MiR-16-5p, a member of the miR-16 family, has been reported to be abnormal expression in tumor tissues and blood of tumor patients, and also downregulated in most cancer cell lines. Aberrant expression of miR-16-5p promotes tumor cell proliferation, invasion, metastasis, angiogenesis, and can also affect the treatment sensitivity, such as radiotherapy and chemotherapy. Generally, miR-16-5p plays an anti-tumor role and these diverse functions of miR-16-5p in tumors collectively indicate that miR-16-5p may become an attractive target for novel anticancer therapies and a powerful diagnostic and prognostic biomarker for early tumor detection and population risk screening. Herein we review the role and utilization of miR-16-5p in malignant tumor in detail.

The objective of the study is to test whether three-dimensional (3D)-printed template can be used reproducibly for guiding malignant tumors brachytherapy and study the dosimetric consistency and adequacy between pre- and post-plan. Between January and December 2016 in our hospital, a total of 14 patients underwent 3D-printed template-guided brachytherapy. All the patients were fixed into position using a vacuum cushion before undertaking a computed tomography (CT) scan. After the preplan was designed, the templates were printed. The tumors were punctured through predesigned needle holes. Following this, another CT scan was used to confirm the locations of needles, and then the 125 I radioactive seeds were implanted into the tumor according to the preplan. Postplan was performed after the operation. Data of the D90 (minimum absorbed dose of 90% target volume), V90 (90% prescription dose coverage volume percentage of target volume), V100, V150, and seed number pre- and post-operation were collected and compared. The mean D90, V90, V100, V150, and seed number preoperation were 94.96 ± 16.43 Gy, 94.64% ± 1.43%, 91.21% ± 1.59%, 65.01% ± 5.78%, and 46.67 ± 21.87, respectively. The mean D90, V90, V100, V150, and seed number postoperation were 91.97 ± 17.54 Gy, 93.35% ± 2.45%, 89.35% ± 3.21%, 63.40% ± 6.36%, and 46.60 ± 22.85, respectively. No significant difference between pre- and post-operation was observed across the data (P >0.05). For immobilized malignant tumors, 3D-printed template can be used reproducibly. The dose parameters in preplan can be achieved easily and satisfactorily by 3D-printed template guided brachytherapy, and it may become an easily reproducible standardized procedure in the future.

Rationale: Patients with lung adenocarcinoma harboring EML4-ALK rearrangements respond well to multiple ALK tyrosine kinase inhibitors (TKIs). However, the tumor will invariably progress due to acquired resistance. Comprehensive genomic profiling appears to be a promising strategy to reveal the underlying molecular mechanisms of ALK-TKIs resistance. Patient concerns: A patient with right lung adenocarcinoma harboring an ALK rearrangement received targeted therapy with multiple ALK-TKIs. He sought for follow-up treatment after his disease progressed again. Diagnosis: The patient had a tumor diagnosed with stage I (T1bN0M0) lung adenocarcinoma. Interventions: Due to the surgical contraindication, the patient did not undergo surgical resection. Instead, he received crizotinib as the first-line therapy with the progression-free survival of 20 months. Then he switched to alectinib treatment, however the disease rapidly progressed again. Outcomes: Next-generation sequencing was performed and revealed that 7 somatic mutations were identified. Among them, 2 mutations, ALK I1171T and BRAF V600E, may be responsible for the resistance of this patient to ALK-TKIs. BRAF V600E mutation may explain the patient's resistance to lorlatinib. Lessons: We present a case of ALK-rearranged lung adenocarcinoma with acquired resistance to ALK inhibition, in which the BRAF V600E mutation is a novel resistance mechanism. This provides evidence that BRAF V600E mutation is one mechanism of ALK-TKI resistance.