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crizotinib

✓ Approved

Roche · ALK · Companion diagnostic

What is crizotinib?

crizotinib is a companion diagnostic developed by Roche. It is approved for therapeutic indications via others.

Drug Profile

CompanyRoche
Drug ClassCompanion diagnostic
Molecular TargetALK
RouteOthers
StatusApproved
Sources: ClinicalTrials.gov, Roche

Mechanism of Action

Molecular Targets

crizotinib acts on 1 molecular target:

ALKALK receptor tyrosine kinase (CD246, NBLST3)
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Therapeutic Indications

crizotinib is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Uterine cancer✓ Approved

Related Research Articles

PubMedTherapeutic advances in musculoskeletal disease2026-08-30

Diagnostic performance of salivary gland ultrasonography using the OMERACT scoring system in Sjögren disease: A cross-sectional diagnostic accuracy study.

Hossain Md Ismail MI, Choudhury Minhaj Rahim MR, Majumder Muhammad Shoaib Momen MSM, Shazzad Md Nahiduzzamane MN et al.

Sjögren disease (SjD) is an autoimmune disorder characterized by salivary and lacrimal gland dysfunction. Salivary gland ultrasonography (SGUS) is a non-invasive, accessible imaging modality for assessing glandular structural changes, although its diagnostic performance compared with conventional diagnostic tests requires further evaluation. To evaluate the diagnostic accuracy of OMERACT-scored salivary gland ultrasonography in patients with suspected primary or secondary SjD. This is a cross-sectional diagnostic accuracy study of salivary ultrasonography. This study was conducted in the Department of Rheumatology, Bangladesh Medical University, from February 2023 to February 2024. Patients presenting with sicca symptoms were classified according to the 2016 ACR/EULAR classification criteria, which served as the reference standard. All participants underwent clinical evaluation, Schirmer's test, unstimulated whole salivary flow rate (UWSFR), anti-SSA/anti-SSB antibody testing, and SGUS of the parotid and submandibular glands. SGUS images were scored using the OMERACT semiquantitative grayscale scoring system (0-3 per gland) by a blinded examiner. Diagnostic performance was assessed using sensitivity, specificity, and receiver operating characteristic (ROC) curve analysis. Among 100 participants, 50 fulfilled the 2016 ACR/EULAR classification criteria for SjD. Patients with SjD had significantly higher mean SGUS scores and lower mean UWSFR compared with those without SjD (p < 0.001). An OMERACT SGUS grade ≥2 in at least one gland demonstrated 84% sensitivity and 92% specificity. A total SGUS score ≥4 showed 88% sensitivity and 86% specificity, whereas a score ≥6 provided 100% specificity with reduced sensitivity (64%). SGUS showed excellent diagnostic performance with an area under the ROC curve (AUC) of 0.94 (95% CI: 0.90-0.99). Compared with SGUS, Schirmer's test demonstrated lower diagnostic accuracy (sensitivity 65.3%, specificity 52%), while UWSFR showed high sensitivity (92%) but limited specificity (48%). SGUS score showed a weak positive correlation with disease duration (r = 0.33, p < 0.05). OMERACT-scored salivary gland ultrasonography demonstrated excellent diagnostic accuracy and superior specificity compared with conventional functional tests. SGUS may serve as a valuable non-invasive adjunctive tool in the diagnostic evaluation of patients with suspected SjD.

PMID 42668827
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PubMedPakistan journal of medical sciences2026-08-30

Diagnostic value of platelet-lymphocyte ratio for pediatric sepsis: A systematic review and meta-analysis.

