Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer DOI Creative Commons
María Hernández, Patricia de la Cruz‐Ojeda,

Ma José López-Grueso

и другие.

Redox Biology, Год журнала: 2020, Номер 36, С. 101510 - 101510

Опубликована: Май 23, 2020

Cancer cells have unlimited replicative potential, insensitivity to growth-inhibitory signals, evasion of apoptosis, cellular stress, and sustained angiogenesis, invasiveness metastatic potential. adequately adapt cell metabolism integrate several intracellular redox signaling promote survival in an inflammatory hypoxic microenvironment order maintain/expand tumor phenotype. The administration tyrosine kinase inhibitor (TKI) constitutes the recommended therapeutic strategy different malignancies at advanced stages. There are important interrelationships between status, mitochondrial function, pathways leading survival/death. induction apoptosis cycle arrest widely related antitumoral properties TKIs result from tightly controlled events involving compartments pathways. aim present review is update most relevant studies dealing with impact TKI treatment on function. endoplasmic reticulum (ER) stress Ca2+ disturbances, alteration status phosphatidylinositol 3-kinase (PI3K)-protein B (Akt)-mammalian target rapamycin (mTOR) AMP-activated protein (AMPK) that involve reprogramming cancer will be covered. Emphasis given identify key components integrated molecular pattern including receptor (RTK) downstream signaling, death mitochondria-related appear involved resistance treatments.

Язык: Английский

Colony-stimulating factor 1 receptor (CSF1R) inhibitors in cancer therapy DOI Creative Commons
Michael A. Cannarile, Maja Weisser, Wolfgang Jacob

и другие.

Journal for ImmunoTherapy of Cancer, Год журнала: 2017, Номер 5(1)

Опубликована: Июнь 30, 2017

The tumor-permissive and immunosuppressive characteristics of tumor-associated macrophages (TAM) have fueled interest in therapeutically targeting these cells. In this context, the colony-stimulating factor 1 (CSF1)/colony-stimulating receptor (CSF1R) axis has gained most attention, various approaches either ligands or are currently clinical development. Emerging data on tolerability CSF1/CSF1R-targeting agents suggest a favorable safety profile, making them attractive combination partners for both standard treatment modalities immunotherapeutic agents. specificity their potent blocking activity been substantiated by impressive response rates diffuse-type tenosynovial giant cell tumors, benign connective tissue disorder driven CSF1 an autocrine fashion. malignant disease setting, immunotherapy combinations with pending. As our knowledge macrophage biology expands, it becomes apparent that complex phenotypic functional properties heavily influenced continuum survival, differentiation, recruitment, polarization signals within specific environment. Thus, role regulating tumorigenesis impact depleting and/or reprogramming TAM as therapeutic cancer patients may vary greatly depending organ-specific We review available efficacy provide comprehensive overview ongoing studies. Furthermore, we discuss local tumor-type specificities potential strategies future.

Язык: Английский

Процитировано

841

European LeukemiaNet recommendations for the management and avoidance of adverse events of treatment in chronic myeloid leukaemia DOI
Juan Luis Steegmann, Michele Baccarani, Massimo Breccia

и другие.

Leukemia, Год журнала: 2016, Номер 30(8), С. 1648 - 1671

Опубликована: Апрель 28, 2016

Язык: Английский

Процитировано

425

Drug-Induced Liver Injury DOI Open Access
Michael D. Leise,

John J. Poterucha,

Jayant A. Talwalkar

и другие.

Mayo Clinic Proceedings, Год журнала: 2014, Номер 89(1), С. 95 - 106

Опубликована: Янв. 1, 2014

Язык: Английский

Процитировано

371

Hepatic adverse event profile of inotuzumab ozogamicin in adult patients with relapsed or refractory acute lymphoblastic leukaemia: results from the open-label, randomised, phase 3 INO-VATE study DOI
Hagop M. Kantarjian, Daniel J. DeAngelo, Anjali S. Advani

и другие.

The Lancet Haematology, Год журнала: 2017, Номер 4(8), С. e387 - e398

Опубликована: Июль 4, 2017

Язык: Английский

Процитировано

192

Adverse effects of tyrosine kinase inhibitors in cancer therapy: pathophysiology, mechanisms and clinical management DOI Creative Commons
Sunitha Shyam Sunder, Umesh C. Sharma,

Saraswati Pokharel

и другие.

Signal Transduction and Targeted Therapy, Год журнала: 2023, Номер 8(1)

Опубликована: Июль 7, 2023

Since their invention in the early 2000s, tyrosine kinase inhibitors (TKIs) have gained prominence as most effective pathway-directed anti-cancer agents. TKIs shown significant utility treatment of multiple hematological malignancies and solid tumors, including chronic myelogenous leukemia, non-small cell lung cancers, gastrointestinal stromal HER2-positive breast cancers. Given widespread applications, an increasing frequency TKI-induced adverse effects has been reported. Although are known to affect organs body lungs, liver, tract, kidneys, thyroid, blood, skin, cardiac involvement accounts for some serious complications. The frequently reported cardiovascular side range from hypertension, atrial fibrillation, reduced function, heart failure sudden death. potential mechanisms these unclear, leading critical knowledge gaps development therapy guidelines. There limited data infer best clinical approaches detection therapeutic modulation effects, universal consensus regarding various management guidelines is yet be reached. In this state-of-the-art review, we examine pre-clinical studies curate evidence on pathophysiology, mechanisms, reactions. We expect that review will provide researchers allied healthcare providers with up-to-date information natural history, risk stratification, emerging cancer patients.

