Pituitary metastasis from renal cell carcinoma presenting with significant hyperprolactinemia, case report.

Key Clinical Message: Kidney metastasis to the pituitary gland can cause hyperprolactinemia even above 250 ng/mL. Although the treatment of metastasis is palliative, surgical decompression could play a major role in the recovery of symptoms and improve quality of life. Pituitary metastasis should be considered in the evaluation of an unusual pituitary mass. Abstract: Pituitary tumors are frequently encountered in the neurosurgical setting. Although the majority of them are pituitary adenomas, rare entities encompass pituitary metastasis. They should be differentiated from pituitary adenomas because their management and prognosis are different. We report a 53-year-old female who complained of headache and had remarkable hyperprolactinemia (271.1 ng/mL). Having considered macroprolactinoma as the initial diagnosis, medical treatment was initiated with Cabergoline. Subsequently, the patient's vision deteriorated which prompted us to perform endoscopic endonasal transsphenoidal surgery. Histologic examination of the resected tumor revealed metastatic renal cell carcinoma. Main treatment for these subjects is palliative; and unlike the pituitary adenoma, the prognosis is unfortunately poor. Pituitary metastasis should be considered in the evaluation of an unusual pituitary mass associated with hyperprolactinemia.

Non-coding RNAs and exosomal non-coding RNAs in pituitary adenoma.

Pituitary adenoma (PA) is the third most common primary intracranial tumor in terms of overall disease incidence. Although they are benign tumors, they can have a variety of clinical symptoms, but are mostly asymptomatic, which often leads to diagnosis at an advanced stage when surgical intervention is ineffective. Earlier identification of PA could reduce morbidity and allow better clinical management of the affected patients. Non-coding RNAs (ncRNAs) do not generally code for proteins, but can modulate biological processes at the post-transcriptional level through a variety of molecular mechanisms. An increased number of ncRNA expression profiles have been found in PAs. Therefore, understanding the expression patterns of different ncRNAs could be a promising method for developing non-invasive biomarkers. This review summarizes the expression patterns of dysregulated ncRNAs (microRNAs, long non-coding RNAs, and circular RNAs) involved in PA, which could one day serve as innovative biomarkers or therapeutic targets for the treatment of this neoplasia. We also discuss the potential molecular pathways by which the dysregulated ncRNAs could cause PA and affect its progression.

Non-coding RNAs and Exosomal Non-coding RNAs in Traumatic Brain Injury: the Small Player with Big Actions.

Nowadays, there is an increasing concern regarding traumatic brain injury (TBI) worldwide since substantial morbidity is observed after it, and the long-term consequences that are not yet fully recognized. A number of cellular pathways related to the secondary injury in brain have been identified, including free radical production (owing to mitochondrial dysfunction), excitotoxicity (regulated by excitatory neurotransmitters), apoptosis, and neuroinflammatory responses (as a result of activation of the immune system and central nervous system). In this context, non-coding RNAs (ncRNAs) maintain a fundamental contribution to post-transcriptional regulation. It has been shown that mammalian brains express high levels of ncRNAs that are involved in several brain physiological processes. Furthermore, altered levels of ncRNA expression have been found in those with traumatic as well non-traumatic brain injuries. The current review highlights the primary molecular mechanisms participated in TBI that describes the latest and novel results about changes and role of ncRNAs in TBI in both clinical and experimental research.

Serum neurofilament light chain in LRRK2 related Parkinson's disease: A five years follow-up.

