MétaCan
← all works

Timing the Landmark Events in the Evolution of Clear Cell Renal Cell Cancer: TRACERx Renal

2018· article· en· 560 citations· W2797702016 on OpenAlex· 10.1016/j.cell.2018.02.020

Why is this work in the frame?

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

No Canadian affiliation. An affiliation-only frame — the usual design — would never have seen this work. It is one of the works that make the case for inverting the frame.

Machine scores (provisional)

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Opus teacher head0.024
GPT teacher head0.264
Teacher spread
0.240 · how far apart the two teachers sit on this one work
Validation status
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Abstract

Clear cell renal cell carcinoma (ccRCC) is characterized by near-universal loss of the short arm of chromosome 3, deleting several tumor suppressor genes. We analyzed whole genomes from 95 biopsies across 33 patients with clear cell renal cell carcinoma. We find hotspots of point mutations in the 5' UTR of TERT, targeting a MYC-MAX-MAD1 repressor associated with telomere lengthening. The most common structural abnormality generates simultaneous 3p loss and 5q gain (36% patients), typically through chromothripsis. This event occurs in childhood or adolescence, generally as the initiating event that precedes emergence of the tumor's most recent common ancestor by years to decades. Similar genomic changes drive inherited ccRCC. Modeling differences in age incidence between inherited and sporadic cancers suggests that the number of cells with 3p loss capable of initiating sporadic tumors is no more than a few hundred. Early development of ccRCC follows well-defined evolutionary trajectories, offering opportunity for early intervention.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

The record

Venue
Cell
Topic
Renal cell carcinoma treatment
Field
Medicine
Canadian institutions
Funders
European Research CouncilInstitute of Cancer ResearchMedical Research CouncilCancer Research UKUniversity of CambridgeNovo Nordisk FondenBreast Cancer Research FoundationRosetrees TrustUniversity College LondonNational Institute for Health and Care ResearchWellcome TrustFrancis Crick InstituteProstate Cancer Foundation
Keywords
BiologyLandmarkCellKidney cancerCancerKidneyCancer researchGeneticsCartography
Has abstract in OpenAlex
yes