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Article: TRK inhibitor activity and resistance in TRK fusion-positive cancers in adults.

Harada, Guilherme / Drilon, Alexander

2022 Volume 264-265, Page(s) 33–39

Abstract: NTRK fusions drive oncogenesis in a variety of adult cancers. The approval of the first-generation TRK inhibitors, larotrectinib and entrectinib, for any cancer with an NTRK fusion represented a focal point in tumor-agnostic drug development. These ... ...

Abstract	NTRK fusions drive oncogenesis in a variety of adult cancers. The approval of the first-generation TRK inhibitors, larotrectinib and entrectinib, for any cancer with an NTRK fusion represented a focal point in tumor-agnostic drug development. These agents achieve high response rates and durable disease control, and display intracranial activity. The use of these agents has resulted in a deeper understanding of the clinical consequences of TRK inhibition. These on-target side effects include dizziness, weight gain, and withdrawal pain. The study of TRK inhibitor resistance led to the development of next generation drugs, such as selitrectinib, repotrectinib, taletrectinib, and other agents that maintain disease control against selected acquired kinase domain mutations. This review discusses the clinical efficacy of TRK inhibitors, their safety profiles, and resistance mechanisms with a focus on data in adult cancers.
MeSH term(s)	Adult ; Humans ; Mutation ; Neoplasms/drug therapy ; Neoplasms/genetics ; Oncogene Proteins, Fusion/genetics ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	Oncogene Proteins, Fusion ; Protein Kinase Inhibitors
Language	English
Publishing date	2022-03-16
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2599227-2
ISSN	2210-7762
ISSN	2210-7762
DOI	10.1016/j.cancergen.2022.03.002
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Article ; Online: Rare molecular subtypes of lung cancer.

Harada, Guilherme / Yang, Soo-Ryum / Cocco, Emiliano / Drilon, Alexander

Nature reviews. Clinical oncology

2023 Volume 20, Issue 4, Page(s) 229–249

Abstract: Oncogenes that occur in ≤5% of non-small-cell lung cancers have been defined as 'rare'; nonetheless, this frequency can correspond to a substantial number of patients diagnosed annually. Within rare oncogenes, less commonly identified alterations (such ... ...

Abstract	Oncogenes that occur in ≤5% of non-small-cell lung cancers have been defined as 'rare'; nonetheless, this frequency can correspond to a substantial number of patients diagnosed annually. Within rare oncogenes, less commonly identified alterations (such as HRAS, NRAS, RIT1, ARAF, RAF1 and MAP2K1 mutations, or ERBB family, LTK and RASGRF1 fusions) can share certain structural or oncogenic features with more commonly recognized alterations (such as KRAS, BRAF, MET and ERBB family mutations, or ALK, RET and ROS1 fusions). Over the past 5 years, a surge in the identification of rare-oncogene-driven lung cancers has challenged the boundaries of traditional clinical grade diagnostic assays and profiling algorithms. In tandem, the number of approved targeted therapies for patients with rare molecular subtypes of lung cancer has risen dramatically. Rational drug design has iteratively improved the quality of small-molecule therapeutic agents and introduced a wave of antibody-based therapeutics, expanding the list of actionable de novo and resistance alterations in lung cancer. Getting additional molecularly tailored therapeutics approved for rare-oncogene-driven lung cancers in a larger range of countries will require ongoing stakeholder cooperation. Patient advocates, health-care agencies, investigators and companies with an interest in diagnostics, therapeutics and real-world evidence have already taken steps to surmount the challenges associated with research into low-frequency drivers.
MeSH term(s)	Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Protein-Tyrosine Kinases/genetics ; Proto-Oncogene Proteins/genetics ; ErbB Receptors/genetics ; Mutation ; Molecular Targeted Therapy
Chemical Substances	Protein-Tyrosine Kinases (EC 2.7.10.1) ; Proto-Oncogene Proteins ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2023-02-20
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/s41571-023-00733-6
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Article ; Online: An Ascendant Challenge: Central Nervous System Metastases in ALK+ Lung Cancers.