BACKGROUND: Studies revealed that serum neurofilament light chain (NFL) levels not only increase considerably over time in Parkinson's disease (PD) but also have a significant association with disease progression. However, there is no evidence of the level of serum NFL in PD patients with leucine-rich repeat kinase 2 (LRRK2) mutation (LRRK2-PD) which is the most common mutation that causes familial and sporadic PD. AIM: Here we aimed to investigate the difference and longitudinal alteration of the serum level of NFL in LRRK2-PD and idiopathic PD (iPD) patients. METHODS: We entered 228 iPD and 103 LRRK2-PD patients and 176 healthy controls (HCs) from PPMI. We compared the level of serum NFL at baseline, six months, one year, two years, three years, and five years visits. Also, we used linear mixed models to assess longitudinal changes of serum NFL over six months, one year, two years, three years, and five years within groups. RESULTS: We found a significant difference in the level of serum NFL between three groups at baseline, two years, three years, and five years time points. Also, our analysis showed that LRRK2-PD patients had significantly lower serum NFL compared to iPD subjects at baseline. In the longitudinal analysis, there was no significant change in the HCs group over five years. The level of serum NFL was significantly increased after two, three, and five years from baseline in LRRK2-PD patients. Also, we found similar results for iPD subjects after three and five years from baseline. CONCLUSION: We can conclude that the overall neurodegeneration might be similar in LRRK2-PD and healthy subjects and lower than the idiopathic form of PD at the early stages, which may disappear in the later stages. Moreover, our findings suggest that the serum NFL might be a more accurate biomarker to distinguish iPD from healthy subjects rather than all PD patients or LRRK2-PD from healthy subjects at the early stages.

Can Preoperative Diffusion Tensor Imaging Tractography Predict the Visual Outcomes of Patients with Pituitary Macroadenomas? A Prospective Pilot Study.

OBJECTIVE: Visual impairment has been reported as the most common clinical manifestation of pituitary adenoma (PA) due to the compressive effect of the tumor. This prospective study aimed to evaluate the predictive role of diffusion tensor imaging (DTI) in the visual improvement of patients with PA, who were candidates for endoscopic endonasal surgery. METHODS: A total of 13 patients (male, 8; female, 5) with visual impairment due to pituitary macroadenoma were enrolled in this study. The DTI findings and visual parameters, including visual acuity (VA), visual field (VF), and visual evoked potential (VEP), were recorded for all participants before and 3 months after surgery. RESULTS: Significant recovery was reported in both VA and VF following PA surgery (P < 0.001). The results of perimetry indicated recovery in all quadrants, except for the lower nasal quadrant of the right eye. The tumor volume showed no significant association with the preoperative optic nerve, optic tract, and chiasm fractional anisotropy (FA) or mean diffusivity (MD). The VA and VF recoveries were more likely in patients with a lower preoperative optic nerve MD. Besides, increased preoperative FA of the optic nerve was associated with a higher probability of VA recovery. No significant correlation was found between the optic tract MD and FA values and visual improvement. Overall, MD values below 0.0021 and FA values above 0.1689 could predict a good prognosis of VA recovery after surgery. CONCLUSIONS: DTI may have a predictive value in estimating visual improvement in patients with PA preoperatively.

TRIM8: a double-edged sword in glioblastoma with the power to heal or hurt.

Glioblastoma multiforme (GBM) is an aggressive primary brain tumor and one of the most lethal central nervous system tumors in adults. Despite significant breakthroughs in standard treatment, only about 5% of patients survive 5 years or longer. Therefore, much effort has been put into the search for identifying new glioma-associated genes. Tripartite motif-containing (TRIM) family proteins are essential regulators of carcinogenesis. TRIM8, a member of the TRIM superfamily, is abnormally expressed in high-grade gliomas and is associated with poor clinical prognosis in patients with glioma. Recent research has shown that TRIM8 is a molecule of duality (MoD) that can function as both an oncogene and a tumor suppressor gene, making it a "double-edged sword" in glioblastoma development. This characteristic is due to its role in selectively regulating three major cellular signaling pathways: the TP53/p53-mediated tumor suppression pathway, NFKB/NF-κB, and the JAK-STAT pathway essential for stem cell property support in glioma stem cells. In this review, TRIM8 is analyzed in detail in the context of GBM and its involvement in essential signaling and stem cell-related pathways. We also discuss the basic biological activities of TRIM8 in macroautophagy/autophagy, regulation of bipolar spindle formation and chromosomal stability, and regulation of chemoresistance, and as a trigger of inflammation.