A primary small cell neuroendocrine carcinoma (SCNC) of the oral cavity (cheek mucosa): Description of a case report.

BACKGROUND: Small cell neuroendocrine carcinoma (SCNC) of the oral cavity is a poorly differentiated, high-grade and very aggressive tumor with a poor prognosis. CASE DESCRIPTION: A 64-year-old, Caucasian, smoker man consulted for an ulcero-necrotic, exophytic, lesion of the right retromolar trigone. Haed&neck CT scan showed a right tonsillar tumor lesion. The 18F-PET scan confirmed the presence of a right, highly hypermetabolic tonsillar lesion and two homolateral, cervical lymph nodes. Histology and immunohistochemistry were consisted with the diagnosis of a primary SCNC of the oral cavity. As the tumor was locally advanced and unresectable, the patient underwent a definitive radio-chemotherapy with a cisplatin/etoposide combined regimen (4 cycles). The treatment was well tolerated and led to a complete tumor response. CONCLUSION: The particularity of this case relies on the rarity of the oral SCNC, its difficult and challenging diagnosis, and the complexity of its management that is not validated by large clinical trials, data being extrapolated from small cell lung cancer. In our case, the patient presenting a locally advanced tumor was treated by a combined radio-chemiotherapy leading to a complete tumor regression. The patient's follow up is too short to assess the real benefit of this treatment on overall survival.

A fatal primary gastric melanoma treated by a double immunotherapy with ipilimumab/nivolumab: description of a case report.

Background: Primary gastric melanoma (GM) is a very uncommon tumor with a poor prognosis. Until now, only a few cases have been reported in the literature. Case Description: A 70-year-old, Caucasian, ex-smoker man, presented with asthenia, anorexia, and weight loss of 5 kg during the last 2 months. Biological test showed high levels of transaminases and a microcytic, hypochromic anemia. Whole body CT-scan documented a gastric tumor lesion with concomitant loco-regional lymph node and hepatic metastases. Histology was consisted with the diagnosis of a primary GM. A double immunotherapy with nivolumab and ipilimumab was started but, 2 weeks later, the patient presented an acute hepatic failure quickly leading to his death despite a high dose corticotherapy. Conclusions: The particularity of this case relies on the rarity of GM, its difficult diagnosis representing a clinical challenge, and the complexity of its management that is not validated by large clinical trials, data being extrapolated from the treatment protocols routinely used in cutaneous melanoma. In our case, the patient died 2 weeks after the first cycle of a nivolumab/ipilimumab combined treatment for an acute hepatic failure that could be related to a treatment toxicity or a tumor hyperprogression. The patient's survival was very short not allowing any accurate evaluation of the efficacy of this therapy.

Development of a Clinical-Biological Model to Assess Tumor Progression in Metastatic Pancreatic Cancer: Post Hoc Analysis of the PRODIGE4/ACCORD11 Trial.

Background: The follow-up of pancreatic cancer (PC) is based on computed tomography (CT) assessment; however, there is no consensus on the use of clinical and biological criteria in tumor progression. We aimed to establish a clinical−biological model to highlight the progression of metastatic PC during first-line treatment. Methods: The patients treated with first-line chemotherapy in the phase 2/3 PRODIGE4/ACCORD11 clinical trial were evaluated retrospectively. Clinical and biological markers were evaluated at the time of CT scans and during treatment to determine tumor progression. Results: In total, 196 patients were analyzed, with 355 available tumor assessments. The clinical and biological factors associated with tumor progression in multivariate analysis included gemcitabine, global health status ≤ 33 (OR = 3.38, 95%CI [1.15; 9.91], p = 0.028), quality of life score between 34 and 66 (OR = 2.65, 95%CI [1.06; 6.59], p = 0.037), carcinoembryonic antigen (CEA) ≥ 3 times the standard value without any increase in the CEA level from inclusion (OR = 2.22, 95%CI [1.01; 4.89], p = 0.048) and with an increase in the CEA level from inclusion (OR = 6.56, 95%CI [2.73; 15.78], p < 0.001), and an increase in the carbohydrate antigen 19-9 level from inclusion (OR = 2.59, 95%CI [1.25; 5.36], p = 0.016). Conclusions: The self-assessment of patients' general health status alongside tumor markers is an interesting approach to the diagnosis of the tumor progression of metastatic pancreatic cancer patients during first-line treatment.

Alectinib in the treatment of ALK-positive metastatic non-small cell lung cancer: clinical trial evidence and experience with a focus on brain metastases.

Molecular profiling of metastatic nonsquamous non-small cell lung cancer (NSCLC) is required to guide the treatment strategy. Anaplastic lymphoma kinase ( ALK) gene rearrangements are found in approximately 5% of lung adenocarcinomas and are associated with specific clinical features including a high risk of brain metastases. Crizotinib was the first ALK inhibitor developed and it demonstrated improved outcomes in patients with ALK-positive advanced NSCLC in comparison with chemotherapy. However, despite an initial response, all ALK-positive NSCLC patients develop acquired resistance to crizotinib. Because the most frequent mechanism of resistance is the development of a secondary ALK mutation, second (ceritinib, alectinib, brigatinib) and third-generation (lorlatinib) ALK inhibitors were developed. Alectinib is a second-generation ALK inhibitor and was shown to be effective for a broad spectrum of ALK rearrangements and ALK mutations. It was also shown to have high intracranial efficacy. In this article, we review clinical trial evidence of alectinib efficacy as well as publications reporting the experience of alectinib in daily practice, with a focus on brain metastases.