Murciano-Goroff, Yonina R / Harada, Guilherme / Drilon, Alexander

Clinical cancer research : an official journal of the American Association for Cancer Research

2022 Volume 28, Issue 12, Page(s) 2477–2479

Abstract: Central nervous system (CNS) metastases constitute a challenge for the design of anaplastic lymphoma kinase (ALK) fusion-positive lung cancer trials. The ASCEND-7 study of ceritinib demonstrates the feasibility of broadening CNS eligibility criteria to ... ...

Abstract	Central nervous system (CNS) metastases constitute a challenge for the design of anaplastic lymphoma kinase (ALK) fusion-positive lung cancer trials. The ASCEND-7 study of ceritinib demonstrates the feasibility of broadening CNS eligibility criteria to include symptomatic brain and leptomeningeal disease and highlights design features that contemporary trials will need to incorporate. See related article by Chow et al., p. 2506.
MeSH term(s)	Anaplastic Lymphoma Kinase ; Brain/pathology ; Carcinoma, Non-Small-Cell Lung/pathology ; Central Nervous System ; Central Nervous System Neoplasms/diagnosis ; Humans ; Lung Neoplasms/pathology ; Protein Kinase Inhibitors/therapeutic use ; Pyrimidines ; Receptor Protein-Tyrosine Kinases ; Sulfones
Chemical Substances	Protein Kinase Inhibitors ; Pyrimidines ; Sulfones ; Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; ceritinib (K418KG2GET)
Language	English
Publishing date	2022-04-08
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-22-0341
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Article ; Online: NTRK fusions in lung cancer: From biology to therapy.

Harada, Guilherme / Santini, Fernando C / Wilhelm, Clare / Drilon, Alexander

Lung cancer (Amsterdam, Netherlands)

2021 Volume 161, Page(s) 108–113

Abstract: Fusions involving TRK protein tyrosine kinases are oncogenic drivers in a variety of tumors in children and adults, with a prevalence of ∼0.2% in non-small cell lung cancer. Diagnosis can be challenging due to structural features such as NTRK intron ... ...

Abstract	Fusions involving TRK protein tyrosine kinases are oncogenic drivers in a variety of tumors in children and adults, with a prevalence of ∼0.2% in non-small cell lung cancer. Diagnosis can be challenging due to structural features such as NTRK intron length, but next-generation sequencing (NGS), including RNA-based NGS, increases detection. The first-generation TRK inhibitors, larotrectinib and entrectinib, have demonstrated clinically meaningful antitumor activity in TRK fusion-positive cancers in a tumor-agnostic fashion and should be considered first-line therapeutic options for TRK fusion-positive lung cancers. Furthermore, the first-generation TRK inhibitors are well tolerated. Care should be taken, however, to monitor on-target adverse events, such as dizziness, weight gain, paresthesias, and withdrawal pain. On-target and off-target mechanisms mediating TRK inhibitor resistance may occur. Next-generation TRK inhibitors, such as selitrectinib, repotrectinib, and taletrectinib, are available on ongoing clinical trials and address on-target resistance. This review will focus on NTRK fusions and TRK-directed targeted therapy specifically in the context of lung cancer.
MeSH term(s)	Biology ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Macrocyclic Compounds ; Neoplasms ; Oncogene Proteins, Fusion/genetics ; Protein Kinase Inhibitors/therapeutic use ; Pyrazoles ; Receptor, trkA
Chemical Substances	Macrocyclic Compounds ; Oncogene Proteins, Fusion ; Protein Kinase Inhibitors ; Pyrazoles ; repotrectinib (08O3FQ4UNP) ; Receptor, trkA (EC 2.7.10.1)
Language	English
Publishing date	2021-09-16
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	632771-0
ISSN	1872-8332 ; 0169-5002
ISSN (online)	1872-8332
ISSN	0169-5002
DOI	10.1016/j.lungcan.2021.09.005
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Zs.A 2135: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Brief Report: Tyrosine Kinase Inhibitors for Lung Cancers That Inhibit MATE-1 Can Lead to "False" Decreases in Renal Function.

