Kev Nkag Siab Txog Cov Hom Phiaj Genetic ntawm Cov Neeg Laus B-ALL

Lub Ib Hlis 15, 2025, Shanghai - Ib qho kev tshuaj xyuas tsis ntev los no tau luam tawm hauv phau ntawv xov xwm Ntshav muab kev tshuaj xyuas tob txog cov noob caj noob ces ntawm cov neeg laus B-cell Acute Lymphoblastic Leukemia (B-ALL), uas yog ib qho mob qog nqaij hlav tsis tshua muaj thiab hnyav nrog kev kwv yees tsis zoo hauv cov neeg laus piv rau cov menyuam yaus. Tau ob xyoo dhau los, kev tshawb fawb txog genomic tau txheeb xyuas ntau dua 20 hom noob caj noob ces sib txawv ntawm B-ALL, txhua tus muaj cov txiaj ntsig tshwj xeeb rau kev teb rau kev kho mob thiab kev kwv yees.

Txawm hais tias kev kho mob uas hloov kho raws li kev pheej hmoo ntawm cov noob caj noob ces tau hloov pauv txoj kev kho mob hauv cov menyuam yaus B-ALL, tab sis cov neeg laus B-ALL tseem tsis tau nkag siab zoo. Daim ntawv tshuaj xyuas no qhia txog kev nkag siab tseem ceeb txog kev sib txawv ntawm cov noob caj noob ces hauv cov neeg laus thiab hais txog qhov xav tau kev koom ua ke ntawm kev txheeb xyuas noob caj noob ces rau hauv kev kuaj mob niaj hnub kom ua tau raws li cov tswv yim kho mob rau tus kheej.

Cov Ntsiab Lus Tseem Ceeb:

1. Philadelphia Chromosome-Positive (Ph+) B-ALL:
   Sawv cev rau hom kab mob uas pom ntau tshaj plaws hauv cov neeg laus, tshwj xeeb tshaj yog cov neeg hnub nyoog tshaj 55 xyoos, Ph+ B-ALL yog los ntawm BCR::ABL1 fusion gene. Keeb kwm cuam tshuam nrog kev kwv yees tsis zoo, kev koom ua ke ntawm tyrosine kinase inhibitors (TKIs) thiab cov tshuaj monoclonal antibodies, xws li blinatumomab, tau txhim kho cov nqi ciaj sia. Cov pov thawj tshiab qhia txog kev sib txawv ntawm cov kab mob hauv Ph+ B-ALL, qhia txog qhov tseem ceeb ntawm cov cim molecular zoo li IKZF1 rau kev faib cov kev pheej hmoo thiab kev npaj kho mob.

2. Kev Hloov Pauv Hypodiploidy Tsawg thiab TP53:
   Qhov hypodiploidy qis, uas muaj tus lej chromosomal ntawm 30-39, yog qhov tshwm sim ntau dua rau cov neeg laus thiab muaj feem cuam tshuam nrog cov txiaj ntsig tsis zoo. Cov kev tshawb fawb tsis ntev los no qhia txog lub luag haujlwm ntawm TP53 mutations, feem ntau cuam tshuam nrog clonal hematopoiesis, hauv kev tsav tsheb no subtype muaj kev pheej hmoo siab. Cov kev tshawb pom qhia tias cov mutations no tsis yog tsuas yog cuam tshuam rau qhov pib ntawm tus kab mob tab sis kuj tseem yuav qhia txog cov tswv yim tom qab kev zam txim.

3. Kev Hloov Kho KMT2A:
   Feem ntau pom muaj nyob rau hauv cov neeg laus B-ALL, KMT2A rearrangements txuas nrog rau cov txiaj ntsig tsis zoo. Cov kev kho mob tshiab, xws li menin inhibitors, muaj kev cia siab rau kev daws qhov teeb meem kev tiv thaiv kev kho mob ntawm cov subtype no.

4. Cov Hom Mob Tsis Tshua Muaj Thiab Cov Kev Kho Mob Tshiab:
   Cov hom kab mob me xws li TCF3::PBX1 thiab TCF3::HLF fusions, txawm tias tsis tshua muaj, qhia txog ntau yam kab mob thiab kev kho mob. Cov ntaub ntawv preclinical txhawb kom pom tias lawv muaj kev rhiab heev rau cov tshuaj tshiab xws li venetoclax thiab BET inhibitors, uas yog txoj hauv kev rau cov kev kho mob tshiab.

Cov Kev Cuam Tshuam Hauv Kev Kho Mob:

Daim kev tshuaj xyuas no hu kom muaj kev siv cov txheej txheem txheeb xyuas cov noob caj noob ces zoo heev, suav nrog kev txheeb xyuas cov noob caj noob ces tag nrho, los txheeb xyuas cov noob caj noob ces tshwj xeeb ntawm cov neeg laus B-ALL. Txoj hauv kev no tuaj yeem txhim kho kev faib cov kev pheej hmoo, coj kev txiav txim siab kho mob, thiab txhim kho kev saib xyuas cov kab mob seem tsawg kawg nkaus (MRD).