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Intratumoral heterogeneity in lung cancer is essential for evasion of immune surveillance by tumor cells and establishment of immunosuppression. Gathering data reveal that circular RNAs (circRNAs), play a role in the pathogenesis and progression of lung cancer. Particularly Kras-driven circRNA signaling triggers infiltration of myeloid-associated tumor macrophages in lung tumor microenvironment thus establishing immune deregulation, and immunosuppression but the exact pathogenic mechanism is still unknown. In this study, we investigate the role of oncogenic Kras signaling in circRNA-related immunosuppression and its involvement in tumoral chemoresistance. The expression pattern of circRNAs HIPK3 and PTK2 was determined using quantitative polymerase chain reaction (qPCR) in lung cancer patient samples and cell lines. Apoptosis was analyzed by Annexin V/PI staining and FACS detection. M2 macrophage polarization and MDSC subset analysis (Gr1 − /CD11b − , Gr1 − /CD11b + ) were determined by flow cytometry. Tumor growth and metastatic potential were determined in vivo in C57BL/6 mice. Findings reveal intra-epithelial CD163 + /CD206 + M2 macrophages to drive Kras immunosuppressive chemoresistance through myeloid differentiation. In particular, monocytic MDSC subsets Gr1 − /CD11b − , Gr1 − /CD11b + triggered an M2-dependent immune response, creating an immunosuppressive tumor-promoting network via circHIPK3/PTK2 enrichment. Specifically, upregulation of exosomal cicHIPK3/PTK2 expression prompted Kras-driven intratumoral heterogeneity and guided lymph node metastasis in C57BL/6 mice. Consequent co-inhibition of circPTK2/M2 macrophage signaling suppressed lung tumor growth along with metastatic potential and prolonged survival in vivo . Taken together, these results demonstrate the key role of myeloid-associated macrophages in sustaining lung immunosuppressive neoplasia through circRNA regulation and represent a potential therapeutic target for clinical intervention in metastatic lung cancer.

The tumor microenvironment plays a key role in progression of tumorigenesis, tumor progression, and metastasis. Accumulating data reveal that dendritic cells (DCs) appear to play a key role in the development and progression of metastatic neoplasia by driving immune system dysfunction and establishing immunosuppression, which is vital for tumor evasion of host immune response. Consequently, in this review, we will discuss the function of tumor-infiltrating DCs in immune cell signaling pathways that lead to treatment resistance, tumor recurrence, and immunosuppression. We will also review DC metabolism, differentiation, and plasticity, which are essential for metastasis and the development of lung tumors. Furthermore, we will take into account the interaction between myeloid cells and DCs in tumor-related immunosuppression. We will specifically look into the molecular immune-related mechanisms in the tumor microenvironment that result in reduced drug sensitivity and tumor relapse, as well as methods for combating drug resistance and focusing on immunosuppressive tumor networks. DCs play a crucial role in modulating the immune response. Especially, as cancer progresses, DCs may switch from playing an immunostimulatory to an inhibitory role. This article’s main emphasis is on tumor-infiltrating DCs. We address how they affect tumor growth and expansion, and we highlight innovative approaches for therapeutic modulation of these immunosuppressive DCs which is necessary for future personalized therapeutic approaches.

Ovarian cancer is a malignant disease that affects thousands of patients every year. Currently, we use surgical techniques for early-stage cancer and chemotherapy treatment combinations for advanced stage cancer. Several novel therapies are currently being investigated, with gene therapy and stem cell therapy being the corner stone of this investigation. We conducted a thorough search on PubMed and gathered up-to-date information regarding epithelial ovarian cancer therapies. We present, in the current review, all novel treatments that were investigated in this field over the past five years, with a particular focus on local treatment.

This study aimed to review the current evidence on the independent and combined effects of diet and exercise and their impact on skeletal muscle mass in the elderly population. Skeletal muscle makes up approximately 40% of total body weight and is essential for performing daily activities. The combination of exercise and diet is known to be a potent anabolic stimulus through stimulation of muscle protein synthesis from amino acids. Aging is strongly associated with a generalized deterioration of physiological function, including a progressive reduction in skeletal muscle mass and strength, which in turn leads to a gradual functional impairment and an increased rate of disability resulting in falls, frailty, or even death. The term sarcopenia, which is an age-related syndrome, is primarily used to describe the gradual and generalized loss of skeletal muscle mass (mainly in type II muscle fibers) and function. Multimodal training is emerging as a popular training method that combines a wide range of physical dimensions. On the other hand, nutrition and especially protein intake provide amino acids, which are essential for muscle protein synthesis. According to ESPEN, protein intake in older people should be at least 1 g/kgbw/day. Essential amino acids, such as leucine, arginine, cysteine, and glutamine, are of particular importance for the regulation of muscle protein synthesis. For instance, a leucine intake of 3 g administered alongside each main meal has been suggested to prevent muscle loss in the elderly. In addition, studies have shown that vitamin D and other micronutrients can have a protective role and may modulate muscle growth; nevertheless, further research is needed to validate these claims. Resistance-based exercise combined with a higher intake of dietary protein, amino acids, and/or vitamin D are currently recognized as the most effective interventions to promote skeletal muscle growth. However, the results are quite controversial and contradictory, which could be explained by the high heterogeneity among studies. It is therefore necessary to further assess the impact of each individual exercise and nutritional approach, particularly protein and amino acids, on human muscle turnover so that more efficient strategies can be implemented for the augmentation of muscle mass in the elderly.

