Brain metastases of the mucoepidermoid lung carcinoma: a case report.

Mucoepidermoid carcinoma, a salivary gland tumor, rarely occurs in bronchial mucous glands. Brain metastases are rarely seen which makes for a challenging diagnosis and treatment approach. A 40-year-old woman presented with confusion, and ataxia, accompanied by a declining Glasgow Coma Score. Brain computerized tomography revealed two hyperdense, postcontrast-enhanced infra- and supratentorial lesions with perifocal edema. First causing obstructive hydrocephalus. The initial surgery involved external ventricular drainage system placement leading to the patient's clinical improvement. After radiological diagnostics, both lesions were resected without complications. Histopathological analysis revealed solid clusters of atypical, polygonal epithelial cells exhibiting mucin production, classified as a poorly differentiated mucoepidermoid carcinoma metastasis which originated from the upper lobe's apicoposterior segment and left lung. The correct treatment approach remains elusive due to the infrequent occurrence and challenging diagnosis. While new oncological and radiosurgery options promise improved overall survival rates, radical resection remains the preferred initial option.

ABCG2 Expression as a Potential Survival Predictor in Human Gliomas.

Gliomas are notably challenging to treat due to their invasive nature and resistance to conventional therapies. The ABCG2 protein has attracted attention for its role in multidrug resistance, complicating treatment effectiveness. This study scrutinized the relationship between ABCG2 expression and glioma grade and the role of ABCG2 in the process of glioma progression, aiming to evaluate ABCG2 expression as a predictive factor of tumor progression and patient survival. Conducted at Dubrava University Hospital, Zagreb, Croatia, the study analyzed 152 glioma specimens from 2013 to 2022, assessing ABCG2 expression alongside standard clinical markers. A significant association was found between patients' survival and the ABCG2 profile (p = 0.003, r = 0.24), separately for patients who underwent chemotherapy (p = 0.0004, r = 0.32) and radiotherapy (p = 0.003, r = 0.29). Furthermore, the ABCG2 profile was significantly associated with disease progression (p = 0.007, r = 0.23), tumor grade (p = 0.0002, r = 0.31), and Ki67 expression (p = 0.0004, r = 0.31). ABCG2-positive tumor cells only showed association with Ki67 expression (p = 0.002, r = 0.28). The ABCG2 profile was found to affect the overall patient survival (p = 0.02) and represent a moderate indicator of tumor progression (p = 0.01), unlike the percentage of ABCG2-positive tumor cells. ABCG2 may serve as a marker of angiogenesis and vascular abnormalities within tumors, predicting glioma progression and treatment response. Targeting ABCG2 could enhance chemoradiotherapy efficacy and improve patient outcomes, which highlights its value in assessing tumor aggressiveness and designing treatment strategies.

The vicious interplay between disrupted sleep and malignant brain tumors: a narrative review.

Malignant brain tumors are among the most aggressive human neoplasms. One of the most common and severe symptoms that patients with these malignancies experience is sleep disruption. Disrupted sleep is known to have significant systemic pro-tumor effects, both in patients with other types of cancer and those with malignant brain lesions. We therefore provide a review of the current knowledge on disrupted sleep in malignant diseases, with an emphasis on malignant brain tumors. More specifically, we review the known ways in which disrupted sleep enables further malignant progression. In the second part of the article, we also provide a theoretical framework of the reverse process. Namely, we argue that due to the several possible pathophysiological mechanisms, patients with malignant brain tumors are especially susceptible to their sleep being disrupted and compromised. Thus, we further argue that addressing the issue of disrupted sleep in patients with malignant brain tumors can, not just improve their quality of life, but also have at least some potential of actively suppressing the devastating disease, especially when other treatment modalities have been exhausted. Future research is therefore desperately needed.

Hemoglobin A1c in Patients with Glioblastoma-A Preliminary Study.

