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Complete response of metastatic BRAF V600-mutant anaplastic thyroid cancer following adjuvant dabrafenib and trametinib treatment:A case report

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世界临床病例杂志 2023年第27期11卷 6664-6669页

作者： Sang Jae Lee Si-Youn Song Min Kyoung Kim Hyung Gyun Na Chang Hoon Bae Yong-Dae Kim Yoon Seok Choi Department of Otorhinolaryngology-Head and Neck Surgery College of MedicineYeungnam UniversityDaegu 42415South Korea Division of Hematology-Oncology Department of Internal MedicineCollege of MedicineYeungnam UniversityDaegu 42415South Korea Regional Center for Respiratory Diseases Yeungnam University Medical CenterDaegu 42415South Korea

BACKGROUND Anaplastic thyroid cancer(ATC)is a rare but aggressive type of thyroid carcinoma.BRAF V600E-mutation,which is found in 10%-50%of ATCs,is associated with poor prognosis.A recent clinical trial reported a substantial clinical benefit of concomitant treatment of dabrafenib(BRAF inhibitor)and trametinib(MEK inhibitor)for treating BRAF V600E-mutant ATC.However,reports on patients with ATC treated with this regimen following surgery are lacking.CASE SUMMARY We report the case of a 63-year-old female patient diagnosed with BRAF V600Emutant ATC.Following three surgeries—total thyroidectomy,total laryngectomy,and neck dissection—she was diagnosed with lung metastasis during follow-up.The metastatic ATC was successfully treated with dabrafenib and trametinib.The patient achieved a complete response at the 32-mo follow-up.CONCLUSION Adjuvant chemotherapy with dabrafenib plus trametinib is efficacious for treatment and prevention of recurrent ATC with BRAF mutation following surgery.

关键词： Thyroid carcinoma Anaplastic BRAF dabrafenib Trametinib Chemotherapy Adjuvant Case report

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dabrafenib,an inhibitor of RIP3 kinase-dependent necroptosis,reduces ischemic brain injury

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Neural Regeneration Research 2018年第2期13卷 252-256页

作者： Shelly A.Cruz Zhaohong Qin Alexandre E R.Stewart Hsiao-Huei Chen Ottawa Hospital Research Institute OttawaCanada University of Ottawa Brain and Mind InstituteOttawaCanada University of Ottawa Heart Institute OttawaCanada Canadian Partnership for Storke Recovery OttawaCanada

Ischemic brain injury triggers neuronal cell death by apoptosis via caspase activation and by necroptosis through activation of the receptor-interacting protein kinases （RIPK） associated with the tumor necrosis factor-alpha （TNF-a）/death receptor. Recent evidence shows RIPK inhibitors are neuroprotective and al- leviate ischemic brain injury in a number of animal models, however, most have not yet undergone clinical trials and safety in humans remains in question. dabrafenib, originally identified as a B-raf inhibitor that is currently used to treat melanoma, was later revealed to be a potent RIPK3 inhibitor at micromolar con- centrations. Here, we investigated whether dabrafenib would show a similar neuroprotective effect in mice subjected to ischemic brain injury by photothrombosis. dabrafenib administered intraperitoneally at 10 mg/ kg one hour after photothrombosis-induced focal ischemic injury significantly reduced infarct lesion size in C57BL6 mice the following day, accompanied by a markedly attenuated upregulation of TNF-u. However, subsequent lower doses （5 mg/kg/day） failed to sustain this neuroprotective effect after 4 days. dabrafenib bl ocked lipopolysaccharides-induced activation of TNF-ct in bone marrow-derived macrophages, suggesting that dabrafenib may attenuate TNF-ct-induced necroptotic pathway after ischemic brain injury. Since Dab- rafenib is already in clinical use for the treatment of melanoma, it might be repurposed for stroke therapy.

关键词： ischemic brain injury inflammation macrophage dabrafenib tumor necrosis factor-alpha photothrombosis receptor-interacting protein kinases necroptosis microgIia stroke neural regeneration

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Radiation recall dermatitis with dabrafenib and trametinib: A case report

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World Journal of Clinical Cases 2020年第3期8卷 522-526页

作者： Mesut Yilmaz Ugur Celik Seyhan Hascicek Medical Oncology Department Bakirköy Dr.Sadi Konuk Training and Research HospitalIstanbul 34144Turkey Dermatology Department Medipol Kosuyolu HospitalIstanbul 34134Turkey Pathology Department Sisli Hamidiye Etfal Training and Research HospitalIstanbul 34134Turkey

BACKGROUND Radiation recall dermatitis has been defined as the "recalling" by skin of previous radiation exposure in response to the administration of certain response-inducing drugs. Although the phenomenon is relatively well known in the medical world,an exact cause has not been documented.CASE SUMMARY Here, we report the rare occurrence of radiation recall dermatitis after palliative radiotherapy for bone metastases in a metastatic melanoma patient treated with a combination of dabrafenib and trametinib.CONCLUSION We present a case of radiation recall dermatitis after completion of palliative radiotherapy while being treated with a combination of dabrafenib and trametinib. This is a very rare toxic event, and there is insufficient data to describe prevention strategies. Increased awareness and reporting of cases will help to better explain the association between targeted therapy and the radiation recall phenomenon.

