KẾT QUẢ ĐIỀU TRỊ BƯỚC HAI PEMETREXED – CARBOPLATIN UNG THƯ PHỔI KHÔNG TÉ BÀO NHỎ SAU KHÁNG THỨ PHÁT THUỐC ỨC CHẾ TYROSINE KINASE

Mục tiêu: Đánh giá kết quả điều trị của phác đồ Pemetrexed – Carboplatin trên bệnh nhân ung thư phổi không tế bào nhỏ sau kháng thuốc ức chế Tyrosin Kinase (TKIs). Đối tượng và phương pháp: Hồi cứu 46 bệnh nhân sau kháng thứ phát EGFR TKIs, điều trị phác đồ Pemetrexed – Carboplatin, có theo dõi dọc. Kết quả: Tỷ lệ đáp ứng khách quan 50%; đáp ứng hoàn toàn 0%; kiểm soát bệnh 78,3%. Các yếu tố tiên lượng đáp ứng kém: toàn trạng PS1, giai đoạn IV, di căn thần kinh trung ương. Sống thêm không bệnh tiến triển trung vị : 4 tháng. Kết luận: Phác đồ Pemetrexed – Carboplatin là lựa chọn điều trị hợp lý cho bệnh nhân ung thư phổi không tế bào nhỏ sau kháng thuốc ức chế Tyrosin Kinase

Nilai Prognostik FLT3 Pada Pasien Leukemia Mieloid Akut

Acute myeloid leukemia (AML) is a disease characterized by neoplastic transformation and abnormality of progenitor cells differentiation from myeloid cells. In AML there is a heterogeneous abnormality in hematopoietic progenitor cells, this abnormality has been identified and affects the balance between proliferation, survival and differentiation of body cells. Mutation of FMS-like tyrosin kinase 3 (FLT3) gene causes overexpression which is one of the most often found mechanism that has been identified could trigger genetic changes that can disturb intracellular signaling tissue in pathogenesis of leukemia. Besides being used as a diagnostic tool, FLT3 overexpression can also be used to assess the prognosis of AML.

Synthesis of (Z)-3-[amino(phenyl)methylidene]-1,3-dihydro-2H-indol-2-ones using an Eschenmoser coupling reaction

A highly modular method for the synthesis of (Z)-3-[amino(phenyl/methyl)methylidene]-1,3-dihydro-2H-indol-2-ones starting from easily available 3-bromooxindoles or (2-oxoindolin-3-yl)triflate and thioacetamides or thiobenzamides is described. A series of 49 compounds, several of which have previously been shown to possess significant tyrosin kinase inhibiting activity, was prepared in yields varying mostly from 70 to 97% and always surpassing those obtained by other published methods. The method includes an Eschenmoser coupling reaction, which is very feasible (even without using a thiophile except tertiary amides) and scalable. The (Z)-configuration of all products was confirmed by NMR techniques.

SUN-485 Combined Treatment with Laser Ablation and Tyrosin Kinase Inhibitors. a Novel Multimodality Approach to Locally Advanced Thyroid Cancer?

Background. Direct loco-regional treatments are considered for local control of cervical metastasis of thyroid cancer. In our feasibility study, laser ablation was employed for initial debulking of an unresectable radioiodine-refractory thyroid cancer in a combined treatment with tyrosin kinase inhibitors (TKI). Clinical case. On June 2016, a 69-year-old woman underwent partial resection of a papillary thyroid cancer with extensive tracheal infiltration. On August 2016, whole body scan performed after 131-I treatment (8140 MBq) demonstrated nearly absent thyroid bed uptake. Due to progressive increase of the cervical mass, the patient experienced dysphonia and dysphagia and, after multidisciplinary consultation, was treated with laser ablation (LTA). After local anesthesia, two 300 nm fiberoptics were inserted into the lesion through 21G spinal needles. Two illuminations with 4-watt output power and 3600 Joules energy delivery were peformed with a diode-laser source. LTA resulted in rapid mass volume decrease (28 x12 x16 mm, 2.8 mL, vs 52 x 29 x 29 mm, 22.7 mL) and improvement of pressure symptoms that lasted 6 months. In May 2017, due to initial regrowth of the tumor mass, the patient started therapy with Lenvatinib, at 10-24 mg/day. The cervical tumor burden remained controlled until April 2019, when occurred rapid disease progression and death of the patient. Discussion. These preliminary results suggest that locally-advanced unresectable and radioiodine-refractory thyroid tumors can be managed with preliminary LTA mass debulking, for rapid control of local disease, followed by long-term TKI treatment. References. Mauri G et al. Cardiovasc Intervent Radiol. 2016 Jul; 39(7):1023-30; Park KW et al. Ann Surg Oncol 2011; 18:2564-2568. Schlumberger M et al. NEJM 2015 12; 372(7):621-30.

Effekt des oralen BTK-Inhibitors Evobrutinib auf Multiple Sklerose

Die Bruton-Tyrosin-Kinase (BTK) ist ein Enzym, welches die Funktion von Immunzellen wie B-Zellen und Myeloidzellen reguliert. Diese Zellarten spielen bei der Pathogenese von Multipler Sklerose (MS) eine bedeutende Rolle. Im Rahmen dieser Phase-II-Studie untersuchten die Forscher, wie sich die orale Einnahme verschiedener Dosen des BTK-Inhibitors Evobrutinib auf die Entstehung von Läsionen im Gehirn von MS-Patienten auswirkt.