BACKGROUND: Glioblastomas are among the most common primary brain tumors with an abysmal prognosis. The significance of glucose metabolism in glioblastoma cell metabolism and proliferation is well-known. However, a significant correlation between the systemic metabolic status of the patient and the cellular proliferation of the glioblastoma has not yet been established. METHODS: Our aim was to observe and analyze for a possible correlation between glioblastoma cellular proliferation and patients' glycated hemoglobin (HbA1c) levels as a marker of chronic systemic glycemia. We analyzed the data from 25 patients and compared their Ki-67 values with their preoperative HbA1c values. RESULTS: We observed a statistically significant correlation (P < 0.03) between chronic glycemia (measured using HbA1c) and the cellular proliferation of glioblastoma (measured by cellular Ki-67 expression). CONCLUSIONS: These results imply a possible positive correlation between glioblastoma cell proliferation and chronic systemic glycemia, a correlation that, to the best of our knowledge, has not yet been reported. Further research in this area could not only lead to a better understanding of glioblastoma but also have significant clinical applications in treating this devastating disease.

Dynamics of inflammatory factors expression in ischemic brain tissue injury.

Ischemic stroke is one of the most common cause of mortality and disability in the modern world. Still, therapeutic options remain modest. Aim of the study was to present dynamics of inflammatory factors expression (C reactive protein, procalcitonin, interleukin 10) in patients after ischemic stroke. Our study included 101 patients divided in thrombolised and nonthrombolised groups. Inflammatory factors concentration in serum was determinate at admission, 24, 48 hours and seven days after the initial onset, while neurological assessment was measured at the admission, 24 hours, seven days and three months after the initial onset using National Institute of Health Stroke Scale and Rankin Scale. Certain pattern was observed in dynamics of inflammatory factors: intensive increase in first and second day after the stroke, followed by decrease till day seven in both groups. Additionally, thrombolised group showed significant neurological improvement. Although well investigated, the role of inflammatory factors in the ischemic stroke still stays controversial. High association of C reactive protein and interleukin 10 values suggest potential prognostic role in patient's follow-up, while the role of procalcitonin values still remains unclear.

Intraspinal calcinosis mimicking intervertebral disc extrusion: A clinical and surgical case report.

BACKGROUND: Subcutaneous calcinosis is a well-recognized manifestation of systemic sclerosis that usually involves multiple pressure points and may also be found in the paraspinal or intraspinal regions. In this case, intraspinal calcinosis uniquely led to a severe neurological deficit. CASE DESCRIPTION: A patient with severe systemic sclerosis/calcinosis exhibited left greater than right lower extremity radiculopathy attributed to intraspinal left-sided L4-L5 calcinosis. On examination, the patient exhibited bilateral positive Lasegue signs, distal lower extremity weakness (left greater than right), and bilaterally decreased Achilles responses. When the magnetic resonance imaging (MRI) revealed a significant intracanalicular mass on the left side at the L4-L5 level, the patient underwent a left-sided L4-L5 decompressive laminectomy. The MRI scan 5 years later revealed no recurrence of the calcinosis, and the patient had no residual neurological deficit. CONCLUSIONS: Spinal calcinosis rarely involves the lumbar spinal canal. Here, a patient with a large left-sided L4-L5 focus of intraspinal calcinosis, mimicking a disc herniation, required a laminectomy to resect the lesion. Lumbar calcinosis should be radiologically evaluated utilizing using X-ray, MRI, and computed tomography studies to adequately document the pathology. Patients, when symptomatic, may require surgical decompression and excision of these lesions.

Intracranial recurrence and distant metastasis of scalp dermatofibrosarcoma protuberans.

Only few cases of scalp dermatofibrosarcoma protuberans with intracranial and distant metastasis have been reported. Here we report a case of scalp dermatofibrosarcoma protuberans with frequent local recurrence, intracranial invasion and with distant lung metastasis during 6 years of treatment. We would like to emphasize difficulties in surgical treatment of such invasive and locally recurrent tumors of scalp, and necessity to understand new molecular pathogenesis of dermatofibrosarcoma protuberans and potential treatment strategy with imatinib for patients with surgically untreatable disease. Close surveillance of patients with scalp dermatofibrosarcoma is necessary due recurrence nature of tumor.