Background and Objectives: Interstitial lung diseases have always been an issue for pulmonary and rheumatology physicians. Computed tomography scans with a high-resolution protocol and bronchoalveolar lavage have been used along with biochemical blood tests to reach a diagnosis. Materials and Methods: We included 80 patients in total. First, all patients had their diagnosis with computed tomography of the thorax, serological/ immunological blood tests and bronchoalveolar lavage. However; after 3 months, all were divided into 2 groups: those who had bronchoalveolar lavage again and those who had cryobiopsy instead of bronchoalveolar lavage (40/40). Positron emission-computed tomography was also performed upon the first and second diagnosis. The patients’ follow-up was 4 years from diagnosis. Results: Patients suffered most from chronic obstructive pulmonary disease (56, 70%), while lung cancer was rarely encountered in the sample (7, 9.75%). Age distribution ranged between 53 and 68 years with a mean value of 60 years. The computed tomography findings revealed 25 patients with typical diagnosis (35.2%), 17 with interstitial pulmonary fibrosis (23.9%) and 11 with probable diagnosis (11%). The cryobiopsy technique led to a new diagnosis in 28 patients (35% of the total sample). Patients who had a new diagnosis with cryobiopsy had a mean survival time of 710 days (<1460). Positron emission-computed tomography SUV uptake was positively associated with the cryobiopsy technique/new disease diagnosis and improved all respiratory functions. Discussion: Positron emission-computed tomography is a tool that can be used along with respiratory functions for disease evaluation. Conclusions: Cryobiopsy is a safe tool for patients with interstitial lung disease and can assist in the diagnosis of interstitial lung diseases. The survival of patients was increased in the cryobiopsy group versus only bronchoalveolar lavage for disease diagnosis.

Background and Objectives: Cancer treatments can adversely influence body weight status, body composition, phase angle (PhA), and resting metabolic rate (RMR), which could possibly affect disease course. Τhe aim was to assess differences in body composition, PhA, RMR, and related parameters in non-small-cell lung cancer (NSCLC) patients after treatment. Methods: The sample consisted of 82 NSCLC (stage IV) male patients (chemotherapy (C) 15.7%; immunotherapy (I) 13.3%; C + I 25.3%; (C) + radiotherapy (R) 22.9 %; and other 15.5%). Body weight and body composition, PhA, RMR, oxygen consumption (VO2), ventilation rate, and diet were assessed at baseline and at 3 months after initiation of therapy. Results: Reductions in PhA, RMR, VO2, ventilation rate, and intracellular water were observed at follow up. Weight loss was evident for 45% of patients who also had a reduction in lean body mass. In the group under C, lean mass was reduced at follow up (55.3 ± 11.53 vs. 52.4 ± 12.6, p = 0.04) without significant weight changes. In subjects with a low adherence to the Mediterranean diet (MedDietScore < 30), RMR (1940 ± 485 vs. 1730 ± 338 Kcal, p = 0.001), VO2 (277.1 ± 70.2 vs. 247 ± 49.1 mL/min, p = 0.001), and ventilation rate (10.1 ± 2.28 vs. 9. ± 2 2.2 L/min, p = 0.03) were significantly reduced. The changes in body weight were positively related to % of change in fat mass (rho = 0.322, p = 0.003) and absolute lean mass change (rho = 0.534, p < 0.001) and negatively associated with % of change in total body water (rho = −0.314, p = 0.004) (Spearman correlation coefficients). Conclusions: In conclusion, cancer therapy related to reductions in PhA and RMR, while lean mass reduction may be related to the type of treatment. Our results emphasize the importance of a more holistic nutritional and body composition assessment beyond body weight, to better address patients’ needs in clinical practice.

