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

Author: Grafiati

Published: 14 March 2023

Last updated: 31 July 2025

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1

Minchom, Anna, Wei Yuan, Mateus Crespo, 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 (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

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2

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 (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 classifie

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3

Sokol, Ethan, Natalie Danziger, Dean Pavlick, 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 (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 m

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4

Lujambio, Amaia. "The more (mutations), the better." Science Translational Medicine 11, no. 477 (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 (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 co

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6

Pavlov, A. Yu, A. G. Dzidzaria, R. A. Gafanov, et al. "Metastatic castration-resistant prostate cancer and immune checkpoint inhibitors." Cancer Urology 20, no. 1 (2024): 153–63. http://dx.doi.org/10.17650/1726-9776-2024-20-1-153-163.

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Therapeutic landscape of several genitourinary malignancies has been revolutionized by the development of immune checkpoint inhibitors; however, the utility of immunotherapies in prostate cancer has been limited, partly due to the immunologically “cold” tumor microenvironment of prostate cancer. As of today, pembrolizumab is the only immune checkpoint inhibitor approved for treatment of metastatic castration-resistant prostate cancer (mCRPC) in a select group of patients with high microsatellite instability, deficient mismatch repair, or high tumor mutational burden. Currently, several combina

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Barroso-Sousa, Romualdo, Jana Priscila Pacífico, Sarah Sammons, and Sara M. Tolaney. "Tumor Mutational Burden in Breast Cancer: Current Evidence, Challenges, and Opportunities." Cancers 15, no. 15 (2023): 3997. http://dx.doi.org/10.3390/cancers15153997.

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Tumor mutational burden (TMB) correlates with tumor neoantigen burden, T cell infiltration, and response to immune checkpoint inhibitors in many solid tumor types. Based on data from the phase II KEYNOTE-158 study, the anti-PD-1 antibody pembrolizumab was granted approval for treating patients with advanced solid tumors and TMB ≥ 10 mutations per megabase. However, this trial did not include any patients with metastatic breast cancer; thus, several questions remain unanswered about the true role of TMB as a predictive biomarker of benefit to immune checkpoint inhibitor therapy in breast cancer

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8

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 (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 contrib

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9

Albertí-Valls, Manel, Sara Olave, Anna Olomí, Anna Macià, and Núria Eritja. "Advances in Immunotherapy for Endometrial Cancer: Insights into MMR Status and Tumor Microenvironment." Cancers 16, no. 23 (2024): 3918. http://dx.doi.org/10.3390/cancers16233918.

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Endometrial cancer is one of the most common gynecological malignancies, and while early-stage cases are highly treatable, recurrent or advanced EC remains challenging to manage. Immunotherapy, particularly immune checkpoint inhibitors, has revolutionized treatment approaches in oncology, and its application in EC has shown promising results. Key to immunotherapy efficacy in EC is the tumor’s mismatch repair status, with MMR-deficient tumors demonstrating a higher tumor mutational burden and increased PD-L1 expression, making them more susceptible to immune checkpoint inhibitors (ICIs) such as

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10

Smith, Katherine E. R., and Svetomir N. Markovic. "Persistent Tumor Mutational Burden (pTMB) May Predict Response to Immune Checkpoint Inhibitors." Clinical Chemistry 70, no. 1 (2024): 25–26. http://dx.doi.org/10.1093/clinchem/hvad128.

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11

Duchemann, Boris, Jordi Remon, Marie Naigeon, et al. "Integrating Circulating Biomarkers in the Immune Checkpoint Inhibitor Treatment in Lung Cancer." Cancers 12, no. 12 (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 heterogenei

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12

Sicard, Guillaume, Frédéric Fina, Raphaelle Fanciullino, Fabrice Barlesi, and Joseph Ciccolini. "Like a Rolling Stone: Sting-Cgas Pathway and Cell-Free DNA as Biomarkers for Combinatorial Immunotherapy." Pharmaceutics 12, no. 8 (2020): 758. http://dx.doi.org/10.3390/pharmaceutics12080758.

