1. O'pka saratonining diagnostikasi va birinchi davolash
Bemor Luga 26 yil 2005 avgustda o'pka adenokarsinomasi va limfa tugunlarida metastaz tashxisi qo'yilgan. 22 yil 2005 sentyabrda chap pastki lobektomiya o'tkazilgan. Operatsiyadan keyin 4 marta karboplatin taksoter bilan birgalikda ishlatilgan. 3 yil 2007 avgustda plevral efüzyon tufayli tashxisning takrorlanishi tasdiqlandi va u Tarceva bilan davolandi (tsikllar soni noma'lum). 8 yil 2008 yanvarda qayta tekshiruvda saraton rivojlanishi aniqlandi, keyin Tarceva bilan davolash to'xtatildi va 16 tsikl uchun Libita bilan davolash boshlandi. Shu bilan birga, vertebral kestirib, metastaz topildi va Zetai 4 tsikli amalga oshirildi.
2. Birinchi marta klinik sinovlarda ishtirok etish, holat nazorat ostida.
In July 2010, Mr. Lu reexamined a large area of brain metastasis and found dozens of small lesions in the brain. He also tested positive for the EML4-ALK fusion gene at the University of Chicago School of Medicine. The whole brain radiation therapy was then used to control the lesions, and the second phase of crizotinib drug trial was started at St. Louis University Hospital. During the treatment, the condition was stably controlled, but a re-examination in May 2012 found that the cancer had progressed slightly, and the shish was suspected to be resistant to crizotinib. He stopped crizotinib on July 18, 2012.
3. Ikkinchi klinik sinovda o'simta aniq yo'qoldi.
On August 6, 2012, Mr. Lu participated in the AP26113 drug klinik tadqiqotlar at Denver Hospital. In October, the PET examination showed that the tumor disappeared and the miyada shish decreased and became large.
4. Noyob gen mutatsiyalarini kashf qiling va yangi klinik sinovlarda qatnashishni intiqlik bilan kuting
2014 yil iyul oyida qayta tekshirilganda, butun tanadagi PET shuni ko'rsatdiki: miya shikastlanishlari asosan barqaror, ko'krak qafasi esa aniq progressiv edi. 12-yil 2014-mayda AP26113 ga qarshi gumon qilingan limfa (3 hujayra, eng kattasi 1.1 sm) ekilgan hujayra liniyalari Massachusets umumiy kasalxonasida amalga oshirildi va AP26113 ni qabul qilishni davom ettirdi.
In August 2014, the doctor called and found that Mr. Lu’s new tumor tissue sequencing detected rare or unseen mutations. This mutation was only reported in ALK-positive children’s neyroblastoma and inflammatory myofibroblastoma. Previous research reports and medical evidence have shown that crizotinib cannot cope with the resistant neuroblastoma caused by this mutation. New genetic test results indicate that Mr. Lu may need to find new drugs for treatment.
On December 8, 2014, after a doctor’s analysis and decision, Mr. Lu was approved to increase the dosage of AP26113 and changed it to 240 mg per day, so the drug replacement plan was temporarily delayed. After observing the efficacy, he decided whether to change the drug and participate in other clinical trials. The patient learned through the hospital that NIVOLUMAB monoclonal antibody immunoterapiya phase 3/4 drug test is recruiting lung cancer patients on a large scale, and Mr. Lu is fully confident of the future anti-cancer.
