Musculoskeletal Pitfalls on Molecular Imaging Studies of Oncologic Patients: How to Stay Out of Trouble.

An increasing amount of molecular imaging studies are ordered each year for an oncologic population that continues to expand and increase in age. The importance of these studies in dictating further care for oncologic patients underscores the necessity of differentiating benign from malignant findings, particularly for a population in whom incidental findings are common. The aim of this review is to provide pictorial examples of benign musculoskeletal pathologies which may be found on molecular imaging and which may be mistaken for malignant processes. Imaging examples are provided in the form of radiographs, bone scintigraphy, computed tomography, and fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) scans. Special attention is paid to specific features that help narrow the differential diagnosis and distinguish benign from malignant processes, with the goal of avoiding unnecessary invasive procedures.

The Utility of PET/CT for the Diagnosis of Periosteal Chondrosarcoma in a Patient With Maffucci's Syndrome.

Maffucci's syndrome is a rare congenital nonhereditary syndrome with less than 300 cases having been reported in the United States. It is characterized by multiple enchondromas, hemangiomas, and rarely lymphangiomas. Enchondromas may undergo malignant transformation to chondrosarcomas. Surveillance plays a vital role in detecting early malignant transformation. Fluorodeoxyglucose (FDG) PET/CT, although falling out of favor, may be utilized as an imaging modality by physicians to determine such transformation, allowing for timely management and intervention. In this report, we share our experience with such a case.

Axitinib plus pembrolizumab in patients with advanced sarcomas including alveolar soft-part sarcoma: a single-centre, single-arm, phase 2 trial.

BACKGROUND: VEGF promotes an immunosuppressive microenvironment and contributes to immune checkpoint inhibitor resistance in cancer. We aimed to assess the activity of the VEGF receptor tyrosine-kinase inhibitor axitinib plus the anti-PD-1 immune checkpoint inhibitor pembrolizumab in patients with sarcoma. METHODS: This single-centre, single-arm, phase 2 trial was undertaken at a tertiary care academic medical centre in Miami, FL, USA, and participants were recruited from all over the USA and internationally. Patients were eligible if they were aged 16 years or older, and had histologically confirmed advanced or metastatic sarcomas, including alveolar soft-part sarcoma (ASPS); measurable disease with one site amenable to repeated biopsies; an ECOG performance status of 0-1; and progressive disease after previous treatment with at least one line of systemic therapy (unless no standard treatment existed or the patient declined therapy). The first five patients were enrolled in a lead-in cohort and were given axitinib 5 mg orally twice daily and pembrolizumab 200 mg intravenously for 30 min on day 8 and every 3 weeks for cycles of 6 weeks for up to 2 years. Thereafter, patients received escalating doses of axitinib (2-10 mg) plus flat dose pembrolizumab according to the schedule above. The primary endpoint was 3-month progression-free survival. All patients were evaluable for survival and safety analyses. This study is registered with ClinicalTrials.gov, number NCT02636725, and is closed to accrual. FINDINGS: Between April 19, 2016, and Feb 7, 2018, of 36 patients assessed for eligibility, 33 (92%) were enrolled and given study treatment (intention-to-treat population and safety population), 12 (36%) of whom had ASPS. With a median follow-up of 14·7 months (IQR 10·1-19·1), 3-month progression-free survival for all evaluable patients was 65·6% (95% CI 46·6-79·3). For patients with ASPS, 3-month progression-free survival was 72·7% (95% CI 37·1-90·3). The most common grade 3 or 4 treatment-related adverse events included hypertension (five [15%] of 33 patients), autoimmune toxicities (five [15%]), nausea or vomiting (two [6%]), and seizures (two [6%]). Serious treatment-related adverse events occurred in seven (21%) patients, including autoimmune colitis, transaminitis, pneumothorax, haemoptysis, seizures, and hypertriglyceridemia. There were no treatment-related deaths. INTERPRETATION: Axitinib plus pembrolizumab has manageable toxicity and preliminary activity in patients with advanced sarcomas, particularly patients with ASPS, warranting further investigation in randomised controlled trials. FUNDING: Merck, Pfizer, American Cancer Society, and Sylvester Comprehensive Cancer Center.

The sodium-iodine symporter and the proton-pump inhibitors in - related to the side effects of- the treatment of thyroid cancer with iodine-131.

Iodine-131 ((131)I) administered to patients for imaging or treatment, concentrates in the gastrointestinal tract, including the salivary glands, stomach and bowel. In Nuclear Medicine practice this biological property of iodine causes side effects when the therapeutic dose of (131)I is large. This occurs during the treatment of patients with differentiated thyroid carcinoma (DTC). During this clinical application, the dose of (131)I is higher than 3.7 GBq. Side effects of this treatment with respect to the stomach, include gastritis as an inflammatory reaction to radiation, anorexia due to gastric atrophy and rarely megaloblastic anemia due to lack of the endogenous factor. Side effects can also include xerostomia. We have recently tried to prevent gastric side effects by prescribing proton pump inhibitors (PPI) for patients with DTC prior to treatment with (131)I. PPI block the excretion of hydrochloric acid from the gastric mucosa and are utilized for the prevention and treatment of gastritis, gastric ulcers and gastroesophageal reflux. Whole body scans before or after the administration of PPI, showed that PPI do not interfere with the biologic distribution of (131)I. These findings were not surprising. Recent studies in animals and humans have shown that the accumulation and concentration of iodine by the thyroid gland is the result of the selective action of sodium iodine symporter (Na+I+symporter, NIS). Furthermore, it was shown that the accumulation and concentration of (131)I in the parietal cells of the gastric mucosa, the ductal cells of the salivary glands and the alveolar epithelial cells of the mammary glands, is analogous to the biologic action of NIS in the thyroid cells. The gastric mucosa accumulates iodine from the capillaries via the extracellular/extravascular space and finally excretes it into the lumen of the stomach, from where it is passively transferred into the bowel, where it is partially reabsorbed to once again enter its metabolic cycle. On the contrary, as it is now known, the PPI have an entirely different metabolic action, which is unrelated to that of the NIS, although both mechanisms coexist in the parietal cells of the gastric mucosa. Thus, during the application of (131)I for imaging or for the treatment of DTC patients, except for the short period of time immediately after the oral administration, when the radionuclide passes through the stomach, the concentration of (131)I in the gastrointestinal tract is due to its active accumulation and excretion by the gastric mucosa. PPI act only on the hydrochloric acid secretion not affecting the biologic properties of iodine.