Kupisa uye kunotonhora pancreatic kenza mamota

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Boka rekutsvagisa kubva kuAbramson Cancer Center (ACC) paYunivhesiti yePennsylvania Chikoro cheMishonga chakawana kuti bundu rinopisa kana kutonhora rinotemwa neruzivo rwakaiswa mumaseru egomarara pachawo. “Hot” tumors are often considered more sensitive to immunotherapy. In a new study published this week in Immunity, the researchers explored the role of “tumor heterogeneity”, namely the ability of tumor cells to move, replicate, metastasize and respond to treatment. These new findings can help oncologists more accurately tailor the unique tumarara composition of patients.

Ben Stanger, purofesa we gastroenterology uye cell uye yekuvandudza biology paUniversity yePennsylvania Perelman Chikoro cheMishonga, akataura kuti mwero uyo masero eT anokwezva kumamota anotariswa neakazvarwa-chaiwo majini. Kuti mamota akure, vanofanirwa kudzivirira kurwiswa nema immune system. Pane nzira mbiri: kukura kuva mamota anotonhora, kana mapundu anopisa anogona kupedza masero eT, achinyatso chengetedza maseru emota kubva mukukuvara kune immune system yemurwere.

In this study, researchers found that whether a tumor is hot or cold determines whether it will respond to immunotherapy. Cold tumor cells produce a compound called CXCL1, which can instruct bone marrow cells to enter the tumor, keep T cells away from the tumor, and ultimately make the immunotherapy insensitive. In contrast, knocking out CXCL1 in cold tumors promotes T cell infiltration and sensitivity to immunotherapy.

Chikwata chakagadzira nhevedzano yemasero mitsara inoteedzera hunhu hwepancreatic tumors, kusanganisira mhando dzemaseru ekudzivirira avanayo. Mune ramangwana, idzi tumarara maseru mitsara inogona kubatsira kuwedzera kuzivisa uye kugadzirisa kurapwa kweakasarudzika madiki evarwere vane akasiyana bundu heterogeneity nyika.

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