Iimbalasane
Kwi-AML ebuyela umva kunye nephikisayo ngokusinda kweminyaka emi-5 ye-25% kuphela, isifundo sonyango ngokuthelekisa unyango ekujoliswe kulo kunye ne-salvage cytotoxic chemotherapy ibonakalise unyango ekujolise kulo ngokusekwe kwi-genomic kunye ne-molecular profiling inokuba neziphumo ezingcono ezinamaxesha asezantsi eziganeko ezimbi, xa kuthelekiswa nekhemotherapy.
I-Acute Myeloid Leukemia (AML) yi a umhlaza yegazi kunye neeseli zomongo wethambo kwaye ichaphazela kakhulu abantu abadala. I-AML ibonakala ngokukhula okungalawulekiyo kunye nokugqithisileyo kwegazi elikhulayo elenza iiseli ze-myeloblast kumongo wethambo ezixinzelela ngaphandle kweeseli zegazi eziqhelekileyo. Injongo yonyango lwe-AML kukuphelisa zonke iiseli ze-leukemia ezingaqhelekanga kwaye ufumane isigulane kwi-remission. Nangona kunjalo, kwiimeko ezininzi, ukuba zonke iiseli ze-leukemia azizange zicinywe ngonyango, isifo sinokuphinda sibuyele emva kokuba sixolelwe ixesha elithile. Kwezinye izigulana, i-leukemia iyaxhathisa kumgangatho wonyango lwe-chemotherapy kwaye ithathwa njengento ephikisayo.
Ukutya okuTyiwa emva kokuChongwa koMhlaza!
Akukho mhlaza mibini ifanayo. Yiya ngaphaya kwezikhokelo zesondlo esiqhelekileyo kuwo wonke umntu kwaye wenze izigqibo ezizezakho malunga nokutya kunye nezongezo ngokuzithemba.
Kukuphi okungcono- unyango olujolisiweyo okanye iChemotherapy?
Kwiimeko ze-AML ebuyele umva okanye i-refractory, iprofayili ye-genomic ye-tumor inika ulwazi oluninzi kwiimpawu ze-molecular eziphantsi umhlaza ezinokuthi ke zinyangwe ngonyango ekujoliswe kulo. Enye into engaqhelekanga yofuzo efunyenwe kwi-30% yezigulane ze-AML yi-FMS-efana ne-tyrosine kinase 3 (FLT3) receptor, ukuba ikhona, ngumqhubi wesifo kunye nesizathu sokuchasana ne-chemotherapy (UPapaemmanuil E et al, Entsha Engl. UJ Med., 2016). Zimbini iintlobo eziphambili ze-FLT2 yokungaqheleki okuye kwafunyanwa kwi-AML genomes: ukuphindwaphindwa kwetand ye-FLT3 gene (ITD) okanye utshintsho kwi-tyrosine kinase domain ye-FLT3 gene (TKD). Zombini ezi mpazamo zikhokelela ekusebenziseni kakhulu indlela ye-FLT3 receptor signaling pathway eqhuba ukukhula okungalawulekiyo kwe-leukemia kwaye iyenze ukuba inganyamezeli kwimigangatho yokhetho lwe-chemotherapy. Ibhokisi yezixhobo ekujoliswe kuyo ngamachiza ahlukeneyo ngokhetho, amandla kunye nemisebenzi yeklinikhi, evunyiweyo okanye kuphuhliso lwe-FLT3 ye-AML eguqulweyo zezi:
- Midostaurin, iziyobisi ekujoliswe kuzo ezininzi, zamkelwe ngokudibeneyo kunye ne-7 + 3 esemgangathweni (icytarabine + daunorubicin) ichemotherapy kwizigulana ezisandula kufunyaniswa ukuba zine-AML enokutshintsha kwe-FLT3. Kodwa kwizigulana ezibuyise umva okanye ezinqabileyo kwi-AML, i-midostaurin ayibonisanga sibonelelo sonyango esihlala sihleli njengearhente enye. (Ilitye le-RM okqhubekayo, eNtsha Engl. UJ Med., 2017; Fisher T, et al, J Clin Ongo-2010)
- I-Sorafenib, enye ichiza elijolise kwi-kinase, ibonakalise imisebenzi yeklinikhi kwizigulana ezine-FLT3-mutated AML. (UBorthakur G, et al, Haematologica, 2011)
- I-Quizartinib, iklasi entsha ye-FLT3 inhibitor ekujoliswe kuyo ibonise umsebenzi we-arhente enye kwizigulana ezibuyileyo neziphikisayo ezine-FLT3-ITD kodwa impendulo yayihleli ixesha elifutshane ngenxa yokungajolisisi utshintsho lwe-FLT3 TKD olunokuvela ngexesha lonyango. (ICortes JE okqhubekayo, Lancet Oncol., 2019)
