Sci­en­tists make im­por­tant pan­cre­atic can­cer dis­cov­ery

Miami Herald - - FRONT PAGE -

NEW YORK — Sci­en­tists at Cold Spring Har­bor Lab­o­ra­tory have dis­cov­ered a key bi­o­log­i­cal mech­a­nism that drives the spread of pan­cre­atic can­cer and helps ex­plain why one of the most com­mon forms of the dis­ease is so deadly.

The re­searchers, in the just-re­leased is­sue of the jour­nal Cell, de­scribe how work­ing with tiny pan­cre­atic organoids — minia­ture liv­ing mod­els of the pan­creas — led to their sig­nif­i­cant step in un­der­stand­ing DNA se­quences that un­der­lie the spread of pan­cre­atic duc­tal car­ci­noma.

Can­cer of the pan­creas has the rep­u­ta­tion of be­ing one of the most lethal ma­lig­nan­cies be­cause of its over­whelm­ing ten­dency to metas­ta­size, spread­ing to sites be­yond the gland it­self, re­searchers said.

Pan­cre­atic duc­tal can­cer, a widely di­ag­nosed form of the dis­ease, of­ten is called a “silent killer” be­cause it pro­duces no overt symp­toms in its early de­vel­op­ment.

There is no method of rou­tine screen­ing to de­tect the ma­lig­nancy in its ear­li­est evo­lu­tion. By the time most pan­cre­atic duc­tal can­cers are found, the dis­ease al­ready has spread else­where in the body.

Cold Spring Har­bor Lab­o­ra­tory sci­en­tists in the lab of Dr. David Tu­ve­son, di­rec­tor of can­cer ther­a­peu­tics, un­masked one of the can­cer’s long­est-held se­crets: Pan­cre­atic can­cer spreads be­cause metastatic cells carry short se­quences of DNA, called en­hancers, that drive the can­cer’s spread.

Th­ese DNA en­hancers are not ev­i­dent in “pri­mary” pan­cre­atic tu­mor cells, which make up the can­cer in its ear­li­est stages of evo­lu­tion.

Th­ese en­hancers, the sci­en­tists found, ac­tively di­rect the can­cer’s spread be­yond the pan­creas.

“We show that to metas­ta­size, the cell has to change. In ef­fect, its whole telecom­mu­ni­ca­tions net­work — its en­hancers — are be­ing re­pro­grammed,” Dr. Christo­pher Vakoc, a co-au­thor of the study, said in a state­ment.

The team was able to de­ci­pher the role that the en­hancers play by de­vel­op­ing organoids that were both repli­cas of pri­mary tu­mor cells and repli­cas of metastatic ones — those that pos­sess the wan­der­lust to travel to dis­tant sites, he said.

In the lab­o­ra­tory, organoids are small, glis­ten­ing spheres, whether pri­mary or metastatic. Each pint-size organoid is about the size of the pe­riod at the end of a sen­tence.

The minia­ture mod­els al­low re­searchers to un­der­stand why the can­cer forms in the first place and how it re­ceives ge­netic mes­sages to spread.

Tu­ve­son also is di­rec­tor of re­search for The Lust­garten Foun­da­tion, the na­tion’s largest pri­vate sup­porter of pan­cre­atic can­cer sci­en­tific and med­i­cal re­search. He has long said that can­cer of the pan­creas is one of the most con­found­ing hu­man dis­eases. Only 7 per­cent of pa­tients sur­vive five years af­ter di­ag­no­sis.

This year, the can­cer is ex­pected to be di­ag­nosed in about 53,070 peo­ple na­tion­wide — about 27,670 men and 25,400, ac­cord­ing to the Amer­i­can Can­cer So­ci­ety.

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