ly ▁create ▁a ▁clone ( s ) ▁of ▁pl asma ▁cells ▁that ▁cause ▁the ▁more ▁serious ▁but ▁still ▁prem align ant ▁dis order ▁of ▁sm older ing ▁multiple ▁my el oma , ▁over t ▁my el oma ▁cancer , ▁and ▁ultimately ▁s P CL . ▁In ▁contrast ▁to ▁s P CL , ▁p P CL ▁presents ▁de ▁nov o ▁with ▁a ▁broad ▁range ▁of ▁gen etic ▁ab normal ities . ▁For ▁example , ▁advanced ▁methods ▁for ▁exam ining ▁the ▁gen ome ▁viz ., ▁whole - ex ome ▁sequ encing ▁and ▁gene ▁expression ▁profil ing , ▁have ▁identified ▁ 1 6 6 ▁non - sil ent ▁gene ▁variants ▁per ▁p P CL ▁patient ▁sample ▁at ▁the ▁time ▁of ▁diagn osis . ▁These ▁ab normal ities ▁are ▁similar ▁but ▁not ▁identical ▁to ▁those ▁detected ▁in ▁s P CL ▁while ▁the ▁ab normal ies ▁detected ▁in ▁s P CL ▁more ▁closely ▁res emble ▁those ▁detected ▁in ▁multiple ▁my el oma ▁than ▁do ▁those ▁of ▁p P CL : ▁the ▁gen etic ▁data ▁support ▁the ▁clin ical ▁data ▁in ▁suggesting ▁that ▁s P CL ▁and ▁p P CL ▁are ▁distinct ▁dise ases ▁with ▁s P CL ▁among ▁the ▁two ▁P CL s ▁being ▁more ▁closely ▁related ▁to ▁multiple ▁my el oma . ▁Ex am ination ▁of ▁pl asma ▁cell ▁imm un oph en ot ype ▁by ▁meas uring ▁certain ▁of ▁their ▁cell ▁surface ▁ant ig ens , ▁particularly ▁Cl uster ▁of ▁different iation . ▁CD ▁markers ▁on ▁pl asma ▁cells ▁from ▁patients ▁with ▁p P CL ▁differ