Chen Li L, Yang Qiuping Q

Early diagnosis of pediatric sepsis remains challenging due to limitations of conventional biomarkers. The platelet-to-lymphocyte ratio (PLR), derived from routine blood tests, has emerged as a potential diagnostic marker. This study aimed to evaluate the diagnostic accuracy of PLR for pediatric sepsis. A systematic search of PubMed, Embase, Web of Science, and Scopus was conducted from inception to March 15, 2026. Studies assessing the diagnostic performance of PLR in pediatric sepsis and reporting sufficient data to construct 2×2 contingency tables were included. Pooled sensitivity and specificity were calculated using a random-effects model. Summary receiver operating characteristic (SROC) analysis and Deeks' funnel plot were performed. Fifteen studies with 1,980 patients were included. The pooled sensitivity and specificity of PLR for diagnosing pediatric sepsis were 0.81 (95% CI: 0.73-0.87) and 0.72 (95% CI: 0.60-0.82), respectively. The SROC curve demonstrated an area under the curve of 0.79, indicating moderate diagnostic accuracy. Significant heterogeneity was observed. Subgroup analysis showed better performance in larger studies (≥150 patients) and studies using higher PLR cut-offs (>50). Deeks' funnel plot showed no evidence of publication bias (p = 0.536). Evidence from studies with high-risk of bias indicates that PLR may have moderate diagnostic accuracy for pediatric sepsis and may serve as a simple, cost-effective adjunctive biomarker. Since, most studies were on neonatal population, evidence may not be generalized to older pediatric populations. Further large-scale prospective studies are needed to establish standardized cut-off values and validate its clinical utility.Registration No: PROSPERO (No. CRD420261338676).

PMID 42668943
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PubMedEuropean heart journal. Case reports2026-08-30

Phenotypic overlap masking MELAS in Turner syndrome: a diagnostic challenge.

Shinozaki Tomoya T, Sumiyoshi Hironobu H, Ueshima Daisuke D, Onaka Joe J et al.

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) is a multisystemic disorder that can present with diverse clinical features, including cardiomyopathy and chronic intestinal pseudo-obstruction. However, diagnosing MELAS can be challenging when its manifestations overlap with other genetic syndromes, leading to diagnostic anchoring and potential mismanagement. A 51-year-old woman with mosaic Turner syndrome presented with concentric left ventricular hypertrophy and mildly reduced systolic function (left ventricular ejection fraction 45%). Her medical history included childhood-onset hearing loss, hypothyroidism, and recurrent intestinal obstruction of unknown etiology, which had been previously attributed to Turner syndrome or its comorbidities. Despite resolution of bowel symptoms during prior hospitalizations, she exhibited persistent hyperlactataemia (4.55 mmol/L), a diagnostic red flag. Cardiac magnetic resonance imaging showed patchy mid-wall late gadolinium enhancement, suggesting a non-ischaemic process. Family history revealed a maternal pattern of cardiomyopathy and stroke-like episodes. Genetic analysis confirmed the m.3243A > G mitochondrial DNA mutation (heteroplasmy 23%), establishing a diagnosis of MELAS. Earlier recognition of mitochondrial dysfunction might have avoided a previous unnecessary laparotomy performed for suspected intestinal ischaemia. This case illustrates the clinical challenge of phenotypic masking; features of Turner syndrome masked the underlying MELAS, resulting in a significant diagnostic delay. The coexistence of unexplained cardiomyopathy, recurrent pseudo-obstruction, and persistent hyperlactataemia should prompt consideration of mitochondrial disease, even in patients with an established genetic diagnosis. Clinicians must remain vigilant for multisystemic 'red flags' to avoid diagnostic anchoring and ensure appropriate metabolic and genetic evaluation.

PMID 42668775
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PubMedCureus2026-08-30

The Great Mimickers: Navigating Diagnostic Pitfalls in Modern Rheumatology.

Assabag Yarden Y

Background Rheumatological mimics frequently cause diagnostic errors and unnecessary immunosuppression due to overreliance on positive serology or non-specific imaging. This review evaluates eight illustrative cases where initial objective findings heavily conflicted with the final, etiology-driven diagnosis. Methods A retrospective chart review of eight patients from a tertiary rheumatology practice was performed. Cases were selected based on significant incongruence between initial laboratory or high-sensitivity imaging profiles and the final clinical etiology. A literature search across PubMed and Google Scholar up to June 2026 contextualized these pitfalls. Results The cohort highlighted critical diagnostic traps: crystal arthropathy misdiagnosed as systemic vasculitis, lupus phenocopies, and structural/functional disorders (e.g., temporomandibular joint dysfunction) misattributed to fibromyalgia. Comprehensive clinical re-evaluation led to the cessation of inappropriate immunomodulatory treatments and the initiation of targeted, etiology-specific therapies. Comprehensive re-evaluation led to the cessation of inappropriate immunomodulatory treatments in all eight patients, with six receiving targeted etiology-specific therapies and two benefiting from lifestyle or occupational modifications. Conclusions Isolated laboratory titers and imaging findings must never supersede strict clinical correlation. Recognizing these common mimics is essential to halt diagnostic momentum and prevent treatment-related morbidity.