According to population-based studies, lung cancer is the prominent reason for cancer-related mortality worldwide in males and is also rising in females at an alarming rate. Sorafenib (SOR), which is approved for the treatment of hepatocellular carcinoma and renal cell carcinoma, is a multitargeted protein kinase inhibitor. Additionally, SOR is the subject of interest for preclinical and clinical trials in lung cancer. This study was designed to assess in vivo the possible effects of sorafenib (SOR) in diethylnitrosamine (DEN)-induced lung carcinogenesis and examine its probable mechanisms of action. A total of 30 adult male rats were divided into three groups (1) control, (2) DEN, and (3) DEN + SOR. The chemical induction of lung carcinogenesis was performed by injection of DEN intraperitoneally at 150 mg/kg once a week for two weeks. The DEN-administered rats were co-treated with SOR of 10 mg/kg by oral gavage for 42 alternate days. Serum and lung tissue samples were analyzed to determine SRY-box transcription factor 2 (SOX-2) levels. The tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) levels were measured in lung tissue supernatants. Lung sections were analyzed for cyclooxygenase-2 (COX-2) and c-Jun N-terminal kinase (JNK) histopathologically. In addition, cyclooxygenase-2 (COX-2) and c-Jun N-terminal kinase (JNK) were analyzed by immunohistochemistry and immunofluorescence methods, respectively. SOR reduced the level of SOX-2 that maintenance of cancer stemness and tumorigenicity, and TNF-α and IL-1β levels. Histopathological analysis demonstrated widespread inflammatory cell infiltration, disorganized alveolar structure, hyperemia in the vessels, and thickened alveolar walls in DEN-induced rats. The damage was markedly reduced upon SOR treatment. Further, immunohistochemical and immunofluorescence analysis also revealed increased expression of COX-2 and JNK expression in DEN-intoxicated rats. However, SOR treatment alleviated the expression of these inflammatory markers in DEN-induced lung carcinogenesis. These findings suggested that SOR inhibits DEN-induced lung precancerous lesions through decreased inflammation with concomitant in reduced SOX-2 levels, which enables the maintenance of cancer stem cell properties.

Introduction: Concomitant surgeries have been performed previously in several centers with experience in laparoscopic surgeries. These surgeries are performed in one patient under one operation with anesthesia. Methods: We performed a retrospective unicenter study from October 2021 to December 2021 analyzing patients who underwent laparoscopic hiatal hernia repair with cholecystectomy. We extracted data from 20 patients who underwent hiatal hernia repair together with cholecystectomy. Grouping of data by hiatal hernia type showed 6 type IV hernias (complex hernia), 13 type III hernias (mixed type) and 1 type I hernia (sliding hernia). Out of the 20 cases analyzed, 19 were patients suffering from chronic cholecystitis and 1 patient presented with acute cholecystitis. The average operating time was 179 min. Minimum blood loss was achieved. Cruroraphy was performed in all cases, mesh reinforcement was added in five cases, and fundoplication was performed in all cases, with 3 Toupet, 2 Dor and 15 floppy Nissen fundoplication procedures performed. Fundopexy was routinely performed in cases of Toupet fundoplication. A total of 1 bipolar and 19 retrograde cholecystectomies were performed. Results: All patients had favorable postoperative hospitalization. Patient follow-up took place at 1 month, 3 months and 6 months, with no sign of recurrence of hiatal hernia (anatomical or symptomatic) and no symptoms of postcholecystectomy syndrome. In two patients, we had to perform colostomy. Conclusion: Concomitant laparoscopic hiatal hernia repair and cholecystectomy is safe and feasible.

Introduction: Non-small-cell lung cancer is still diagnosed at an inoperable stage and systematic treatment is the only option. Immunotherapy is currently considered to be the tip of the arrow as the first-line treatment for patients with a programmed death-ligand 1 ≥ 50. Sleep is known to be an essential part of our everyday life. Patients and Methods: We investigated, upon diagnosis and after nine months, 49 non-small-cell lung cancer patients undergoing immunotherapy treatment with nivolumab and pemprolisumab. A polysomnographic examination was conducted. Moreover, the patients completed the Epworth Sleepiness Scale (ESS), the Pittsburgh Sleep Quality Index (PSQI), the Fatigue Severity Scale (FSS) and the Medical Research Council (MRC) dyspnea scale. Results: Tukey mean-difference plots, summary statistics, and the results of paired t-test of five questionnaire responses in accordance with the PD-L1 test across groups were examined. The results indicated that, upon diagnosis, patients had sleep disturbances which were not associated with brain metastases or their PD-L1 expression status. However, the PD-L1 status and disease control were strongly associated, since a PD-L1 ≥80 improved the disease status within the first 4 months. All data from the sleep questionnaires and polysomnography reports indicated that the majority of patients with a partial response and complete response had their initial sleep disturbances improved. There was no connection between nivolumab or pembrolisumab and sleep disturbances. Conclusion: Upon diagnosis, lung cancer patients have sleep disorders such as anxiety, early morning wakening, late sleep onset, prolonged nocturnal waking periods, daytime sleepiness, and unrefreshing sleep. However, these symptoms tend to improve very quickly for patients with a PD-L1 expression ≥80, because disease status improves also very quickly within the first 4 months of treatment.

We present a case of a 65-year-old male with a difficulty to diagnose mesothelioma. To be specific, three attempts were made to diagnose the disease, and only with a large sample performed with robot-assisted surgery, our pathologists were able to identify the malignancy. The novelty for our case is mostly based on the timeline of the diagnosis along with the tissue samples where we present the course of the transformation from benign to malignancy. All tissue biopsies were checked by two independent pathologists. Conclusively, diagnosis for small local lesions should be performed with an endoscopic method, video-assisted or robot-assisted.