HGF/MET pathway aberrations as diagnostic, prognostic, and predictive biomarkers in human cancers

被引:150
作者
Moosavi, Fatemeh [1 ]
Giovannetti, Elisa [2 ,3 ]
Saso, Luciano [4 ]
Firuzi, Omidreza [1 ]
机构
[1] Shiraz Univ Med Sci, Med & Nat Prod Chem Res Ctr, 1 Neshat St, Shiraz 7144816645, Iran
[2] Vrije Univ Amsterdam, Med Ctr VUmc, Amsterdam UMC, Dept Med Oncol,Canc Ctr Amsterdam, Amsterdam, Netherlands
[3] Fdn Pisana Sci Onlus, AIRC Start Unit, Canc Pharmacol Lab, Pisa, Italy
[4] Sapienza Univ, Dept Physiol & Pharmacol, Rome, Italy
关键词
Receptor tyrosine kinases; c-MET; neoplasms; biomarker discovery; targeted therapy; HEPATOCYTE GROWTH-FACTOR; CELL LUNG-CANCER; SOLUBLE C-MET; RECEPTOR TYROSINE KINASE; RANDOMIZED PHASE-II; GENE COPY NUMBER; BREAST-CANCER; GASTRIC-CANCER; CLINICAL-SIGNIFICANCE; HUMAN-PAPILLOMAVIRUS;
D O I
10.1080/10408363.2019.1653821
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Cancer is a major cause of death worldwide. MET tyrosine kinase receptor [MET, c-MET, hepatocyte growth factor (HGF) receptor] pathway activation is associated with the appearance of several hallmarks of cancer. The HGF/MET pathway has emerged as an important actionable target across many solid tumors; therefore, biomarker discovery becomes essential in order to guide clinical intervention and patient stratification with the aim of moving towards personalized medicine. The focus of this review is on how the aberrant activation of the HGF/MET pathway in tumor tissue or the circulation can provide diagnostic and prognostic biomarkers and predictive biomarkers of drug response. Many meta-analyses have shown that aberrant activation of the MET pathway in tumor tissue, including MET gene overexpression, gene amplification, exon 14 skipping and other activating mutations, is almost invariably associated with shorter survival and poor prognosis. Most meta-analyses have been performed in non-small cell lung cancer (NSCLC), breast, head and neck cancers as well as colorectal, gastric, pancreatic and other gastrointestinal cancers. Furthermore, several studies have shown the predictive value of MET biomarkers in the identification of patients who gain the most benefit from HGF/MET targeted therapies administered as single or combination therapies. The highest predictive values have been observed for response to foretinib and savolitinib in renal cancer, as well as tivantinib in NSCLC and colorectal cancer. However, some studies, especially those based on MET expression, have failed to show much value in these stratifications. This may be rooted in lack of standardization of methodologies, in particular in scoring systems applied in immunohistochemistry determinations or absence of oncogenic addiction of cancer cells to the MET pathway, despite detection of overexpression. Measurements of amplification and mutation aberrations are less likely to suffer from these pitfalls. Increased levels of MET soluble ectodomain (sMET) in circulation have also been associated with poor prognosis; however, the evidence is not as strong as it is with tissue-based biomarkers. As a diagnostic biomarker, sMET has shown its value in distinguishing cancer patients from healthy individuals in prostate and bladder cancers and in melanoma. On the other hand, increased circulating HGF has also been presented as a valuable prognostic and diagnostic biomarker in many cancers; however, there is controversy on the predictive value of HGF as a biomarker. Other biomarkers such as circulating tumor DNA (ctDNA) and tumor HGF levels have also been briefly covered. In conclusion, HGF/MET aberrations can provide valuable diagnostic, prognostic and predictive biomarkers and represent vital assets for personalized cancer therapy.
引用
收藏
页码:533 / 566
页数:34
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