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Combining immune checkpoint inhibitors with other treatments likely to harness tumor immunity is a rising strategy in oncology. The exact modalities of such a combinatorial regimen are yet to be defined, and most attempts have relied so far on concomitant dosing, rather than sequential or phased administration. Because immunomodulating features are likely to be time-, dose-, and-schedule dependent, the need for biomarkers providing real-time information is critical to better define the optimal time-window to combine immune checkpoint inhibitors with other drugs. In this review, we present the

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Lanka, Sree M., Nicholas A. Zorko, Emmanuel S. Antonarakis, and Pedro C. Barata. "Metastatic Castration-Resistant Prostate Cancer, Immune Checkpoint Inhibitors, and Beyond." Current Oncology 30, no. 4 (2023): 4246–56. http://dx.doi.org/10.3390/curroncol30040323.

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The therapeutic landscape of several genitourinary malignancies has been revolutionized by the development of immune checkpoint inhibitors (ICIs); however, the utility of immunotherapies in prostate cancer has been limited, partly due to the immunologically “cold” tumor terrain of prostate cancer. As of today, pembrolizumab is the only immune checkpoint inhibitor approved for the treatment of metastatic castration resistant prostate cancer (mCRPC) in a select group of patients with high microsatellite instability (MSI-H), deficient mismatch repair (dMMR), or high tumor mutational burden (TMB).

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14

Longo, Vito, Oronzo Brunetti, Amalia Azzariti, et al. "Strategies to Improve Cancer Immune Checkpoint Inhibitors Efficacy, Other Than Abscopal Effect: A Systematic Review." Cancers 11, no. 4 (2019): 539. http://dx.doi.org/10.3390/cancers11040539.

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Despite that the impact of immune checkpoint inhibitors on malignancies treatment is unprecedented, a lack of response to these molecules is observed in several cases. Differently from melanoma and non-small cell lung cancer, where the use of immune checkpoint inhibitors results in a high efficacy, the response rate in other tumors, such as gastrointestinal cancers, breast cancer, sarcomas, and part of genitourinary cancers remains low. The first strategy evaluated to improve the response rate to immune checkpoint inhibitors is the use of predictive factors for the response such as PD-L1 expre

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15

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 (2018): 873–75. http://dx.doi.org/10.1007/s00066-018-1341-z.

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16

Hong, Xin, Ryan J. Sullivan, Mark Kalinich, et al. "Molecular signatures of circulating melanoma cells for monitoring early response to immune checkpoint therapy." Proceedings of the National Academy of Sciences 115, no. 10 (2018): 2467–72. http://dx.doi.org/10.1073/pnas.1719264115.

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A subset of patients with metastatic melanoma have sustained remissions following treatment with immune checkpoint inhibitors. However, analyses of pretreatment tumor biopsies for markers predictive of response, including PD-1 ligand (PD-L1) expression and mutational burden, are insufficiently precise to guide treatment selection, and clinical radiographic evidence of response on therapy may be delayed, leading to some patients receiving potentially ineffective but toxic therapy. Here, we developed a molecular signature of melanoma circulating tumor cells (CTCs) to quantify early tumor respons

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17

Acosta-Medina, Aldo A., Jithma P. Abeykoon, Surendra Dasari, et al. "Tumor Mutational Burden in Histiocytic Neoplasms." Blood 138, Supplement 1 (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 pe

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18

Bielska, Agata A., Walid K. Chatila, Henry Walch, et al. "Tumor Mutational Burden and Mismatch Repair Deficiency Discordance as a Mechanism of Immunotherapy Resistance." Journal of the National Comprehensive Cancer Network 19, no. 2 (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 im

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19

Patel, Amol, Dharmesh Soneji, Purvish Parikh, and Manish Kumar. "Biomarkers in immuno-oncology: A review article." International Journal of Molecular & Immuno Oncology 4 (May 20, 2019): 41–49. http://dx.doi.org/10.25259/ijmio-4-041.

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Immunotherapy is the new addition to the armamentarium against cancer. Role of immune checkpoint inhibitors is proven, but with limitations of benefit in around 20% of the patients. The cost of therapy and to some extent the toxicities are deterrent for generalized use. Biomarker is urgently needed to rationalize the use of immunotherapy. Tumor mutational burden, programmed death-ligand 1 expression, microsatellite instability, tumor-infiltrating lymphocytes, T-cell repertoire, and various other biomarkers have shown early promise in predicting response and benefit from immune checkpoint inhib

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20

Akhaladze, D. G., G. S. Rabaev, N. V. Zhukov, et al. "INITIAL EXPERIENCE IN ESTIMATING TUMOR MUTATION BURDEN IN PEDIATRIC HEPATOCELLULAR CARCINOMA." Pediatria. Journal named after G.N. Speransky 100, no. 3 (2021): 193–99. http://dx.doi.org/10.24110/0031-403x-2021-100-3-193-199.