Chen, Monica F / Harada, Guilherme / Liu, Dazhi / DeMatteo, Ray / Falcon, Christina / Wilhelm, Clare / Kris, Mark G / Drilon, Alexander / Gutgarts, Victoria

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer

2023 Volume 19, Issue 1, Page(s) 153–159

Abstract: Introduction: Select tyrosine kinase inhibitors (TKIs) used to treat oncogene-driven lung cancers also inhibit MATE-1. When MATE-1 is blocked, creatinine is retained in the serum. Elevated creatinine levels raise the specter of drug-induced intrarenal ... ...

Abstract	Introduction: Select tyrosine kinase inhibitors (TKIs) used to treat oncogene-driven lung cancers also inhibit MATE-1. When MATE-1 is blocked, creatinine is retained in the serum. Elevated creatinine levels raise the specter of drug-induced intrarenal insufficiency despite the lack of true renal injury. We conducted a systematic analysis of MATE-1 inhibitor (MATEi)-treated patients to comprehensively characterize this phenomenon. Methods: Patients with oncogene-driven lung cancer treated with a wide variety of MATEi TKIs (brigatinib, cabozantinib, capmatinib, crizotinib, entrectinib, lorlatinib, pralsetinib, selpercatinib, and tepotinib) were eligible for an analysis of renal dysfunction. Acute kidney injury was classified on the basis of creatinine levels (Kidney Disease: Improving Global Outcomes criteria) as stage 1 (≥1.5× but <2× baseline), stage 2 (≥2× but <3× baseline), or stage 3 (>3× baseline). When available, cystatin C, a marker of kidney function unaffected by MATE-1, was used to evaluate the glomerular filtration rate (GFR). Results: We identified 863 patients receiving MATEi TKIs including crizotinib (39%, n = 333), lorlatinib (17%, n = 144), cabozantinib (10%, n = 87), selpercatinib (10%, n = 82), capmatinib (9%, n = 77), brigatinib (6%, n = 53), entrectinib (5%, n = 45), tepotinib (5%, n = 41), and pralsetinib (0.1%, n = 1). Of the 90 patients (10%) with acute kidney injury, Kidney Disease: Improving Global Outcomes stages 1, 2, and 3 were observed in 72% (n = 65), 21% (n = 19), and 7% (n = 6) of patients, respectively. Concurrently drawn creatinine and cystatin C levels on TKI therapy were available for 17 patients. In most cases (n = 15 of 17), the calculated GFR was higher using cystatin C versus creatinine. The percentage of patients whose GFR was higher using cystatin C versus creatinine by less than 10 mL/min, 10 to 19 mL/min, 20 to 29 mL/min, and more than or equal to 30 mL/min was 27% (n = four of 15), 20% (n = three of 15), 20% (n = three of 15), and 33% (n = five of 15), respectively. Long-term data in three patients that spanned 3 years revealed that GFR was higher using cystatin C versus creatinine in 96% (n = 49 of 51) of all time points. Using a virtual clinical trial GFR cutoff of 40 mL/min, the percentage of eligible patients rose from 41% (n = seven of 17) using creatinine calculations to 71% (n = 12 of 17) using cystatin C calculations. Conclusions: The calculated GFR in patients with cancer receiving MATEi TKIs was higher in almost all cases when using cystatin C. When serum creatinine level seems elevated in patients receiving MATE-1 inhibitors, we recommend recalculating GFR using cystatin C before searching for other etiologies of kidney injury and reducing or stopping TKI therapy.
MeSH term(s)	Humans ; Cystatin C ; Tyrosine Kinase Inhibitors ; Creatinine ; Lung Neoplasms/drug therapy ; Crizotinib ; Glomerular Filtration Rate ; Kidney ; Acute Kidney Injury ; Biomarkers
Chemical Substances	entrectinib (L5ORF0AN1I) ; Cystatin C ; capmatinib (TY34L4F9OZ) ; brigatinib (HYW8DB273J) ; cabozantinib (1C39JW444G) ; lorlatinib (OSP71S83EU) ; Tyrosine Kinase Inhibitors ; Creatinine (AYI8EX34EU) ; Crizotinib (53AH36668S) ; Biomarkers
Language	English
Publishing date	2023-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2432037-7
ISSN	1556-1380 ; 1556-0864
ISSN (online)	1556-1380
ISSN	1556-0864
DOI	10.1016/j.jtho.2023.09.1444
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Zs.MO 652: Show issues

