Ciwon_Huhun_Daji
Umarnin Bincike
Umarnin bincike Ana ci gaba da neman sabbin zaɓuɓɓukan magani. Yawancin gwaje-gwaje na asibiti da suka haɗa da aikin rediyo, tiyata, masu hana EGFR, masu hana microtubule da immunotherapy suna gudana a halin yanzu.[206] Umarnin bincike don maganin ciwon huhu na huhu sun haɗa da immunotherapy, [207] [208] wanda ke ƙarfafa tsarin garkuwar jiki don kai hari ga ƙwayoyin tumo, epigenetics, da sabon haɗin chemotherapy da radiotherapy, duka a kan kansu kuma tare. Yawancin waɗannan sabbin jiyya suna aiki ta hanyar toshe wuraren bincike na rigakafi, suna ɓata ikon kansa na guje wa tsarin garkuwar jiki.[207][208] Ipilimumab yana toshe sigina ta hanyar mai karɓa akan ƙwayoyin T da aka sani da CTLA-4, wanda ke lalata tsarin rigakafi. Hukumar Abinci da Magunguna ta Amurka ta amince da ita don maganin cutar sankarau, kuma tana fuskantar gwaji na asibiti na NSCLC da SCLC.[207] Sauran jiyya na immunotherapy suna tsoma baki tare da ɗaure furotin da aka tsara na mutuwar kwayar halitta 1 (PD-1) tare da ligand PD-1 ligand 1 (PD-L1), kuma an yarda da su azaman jiyya na farko- da na gaba-gaba don ɓangarori daban-daban na cututtukan huhu. [208] Yin sigina ta hanyar PD-1 yana hana ƙwayoyin T. Wasu ƙwayoyin kansa suna bayyana suna amfani da wannan ta hanyar bayyana PD-L1 don kashe ƙwayoyin T waɗanda zasu iya gane su a matsayin barazana. Monoclonal rigakafi da ke niyya duka PD-1 da PD-L1, irin su pembrolizumab, nivolumab, [65] atezolizumab, da durvalumab[208] a halin yanzu suna cikin gwaji na asibiti don maganin ciwon huhu.[207][208] Epigenetics shine nazarin ƙananan gyare-gyaren kwayoyin halitta - ko "tags" - waɗanda ke ɗaure ga DNA kuma suna canza matakan bayyanar kwayoyin halitta. Yin niyya ga waɗannan alamun da kwayoyi na iya kashe ƙwayoyin cutar kansa. Binciken farko-farko a cikin NSCLC ta amfani da kwayoyi da ke nufin gyare-gyaren epigenetic ya nuna cewa toshe fiye da ɗaya daga cikin waɗannan alamun zai iya kashe kwayoyin cutar kansa tare da ƙananan sakamako masu illa.[209] Nazarin ya kuma nuna cewa ba wa mutane waɗannan magungunan kafin daidaitaccen magani na iya inganta tasirinsa. Ana gudanar da gwaje-gwaje na asibiti don tantance yadda waɗannan magungunan ke kashe ƙwayoyin cutar kansar huhu a cikin mutane.[209] Magunguna da yawa waɗanda ke da alaƙa da hanyoyin epigenetic suna cikin haɓakawa. Histone deacetylase inhibitors a cikin ci gaba sun haɗa da valproic acid, vorinostat, belinostat, panobinostat, entinostat, da romidepsin. Masu hana DNA methyltransferase a cikin haɓakawa sun haɗa da decitabine, azacytidine, da hydralazine.[61] Aikin TRACERx yana duban yadda NSCLC ke tasowa da haɓakawa, da kuma yadda waɗannan ciwace-ciwacen suka zama masu jure wa jiyya.[210] Aikin zai duba samfuran ƙari daga mutane 850 masu NSCLC a matakai daban-daban ciki har da ganewar asali, bayan jiyya na farko, bayan magani, da sake dawowa.[211]. Ta hanyar nazarin samfurori a wurare daban-daban na ci gaban ƙwayar cuta, masu binciken suna fatan gano canje-canjen da ke haifar da ci gaban ƙwayar cuta da juriya ga jiyya. Sakamakon wannan aikin zai taimaka wa masana kimiyya da likitoci su sami kyakkyawar fahimta game da NSCLC da yiwuwar haifar da ci gaba da sababbin magungunan cutar.[210]. Don cututtukan daji na huhu waɗanda ke haɓaka juriya ga mai karɓar haɓakar haɓakar epidermal (EGFR) da anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors, sabbin magunguna suna cikin haɓakawa. Masu hana EGFR sun haɗa da erlotinib, gefitinib, afatinib da icotinib (na ƙarshe yana samuwa a China kawai).[146] Madadin hanyar sigina, c-Met, na iya hana tivantinib da onartuzumab. Sabbin masu hana ALK sun haɗa da crizotinib da ceritinib.[212] Idan hanyar MAPK/ERK ta shiga, mai hana BRAF kinase dabrafenib da MAPK/MEK inhibitor trametinib na iya zama da amfani.[213] An bincika hanyar PI3K azaman manufa don maganin ciwon huhu. Mafi kyawun dabarun tunkarar wannan tafarki kamar hanawa ɗaya ko fiye da membobi na aji I PI3Ks ne, tare da hana wannan hanyar tare da wasu kamar MEK[214]. Kwayoyin ciwon daji na huhu galibi suna jure wa na al'ada.