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The level of tumor mutation burden (TMB) is a predictive factor of immune checkpoints that determines the potential effectiveness of immune checkpoint inhibitors and indications for their prescription regardless of the type of tumor in adults and children. However, the prevalence of tumors with high TMB in the pediatric population has not been well studied. Objective of the research: to assess the detection frequency of high TMB (>10 mutations per megabase) in pediatric hepatocellular carcinoma (HCC). Materials and methods of research: Next Generation Sequencing, Ion AmpliSeq™ Comprehensive

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21

Corrò, Claudia, Valérie Dutoit, and Thibaud Koessler. "Emerging Trends for Radio-Immunotherapy in Rectal Cancer." Cancers 13, no. 6 (2021): 1374. http://dx.doi.org/10.3390/cancers13061374.

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Rectal cancer is a heterogeneous disease at the genetic and molecular levels, both aspects having major repercussions on the tumor immune contexture. Whilst microsatellite status and tumor mutational load have been associated with response to immunotherapy, presence of tumor-infiltrating lymphocytes is one of the most powerful prognostic and predictive biomarkers. Yet, the majority of rectal cancers are characterized by microsatellite stability, low tumor mutational burden and poor T cell infiltration. Consequently, these tumors do not respond to immunotherapy and treatment largely relies on r

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C Guven, Deniz, Taha K. Sahin, Omer Dizdar, and Saadettin Kilickap. "Predictive biomarkers for immunotherapy efficacy in non-small-cell lung cancer: current status and future perspectives." Biomarkers in Medicine 14, no. 14 (2020): 1383–92. http://dx.doi.org/10.2217/bmm-2020-0310.

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In recent years, immune checkpoint inhibitors have rapidly changed treatment paradigms and have been pivotal for the treatment of advanced NSCLC patients. However, many patients don't respond to immunotherapy, and toxicities are a concern. Mounting evidence suggests that PD-L1 expression and tumor mutational burden are useful biomarkers in NSCLC and widely used in clinical practice. Given various limitations of PD-L1 and tumor mutational burden, many candidate biomarkers have emerged. From these biomarkers, peripheral blood-based biomarkers are promising options for the prediction of immunothe

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El-Sayes, Nader, Alyssa Vito, Omar Salem, Samuel Tekeste Workenhe, Yonghong Wan, and Karen Mossman. "A Combination of Chemotherapy and Oncolytic Virotherapy Sensitizes Colorectal Adenocarcinoma to Immune Checkpoint Inhibitors in a cDC1-Dependent Manner." International Journal of Molecular Sciences 23, no. 3 (2022): 1754. http://dx.doi.org/10.3390/ijms23031754.

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Immune checkpoint therapy has shown great promise in the treatment of cancers with a high mutational burden, such as mismatch repair-deficient colorectal carcinoma (dMMR CRC). However, many patients fail to respond to immune checkpoint therapy. Using a mouse model of dMMR CRC, we demonstrated that tumors can be further sensitized to immune checkpoint therapy by using a combination of low-dose chemotherapy and oncolytic HSV-1. This combination induced the infiltration of CD8+ and CD4+ T cells into the tumor and the upregulation of gene signatures associated with the chemoattraction of myeloid c

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Boutin, Mélina, and Sharlene Gill. "Controversies and management of deficient mismatch repair gastrointestinal cancers in the neoadjuvant setting." Therapeutic Advances in Medical Oncology 15 (January 2023): 175883592311625. http://dx.doi.org/10.1177/17588359231162577.