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Article: TKI Type Switching Overcomes ROS1 L2086F in ROS1 Fusion-Positive Cancers.

Thawani, Rajat / Repetto, Matteo / Keddy, Clare / Nicholson, Katelyn / Jones, Kristen / Nusser, Kevin / Beach, Catherine Z / Harada, Guilherme / Drilon, Alexander / Davare, Monika A

bioRxiv : the preprint server for biology

2024

Abstract: Purpose: Despite the robust efficacy of ROS1 tyrosine kinase inhibitors (TKIs) in ROS1-positive non-small cell lung cancer, TKI resistance continues to hamper durability of the therapeutic response. The resistance liabilities of next-generation ROS1 TKI ...

Abstract	Purpose: Despite the robust efficacy of ROS1 tyrosine kinase inhibitors (TKIs) in ROS1-positive non-small cell lung cancer, TKI resistance continues to hamper durability of the therapeutic response. The resistance liabilities of next-generation ROS1 TKI are sparsely characterized. Design: We compared the activity of type I TKIs (crizotinib, entrectinib, taletrectinib, lorlatinib, and repotrectinib) to the type II TKIs (cabozantinib and merestinib), and to the type I FLT3 inhibitor, gilteritinib, in CD74-ROS1 wildtype and F2004C, L2026M, G2032R, or L2086 mutant Ba/F3 cells. The findings from the Ba/F3 cell model were confirmed using NIH3T3 colony formation assays and in vivo tumor growth. CRISPR/Cas9 gene editing was used to generate isogenic wildtype and L2086F mutant TPM3-ROS1 expressing patient-derived cell lines. These lines were used to further evaluate TKI activity using cell viability and immunoblotting methods. Molecular modeling studies enabled the characterization of structural determinants of TKI sensitivity in wildtype and mutant ROS1 kinase domains. We also report clinical cases of ROS1 TKI resistance that were treated with cabozantinib. Results: ROS1 L2086F mutant kinase is resistant to type I TKI including crizotinib, entrectinib, lorlatinib, repotrectinib, taletrectinib, while the type II TKI cabozantinib and merestinib retain activity. Additionally, we found that gilteritinib, a type I FLT3 inhibitor, inhibited wildtype and L2086F mutant ROS1, however ROS1 G2032R solvent front mutation imposed resistance. The specific binding poses adopted by cabozantinib in the DFG-out kinase conformation and gilteritinib in the DFG-in kinase, provide rationale for their activity in the ROS1 mutants. Clinical cases demonstrated response to cabozantinib in tumors developing TKI resistance due to the ROS1 L2086F mutation. Conclusion: Cabozantinib and gilteritinib effectively inhibit ROS1 L2086F. Clinical activity of cabozantinib is confirmed in patients with TKI-resistant, ROS1 L2086F mutant NSCLC. Gilteritinib may offer an alternative with distinct off-target toxicities, however further studies are required. Since cabozantinib and gilteritinib are multi-kinase inhibitors, there is a persistent unmet need for more selective and better-tolerated TKI to overcome ROS1 L2086F kinase-intrinsic resistance. Translational relevance: ROS1 L2086F is an emerging recurrent resistance mutation to type I ROS1 TKIs, including later generation TKIs. Here, we show corroborating preclinical and clinical evidence for the activity of the quinolone-based type II TKI, cabozantinib, in ROS1
Language	English
Publishing date	2024-01-19
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.16.575901
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Article ; Online: Cushing's syndrome due to ectopic adrenocorticotropin secretion by a parotid carcinoma.

