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There have been studies on antibiotic use concerning lung cancer and its potential impact on carcinogenesis and microbiome. However, subsequent research has failed to support these associations consistently. In terms of the potential carcinogenic of antibiotics on lung cancer, the available evidence has not been sufficient to draw any definitive conclusions. Maintaining immune homeostasis and preventing pathogen invasion is critically dependent on the microbiome. The subtle balance of the body microbiota, including the lungs, is susceptible to disruption by antibiotic use. There is an association between disruptions of the lung microbiome and respiratory diseases, including lung cancer, and decreased efficacy of treatments. Patients with lung cancer are often indicated for antibiotic treatment due to respiratory infections or other comorbidities. Pulmonary infections in the area of undetected lung tumors are not uncommon. They can be an early sign of malignancy, which may explain the association between antibiotic use and lung cancer diagnosis. Antibiotic use can also affect the effectiveness of immune checkpoint inhibitor therapy. Studies suggest that antibiotic use can impair the efficacy of immune checkpoint inhibitor therapy in lung cancer patients, particularly around the time when treatment is initiated. These findings require further study, understanding underlying mechanisms, and identifying microbiota signatures associated with treatment response.

Lung malignancies have a substantial impact on cancer incidence and mortality worldwide. Even though many factors involved in the development of the disease are known, many questions remain unanswered. Previous studies suggest that the intestinal microbiota may have a role in developing malignant diseases. According to some findings, the microbiota has proven to be a key modulator of carcinogenic processes and the immune response against cancer cells, potentially influencing the effectiveness of immunotherapy. In our study, we characterized culturable microorganisms associated with non-small cell lung cancer (NSCLC) that can be recovered from rectal swabs and mouthwash. In addition, we also explored differences in the culturable microbiota with two main types of NSCLC – adenocarcinoma (ADC) and squamous cell carcinoma (SCC). With 141 patients included in the study (86 ADC and 55 SCC cases), a significant difference was observed between the two types in seven bacterial species (Collinsella, Corynebacterium, Klebsiella, Lactobacillus, Neisseria, Rothia, and Streptococcus), including the site of origin. The relationship between microbial dysbiosis and lung cancer is poorly understood; future research could shed light on the links between gut microbiota and lung cancer development.

Idiopathic pulmonary fibrosis (IPF) is a severe and currently incurable disease that is associated with irreversible fibrotic remodeling of the lung parenchyma. Pathological remodeling of the lung leads to damage of the alveolo-capillary barrier. There is a reduction in the diffusing capacity of the lungs for respiratory gases. Later, changes in the mechanical properties of lung tissue occur - their compliance decreases and respiratory work increases. Impaired respiratory gases exchange with restrictive ventilatory failure lead to tissue hypoxia and muscle weakness. Progressive respiratory insufficiency develops. The triggers of fibrotic remodeling of the lung are currently unknown, as are the pathomechanisms that keep this process active. IPF can only be slowed pharmacologically, not reversed. It is therefore very important to start its treatment as soon as possible. Early detection of IPF patients requires a multidisciplinary approach. Diagnosis, treatment initiation, and monitoring in specialized centers offer the best chance of slowing disease progression, enhancing quality of life, and extending patient survival. In addition to antifibrotic therapy, good lifestyle management, maintenance of physical fitness and treatment of associated chronic diseases such as diabetes and cardiac comorbidities are important. Lung transplantation is an option for some patients with IPF. This is a challenging treatment modality, requiring close collaboration with transplant centers and expert selection of suitable candidates, influenced, among other things, by the availability of suitable donor lungs. Our article aims to provide current information about IPF, focusing on its functional consequences and clinical manifestation. We discuss the molecular and cellular mechanisms potentially involved in IPF development, as well as the morphological changes observed in lung biopsies and high-resolution computed tomography (HRCT) images. Finally, we summarize the existing treatment options. [ABSTRACT FROM AUTHOR]

