Reporting recommendations for tumour MARKer prognostic studies (REMARK)

US National Cancer Institute, Bethesda, MD 20892, USA.
British Journal of Cancer (Impact Factor: 4.82). 09/2005; 93(4). DOI: 10.1093/jnci/dji237
Source: OAI

ABSTRACT Despite years of research and hundreds of reports on tumor markers in oncology, the number of markers that have emerged as clinically useful is pitifully small. Often, initially reported studies of a marker show great promise, but subsequent studies on the same or related markers yield inconsistent conclusions or stand in direct contradiction to the promising results. It is imperative that we attempt to understand the reasons that multiple studies of the same marker lead to differing conclusions. A variety of methodologic problems have been cited to explain these discrepancies. Unfortunately, many tumor marker studies have not been reported in a rigorous fashion, and published articles often lack sufficient information to allow adequate assessment of the quality of the study or the generalizability of study results. The development of guidelines for the reporting of tumor marker studies was a major recommendation of the National Cancer Institute–European Organisation for Research and Treatment of Cancer (NCI-EORTC) First International Meeting on Cancer Diagnostics in 2000. As for the successful CONSORT initiative for randomized trials and for the STARD statement for diagnostic studies, we suggest guidelines to provide relevant information about the study design, preplanned hypotheses, patient and specimen characteristics, assay methods, and statistical analysis methods. In addition, the guidelines suggest helpful presentations of data and important elements to include in discussions. The goal of these guidelines is to encourage transparent and complete reporting so that the relevant information will be available to others to help them to judge the usefulness of the data and understand the context in which the conclusions apply.

  • Source
    • "This lack of an ideal biomarker for HCC diagnosis, prognosis and therapy currently poses a major challenge to HCC management [9]. The identification of a biochemical marker with better sensitivity and/or specificity than AFP could be extremely helpful in improving the early diagnosis of HCC [10] and such early recognition would help clinicians select more effective therapies for patients, thus improving HCC prognosis [11] [12]. An ideal marker for early diagnosis would meet the following requirements: i) high accuracy; ii) specimen collection that is both easy and non-invasive; and iii) cost-effective [13]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Viral hepatitis is the most significant predisposing factor for hepatocellular carcinoma (HCC). Liver cancer grows silently with mild or no symptoms until the disease is advanced and with little hope of cure. Early recognition of the onset of HCC would help to select more effective therapies for patients leading to a better prognosis and life span. The current study aims to evaluate two diagnostic and prognostic markers – Prothrombin induced by vitamin K absence-II (PIVKA-II) and macrophage migration inhibitory factor (MIF) in the serum of patients with HCC and those with a high risk of developing hepatic cancers. Serum samples from hepatocellular carcinoma, hepatitis C and normal subjects were subjected to quantitative determinations of different parameters including alpha-fetoprotein (AFP), PIVKA-II and MIF. Significant differences between the various groups were recorded. PIVKA-II and AFP showed a higher specificity and sensitivity compared to MIF, and there was considerable correlation between AFP and both PIVKA and MIF. It is concluded that analysis of PIVKA-II and AFP can serve as useful non-invasive markers for the early detection of HCC with good sensitivity and specificity.
    Microbial Pathogenesis 10/2014; 77. DOI:10.1016/j.micpath.2014.10.009 · 2.00 Impact Factor
  • Source
    • "In addition, there must be increased efforts to understand the molecular effects of novel drugs prior to clinical testing, with animal models such as patientderived xenografts and genetically engineered mouse models used to screen novel drugs targeting rare mutations. The development of biomarkers that predict response to these novel agents is also crucial, though any potential markers should be evaluated carefully to ensure effective development, with validation undertaken according to the REporting recommendations for tumour MARKer prognostic studies (REMARK) guidelines [115] [116]. Further aspects that must be taken into account in biomarker development include factors associated with the drug itself, as well as its impact on the stroma and target cell. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC), which accounts for more than 90% of all pancreatic tumours, is a devastating malignancy with an extremely poor prognosis, as shown by a 1-year survival rate of around 18% for all stages of the disease. The low survival rates associated with PDAC primarily reflect the fact that tumours progress rapidly with few specific symptoms and are thus at an advanced stage at diagnosis in most patients. As a result, there is an urgent need to develop accurate markers of pre-invasive pancreatic neoplasms in order to facilitate prediction of cancer risk and to help diagnose the disease at an earlier stage. However, screening for early diagnosis of prostate cancer remains challenging and identifying a highly accurate, low-cost screening test for early PDAC for use in clinical practice remains an important unmet need. More effective therapies are also crucial in PDAC, since progress in identifying novel therapies has been hampered by the genetic complexity of the disease and treatment remains a major challenge. Presently, the greatest step towards improved treatment efficacy has been made in the field of palliative chemotherapy by introducing FOLFIRINOX (folinic acid, 5-fluorouracil, irinotecan and oxaliplatin) and gemcitabine/nab-paclitaxel. Strategies designed to raise the profile of PDAC in research and clinical practice are a further requirement in order to ensure the best treatment for patients. This article proposes a number of approaches that may help to accelerate progress in treating patients with PDAC, which, in turn, may be expected to improve the quality of life and survival for those suffering from this devastating disease.
    Pancreatology 10/2014; 15(1). DOI:10.1016/j.pan.2014.10.001 · 2.50 Impact Factor
  • Source
    • "The Reporting Recommendations for Tumour Marker Prognostic Studies criteria, recommended by McShane et al. [15], were followed throughout this study. This work was approved by the Nottingham Research Ethics Committee. "
    [Show abstract] [Hide abstract]
    ABSTRACT: ATM-Chk2 network is critical for genomic stability and its deregulation may influence breast cancer pathogenesis. We investigated ATM and Chk2 protein levels in two cohorts [cohort 1 (n=1650) and cohort 2 (n= 252)]. ATM and Chk2 mRNA expression was evaluated in the Metabric cohort (n=1950). Low nuclear ATM protein level was significantly associated with aggressive breast cancer including larger size tumours, higher tumour grade, higher mitotic index, pleomorphism , tumour type , lymphovascular invasion, ER- , PR-, AR-, triple negative and basal-like phenotypes (ps<0.05). BRCA1 negative, low XRCC1, low SMUG1, high FEN1, high MIB1, p53 mutants, low MDM2, low Bcl-2, low p21, low Bax, high CDK1 and low Chk2 were also more frequent in tumours with low nuclear ATM level (ps<0.05). Low ATM protein level was significantly associated with poor survival including in patients with ER- negative tumours who received adjuvant anthracycline or CMF based adjuvant chemotherapy (ps<0.05). Low nuclear Chk2 protein was likely in ER-/PR-/AR-, HER- 2 positive, BRCA1 negative, low XRCC1, low SMUG1, low APE1, low polβ, low DNA-PKcs, low ATM, low Bcl-2 and low TOPO2A tumours (p<0.05). In patients with ER+ tumours who received endocrine therapy or ER- negative tumours who received chemotherapy, nuclear Chk2 levels did not significantly influence survival. In p53 mutant tumours, low ATM (p<0.000001) or high Chk2 (p<0.01) was associated with poor survival. When investigated together, low ATM/high Chk2 tumours have the worst survival (p=0.0033). Our data suggests that ATM-Chk2 levels in sporadic breast cancer may have prognostic and predictive significance.
    Neoplasia 09/2014; 16(11). DOI:10.1016/j.neo.2014.09.009 · 5.40 Impact Factor
Show more