Treatment of poorly differentiated neuroendocrine carcinoma of the pancreas.

Poorly differentiated neuroendocrine carcinoma is a rare malignancy that remains a challenge to treat. Poorly differentiated neuroendocrine carcinoma occurs at an incidence of 2% annually in United States. The current standard of care is based largely upon retrospective data. There remains a need for large prospective cooperative group trials in the management of poorly differentiated neuroendocrine carcinoma. In this paper, we will review abstract #e15096 (Paclitaxel, carboplatin, and etoposide (TCE) in advanced poorly differentiated neuroendocrine carcinoma) by Loeffler et al. and #e15071 (Poorly differentiated neuroendocrine carcinoma (NEC G3): prognostic factors and potential novel targets) by Heetfeld et al. presented at the 2013 ASCO Annual Meeting highlighting treatment options in first and second lines for poorly differentiated neuroendocrine carcinoma.

Biomarkers in neuroendocrine tumors.

Neuroendocrine tumors are a heterogeneous group of tumors with cells of neuroendocrine differentiation that arise from diverse anatomic sites with varying morphologic and clinical features. Since the natural history and prognosis varies widely between individual neuroendocrine tumor types, there is a critical need to identify accurate prognostic and predictive biomarkers and markers predictive of therapeutic efficacy. To date, plasma chromogranin-A levels have generally been accepted as the most useful biomarker, despite the fact that there are substantial concerns in sensitivity and discrepancies in measurement techniques. As a consequence, considerable attention has been focused upon the development of novel biomarkers that can be utilized with more clinical efficacy than chromogranin-A. In addition to amplifying the diagnostic/prognostic landscape, the need to calibrate the efficacy of biological targeted therapy has further accelerated the development of molecular biomarkers. At the 2013 American Society of Clinical Oncology (ASCO) Annual Meeting, Chou et al. (Abstract #e15151) presented data that chromogranin A levels can be monitored during treatment to predict clinical outcome. Modlin et al. (Abstract #4137), demonstrated a promising novel biomarker, serum multi-transcript molecular signature. Grande et al. (Abstract #4140), Heetfield et al. (Abstract #e15071) and Casanovas et al. (Abstract #4139) described sVEGFR2, p-mTOR and IGF1R as molecular markers with potential for use in targeted therapy trials. The authors review and summarize these abstracts in this article.

Use of supportive care for symptom management in pancreatic cancer: application of clinical research to patient care.

In this paper, we will be discussing Abstracts #9061, #9062, #9065, #9072 and #9097 presented at the recent 2012 American Society of Clinical Oncology (ASCO) Annual Meeting. All of these abstracts explore innovative ways to control symptoms in cancer patients. We are hopeful that these methods are able to be used in symptomatic pancreatic cancer patients.

A Rare Case of White Piedra Caused by Candida parapsilosis in the Sub-Himalayan Region of North India.

White piedra is a superficial fungal infection of the hair shaft, caused by Trichosporon, a noncandidal yeast characterized by the presence of numerous, discrete, asymptomatic nodules attached to the infected hair shafts. White piedra is considered a disease of tropical regions and occasionally reported from temperate countries. Although Candida parapsilosis such as Candida albicans is well known to cause cutaneous infections, it has been reported as a co-isolate for white piedra along with Trichosporon. We report a case of white piedra from a temperate region caused by C. parapsilosis.

Pattern of Marginal Local Failure in a Phase II Trial of Neoadjuvant Chemotherapy and Stereotactic Body Radiation Therapy for Resectable and Borderline Resectable Pancreas Cancer.

OBJECTIVES: The main objectives of this study were to prospectively evaluate the safety and efficacy of stereotactic body radiation therapy (SBRT) in the neoadjuvant setting for resectable or borderline resectable pancreatic cancer. MATERIALS AND METHODS: Eighteen patients were enrolled from November 2014 to June 2017. Following 3 cycles of chemotherapy, SBRT was delivered to the tumor and abutting vessel and a 3 mm planning target volume (PTV) margin to 33 Gy (6.6 Gy×5) with an optional elective PTV to 25 Gy (5 Gy×5) customized to the nodal space and mesenteric vessels. The primary endpoint is ≥grade 3 acute and late gastrointestinal toxicity. RESULTS: Fifteen patients had borderline resectable tumors due to arterial abutment (n=7) or superior mesenteric vein encasement (n=8); 3 patients had resectable tumors. There were no ≥grade 3 acute or late gastrointestinal events. Following SBRT, surgery was performed in 12 patients (67%) with 11 (92%) R0 resections. The median overall survival and progression-free survival was 21 months (95% CI: 18-29) and 11 months (95% CI: 8.4-16). Progression occurred in 83% (10/12) of resected patients (distant [n=4, 40%], local-only [n=4, 40%], and local and distant [n=2, 20%]). The cumulative incidence of local failure (LF) at 12 months from resection was 50% (95% CI: 20-80). All LF were outside to the PTV33. CONCLUSIONS: Neoadjuvant SBRT was well tolerated, however LFs were predominantly observed outside the PTV33 volume that would have been covered with conventional RT volumes. The durability of local control after SBRT in the neoadjuvant setting merits examination relative to chemoradiation before incorporation into routine practice.

Therapeutic human monoclonal antibodies against cancer.

There are over 30 monoclonal antibodies that are FDA approved for a variety of diseases ranging from malignancies to autoimmune diseases to macular degeneration. These antibodies include murine, fully humanized, and chimeric antibodies. There are a number of monoclonal antibodies used in the treatment of malignancies; in fact, three of the top five grossing antibodies (bevacizumab, trastuzumab, and rituximab) are used in oncology Scolnik (mAbs 1:179-184, 2009).