Antonacio, Fernanda F / Harada, Guilherme / Vilela, Rafael S / Freitas, Thais C / Lima, Jose V / Kowalski, Luiz Paulo / Almeida, Madson Q / de Castro, Gilberto

Archives of endocrinology and metabolism

2022 Volume 66, Issue 1, Page(s) 92–96

Abstract: We report a rare case of Cushing's syndrome in a 37-year-old female who initially presented with localized acinic cell carcinoma of the parotid gland. In January 2014, she underwent a right parotidectomy with facial nerve preservation and adjuvant ... ...

Abstract	We report a rare case of Cushing's syndrome in a 37-year-old female who initially presented with localized acinic cell carcinoma of the parotid gland. In January 2014, she underwent a right parotidectomy with facial nerve preservation and adjuvant radiotherapy. In August 2018, she presented a histologically-proven local regional relapse. The patient was considered for salvage surgery with facial nerve sacrifice and remained with no evidence of disease. One year later the patient developed pulmonary dissemination and started to gain weight and developed facial plethora and acne on the face and upper trunk. In a physical examination, the patient presented moon face, buffalo hump, acne and stage 2 hypertension. Biochemical evaluation confirmed ACTH-dependent Cushing's syndrome. IHC for ACTH in the lung biopsy revealed strong positive staining for ACTH confirming a diagnosis of ectopic ACTH secretion by a metastatic parotid acinic cell carcinoma. Ketoconazole (600 mg/d) was started to treat the CS. In addition, as chemotherapy was initiated to treat the metastatic disease. After the fifth cycle of chemotherapy, ketoconazole was suspended and the patient remained in remission of CS for four months, when CS recurred. A unique feature of this case is related to the clinical CS relapse associated with disease progression, which needed prompt treatment with ketoconazole, resulting in a significant improvement in the patient's condition. Although rare, should be attentive for possible CS features in patients with high-grade salivary gland carcinomas, since the diagnosis of ectopic secretion of ACTH may significantly impact their management and outcomes.
MeSH term(s)	ACTH Syndrome, Ectopic/complications ; ACTH Syndrome, Ectopic/diagnosis ; Adrenocorticotropic Hormone ; Adult ; Carcinoma/complications ; Cushing Syndrome/diagnosis ; Cushing Syndrome/etiology ; Female ; Humans ; Neoplasm Recurrence, Local ; Parotid Neoplasms/complications
Chemical Substances	Adrenocorticotropic Hormone (9002-60-2)
Language	English
Publishing date	2022-01-13
Publishing country	Brazil
Document type	Case Reports
ISSN	2359-4292
ISSN (online)	2359-4292
DOI	10.20945/2359-3997000000426
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Article: Cardiovascular toxicity following immune checkpoint inhibitors: A systematic review and meta-analysis.

Xavier, Camila Bragança / Lopes, Carlos Diego Holanda / Harada, Guilherme / Peres, Eduardo Dante Bariani / Katz, Artur / Jardim, Denis Leonardo

Translational oncology

2022 Volume 19, Page(s) 101383

Abstract: Background: Immune checkpoint inhibitors may be associated with multiple immune-related toxicities. Cardiovascular adverse effects are underreported in clinical trials.: Methods: We conducted a systematic review and meta-analysis to evaluate ... ...

