The detection of synchronous or metachronous malignancies is on the rise with the advent of whole-body F-FDG PET/CT. It has shown its utility in detecting second primary carcinoma in patients undergoing imaging for evaluation of primary carcinoma, influencing the management and overall survival. Primary malignant melanoma of the lung is an extremely rare entity, accounting for 0.01% of all lung tumors. It is an even rare occurrence as a synchronous malignancy. We present the case of a 33-year-old woman with primary parotid myoepithelial carcinoma and incidental detection of second primary malignant melanoma of lung during F-FDG PET/CT imaging.
To describe a rare case of sarcomatoid squamous cell carcinoma of alveolus. A 53-year-old female with complaints of non-healing ulcerative growth over the left side of the hard palate, which was associated with pain for two months. She underwent extraction and a Histo-pathological examination of teeth with attached soft tissue was suggestive of Sarcomatoid Carcinoma. The patient underwent Left infrastructure maxillectomy with wide local excision with left modified radical neck dissection type II. Histopathology showed lympho-vascular infiltration and perineural infiltration. All margins were free. Out of 8 lymph nodes that were dissected, 1 showed metastatic disease. The patient received adjuvant concurrent radio-chemotherapy 66Gy in 33 fractions (2Gy/day) in two phases along with weekly Injection Cisplatin 40 mg/m2. Sarcomatoid squamous carcinoma is a rare and uncommon variant of squamous cell carcinoma. It is aggressive in nature and shows early recurrence and metastasis. Thus, associated with a poor prognosis. There is no defined treatment protocol for this variant. We have discussed a case of sarcomatoid carcinoma of the alveolus that was operated and followed by adjuvant chemo-radiotherapy.
Introduction and Objective: Although Paclitaxel has demonstrated antitumor activity against several cancers, the acquisition of resistance during treatment remains a significant problem. Several potential mechanisms were proposed and the recent studies determined that drug resistance may involve histone H3 acetylation. Histone deacetylases (HDACs) are overexpressed in prostate cancer (PCa) and HDAC inhibitors have greater anti-proliferative activity against prostate and breast cancer models. We have investigated the interaction of the HDAC inhibitors Valproic Acid (VPA) and SAHA (Vorinostat) with Paclitaxel in both susceptible and resistance PCa cell lines. We evaluated anti-proliferative activity, nuclear morphometry, expression of apoptotic genes: Caspases 3 and 9 and Annexin A5, and three keratins (8, 18 and 19) which are involved in cell differentiation. Methods: Four PCa cell lines PC3, PC3-TxR (Paclitaxel resistant), DU145 and DU145-TxR (Paclitaxel resistant) were grown in 96 well & 24 well tissue culture plates. After a day, the cells were exposed to 1.2mM of VPA and 5μM of SAHA for 24 hours followed by treatment with 4.5nM Paclitaxel for 48 hours. WST-1 cytotoxicity assay was performed in the 96 well plates. From the 24 well plates, RNA was isolated and the real-time PCR for expression of specific genes was done using gene specific primers and β-actin (to calculate relative expression). Nuclear morphometry was done in Feulgen stained nuclei using AutoCyteTM Pathology Workstation and QUIC-DNA software. Results: We found after 24hrs treatment: (i) VPA (1.2mM) reversed Paclitaxel resistance only in PC3 cell lines (50%) while (ii) SAHA made all the PCa cell lines more susceptible to Paclitaxel (50-60%). We observed specific changes in DNA ploidy and in nuclear structure in Paclitaxel resistant DU145-TxR cell lines when compared to DU145 cells. Our results showed different patterns of apoptotic and keratin gene expression occurred in DU145 and DU145-TxR cell lines following treatment with SAHA but no significant changes in PC3 and PC3-TxR cell lines. Expressions of Caspase 3, Caspase 9 and Annexin A5 were increased significantly in SAHA treated DU145-TxR cells, and KRT-8 and KRT-19 (keratins) were significantly downregulated in DU145-TxR cell lines irrespective of treatment. Conclusions: Hence, resistance to Paclitaxel can be rescued by HDAC inhibitors VPA and SAHA, but likely by different mechanisms that are yet to be established. Also, altered expression of apoptotic biomarkers, but not keratins shows that the rescue by SAHA involves apoptosis but not epithelial mesenchymal transition. Source of funding: National Cancer Institute of the National Institutes of Health through awards funded under Grant number 1U54CA143868-03 Citation Format: Christhunesa S. Christudass, Karan Sood, David Yeater, Robert W. Veltri. Paclitaxel resistance in prostate cancer: rescue of resistance using HDAC inhibitor SAHA involves apoptosis. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 979. doi:10.1158/1538-7445.AM2013-979
I studied a new approach called Capsule networks to overcome the drawbacks of convolutional neural networks.
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