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KIT ATP袋结构域的一个新突变导致胃肠间质肿瘤患者对伊马替尼获得性耐药

世界核心医学期刊文摘（胃肠病学分册） 2005年第2期1卷 28-28页

作者： tamborini e. Bonadiman L. Gre.o A. S. Pilotti 翟惠虹 U.of e.p. Mole.ular Pat hology Department of PathologyIst. Naz. Stud. e Al Cura dei Tumori Milan Ita ly

Background &Aims: Imatinib, a tyrosine.kinase.inhibitor of BCR-ABL, KIT, and plate.e.-de.ive. growth factor re.e.tor, is use. in patie.ts with chronic mye. oge.ous le.ke.ia (CML)and gastrointe.tinal stromal tumors (GIST). Primary and ac quire. re.istance.to the.drug can occur in both dise.se.. Mole.ular me.hanisms h ave.be.n re.orte. in CML and GIST for primary re.istance. whe.e.s e.te.sive.stud ie. on the.me.hanisms re.ponsible.for se.ondary re.istance.have.be.n almost e.cl usive.y re.orte. for CML. Me.hods: In a patie.t with advance. GIST unde.going im atinib the.apy,an isolate. progre.sing pe.itone.l mass was e.cise., along with 2 still-re.ponding le.ions. Comple.e.tary DNA and ge.omic DNA we.e.analyze. by s e.ue.cing for c-Kit ge.e.mutations. KIT re.e.tor e.pre.sion and phosphorylation status we.e.asse.se. by immunopre.ipitation and We.te.n blot. Transie.t-transf e.tion e.pe.ime.ts we.e.pe.forme. with mutage.ize. KIT constructs, and the.r act ivation status was asse.se.. Re.ults: In addition to an e.on11 mutation, share. among all of the.analyze. le.ions, a nove. point mutation in c-Kit e.on 14 re.u lting in T670I substitution was found only in the.progre.sing le.ion, which harb ore. aphosphorylate. re.e.tor, as oppose. to the.finding of an inactive.re.e.tor in re.ponding le.ions. Functional analyse. showe. that KIT/T670I is inse.sitive.to imatinib and that T670I mutation,introduce. in a re.e.tor re.ponding to imat inib, subve.te. its se.sitivity to the.drug. Conclusions: This ne. mutation was confine. to the.progre.sing le.ion; the.re.ulting amino acidic substitution, T67 0I, affe.ting the.ATP/imatinib pocke. of KIT,make. it inse.sitive.to the.drug. I nte.e.tingly, this substitution is a homologue.to the.T315I mutation alre.dy re. orte. in CML,whe.e.it is re.ponsible.for acquire. re.istance.to imatinib.

关键词：间质肿瘤 KIT ATP 伊马替尼获得性耐药结构域肾上腺素注射慢性髓性白血病免疫沉淀法消化性溃疡出血胶圈套扎

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The.soluble.glycoprote.n NMB(GPNMB)produce. by macrophage. induce. cance. ste.nne.s and me.astasis via CD44 and IL-33

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Ce.lular & Mole.ular Immunology 2021年第3期18卷 711-722页

作者： M.Liguori e.Digifico A.Vacchini R.Avigni F.S.Colombo e.M.Borroni F.M.Farina S.Milane.i A.Castagna L.Mannarino I.Craparotta S.Marchini e.e.ba N.Panini M.tamborini V.Rimoldi P.Allave.a C.Be.giovine IRCCS Humanitas Clinical and Re.e.rch Ce.te. Via Manzoni 5620089 RozzanoMlItaly De.artme.t of Biome.ical Scie.ce. Humanitas Universityvia Rita Levi Montalcini 420089 Pieve EmanueleItaly De.artme.t of Me.ical Biote.hnologie. and Translational Me.icine Universita degli Studi di MilanoVia Fratelli Cervi20090 SegrateItaly De.artme.t of Oncology Mario Negri Institute for Pharmacological Research IRCCS20156 MilanItaly

In cance.,mye.oid ce.ls have.tumor-supporting *** re.orte. that the.prote.n GPNMB(glycoprote.n nonme.astatic B)was profoundly upre.ulate. in macrophage. inte.acting with tumor ***,using mouse.tumor mode.s,we.show that macrophage.de.ive. soluble.GPNMB incre.se. tumor growth and me.astasis in Gpnmb-mutant mice.DBA/2J).GPNMB trigge.s in the.cance. ce.ls the.formation of se.f-re.e.ing sphe.oids,which are.characte.ize. by the.e.pre.sion of cance. ste. ce.l marke.s,prolonge. ce.l survival and incre.se. tumor-forming *** the.CD44 re.e.tor,GPNMB me.hanistically activate. tumor ce.ls to e.pre.s the.cytokine.IL-33 and its re.e.tor UR1L. We.also de.e.mine. that re.ombinant IL-33 binding to IL-1R1L is sufficie.t to induce.tumor sphe.oid formation with fe.ture. of cance. ste. ***,our re.ults re.e.l a ne. paracrine.axis,GPNMB and IL-33,which is activate. during the.cross talk of macrophage. with tumor ce.ls and e.e.tually promote. cance. ce.l survival,the.e.pansion of cance. ste. ce.ls and the.acquisition of a me.astatic phe.otype.

关键词： cance. ste. ce.ls GPNMB IL-33 me.astasis tumor associate. macrophage.

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