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High microsatellite instability (MSI-H)/deficient mismatch repair (dMMR) phenotype is a distinct molecular signature across gastrointestinal cancers characterized by high tumor mutational burden and high neoantigen load. Tumors harboring dMMR are highly immunogenic and heavily infiltrated by immune cells; consequently, they are uniquely vulnerable to therapeutic strategies enhancing immune antitumor response such as checkpoint inhibitors. The MSI-H/dMMR phenotype arose as a powerful predictor of response to immune checkpoint inhibitors with evidence supporting significantly improved outcomes i

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Ottini, Arianna, Pierangela Sepe, Teresa Beninato, et al. "Biomarker-driven immunotherapy for precision medicine in prostate cancer." Personalized Medicine 19, no. 1 (2022): 51–66. http://dx.doi.org/10.2217/pme-2021-0079.

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Although immunotherapy has recently revolutionized standard of care in different cancer types, prostate cancer has generally failed to show dramatic responses to immune checkpoint inhibitors. As in other tumors, the goal in prostate cancer is now to target treatments more precisely on patient’s individual characteristics through precision medicine. Defects in mismatch repair, mutations in the exonuclease domain of the DNA polymerase epsilon ( POLE), high tumor mutational burden and the presence of biallelic loss of CDK12 among others, are predictive biomarkers of response to immunotherapy. In

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Citra Wahyudin, Hendris Utama, Afriani Afriani, Fenty Anggrainy, and Sabrina Ermayanti. "Immunotherapy in Lung Cancer: A Narrative Literature Review." Bioscientia Medicina : Journal of Biomedicine and Translational Research 7, no. 1 (2023): 3024–30. http://dx.doi.org/10.37275/bsm.v7i1.755.

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Lung cancer is the most common cause of death from cancer in both men and women worldwide. Cancers with low immunogenicity often do not present antigens, so immune responses can be avoided. Uncontrolled growth of tumor cells occurs due to various factors such as activation of immunosuppressive mechanisms, induction of various immunosuppressive cells, and expression of immune checkpoint molecules. The development of lung cancer management has progressed since the discovery of molecular-based target therapy and immunotherapy. The high expression of tumor mutational burden in lung cancer indicate

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Yu, Jiangnan, Zhikun Guo, and Lei Wang. "Progress and Challenges of Immunotherapy Predictive Biomarkers for Triple Negative Breast Cancer in the Era of Single-Cell Multi-Omics." Life 13, no. 5 (2023): 1189. http://dx.doi.org/10.3390/life13051189.

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Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer with a poor prognosis. Despite conventional treatments, including surgery, radiation, and chemotherapy, the overall response rate to PD-1/PD-L1 immune checkpoint inhibitors remains low, with limited predictive significance from current biomarkers such as PD-L1 expression, tumor-infiltrating lymphocytes (TILs), and tumor mutational burden (TMB). To address this challenge, recent advancements in single-cell sequencing techniques have enabled deeper exploration of the highly complex and heterogeneous TNBC tumor m

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Chen, Nan, Nicole Higashiyama, and Valentina Hoyos. "Predictive Biomarkers of Immune Checkpoint Inhibitor Response in Breast Cancer: Looking beyond Tumoral PD-L1." Biomedicines 9, no. 12 (2021): 1863. http://dx.doi.org/10.3390/biomedicines9121863.

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Immune checkpoint inhibitors utilize the immune system to kill cancer cells and are now widely applied across numerous malignancies. Pembrolizumab has two breast-specific indications in triple-negative disease. Currently, programmed death ligand-1 (PD-L1) expression on tumor and surrounding immune cells is the only validated predictive biomarker for immune checkpoint inhibitors (ICIs) in breast cancer; however, it can be imprecise. Additional biomarkers are needed to identify the patient population who will derive the most benefit from these therapies. The tumor immune microenvironment contain

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Kinget, Lisa, Oliver Bechter, Kevin Punie, et al. "Multitumor Case Series of Germline BRCA1, BRCA2 and CHEK2-Mutated Patients Responding Favorably on Immune Checkpoint Inhibitors." Current Oncology 28, no. 5 (2021): 3227–39. http://dx.doi.org/10.3390/curroncol28050280.

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In recent years, immune checkpoint inhibitors (ICPI) have become widely used for multiple solid malignancies. Reliable predictive biomarkers for selection of patients who would benefit most are lacking. Several tumor types with somatic or germline alterations in genes involved in the DNA damage response (DDR) pathway harbor a higher tumor mutational burden, possibly associated with an increased tumoral neoantigen load. These neoantigens are thought to lead to stronger immune activation and enhanced response to ICPIs. We present a series of seven patients with different malignancies with germli

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30

Mazloom, Anita, Nima Ghalehsari, Victor Gazivoda, et al. "Role of Immune Checkpoint Inhibitors in Gastrointestinal Malignancies." Journal of Clinical Medicine 9, no. 8 (2020): 2533. http://dx.doi.org/10.3390/jcm9082533.