- I-Gilteritinib lelinye iklasi elitsha leziyobisi kuphuhliso lweklinikhi, ekhetha zombini utshintsho lwe-ITD kunye ne-TKD. Kwinqanaba 1-2 lokufundwa kweklinikhi, iipesenti ezingama-41 zezigulana ezinokubuyela umva kunye nokukhanyela i-AML zazinokuxolelwa ngokupheleleyo. (I-Perl AE, et al, iLancet Oncol., 2017)
Isigaba se-3 solingo lwezonyango olungenamsebenzi xa kuthelekiswa nefuthe lonyango ekujolise kulo uGilteritinib ngokuchasene ne-salvage chemotherapy kwi-371 ebuyileyo kunye ne-refractory ye-AML yezigulana (Trial No. NCT02421939). Kwizigulana ezingama-371 eziphinda zibuye zibuye zaphinde zaphika, i-247 yabelwa ngokungacwangciswanga kwiqela laseGilteritinib kunye ne-124 kwiqela lokusindisa i-chemotherapy. Umlinganiso wokubuyela umva kunye nokuphikisa kuwo omabini amaqela wawumalunga ne-60: 40. Ukhetho lokusindisa i-chemotherapy lwalulunyango oluphezulu kakhulu: iMitoxantrone, i-Etoposide, iCytarabine (MEC), okanye iFludarabine, iCytarabine, iGranulocyte colony-stimulating factor kunye ne-Idarubicin (FLAG-IDA); okanye ukhetho oluphantsi lonyango: idosi esezantsi yeCytarabine, okanye iAzacitidine. Iziphumo ezisandula ukupapashwa zolu vavanyo zibonise ukuba iqela ekujoliswe kulo kunyango kunye noGilteritinib lalinokusinda kwiinyanga eziyi-9.3 xa kuthelekiswa neenyanga ezi-5.6 neqela le-salvage chemotherapy. Kwakukho abaguli abangama-34% abafumene ukuxolelwa okupheleleyo kunye nokubuyiswa okupheleleyo okanye okupheleleyo kwe-hematologic kwiqela laseGilteritinib, ngelixa kuphela i-15.3% kwiqela le-chemotherapy. Kwakhona, iziganeko ezibi kakhulu zebanga lesi-3 okanye ngaphezulu ziye zafunyanwa zivela qho kwiqela ekujoliswe kulo kwiqela le-chemotherapy (I-Perl AE, et al, Entsha Engl. UJ Med., 2019).
Idatha engentla ixhasa ukuba koku kunzima ukunyanga i-AML ebuyayo kunye nephikisayo ngesifo esingalunganga kunye nokusinda kweminyaka emi-5 kuphela, unyango ekujolise kulo ngokusekwe kwiprofayili ye-genomic kunye nemolekyuli inokuba neziphumo ezingcono kunye nokuhamba rhoqo kweziganeko ezimbi, xa kuthelekiswa nokuqhubeka Unyango lwe-chemotherapy.
Kukuphi ukutya okutyayo kwaye okuncedisayo kukuthatha sisigqibo osithathayo. Isigqibo sakho kufuneka sibandakanye ukuthathelwa ingqalelo kotshintsho lomhlaza kuhlobo lomhlaza, unyango oluqhubekayo kunye nezongezelelo, nakuphi na ukwaliwa, ulwazi ngobomi bakho, ubunzima, ukuphakama kunye nemikhwa.
Isicwangciso sesondlo somhlaza esivela kwi-addon asisekelwanga kukhangelo lwe-Intanethi. Isebenza ngokuzenzekelayo ukwenza izigqibo zakho kusekwe kwisayensi yemolekyuli ephunyezwe ngoososayensi kunye neenjineli zesoftware. Nokuba ukhathalele na ukuqonda iindlela ezisisiseko seemolekyuli okanye hayi - zokucwangciswa kwesondlo somhlaza ukuqonda kuyafuneka.
Qalisa NGOKU ngokucwangciswa kwesondlo ngokuphendula imibuzo ngegama lomhlaza, uguquko kwimfuza, unyango oluqhubekayo kunye nezincedisi, nakuphi na ukwaliwa, imikhwa, indlela yokuphila, iqela lobudala kunye nesini.
ISondlo esiSiqu soMhlaza!
Umhlaza uyatshintsha ngokuhamba kwexesha. Yenza ngokwezifiso kwaye uguqule isondlo sakho ngokusekwe kwisalathiso somhlaza, unyango, indlela yokuphila, ukhetho lokutya, i-allergies kunye nezinye izinto.
Izigulana ezinomhlaza zihlala zisebenza ngeendlela ezahlukeneyo iziphumo ebezingalindelekanga ezichaphazela umgangatho wobomi babo kwaye bajonge ezinye iindlela zonyango lomhlaza. Ukuthatha isondlo esifanelekileyo kunye nezongezelelo ezisekwe kuqwalaselo lwenzululwazi (ukuphepha ukuqagela kunye nokukhetha okungakhethiyo) lolona nyango lulungileyo lwendalo umhlaza kunye neziphumo ebezingalindelekanga ezinxulumene nonyango.