Browsing by Author "Chen, Liling"
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Item The Evaluation of Elongated Styloid Processes in regard to possible Clinical and Pathological Outcomes - A Case Series(2024-03-21) Cornejo, Federico; Desai, Ananya; Cheng, Jack; Chen, Liling; Cruise, Forrest; McKean, John; Menegaz, Rachel A.; Crowe, NicoleBackground: Eagle’s syndrome (ES) is defined as elongation or ossification of the styloid process that may compress adjacent anatomy, producing variable symptomology. ES is subclassified into Classic ES or Stylocarotid syndrome. Classic ES may present asymptomatically, or with dull, recurring cervicofacial pain, and Stylocarotid syndrome may present with parietal headaches, and presyncope/syncopal episodes. The etiology of the abnormal ossification of the styloid process or stylohyoid ligament is unknown but likely caused by reactive metaplasia/hyperplasia or anatomical variance. Although a styloid process greater than 30mm in length is generally considered elongated, clinical guidelines for measuring styloid process length, and specific histological characterizations for ES have not been formally established. However, elongated styloid processes can be structurally classified as uninterrupted (one unsegmented process), pseudo-articulated (two parts in close proximity), or segmented (three or more parts). Styloid processes may also be classified into four calcification patterns including outlined calcification, partial calcification (multiple bone pieces surrounded by a continuous calcified process), nodular calcification (segmented, bumpy surfaced bone pieces due to thickened calcifications), and complete calcification. However, no clinical correlation has been identified between patient presentation and morphology/calcification pattern. Case Information: A 62-year-old deceased Caucasian male (147lbs / 5’6”) with an elongated stylohyoid process was discovered during routine dissection. Medical history was significant for liver and renal disease. Cause of death was reported as “chronic alcoholism”. Social history was significant for off-and-on incarceration for more than 40 years, and chronic alcohol, tobacco, and non-prescription illicit drug use of unknown types, amount, frequency, or duration. No other history was available. The styloid processes of the patient were imaged in-situ using a 3D C-arm X-ray machine. Furthermore, bilateral styloid processes were collected from the patient and seven other anatomical donors (6 M/1 F, age range 61-76) by detaching them from the base of the temporal bone and excising portions of the hyoid bone to maintain the stylohyoid ligament intact. Calipers were used to measure the length of the styloid processes and their calcifications. The primary donor exhibited elongated, asymmetrical processes (31.9 mm left, 37.8 mm right). Significant variation in styloid process lengths were observed in this sample (mean length 28.5 mm; standard deviation 13.5 mm; range 14.5-68.3 mm). Generally, the styloid processes demonstrated bilateral asymmetry across the sample. This asymmetry was notably pronounced in one donor with a significantly elongated styloid process (20.5 mm left, 68.3 mm right), co-occurrent with thyroid cartilage calcification. Conclusions: There is presently no consistent diagnostic measure of an elongated stylohyoid process available for providers to assess patient risk for Eagle’s Syndrome or its future progression. In this study, styloid length was found to be a continuous variable with no clear “cutoff” between elongated and normal lengths at 30mm. Furthermore, the lack of histological evidence detailing the condition's progression hinders diagnostic measures and risk assessment. We recommend further studies perform histologic analysis to better understand the progression of elongated styloid processes. Based on additional samples, a standardized diagnostic measurement can be created to improve treatment regimens and health risk screenings.Item EXPLORING A COMBINATION USING CHEMOTHERAPY AND TOLFENAMIC ACID TO INDUCE ANTI-PROLIFERATIVE RESPONSE IN MEDULLOBLASTOMA CELL LINES(2024-03-21) Chen, Liling; Sankpal, Umesh; Basha, RiyazBackground: Medulloblastoma (MB) is the most common malignant brain tumor in children, with a peak incidence between the ages of 5-9 years old. Originating in the cerebellum, it often metastasizes throughout the CNS via the CSF, making it very difficult to treat. Current treatment options are limited, and includes surgical resection followed by radiation and chemotherapeutic agents. However, these agents are associated with numerous toxicities and long-term neurocognitive deficits in survivors. Our laboratory is interested in identifying drug resistance cell markers and combination therapies that target them to help increase efficacy of the chemotherapeutic agents. We have previously demonstrated that combination therapy of chemotherapeutic agents with Tolfenamic acid (TA), decreased the number of viable cancer cells when compared to the chemotherapeutic agents alone. TA is a non-steroidal anti-inflammatory drug, and its anti-cancer activity can be attributed to its ability to downregulate Specificity Protein 1 (Sp1), a transcription factor responsible for the upregulation of the anti-apoptotic protein, Survivin. Numerous cancerous tumors have been known to express high levels of Sp1 and SurvivIn, however these markers have not been well established in MB. Purpose: The aim of the project is to elucidate the association of Survivin expression in MB cells with the likelihood of patient survival and to test combination treatments of chemotherapeutic agents with the potential Survivin inhibitor, TA. The goal is to reduce the effective dosage of the chemotherapeutic agent Cisplatin, thereby reducing their side effect profiles. Methods: A R2 genomics visualization platform was accessed to obtain data regarding patient survival rates and Survivin expression in MB cells. A Kaplan-Meier curve was then generated to analyze the relationship. MB cell lines, DAOY, and D283 cells were obtained through the ATCC and cultured following standard cell culture conditions. Cells were then treated with vehicle (DMSO) or optimized doses of a chemotherapeutic agents (Vincristine or Cisplatin) with TA. Cell viability was measured at 24h and 48h post-treatment using Cell-TiterGlo kit (Promega) following manufacturer’s instructions. Results: The Kaplan-Meier curve showed that the overexpression of Survivin resulted in a poor prognosis and low survival rates among MB patients. Compared to results of MB cell inhibition with individual agents (Vincristine and Cisplatin) from our previous studies, the combination of TA and Vincristine or TA and Cisplatin showed decreased MB cell growth and downregulation of Survivin. Differential effects of Vincristine and Cisplatin were noted against DAOY and D283 cell lines. Conclusion: These preliminary observations suggest that Survivin expression may be associated with poor prognosis in MB patients and that inhibiting Survivin with TA is inducing the anti-proliferative effects of chemotherapeutic agents in MB cells. Further research involving other chemotherapies is required to understand TA’s role in Survivin inhibition. Understanding the specific effect of Cisplatin can help to design the therapies based on the molecular sub-group of MB.