Ukuqonda okutsha kwiintlobo zezakhi zofuzo zabantu abadala i-B-ALL

Ngomhla we-15 kweyoMqungu, ngowama-2025, eShanghai – Uphononongo lwakutshanje olupapashwe kwijenali Igazi Inika uhlalutyo olunzulu lwee-subtypes ze-genetic ze-B-cell Acute Lymphoblastic Leukemia (B-ALL) yabantu abadala, isifo esingaqhelekanga nesinobundlongondlongo esinokubangela i-prognosis embi kakhulu kubantu abadala xa kuthelekiswa nabantwana. Kwiminyaka engamashumi amabini edlulileyo, uphando lwe-genomic luchonge ii-subtypes ze-genetic ezingaphezu kwama-20 ezahlukeneyo ze-B-ALL, nganye ineempembelelo ezizodwa kwimpendulo yonyango kunye ne-prognosis.

Nangona unyango oluhlengahlengiswe ngumzimba luye lwaguqula iindlela zonyango kwi-B-ALL yabantwana, imeko yemfuza ye-B-ALL yabantu abadala ayikaqondwa kakuhle. Olu phononongo lubonisa ukuqonda okubalulekileyo malunga nokwahluka kwezinto eziphilayo ze-subtypes zemfuza kwizigulane zabantu abadala kwaye lugxininisa imfuneko yokudibanisa iprofayili yemfuza kuxilongo oluqhelekileyo ukuze kuvunyelwe iindlela zonyango ezenzelwe wena.

Iziphumo eziphambili:

1. I-Philadelphia Chromosome-Positive (Ph+) B-ALL:
   Imele uhlobo oluqhelekileyo kubantu abadala, ingakumbi abo bangaphezulu kweminyaka engama-55, i-Ph+ B-ALL ivela kwi-BCR::ABL1 fusion gene. Ngokwembali enxulunyaniswa nokubikezela okubi, ukuhlanganiswa kwe-tyrosine kinase inhibitors (TKIs) kunye nee-antibodies ze-monoclonal ezijoliswe kuzo, ezifana ne-blinatumomab, kuye kwaphucula kakhulu amazinga okusinda. Ubungqina obuvelayo bubonisa ukungafani okukhulu kwebhayoloji ngaphakathi kwe-Ph+ B-ALL, nto leyo egxininisa ukubaluleka kweempawu ze-molecular ezifana ne-IKZF1 zokuhluzwa komngcipheko kunye nocwangciso lonyango.

2. Utshintsho oluphantsi lwe-Hypodiploidy kunye ne-TP53:
   I-hypodiploidy ephantsi, ebonakaliswa yi-chromosome count ye-30-39, ixhaphake kakhulu kubantu abadala kwaye ihambelana neziphumo ezimbi. Izifundo zakutshanje zibonisa indima ye-TP53 mutations, edla ngokunxulunyaniswa ne-clonal hematopoiesis, ekuqhubeni olu hlobo lunobungozi obukhulu. Iziphumo zibonisa ukuba olu tshintsho aluphembeleli nje kuphela ukuqala kwesifo kodwa lunokwazisa neendlela zokulungisa emva kokukhululwa kwisifo.

3. Uhlengahlengiso lwe-KMT2A:
   Okubonwa rhoqo kwi-B-ALL yabantu abadala, ukuhlelwa kwakhona kwe-KMT2A kunxulunyaniswa neziphumo ezimbi. Iindlela ezintsha zonyango, ezifana nezithinteli ze-menin, zithembisa ukujongana nokunganyangeki konyango okuqhelekileyo kolu hlobo.

4. Iintlobo eziNcinci ezingaqhelekanga kunye noNyango oluvelayo:
   Iintlobo ezincinci ezifana ne-TCF3::PBX1 kunye ne-TCF3::HLF fusions, nangona zinqabile, zibonisa umahluko omkhulu webhayoloji kunye noweklinikhi. Ukukhuthaza idatha yangaphambi kweklinikhi kubonisa uvakalelo kwiiarhente ezintsha ezifana ne-venetoclax kunye ne-BET inhibitors, zivula indlela yeendlela ezintsha zonyango.

Iziphumo zeKlinikhi:

Olu phononongo lufuna ukubandakanywa rhoqo kweendlela eziphambili zokuchonga i-genomic, kuquka ulandelelwano lwe-whole-transcriptome, ukuze kuchongwe iintlobo ezithile ze-genetic ze-B-ALL yabantu abadala. Le ndlela inokuphucula ukwahlulwahlulwa komngcipheko, ikhokhele izigqibo zonyango, kwaye iphucule ukujonga isifo esincinci esisele (MRD).