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Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of several solid and hematological malignancies. ICIs are not only able to produce long and durable responses, but also very well tolerated by patients. There are several approved indications of use of ICIs in treatment of metastatic gastrointestinal malignancies including gastric, esophageal, colorectal and hepatocellular carcinoma. In addition, ICIs can be used in microsatellite instability-high (MSI-H) and high tumor mutational burden (TMB) tumors in chemotherapy-resistant setting. Despite having good efficacy and superio

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Chokshi, Chirayu R., Benjamin A. Brakel, Nazanin Tatari, et al. "Advances in Immunotherapy for Adult Glioblastoma." Cancers 13, no. 14 (2021): 3400. http://dx.doi.org/10.3390/cancers13143400.

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Despite aggressive multimodal therapy, glioblastoma (GBM) remains the most common malignant primary brain tumor in adults. With the advent of therapies that revitalize the anti-tumor immune response, several immunotherapeutic modalities have been developed for treatment of GBM. In this review, we summarize recent clinical and preclinical efforts to evaluate vaccination strategies, immune checkpoint inhibitors (ICIs) and chimeric antigen receptor (CAR) T cells. Although these modalities have shown long-term tumor regression in subsets of treated patients, the underlying biology that may predict

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Bailey, Nathanael G. "Visualization of the Effect of Assay Size on the Error Profile of Tumor Mutational Burden Measurement." Genes 13, no. 3 (2022): 432. http://dx.doi.org/10.3390/genes13030432.

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Tumor mutational burden (TMB) refers to the number of somatic mutations in a tumor per megabase and is a biomarker for response to immune checkpoint inhibitor therapy. Immune checkpoint inhibitors are currently approved for tumors with TMB greater than or equal to 10 mutations/megabase. Many laboratories are currently reporting TMB values based upon targeted resequencing panels with limited genomic coverage. Due to sampling variation, this leads to significant uncertainty in the assay’s TMB result, particularly at relatively low TMB levels near the 10 mutation per megabase therapeutic threshol

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Saggese, Pasquale, Cesar Martinez, Linh Tran, et al. "Genotoxic Treatment Enhances Immune Response in a Genetic Model of Lung Cancer." Cancers 13, no. 14 (2021): 3595. http://dx.doi.org/10.3390/cancers13143595.

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Recent advances in immunotherapy have reshaped the clinical management of lung cancer, and immune checkpoint inhibitors (ICIs) are now first-line treatment for advanced lung cancer. However, the majority of patients do not respond to ICIs as single agents, and many develop resistance after initial responses. Therefore, there is urgent need to improve the current ICI strategies. Murine models currently available for pre-clinical studies have serious limitations for evaluating novel immunotherapies. GEMMs are reliable and predictable models driven by oncogenic mutations mirroring those found in

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34

Li, Suoni, Jiequn Ma, Jie Bai, and Zheng Zhao. "Complete remission after pembrolizumab monotherapy in a non-small cell lung cancer patient with PD-L1 negative, high tumor mutational burden, and positive tumor-infiltrating lymphocytes: A case report." Medicine 103, no. 49 (2024): e40369. https://doi.org/10.1097/md.0000000000040369.

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Rationale: Immune checkpoint inhibitors have been used to treat cancer patients. Non-small cell lung cancer (NSCLC) patients with a high expression level of programmed cell death ligand-1 (PD-L1) could benefit from immune checkpoint inhibitor monotherapy. However, treating NSCLC patients with PD-L1 negative is still a clinical challenge. The utilization of new-type tumor markers as predictive indicators of therapeutic efficacy, with the aim of guiding clinical medication strategies, has emerged as a paramount focus of clinical investigation and interest. Patient concerns and diagnoses: We repo

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Koustas, Evangelos, Panagiotis Sarantis, Athanasios G. Papavassiliou, and Michalis V. Karamouzis. "The Resistance Mechanisms of Checkpoint Inhibitors in Solid Tumors." Biomolecules 10, no. 5 (2020): 666. http://dx.doi.org/10.3390/biom10050666.

