cycles of tremelimumab combined with durvalumab achieving partial response (PR) or stable disease (SD) followed by progressive disease (PD) during the maintenance with only durvalumab or the follow-up phase. Subjects who met the re-treatment criteria received tremelimumab (1 mg/Kg i.v.) and durvalumab (20 mg/Kg i.v.) every four weeks (Q4W) for four doses (“re-induction phase”), followed by durvalumab (20 mg/Kg, i.v.) Q4W for additional nine doses (“maintenance phase of re-treatment”). The evaluated endpoints were objective response rate (ORR), disease control rate (DCR), per immune-related (ir)-modified RECIST criteria, overall survival (OS) and safety. A post-hoc analysis was conducted to evaluated tumor mutational burden (TMB) on all patients enrolled, whose paraffin tumor sample was available before starting treatment. Median values of TMB were calculated and used as a cut-off to divide patients in equal number groups for comparisons with survival. Survival times were analyzed with the Kaplan-Meier method and differences between curves were evaluated with the log-rank test. P values < 0.05 were considered as significant. Results: Seventeen (42.5%) of the 40 patients enrolled in the NIBIT-MESO-1 study met the criteria for re-treatment and received therapy. Among them, 8 (47%) completed the re-induction phase, 7 (41.2%) went on maintenance phase of re-treatment, and 1 (5%) passed to follow-up phase. At data cut-off, April 30, 2020, all 17 patients were discontinued during re-treatment because of PD, and 13 (73%) received additional lines of therapy (chemotherapy or immunotherapy). Seven (41%) of the 17 re-treated subjects had an ir-SD, while no ir-ORR was observed. From the start of re-treatment to a median follow-up of 24 months, median OS (mOS) was 12.5 months. Grade 1-2 ir-adverse events (AEs) occurred in 6 (35%) re-treated patients, were most frequently dermatological and reversible per protocol guidelines; no grade 3-4 ir-AEs were observed. At a median follow-up of 46 months, mOS of re-treated patients was significantly (p=0.01) higher (25.6 months, 95% CI: 9.6-41.6) as compared to the 23 subjects who were not re-treated (9.9 months, 95% CI: 7.7-12.1). In a post-hoc analysis on the 28 patients for whom tumour tissue before treatment was available, TMB values higher than the median cut-off of 8.3 mutations per Mb were associated with a higher mOS compared with lower TMB, but this difference was non-significant (p=0.06). Moreover, when patients were additionally stratified for ICI re-treatment (n=13), there was a significant difference in survival between those with a TMB higher than 8.3 mutations per Mb and those with lower TMB values in the re-treated cohort (1256 days vs 528 days; p=0·02). Conclusions: Re-treatment with tremelimumab and durvalumab of MM patients who developed resistance to therapy in the NIBIT-MESO-1 study seems to be clinically effective and safe in a sizeable proportion of re-treated subjects, suggesting its potential application in the clinical practice. Further studies on a larger sample will be needed to validate the predictive role of TMB, either as an independent predictive biomarker or associated with others potential predictive immune biomarkers.
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Book chapters on the topic "Mesothelioma, immune-checkpoint inhibitors, tumor mutational burden"

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Emancipator, Kenneth, Jianda Yuan, Razvan Cristescu, Deepti Aurora-Garg, and Priti S. Hegde. "Predictive Biomarkers (Programmed Death Ligand 1 Expression, Microsatellite Instability, and Tumor Mutational Burden) for Response to Immune Checkpoint Inhibitors." In Cancer Immunotherapy Principles and Practice. 2nd ed. New York, NY: Springer Publishing Company, 2021. http://dx.doi.org/10.1891/9780826137432.0045.

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Conference papers on the topic "Mesothelioma, immune-checkpoint inhibitors, tumor mutational burden"

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Sousa, Romualdo Barroso, Svitlana Tyekucheva, Pedro Exman, Renato Umeton, F. Stephen Hodi, Eric P. Winer, Nancy U. Lin, and Sara M. Tolaney. "TUMOR MUTATIONAL BURDEN (TMB) IS A POTENTIAL PREDICTOR OF RESPONSE TO IMMUNE CHECKPOINT INHIBITORS (ICI) IN METASTATIC TRIPLE-NEGATIVE BREAST CANCER (MTNBC)." In Brazilian Breast Cancer Symposium. v29s1, 2019. http://dx.doi.org/10.29289/259453942019v29s1g04.

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Hsieh, Yi-Lin, Pei-Ning Yu, Yi-Hua Jan, Meng-Shao Lai, Woei-Fuh Wang, De-Wei Zhuo, Shu-Jen Chen, Jen-Hao Cheng, Kien Thiam Tan, and Yu-Li Su. "Abstract 3177: Panel-derived tumor mutational burden (TMB) is associated with the response to the immune checkpoint inhibitors (ICIs) in urothelial cancers." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3177.

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Hu, Jing, Bixun Li, Bing Zou, Senming Wang, Ye Qiu, Maolin Yan, Zhiming Zeng, et al. "Abstract 620: Associations of genomic alteration, tumor mutational burden with PD-L1 expression and response to immune checkpoint inhibitors in Chinese lung patients." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-620.

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Barroso-Sousa, R., S. Tyekucheva, S. Pernas-Simon, P. Exman, E. Jain, AC Garrido-Castro, M. Hughes, et al. "Abstract P5-12-02:PTENalterations and tumor mutational burden (TMB) as potential predictors of resistance or response to immune checkpoint inhibitors (ICI) in metastatic triple-negative breast cancer (mTNBC)." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p5-12-02.

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