The incidence and mortality of cancer have increased over the past decades. Significant progress has been made in understanding the underpinnings of this disease and developing therapies. Despite this, cancer still remains a major therapeutic challenge. Current therapeutic research has targeted several aspects of the disease such as cancer development, growth, angiogenesis and metastases. Many molecular and cellular mechanisms remain unknown and current therapies have so far failed to meet their intended potential. Recent studies show that glycans, especially oligosaccharide chains, may play a role in carcinogenesis as recognition patterns for galectins. Galectins are members of the lectin family, which show high affinity for β-galactosides. The galectin–glycan conjugate plays a fundamental role in metastasis, angiogenesis, tumor immunity, proliferation and apoptosis. Galectins’ action is mediated by a structure containing at least one carbohydrate recognition domain (CRD). The potential prognostic value of galectins has been described in several neoplasms and helps clinicians predict disease outcome and determine therapeutic interventions. Currently, new therapeutic strategies involve the use of inhibitors such as competitive carbohydrates, small non-carbohydrate binding molecules and antibodies. This review outlines our current knowledge regarding the mechanism of action and potential therapy implications of galectins in cancer.

Tumor microenvironment (TME) is characterized by mutual interactions of the tumor, stromal and immune cells. Early and advanced colorectal tumors differ in structure and present altered serum cytokine levels. Mutual crosstalk among TME infiltrating cells may shift the balance into immune suppressive or pro-inflammatory, antitumor response this way influencing patients’ prognosis. Cancer-related inflammation affects all the body and this way, the systemic level of cytokines could reflect TME processes. Despite numerous studies, it is still not known how systemic cytokines levels change during colorectal cancer (CRC) tumor development. Better understanding tumor microenvironment processes could help in planning therapeutic interventions and more accurate patient prognosis. To contribute to the comprehension of these processes within TME, we reviewed cytokines levels from clinical trials in early and advanced colorectal cancer. Presented data were analyzed in the context of experimental studies and studies analyzing tumor infiltration with immune cells. The review summarizes clinical data of cytokines secreted by tumor microenvironment cells: lymphocytes T helper 1 (Th1), lymphocytes T helper 2 (Th2), lymphocytes T helper 17 (Th17), regulatory T cells (Treg cells), regulatory T cells (Breg cells), M1/M2 macrophages, N1/N2 neutrophils, myeloid-derived suppressor cells (MDSC), dendritic cells (DC), innate lymphoid cells (ILC) natural killer (NK) cells and tumor cells.

Comparison of 14 cytokines levels between a control group and prospectively enrolled CRC patients to confirm their significance in CRC development. We tested if a model based on 14 cytokines levels could predict prognosis in Caucasian CRC patients treated with 5-FU based chemotherapy. Novel prognostic tools in colorectal cancer (CRC) are necessary to optimize treatment, reduce toxicity and chemotherapy (CHT) costs. We assessed prognostic significance of 14 cytokines: IL-1 beta, IL-1RA, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, IL12p70, IL-13, IL-17A in 75 prospectively enrolled CRC patients before initiation of palliative or adjuvant CHT and in 22 control subjects. Readings were taken using the Bio-Plex 200 System. Response to treatment was assessed after 6 months from initiation of CHT. The treated group was divided depending on the response into a progressors (death, progression of disease) and non-progressors group (stable disease, partial response, complete response). We found that increased concentration of IL-8 was a negative prognostic factor in the whole group and palliative subgroup, whereas increased level of IL-10, IL-7, and IL-12p70 was a negative predictor in the adjuvant group CHT. We proposed a statistical model based on circulating cytokine levels, showing a good prognostic value in prediction of the response to CHT (AUC = 0.956). The model, including combined IL-2, IL-8, IL-10 and IL-13 levels, established in the whole treated group, should be validated in larger trials.

Injuries in children are one of the most frequent causes of high morbidity and mortality, and they present a challenge to the treating physician. Fortunately, spinal trauma in pediatric patient is relatively rare. Brown-Séquard syndrome is a rare form of incomplete spinal cord injury consisting of ipsilateral upper motor neuron paralysis (hemiplegia) and loss of proprioception with contralateral pain and temperature sensation deficits resulting from hemisection or lateral injury to the spinal cord. A 11-year-old girl was admitted to our Pediatric Trauma Emergency Department after she had suffered a penetrating back injury. Neurological examination demonstrated left lower extremity paresis and moderate spastic paralysis of the right lower extremity. The examination showed loss of temperature sensation contralateral to and below the lesion. The examination of the pain sensation was difficult because the patient was in pain shock, but it was diminished on the side opposite to the damage. Multislice spiral computed tomography (MSCT) demonstrated a triangular foreign body in spinal canal at the level of the Th11–Th12. After a Th₁₁–L₂ laminectomy and retrieval of foreign bodies, dura repair was performed. Patient was discharged from the hospital with partial recovery. Operative decompression of the neural elements in case of spinal canal compromise is the treatment of choice. Indication for surgical intervention in existing cerebrospinal fluid fistula includes closure of the dura and reducing neural elements compression and lowering the risk of infectious complications by removing bone or foreign body fragments. Patients with Brown-Séquard syndrome have good prognosis for functional recovery.

Galectins are a family of lectins characterized by an affinity for β-galactosides through the carbohydrate recognition domain (CRD). The extracellular and intracellular presence of Galectins has been described. Their activity and functions are mainly attributed to cell type. The tumor microenviroment is a complex milieu connected with immunosupression, angiogenesis and hypoxic compartments. The studies of interactions between Glycans-Lectins are highly advanced and promising. We are not able to explain the pathogenesis of many diseases only by protein-protein interactions, that is why in these studies is a chance to find a new therapeutic targets. Galectins play a fundametal functions in tumor growth and progression, angiogenesis, adhesion, tumor immune-escape. They are also active in inflammation, fibrosis, organogenesis and immunological functions. The most known Galectin is Gal-3. Depending on the localization Gal-3 may exhibit either pro-apoptotic or anti-apoptotic activity. This publication presents role of Galectins in hematological malignancies and shows potencial prognostoic value and new therapeutic possibilities.