Abstract	Background: Immune checkpoint inhibitors may be associated with multiple immune-related toxicities. Cardiovascular adverse effects are underreported in clinical trials. Methods: We conducted a systematic review and meta-analysis to evaluate cardiovascular adverse effects incidence among patients with solid tumors receiving immune checkpoint inhibitors in randomized clinical trials and the relative risk of presenting these effects compared to placebo or best supportive care. The search was conducted through MEDLINE, Embase, and Scopus databases from January 1st, 2010 until July 1st, 2020. Outcomes were reported following Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines. Results: 57 randomized clinical trials including 12,118 patients were included. All grade CV AEs incidence rate was 8.32% (95% CI = 6.35%-10.53%). When only grade 3-5 CV AEs were considered, ICIs were significantly associated with increased risk than placebo or BSC (RR = 1.36; 95% CI = 1.06-1.73; p = 0.01). Conclusion: This meta-analysis corroborates the hypothesis of increased CV risk related to immune checkpoint inhibitors.
Language	English
Publishing date	2022-03-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2443840-6
ISSN	1936-5233
ISSN	1936-5233
DOI	10.1016/j.tranon.2022.101383
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Article ; Online: The importance of molecular characterization in lung cancer.

Castro Junior, Gilberto de / Harada, Guilherme / Mello, Evandro Sobroza de

Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia

2019 Volume 45, Issue 3, Page(s) e20190139

MeSH term(s)	Brazil ; Carcinoma, Non-Small-Cell Lung ; Humans ; Lung Neoplasms
Language	Portuguese
Publishing date	2019-06-03
Publishing country	Brazil
Document type	Editorial ; Comment
ZDB-ID	2223157-2
ISSN	1806-3756 ; 1806-3713
ISSN (online)	1806-3756
ISSN	1806-3713
DOI	10.1590/1806-3713/e20190139
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Article ; Online: TRK Inhibitors in Non-Small Cell Lung Cancer.

Harada, Guilherme / Gongora, Aline Bobato Lara / da Costa, Cesar Martins / Santini, Fernando Costa

Current treatment options in oncology

2020 Volume 21, Issue 5, Page(s) 39

Abstract: Opinion statement: Care should be taken to ensure that the diagnostic strategy for a recently diagnosed advanced non-small cell lung cancer includes NTRK fusion testing. RNA sequencing is the gold standard method of detection of NTRK fusion; however, ... ...

Abstract	Opinion statement: Care should be taken to ensure that the diagnostic strategy for a recently diagnosed advanced non-small cell lung cancer includes NTRK fusion testing. RNA sequencing is the gold standard method of detection of NTRK fusion; however, pan-TRK immunohistochemistry could be used as a screening method with good sensitivity. Larotrectinib and entrectinib are approved therapies for TRK fusion-positive lung cancers as first or subsequent lines of therapy. TRK inhibition has demonstrated clinically meaningful, deep, and durable systemic and central nervous system responses. Larotrectinib and entrectinib have a manageable safety profile, including some TRK-related adverse events, such as dizziness and weight gain. At disease progression on first-generation TRK inhibitors, enrollment on a clinical trial should be encouraged, as new-generation TRK inhibitors are being tested.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor ; Carcinoma, Non-Small-Cell Lung/diagnosis ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/etiology ; Carcinoma, Non-Small-Cell Lung/mortality ; Disease Management ; Disease Susceptibility ; Humans ; Lung Neoplasms/diagnosis ; Lung Neoplasms/drug therapy ; Lung Neoplasms/etiology ; Lung Neoplasms/mortality ; Molecular Diagnostic Techniques ; Molecular Targeted Therapy/adverse effects ; Molecular Targeted Therapy/methods ; Neoplasm Metastasis ; Neoplasm Staging ; Prognosis ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors ; Treatment Outcome
Chemical Substances	Antineoplastic Agents ; Biomarkers, Tumor ; Protein Kinase Inhibitors ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2020-04-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2057351-0
ISSN	1534-6277 ; 1527-2729
ISSN (online)	1534-6277
ISSN	1527-2729
DOI	10.1007/s11864-020-00741-z
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