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The emergence of cancer immunotherapy has already shown some remarkable results, having changed the treatment strategy in clinical practice for solid tumors. Despite these promising long-term responses, patients seem to lack the ability to respond to immune checkpoint inhibitors, thus demonstrating a primary resistance to immunotherapy. Moreover, a significant number of patients who initially respond to treatment eventually acquire resistance to immunotherapy. Both resistance mechanisms are a result of a complex interaction among different molecules, pathways, and cellular processes. Several r

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Golkaram, Mahdi, Chen Zhao, Kristina Kruglyak, Shile Zhang, and Sven Bilke. "The interplay between cancer type, panel size and tumor mutational burden threshold in patient selection for cancer immunotherapy." PLOS Computational Biology 16, no. 11 (2020): e1008332. http://dx.doi.org/10.1371/journal.pcbi.1008332.

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The tumor mutational burden (TMB) is increasingly recognized as an emerging biomarker that predicts improved outcomes or response to immune checkpoint inhibitors in cancer. A multitude of technical and biological factors make it difficult to compare TMB values across platforms, histologies, and treatments. Here, we present a mechanistic model that explains the association between panel size, histology, and TMB threshold with panel performance and survival outcome and demonstrate the limitations of existing methods utilized to harmonize TMB across platforms.

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Vivaldi, Caterina, Silvia Catanese, Valentina Massa, et al. "Immune Checkpoint Inhibitors in Esophageal Cancers: Are We Finally Finding the Right Path in the Mist?" International Journal of Molecular Sciences 21, no. 5 (2020): 1658. http://dx.doi.org/10.3390/ijms21051658.

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Esophageal cancer remains a challenging disease due to limited treatment options and poor prognosis. In recent years, immune checkpoint inhibitors (ICI) have been proven to be safe and effective in the treatment of highly lethal malignancies, such as non-small cell lung cancer and melanoma. Recent clinical trials also showed promising activity in immune checkpoint inhibitors in pretreated advanced esophageal carcinoma and a potentially significant impact on the outcome of selected patients, independently of histology. Combination studies evaluating immunotherapy and chemotherapy and, in locali

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Valente, Ana, Amy Gin, Allison Wells, Kai Ding, and Kathleen Moore. "Exploring tumor mutational burden status and clinical benefit of immune checkpoint inhibitors in endometrial cancer." Gynecologic Oncology 164, no. 1 (2022): 3–4. http://dx.doi.org/10.1016/j.ygyno.2021.10.046.

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Kim, Jong Yeob, Andreas Kronbichler, Michael Eisenhut, et al. "Tumor Mutational Burden and Efficacy of Immune Checkpoint Inhibitors: A Systematic Review and Meta-Analysis." Cancers 11, no. 11 (2019): 1798. http://dx.doi.org/10.3390/cancers11111798.

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Tumor mutational burden (TMB) is a genomic biomarker that predicts favorable responses to immune checkpoint inhibitors (ICIs). Here, we set out to assess the predictive value of TMB on long-term survival outcomes in patients undergoing ICIs. We systematically searched PubMed, Embase, CENTRAL and clinicaltrials.gov from inception to 6 August 2019. We included retrospective studies or clinical trials of ICIs that reported hazard ratios (HRs) for overall survival (OS) and/or progression-free survival (PFS) according to TMB. Data on 5712 patients from 26 studies were included. Among patients who r

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Ghidini, Michele, Angelica Petrillo, Andrea Botticelli, et al. "How to Best Exploit Immunotherapeutics in Advanced Gastric Cancer: Between Biomarkers and Novel Cell-Based Approaches." Journal of Clinical Medicine 10, no. 7 (2021): 1412. http://dx.doi.org/10.3390/jcm10071412.

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Despite extensive research efforts, advanced gastric cancer still has a dismal prognosis with conventional treatment options. Immune checkpoint inhibitors have revolutionized the treatment landscape for many solid tumors. Amongst gastric cancer subtypes, tumors with microsatellite instability and Epstein Barr Virus positive tumors provide the strongest rationale for responding to immunotherapy. Various predictive biomarkers such as mismatch repair status, programmed death ligand 1 expression, tumor mutational burden, assessment of tumor infiltrating lymphocytes and circulating biomarkers have

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Li, Zhenxiang, Jiamao Lin, Lijuan Zhang, et al. "Comprehensive analysis of multiple parameters associated with tumor immune microenvironment in ARID1A mutant cancers." Future Oncology 16, no. 29 (2020): 2295–306. http://dx.doi.org/10.2217/fon-2020-0243.