Foci of splenic tissue separated from the spleen can occur as a congenital anomaly. Isolated nodules of splenic tissue are called accessory spleens or spleniculli. However, nodules of splenic tissue can merge with other organs during embryonic development, in which case we speak of spleno-visceral fusions: most often, they merge with the tail of the pancreas (thus forming spleno-pancreatic fusion or an intrapancreatic accessory spleen), with the reproductive gland (i.e., spleno-gonadal fusion), or with the kidney (i.e., spleno-renal fusion). Our case report describes the fusion of heterotopic splenic tissue with the right adrenal gland, which was misinterpreted as a metastasis of a renal cell carcinoma. To the best of our knowledge, this is the first reported case of spleno-adrenal fusion. Spleno-visceral fusions usually represent asymptomatic conditions; their main clinical significance lies in the confusion they cause and its misinterpretation as tumors of other organs. We believe that the cause of retroperitoneal spleno-visceral fusions is the anomalous migration of splenic cells along the dorsal mesentery to the urogenital ridge, together with primitive germ cells, at the end of the fifth week and during the sixth week of embryonic age. This theory explains the possible origin of spleno-visceral fusions, their different frequency of occurrence, and the predominance of findings on the left side.

Glioblastoma is currently considered the most common and, unfortunately, also the most aggressive primary brain tumor, with the highest morbidity and mortality rates. The average survival of patients diagnosed with glioblastoma is 14 months, and only 2% of patients survive 3 years after surgery. Based on our clinical experience and knowledge from extensive clinical studies, survival is mainly related to the molecular biological properties of glioblastoma, which are of interest to the general medical community. Our study examined a total of 71 retrospective studies published from 2016 through 2022 and available on PubMed that deal with mutations of selected genes in the pathophysiology of GBM. In conclusion, we can find other mutations within a given gene group that have different effects on the prognosis and quality of survival of a patient with glioblastoma. These mutations, together with the associated mutations of other genes, as well as intratumoral heterogeneity itself, offer enormous potential for further clinical research and possible application in therapeutic practice. [ABSTRACT FROM AUTHOR]

Foci of splenic tissue separated from the spleen can occur as a congenital anomaly. Isolated nodules of splenic tissue are called accessory spleens or spleniculli. However, nodules of splenic tissue can merge with other organs during embryonic development, in which case we speak of spleno-visceral fusions: most often, they merge with the tail of the pancreas (thus forming spleno-pancreatic fusion or an intrapancreatic accessory spleen), with the reproductive gland (i.e., spleno-gonadal fusion), or with the kidney (i.e., spleno-renal fusion). Our case report describes the fusion of heterotopic splenic tissue with the right adrenal gland, which was misinterpreted as a metastasis of a renal cell carcinoma. To the best of our knowledge, this is the first reported case of spleno-adrenal fusion. Spleno-visceral fusions usually represent asymptomatic conditions; their main clinical significance lies in the confusion they cause and its misinterpretation as tumors of other organs. We believe that the cause of retroperitoneal spleno-visceral fusions is the anomalous migration of splenic cells along the dorsal mesentery to the urogenital ridge, together with primitive germ cells, at the end of the fifth week and during the sixth week of embryonic age. This theory explains the possible origin of spleno-visceral fusions, their different frequency of occurrence, and the predominance of findings on the left side. [ABSTRACT FROM AUTHOR]

Copyright of Czech Radiology / Ceska Radiologie is the property of Czech Medical Association of JE Purkyne and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Czech Radiology / Ceska Radiologie is the property of Czech Medical Association of JE Purkyne and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Czech Radiology / Ceska Radiologie is the property of Czech Medical Association of JE Purkyne and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The topic of pheochromocytomas is becoming increasingly popular as a result of major advances in different medical fields, including laboratory diagnosis, genetics, therapy, and particularly in novel advances in imaging techniques. The present review article discusses current clinical, biochemical, genetic and histopathological aspects of the diagnosis of pheochromocytomas and planning of pre‑surgical preparation and subsequent surgical treatment options. The main part of the paper is focused on the role of morphological imaging methods (primarily computed tomography and magnetic resonance imaging) and functional imaging (scintigraphy and positron emission tomography) in the diagnosis and staging of pheochromocytomas. [ABSTRACT FROM AUTHOR]