关键词： Radiation recall dermatitis Melanoma Radiotherapy dabrafenib Trametinib Case report

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Asian Case of Metastatic Melanoma in Which a Complete Response Was Maintained after Discontinuation of dabrafenib and Trametinib

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Journal of Cosmetics, Dermatological Sciences and Applications 2020年第2期10卷 55-58页

作者： Rikako Deno Atsushi Tanemura Madoka Takafuji Yuma Hanaoka Eiji Kiyohara Noriko Arase Mari Wataya-Kaneda Manabu Fujimoto Department of Dermatology Graduate School of Medicine Osaka University Suita Osaka Japan

A 54-year-old man diagnosed with metastatic melanoma of the right inguinal node with occult primary developed liver and bone metastases. The combination of dabrafenib plus trametinib was initiated, and a complete response (CR) was achieved 24 months after starting treatment. One month later, the target therapy was discontinued at the patient’s decision, and he has remained free from progression for 21 months since discontinuation. To the extent of our knowledge, real-world data in Asian melanoma concerning the discontinuation of dabrafenib plus trametinib after achieving CR have not been published;therefore, our case is a meaningful one for considering to cease target drugs and to rescue their financial toxicity.

关键词： Metastatic Melanoma dabrafenib Trametinib Complete Response Discontinuation

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抗肿瘤药dabrafenib

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药学进展 2013年第2期37卷 93-94页

作者：杨臻峥

Ras／Raf／MEK／ERK信号转导通路是调控细胞生长、分化和增殖最重要的通路之一，其中信号蛋白的过度表达或突变可导致肿瘤的发生和发展。如Raf激酶家族共包括3个成员—A．Raf、B—Raf和C—Raf，B—Raf在这3个成员中的突变率最高，约有7... 详细信息

Ras／Raf／MEK／ERK信号转导通路是调控细胞生长、分化和增殖最重要的通路之一，其中信号蛋白的过度表达或突变可导致肿瘤的发生和发展。如Raf激酶家族共包括3个成员—A．Raf、B—Raf和C—Raf，B—Raf在这3个成员中的突变率最高，约有7％～8％的人类肿瘤发生B-Raf 基因突变，而4-Raf 和c-R妒基因则较少发生突变。最具致命性的皮肤癌——黑色素瘤中B-Raf的突变率最高，约有40％～68％的转移性黑色素瘤发生这种突变，因此，

关键词： dabrafenib 黑色素瘤 B-Raf抑制剂

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RIPK3依赖的程序性坏死在气道上皮细胞损伤中的作用

RIPK3依赖的程序性坏死在气道上皮细胞损伤中的作用

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作者：陈宝先华中科技大学

学位级别：硕士

研究背景急性肺损伤(ALI)和其严重形式急性呼吸窘迫综合征(ARDS)是呼吸科常见急症之一,可由脓毒症诱发。细菌脂多糖(LPS)是革兰氏阴性细菌细胞壁的主要组分之一,作为革兰氏阴性细菌主要致病物质的基础,能在体内引起强烈的免疫反应。气... 详细信息

研究背景急性肺损伤(ALI)和其严重形式急性呼吸窘迫综合征(ARDS)是呼吸科常见急症之一,可由脓毒症诱发。细菌脂多糖(LPS)是革兰氏阴性细菌细胞壁的主要组分之一,作为革兰氏阴性细菌主要致病物质的基础,能在体内引起强烈的免疫反应。气道上皮细胞在启动和维持急性肺损伤(ALI)炎症反应过程中起着重要作用。急性肺损伤患者气道上皮细胞发生损伤、增生、死亡等改变,损伤或者死亡的气道上皮细胞通过分泌多种细胞因子和趋化因子,趋化并活化免疫细胞,启动炎症反应;且气道上皮细胞作为屏障结构被破坏,促进外来抗原直接与粘膜下层免疫细胞接触,加重炎症反应发生。Necroptosis,程序性坏死,是一种新近被发现的细胞程序性死亡方式,受主要信号分子RIPK1、RIPK3、MLKL等调节。程序性坏死被普遍认为是一种高度促炎的细胞死亡方式,在体内多种急慢性炎症中发挥重要作用,但是它是否参与急性肺损伤气道上皮细胞炎症目前国内外尚未见报道。目的:探讨RIPK3依赖的程序性坏死在急性肺损伤气道上皮细胞炎症中的作用。方法:本实验用LPS刺激人气道上皮细胞系HBE,使用流式细胞仪检测气道上皮细胞发生程序性坏死的情况,Western-Blot检测程序性坏死主要信号分子表达量的变化。结果:1.LPS诱导气道上皮细胞发生死亡LPS刺激HBE 24h,结果显示LPS增加HBE死亡比例即Annexin V+/PI++Annexin V+/PI-比例(23.90%±1.749%vs 9.056%±0.8710%,Pdabrafenib(Da)处理,气道上皮细胞的死亡比例即Annexin V+/PI++Annexin V+/PI-比例较直接加LPS刺激明显减少(16.52%±2.264%vs 23.90%±1.749%,P0.05,n=4)。3.RIPK3-MLKL信号通路在LPS诱导的气道上皮细胞炎症中的作用LPS能够促进RIPK3作用底物MLKL的活化,即p-MLKL的表达上调;RIPK3抑制剂dabrafenib抑制RIPK3作用之后,p-MLKL的表达上调受到抑制。结论:实验结果说明LPS能诱导气道上皮细胞发生程序性坏死;LPS促进程序性坏死通路中MLKL信号分子的活化;RIPK3抑制剂dabrafenib可部分缓解LPS诱导引起的气道上皮细胞程序性坏死的发生,减少RIPK3下游信号分子MLKL的活化。

关键词： LPS 气道上皮细胞程序性坏死 dabrafenib RIPK3 MLKL

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