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Aim: To verify the relationship between ARID1A and tumor immune microenvironment thus immune checkpoint inhibitors (ICIs) response. Material & methods: Several public databases were used to characterize the association between ARID1A gene alteration and tumor immunity. Results: The gene mutation frequency was 8.2% in all cancer types. The ARID1A-mutated cancers have higher scores of mutation count, tumor mutational burden, neoantigen load (p < 0.001) and T cell repertoire, B cell repertoire diversity (p < 0.05). The gene mutation has tight association with multiple-activated immune c

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Rauterkus, Grant, Agreen Hadadi, Reagan Barnett, et al. "Blood-based tumor mutational burden from circulating tumor DNA and immune checkpoint inhibitors in advanced prostate cancer." Journal of Clinical Oncology 40, no. 6_suppl (2022): 165. http://dx.doi.org/10.1200/jco.2022.40.6_suppl.165.

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165 Background: A prior study of patients with advanced cancers treated with immune checkpoint inhibitors (ICI) associated improved overall survival with tissue tumor mutational burden above the 80th percentile in each histology (tTMB-H). TMB can also reliably be calculated via liquid biopsy (bTMB), and trends higher than tTMB in analogous tumors. Here, we generate a plasma-informed benchmark for bTMB-H in advanced prostate cancer and report preliminary data from an ongoing multi-institutional case series of patients treated with ICI. Methods: Circulating tumor DNA (ctDNA) next generation sequ

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Miao, Diana, Claire Margolis, Dylan Martini, et al. "Loss-of-function of PBRM1 to predict response to anti-PD-1/PD-L1 therapy in metastatic renal cell carcinoma." Journal of Clinical Oncology 35, no. 15_suppl (2017): 3016. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.3016.

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3016 Background: Immune checkpoint inhibitors targeting programmed cell death-1 (PD-1) substantially improve patient survival in clear-cell renal cell carcinoma (ccRCC), but predictive biomarkers for efficacy have not yet been identified. Methods: We analyzed whole exome sequencing (WES) from a clinical trial of anti-PD-1 monotherapy (nivolumab) for ccRCC (N = 34) to discover genomic predictors of response to immune checkpoint therapy, and validated our findings in 28 ccRCC patients from 2 institutions treated with anti-PD-1 or anti-PD-L1 therapies. We defined 3 response groups: clinical benef

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Truong, Cao-Sang, and So Young Yoo. "Oncolytic Vaccinia Virus in Lung Cancer Vaccines." Vaccines 10, no. 2 (2022): 240. http://dx.doi.org/10.3390/vaccines10020240.

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Therapeutic cancer vaccines represent a promising therapeutic modality via the induction of long-term immune response and reduction in adverse effects by specifically targeting tumor-associated antigens. Oncolytic virus, especially vaccinia virus (VV) is a promising cancer treatment option for effective cancer immunotherapy and thus can also be utilized in cancer vaccines. Non-small cell lung cancer (NSCLC) is likely to respond to immunotherapy, such as immune checkpoint inhibitors or cancer vaccines, since it has a high tumor mutational burden. In this review, we will summarize recent applica

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Ngo, Carine, and Sophie Postel-Vinay. "Immunotherapy for SMARCB1-Deficient Sarcomas: Current Evidence and Future Developments." Biomedicines 10, no. 3 (2022): 650. http://dx.doi.org/10.3390/biomedicines10030650.

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Mutations in subunits of the SWItch Sucrose Non-Fermentable (SWI/SNF) complex occur in 20% of all human tumors. Among these, the core subunit SMARCB1 is the most frequently mutated, and SMARCB1 loss represents a founder driver event in several malignancies, such as malignant rhabdoid tumors (MRT), epithelioid sarcoma, poorly differentiated chordoma, and renal medullary carcinoma (RMC). Intriguingly, SMARCB1-deficient pediatric MRT and RMC have recently been reported to be immunogenic, despite their very simple genome and low tumor mutational burden. Responses to immune checkpoint inhibitors ha

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Alibrahim, Mohamed Nazem, Antonino Carbone, Noor Alsaleh, and Annunziata Gloghini. "Immune Checkpoint Molecules in Hodgkin Lymphoma and Other Hematological Malignancies." Cancers 17, no. 14 (2025): 2292. https://doi.org/10.3390/cancers17142292.

