Colorectal cancer (CRC) is the second most commonly diagnosed cancer among females and third among males worldwide. It also contributes significantly to cancer-related deaths, despite the continuous progress in diagnostic and therapeutic methods. Biomarkers currently play an important role in the detection and treatment of patients with colorectal cancer. Risk stratification for screening might be augmented by finding new biomarkers which alone or as a complement of existing tests might recognize either the predisposition or early stage of the disease. Biomarkers have also the potential to change diagnostic and treatment algorithms by selecting the proper chemotherapeutic drugs across a broad spectrum of patients. There are attempts to personalise chemotherapy based on presence or absence of specific biomarkers. In this review, we update review published last year and describe our understanding of tumour markers and biomarkers role in CRC screening, diagnosis, treatment and follow-up. Goal of future research is to identify those biomarkers that could allow a non-invasive and cost-effective diagnosis, as well as to recognise the best prognostic panel and define the predictive biomarkers for available treatments.

Surgical trauma affects both the innate and acquired immunity. The severity of immune disorders is proportional to the extent of surgical trauma and depends on a number of factors, including primarily the basic disease requiring surgical treatment (e.g. cancer), often coexisting infections and impaired nutritional status. Disorder of the immune response following surgical trauma may predispose to septic complications burdened with the highest mortality rate. Extensive surgery in cancer patients is associated with simultaneous activation of pro- and anti-inflammatory processes defined as SIRS (systemic inflammatory immune response) and CARS (compensatory anti-inflammatory immune response). However, it is generally believed that major surgical trauma is accompanied by sustained postoperative immunosuppression, which is particularly important in patients operated on for cancer, since the suppression of the immune system promotes not only septic complications, but also proliferation and tumor metastasis. This paper reviews the main features of immune response to surgical trauma and possibilities of its regulation.

According to the World Health Organization, post-traumatic mortality rates are still very high and show an increasing tendency. Disorders of innate immune response that may increase the risk of serious complications play a key role in the immunological system response to trauma and infection. The mechanism of these disorders is multifactorial and is still poorly understood. The changing concepts of systemic inflammatory response syndrome (SIRS) and compensatory anti-inflammatory response syndrome (CARS) early inflammatory response, presented in this work, have been extended to genetic studies. Overexpression of genes and increased production of immune response mediators are among the main causes of multiple organ dysfunction syndrome (MODS). Changes in gene expression detected early after injury precede the occurrence of subsequent complications with a typical clinical picture. Rapid depletion of energy resources leads to immunosuppression and persistent inflammation and immune suppression catabolism syndrome (PICS). Early diagnosis of immune disorders and appropriate nutritional therapy can significantly reduce the incidence of complications, length of hospital stay, and mortality. The study presents the development of knowledge and current views explaining the mechanisms of the immune response to trauma and infection.

Pancreatic cancer remains a disease with very poor prognosis (only 5-6% of patients are still alive after five years). Attempts to improve the results of treatment of pancreatic cancer focus on a better understanding of the pathogenesis, and non-invasive diagnostic methods (genetic testing from peripheral blood), which would create the possibility of early diagnosis and early surgical treatment before the onset of metastasis. New hopes for the improvement of early diagnosis and treatment of pancreatic ductal adenocarcinoma (PDAC) are associated with genetic testing of microRNA expression changes. A large body of evidence has revealed that microRNAs are aberrantly expressed in the serum and in cancer tissues and elicit oncogenic or tumour-suppressive functions. Selected microRNAs can distinguish pancreatic ductal adenocarcinoma from non-cancerous lesions of the pancreas. This review focuses on the involvement of microRNAs in the early diagnosis of pancreatic cancer. Research results related to the development of a novel therapeutic strategy based on the modulation of microRNA expressions for a better outcome in patients with pancreatic cancer are also presented.

A steady increase in colorectal cancer (CRC) incidence and mortality has been observed in Europe, despite the continuous advancement in diagnostic and therapeutic methods. Accordingly, further progress is very much desirable in non-invasive diagnostic methods to enable early diagnosis, preand postoperative staging, and to assist in selecting the most suitable neo-adjuvant and adjuvant therapeutic methods and post-treatment follow-up. This review summarizes the current state of knowledge about the role of tumor markers and biomarkers in CRC diagnosis, treatment and follow-up. New biomarkers which are absent in healthy persons and present in CRC are still being investigated, especially those that can be detected at early development stage of the disease and used in screening tests. Unfortunately, no molecule that would meet all of the foregoing criteria has been identified so far. Carcinoembryonic antigen still remains the only tumor marker of recognised efficacy in monitoring patients during and after CRC therapy. Clinical studies and retrospective analyses allowed to discover and introduce to the clinical practice several bioindicators that assist in selecting the proper chemotherapeutic drug. There are attempts to "personalise" chemotherapy based on presence or absence of specific biomarkers. Therapy with anti-EGFR antibodies is desirable in patients with advanced CRC and absence of KRAS or BRAF mutation. Defining tumor phenotype - microsatellite instability (MSI) or microsatellite stability (MSS) and testing for the presence or absence of 18q chromosome deletion is very much desirable in standard 5-FU-based therapy. Analysis of UGT1A1 alleles may be the basis for modified dosing and reducing the potential toxicity of irinotecan. Studies on CRC biomarkers need to continue to closely examine the relationship between therapy and CRC curability. Targeted therapy against membrane receptors appears to be the future of CRC therapy.