Язык: Английский

Процитировано

191

Drug-Induced Liver Injury DOI
Kurt W. Fisher, Raj Vuppalanchi,

Romil Saxena

и другие.

Archives of Pathology & Laboratory Medicine, Год журнала: 2015, Номер 139(7), С. 876 - 887

Опубликована: Июнь 30, 2015

Context Drug-induced liver injury (DILI) represents a diverse set of responses following exposure to any manufactured or naturally occurring chemical compound. is major concern owing the ever increasing number compounds introduced into market for treatment various diseases as well popularity herbals, which lend themselves self-medication but are not rigorously regulated. Objective To provide an overview prevalence, classification, and diagnosis DILI with emphasis on pathogenesis role biopsy. focus most common, emerging, herbal agents that cause histologic pattern observed. Data Sources A review literature was drawn from PubMed (US National Library Medicine) repository, textbooks, online databases. All figures were taken cases seen at our tertiary referral center, 1 12 participating sites in Institutes Health–funded Drug-Induced Liver Injury Network. Conclusions due prescription, over-the-counter, products disease United States around world. Diagnosis challenging because there no single clinical, laboratory, feature specific DILI. Accurate requires establishing causal relationship suspected agent excluding competing causes injury. The biopsy essential component management by offering clues underlying pathogenesis, providing prognostic information, guiding therapy.

Язык: Английский

Процитировано

174

Long-Term Side Effects of Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia DOI

Lauren E. Caldemeyer,

Michael J. Dugan, John Edwards

и другие.

Current Hematologic Malignancy Reports, Год журнала: 2016, Номер 11(2), С. 71 - 79

Опубликована: Фев. 27, 2016

Язык: Английский

Процитировано

139

Current and future directions in the treatment and prevention of drug-induced liver injury: a systematic review DOI
Jonathan G. Stine, James H. Lewis

Expert Review of Gastroenterology & Hepatology, Год журнала: 2015, Номер 10(4), С. 517 - 536

Опубликована: Дек. 3, 2015

While the pace of discovery new agents, mechanisms and risk factors involved in drug-induced liver injury (DILI) remains brisk, advances treatment acute DILI seems slow by comparison. In general, key to treating suspected is stop using drug prior developing irreversible failure. However, predicting when an inexact science, commonly used ALT monitoring ineffective strategy outside clinical trials. The only specific antidote for N-acetylcysteine (NAC) acetaminophen poisoning, although NAC proving be beneficial some cases non-acetaminophen adults. Corticosteroids can effective associated with autoimmune or systemic hypersensitivity features. Ursodeoxycholic acid, silymarin glycyrrhizin have been treat decades, but success anecdotal. Bile acid washout regimens cholestyramine appear more evidenced based, particular leflunomide toxicity. For failure, use support systems still investigational United States emergency transplant limited its availability. Primary prevention appears avoiding need treatment. Pharmacogenomics, including human leukocyte antigen genotyping biomarkers offers significant promise future. This article describes summarizes numerous diverse modalities that are currently available manage DILI.

Язык: Английский

Процитировано

99

Safety and Tolerability of Epidermal Growth Factor Receptor (EGFR) Tyrosine Kinase Inhibitors in Oncology DOI
Rashmi R. Shah,

Devron R. Shah

Drug Safety, Год журнала: 2019, Номер 42(2), С. 181 - 198

Опубликована: Янв. 16, 2019

Язык: Английский

Процитировано

76

KIAA1429 promotes tumorigenesis and gefitinib resistance in lung adenocarcinoma by activating the JNK/ MAPK pathway in an m6A-dependent manner DOI Creative Commons
Xi Lin, Rongyi Ye, Zhiming Li

и другие.

Drug Resistance Updates, Год журнала: 2022, Номер 66, С. 100908 - 100908

Опубликована: Дек. 5, 2022

Non-small cell lung cancer is the leading cause of related mortality worldwide, and adenocarcinoma (LUAD) one most common subtypes. The role N6-methyladenosine (m6A) modification in tumorigenesis drug resistance LUAD remains unclear. In this study, we evaluated effects vir-like m6A methyltransferase-associated protein (KIAA1429) depletion on proliferation, migration, invasion, cells, identified m6A-dependent downstream genes influenced by KIAA1429. We found that KIAA1429 activated Jun N-terminal kinase (JNK) mitogen-activated (MAPK) pathway as a novel signaling event, which responsible for to gefitinib cells. MAP3K2 showed high expression patients' tissues. Knockdown inhibited an methylation-dependent manner, restraining progression cells inhibiting growth gefitinib-resistant HCC827 positively regulated expression, JNK/ MAPK pathway, promoted reproduced vitro results nude mouse xenografted with knockdown Our study mechanism KIAA1429-mediated occurs activating pathway. These findings provide potential targets molecular therapy clinical treatment patients resistance.

Язык: Английский

Процитировано

54