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Immune checkpoints such as PD-1/PD-L1, CTLA-4, LAG-3, TIM-3, and TIGIT play critical roles in regulating anti-tumor immunity and are exploited by hematological malignancies to evade immune surveillance. While classic Hodgkin lymphoma (HL) demonstrates notable responsiveness to immune checkpoint inhibitors (ICIs), which is attributed to genetic alterations like chromosome 9p24.1 amplification, the responsiveness of non-Hodgkin lymphoma (NHL), acute myeloid leukemia (AML), and multiple myeloma (MM) remain inconsistent and generally modest. In NHL, the heterogeneous immune microenvironment, parti

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Modur, Vishnu, and Fukun Guo. "Tumors bearing defective transcription elongation are immune hot but resistant to immune checkpoint inhibitors." Journal of Immunology 208, no. 1_Supplement (2022): 119.11. http://dx.doi.org/10.4049/jimmunol.208.supp.119.11.

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Abstract Tumors infiltrated with abundant T lymphocytes are generally thought to respond to immune checkpoint inhibitors (ICI). However, a significant proportion of immune hot tumors are resistant to ICI. The immune nature of such tumors is poorly understood. We recently reported a tumor type that is defective in transcription elongation (TEdef) and irresponsive to ICI in several clinical cohorts. Here, we show that TEdef tumors are unexpectedly infiltrated with cytotoxic T cells (CTLs) in patients and in animal models. Mechanistically, T cell infiltration is facilitated by cytoplasmic DNA/dou

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Omuro, Antonio. "Immune-checkpoint inhibitors for glioblastoma: what have we learned?" Arquivos de Neuro-Psiquiatria 80, no. 5 suppl 1 (2022): 266–69. http://dx.doi.org/10.1590/0004-282x-anp-2022-s129.

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ABSTRACT Background: Glioblastoma, the most common malignant primary brain tumor, remains a lethal disease with few therapeutic options. Immunotherapies, particularly immune checkpoint inhibitors (ICPi), have revolutionized cancer treatment, but their role in glioblastoma is uncertain. Objective: To review the state of immunotherapies in glioblastoma, with an emphasis on recently published ICPi clinical trials. Methods: In this editorial/opinion article, we critically review results of the first generation of trials of ipilimumab, nivolumab and pembrolizumab in glioblastoma, as well as future

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Polano, Maurizio, Marco Chierici, Michele Dal Bo, et al. "A Pan-Cancer Approach to Predict Responsiveness to Immune Checkpoint Inhibitors by Machine Learning." Cancers 11, no. 10 (2019): 1562. http://dx.doi.org/10.3390/cancers11101562.

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Immunotherapy by using immune checkpoint inhibitors (ICI) has dramatically improved the treatment options in various cancers, increasing survival rates for treated patients. Nevertheless, there are heterogeneous response rates to ICI among different cancer types, and even in the context of patients affected by a specific cancer. Thus, it becomes crucial to identify factors that predict the response to immunotherapeutic approaches. A comprehensive investigation of the mutational and immunological aspects of the tumor can be useful to obtain a robust prediction. By performing a pan-cancer analys

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Pabst, Lucile, Sébastien Lopes, Basil Bertrand, et al. "Prognostic and Predictive Biomarkers in the Era of Immunotherapy for Lung Cancer." International Journal of Molecular Sciences 24, no. 8 (2023): 7577. http://dx.doi.org/10.3390/ijms24087577.

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The therapeutic algorithm of lung cancer has recently been revolutionized by the emergence of immune checkpoint inhibitors. However, an objective and durable response rate remains low with those recent therapies and some patients even experience severe adverse events. Prognostic and predictive biomarkers are therefore needed in order to select patients who will respond. Nowadays, the only validated biomarker is the PD-L1 expression, but its predictive value remains imperfect, and it does not offer any certainty of a sustained response to treatment. With recent progresses in molecular biology,

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