Drug resistance is an important problem in the treatment of patients with lung cancer. Tumours become resistant not only to the drugs used initially, but also to those to which they have not yet been exposed. Data obtained from various sources indicate that multiple mechanisms contribute to drug resistance. Many of them are inter-related or independent of each other, but may exist simultaneously in cancer cells or subpopulation of cells, producing an overall drug-resistant phenotype. The resistance-related proteins P-glycoprotein, glutathione-dependent enzymes, topoisomerases, metallothioneins, thymidylate synthase and 06-alkyl-DNA alkyltransferase have been found in various human lung tumours, but these alone cannot explain the drug-resistant phenotype. Cell-cycle-related proteins, angiogenic factors, protooncogenes, and tumour suppressor genes also play a role in the resistant phenotype. In future, a key challenge will be to determine the relative quantitative contributions of each of these mechanisms to overall resistance. The use of DNA microarray technology in drug resistance in lung cancer will yield insight into the mechanisms of drug resistance and the rational design of more effective strategies to circumvent resistance. [ABSTRACT FROM AUTHOR]

Fractured bones can regenerate and restore their biological and mechanical properties to the state prior to the damage. In some cases, however, the treatment of fractures requires the use of supportive implants. For bone healing, three processes are essential: the inflammatory phase, the repair phase and the remodelling phase. A proper course of the first - inflammatory - stage is important to ensure a successful fracture healing process. In our study, we evaluated tissue samples immunohistochemically from the area surrounding the fractures of upper and lower limbs (bone tissue, soft tissue, and the implant-adhering tissue) for markers: CD11b, CD15, CD34, CD44, CD68, Cathepsin K, and TRAcP that are linked to the aforementioned phases. In soft tissue, higher expressions of CD68, CD34, CD15 and CD11b markers were observed than in other locations. TRAcP and Cathepsin K markers were more expressed in the bone tissue, while pigmentation, necrosis and calcification were more observed in the implant-adhering tissue. Since even the implant materials commonly perceived as inert elicit the observed inflammatory responses, new surface treatments and materials need to be developed., (©The Author(s) 2023. Open Access. This article is licensed under a Creative Commons CC-BY International License.)

Lung cancer is one of the leading causes of cancer-related deaths worldwide, with small cell lung cancer (SCLC) having the worst prognosis. SCLC is diagnosed late in the disease's progression, limiting treatment options. The most common treatment for SCLC is chemotherapy. As the disease progresses, immunotherapy, most commonly checkpoint inhibitor medication, becomes more important. Efforts should be made in the development of immunotherapy to map specific biomarkers, which play a role in properly assigning a type of immunotherapy to the right cohort of patients, where the benefits outweigh any risks or adverse effects. The objective of this review was to provide a thorough assessment of current knowledge about the nature of the tumor process and treatment options for small cell lung cancer, with a focus on predictive biomarkers. According to the information obtained, the greatest potential, which has already been directly demonstrated in some studies, has characteristics such as tumor microenvironment composition, tumor mutation burden, and molecular subtyping of SCLC. Several other aspects appear to be promising, but more research, particularly prospective studies on a larger number of probands, is required. However, it is clear that this field of study will continue to expand, as developing a reliable method to predict immunotherapy response is a very appealing goal of current medicine and research in the field of targeted cancer therapy., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Skopelidou, Strakoš, Škarda, Raška and Kafková-Rašková.)

We report the case of a 42-year - old female with familiar form von Hippel-Lindau disease (VHL) and recurrent endolymphatic sac tumour (ELST), which was presented like non-homogenous, solid and cystic expansion of the left petrous temporal bone. Histologically, there was found lamellae of bone with adjacent ligament and with papillary projections with fibrovascular core. The papillae were lined by a single layer of cuboidal epithelium with hyperchromatic and lightly pleomorphic nuclei. Sporadically, small cystic formations with eosinophilic, PAS positive secretion were noted. Imunohistochemically, the cuboidal cells showed diffuse positivity for vimentin, epithelial membrane antigen (EMA), cytokeratin AE1/AE3 and S100 protein (weakly). Other markers examined, including TTF1, PAX8 and CD10, were negative. Endolymphatic sac tumour is rare low-grade malignant epithelial tumour arising from the endolymphatic sac in the temporal bone, which occurs in 1 out of 30 000 births, with just fewer than 300 cases reported in the literature. About one third of cases are associated with von Hippel- Lindau disease, an autosomal dominant familial cancer syndrome.