PMID 42668922
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PubMedInternational journal of general medicine2026-08-30

Diagnostic Performance of Platelet-to-Lymphocyte Ratio and CA19-9 Added to EUS-FNA for Solid Pancreatic Lesions: A Single-Center Retrospective Study.

Liu Shasha S, Hu Chen C, Fan Yujing Y, Liu Lina L et al.

To evaluate the incremental diagnostic value of the platelet-to-lymphocyte ratio (PLR) and carbohydrate antigen 19-9 (CA19-9) when combined with endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) in patients with solid pancreatic lesions. This retrospective single-center study included 127 consecutive patients who underwent EUS-FNA for solid pancreatic lesions between December 29, 2020, and October 23, 2023. Final diagnoses were established using a reference standard independent of the index EUS-FNA. Malignancy was confirmed by surgical pathology, independent cytologic or histologic evidence, or unequivocal radiologic progression or metastasis. Non-malignancy was established by independent benign pathology or lesion stability or regression without anticancer therapy during at least 24 months of clinical and imaging follow-up. Among 127 patients, 80 had malignant lesions and 47 had non-malignant lesions. EUS-FNA achieved an accuracy of 91.3%, sensitivity of 93.8%, specificity of 87.2%, positive predictive value of 92.6%, and negative predictive value of 89.1%. CA19-9 levels were significantly higher in malignant than in non-malignant lesions (median [IQR], 197.21 [9.51-928.36] vs 14.30 [3.97-211.02] U/mL; P=0.001), with an AUC of 0.692. The PLR plus CA19-9 model yielded an apparent AUC of 0.734 and an optimism-corrected AUC of 0.717. The EUS-FNA plus PLR plus CA19-9 model showed the highest discrimination, with an apparent AUC of 0.986 (bootstrap 95% CI, 0.962-1.000) and an optimism-corrected AUC of 0.981; the corresponding Brier scores were 0.033 and 0.041. EUS-FNA demonstrated high diagnostic accuracy for solid pancreatic lesions. PLR and CA19-9 provided complementary diagnostic value, and the three-variable model showed high diagnostic performance after internal validation.

PMID 42668854
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PubMedCaspian journal of internal medicine2026-08-30

Diagnostic challenges and mimicking disorders of Wilson's Disease: A comprehensive review.

Hashemi Seyyed-Saleh SS, Gholoobi Aida A, Naghipoor Karim K, Hamzehloei Tayebeh T

Wilson disease is classically defined as an autosomal recessive disorder of copper metabolism that leads to neurological and hepatic dysfunction. It is one of the most prevalent genetic liver disorders caused by pathogenic mutations in the ATP7B gene, leading to defective copper transport and toxic accumulation in tissues. Without timely diagnosis and appropriate treatment, Wilson disease can progress to life-threatening hepatic failure and severe neurological impairment, ultimately resulting in death. Clinically, Wilson disease exhibits marked phenotypic heterogeneity, presenting with a wide spectrum of hepatic, neurological, and psychiatric symptoms. Differential diagnosis can be complicated by other inherited metabolic disorders with overlapping clinical and biochemical features, collectively referred to as Wilson's mimicry disease. These disorders may contribute to diagnostic uncertainty, potentially delaying the identification of Wilson disease and timely initiation of effective therapy. In this review, we collated pertinent information on Wilson disease and its related differential diagnoses based on a broad review of the scientific literature. Our findings highlight disorders that closely mimic Wilson disease clinically and biochemically, outlining their distinguishing clinical, biochemical, and genetic features, which can be differentiated through specific diagnostic markers and genetic testing. Enhancing awareness and understanding of these entities is essential to improve diagnostic accuracy in pediatric neurology and hepatology.

PMID 42668699
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