title: [Biomarkers in solid tumors].
abstract: In the past decade the revolutionary development of molecular technology contributed a lot to the increase of our knowledge on cancer. These informations led to the discovery and understanding of those key regulatory changes in the genesis and progression of malignancies that can serve as targets in tumor diagnostics and therapy. One of the main challenges in the research field is to identify the most important molecular networks, the molecular targets, the markers (biomarkers) which can predict therapeutic responsiveness in order to select the appropriate patients, as well as markers to judge the prognosis of the disease. The aims of our study approached some details of the biomarker area and reached certain conclusions: (1) The anti-EGFR therapy, used in the second line or even further, proved to be effective, providing clinical advantage (operability, regression) in 36% of patients carrying wild-type KRAS. G13D mutations were the most frequent among the KRAS-mutants, which, according to current data, could react to anti-EGFR therapy. (2) Extended immunohistochemical (IHC) analysis on colorectal cancer samples (using tissue microarray) found rather few correlations between the IHC estimation and the clinical characteristics related mainly to survival. According to the results with anti-EGFR antibodies in the diagnostic histological samples, the regulatory pathway which rules the proliferation of normal colonic mucosa is also present in colonic cancer cells. This finding is supported by the increased ativity of the downstream members (as RAS, RAF, ERK) of the EGFR signalling. (3) The level of D-dimer increased at least as much as the level of classical tumor markers in the early stages of tumor growth. D-dimer can be considered as a prognostic factor in tumor types studied (breast-, colorectal-, ovarian cancers) and its measurement is advised besides the classical markers. We hope that these results may contribute to the design of a more individual-based and more effective antitumor strategy.
authors.affiliation: Patológiai Tudományok Doktori Iskolája, Semmelweis Egyetem, Budapest, Hungary. zsulacz@chello.hu
authors.forename: Zsuzsanna
authors.initials: Z
authors.lastname: Nagy
mesh_terms: D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D014408:Biomarkers, Tumor / Q000032:analysis* / Q000097:blood / Q000302:isolation & purification* / Q000378:metabolism; D001777:Blood Coagulation; D001943:Breast Neoplasms / Q000737:chemistry / Q000188:drug therapy; D015179:Colorectal Neoplasms / Q000737:chemistry / Q000188:drug therapy; D018450:Disease Progression; D066246:ErbB Receptors / Q000037:antagonists & inhibitors*; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis*; D006495:Heparin, Low-Molecular-Weight / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009369:Neoplasms / Q000737:chemistry* / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D010051:Ovarian Neoplasms / Q000737:chemistry / Q000188:drug therapy; D011237:Predictive Value of Tests; D011379:Prognosis; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras); D015398:Signal Transduction; D046888:Tissue Array Analysis; D016896:Treatment Outcome; D018631:ras Proteins / Q000235:genetics*
chemical_list: D000970:Antineoplastic Agents; D014408:Biomarkers, Tumor; D005338:Fibrin Fibrinogen Degradation Products; D006495:Heparin, Low-Molecular-Weight; C117307:KRAS protein, human; D011518:Proto-Oncogene Proteins; C036309:fibrin fragment D; C512478:EGFR protein, human; D066246:ErbB Receptors; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins