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Glioma progression is shaped by genetic evolution and microenvironment interactions.

Glioma progression is shaped by genetic evolution and microenvironment interactions.

Authors :
Varn, Frederick S
Varn, Frederick S
Johnson, Kevin C
Martinek, Jan
Huse, Jason T
Nasrallah, MacLean P
Wesseling, Pieter
Cooper, Lee AD
Malta, Tathiane M
Wade, Taylor E
Sabedot, Thais S
Brat, Daniel
Gould, Peter V
Wöehrer, Adelheid
Aldape, Kenneth
Ismail, Azzam
Sivajothi, Santhosh K
Barthel, Floris P
Kim, Hoon
Kocakavuk, Emre
Ahmed, Nazia
White, Kieron
Datta, Indrani
Moon, Hyo-Eun
Pollock, Steven
Goldfarb, Christine
Lee, Ga-Hyun
Garofano, Luciano
Anderson, Kevin J
Nehar-Belaid, Djamel
Barnholtz-Sloan, Jill S
Bakas, Spyridon
Byrne, Annette T
D'Angelo, Fulvio
Gan, Hui K
Khasraw, Mustafa
Migliozzi, Simona
Ormond, D Ryan
Paek, Sun Ha
Van Meir, Erwin G
Walenkamp, Annemiek ME
Watts, Colin
Weiss, Tobias
Weller, Michael
Palucka, Karolina
Stead, Lucy F
Poisson, Laila M
Noushmehr, Houtan
Iavarone, Antonio
Verhaak, Roel GW
GLASS Consortium
Varn, Frederick S
Varn, Frederick S
Johnson, Kevin C
Martinek, Jan
Huse, Jason T
Nasrallah, MacLean P
Wesseling, Pieter
Cooper, Lee AD
Malta, Tathiane M
Wade, Taylor E
Sabedot, Thais S
Brat, Daniel
Gould, Peter V
Wöehrer, Adelheid
Aldape, Kenneth
Ismail, Azzam
Sivajothi, Santhosh K
Barthel, Floris P
Kim, Hoon
Kocakavuk, Emre
Ahmed, Nazia
White, Kieron
Datta, Indrani
Moon, Hyo-Eun
Pollock, Steven
Goldfarb, Christine
Lee, Ga-Hyun
Garofano, Luciano
Anderson, Kevin J
Nehar-Belaid, Djamel
Barnholtz-Sloan, Jill S
Bakas, Spyridon
Byrne, Annette T
D'Angelo, Fulvio
Gan, Hui K
Khasraw, Mustafa
Migliozzi, Simona
Ormond, D Ryan
Paek, Sun Ha
Van Meir, Erwin G
Walenkamp, Annemiek ME
Watts, Colin
Weiss, Tobias
Weller, Michael
Palucka, Karolina
Stead, Lucy F
Poisson, Laila M
Noushmehr, Houtan
Iavarone, Antonio
Verhaak, Roel GW
GLASS Consortium
Source :
Cell; vol 185, iss 12, 2184-2199.e16; 0092-8674
Publication Year :
2022

Abstract

The factors driving therapy resistance in diffuse glioma remain poorly understood. To identify treatment-associated cellular and genetic changes, we analyzed RNA and/or DNA sequencing data from the temporally separated tumor pairs of 304 adult patients with isocitrate dehydrogenase (IDH)-wild-type and IDH-mutant glioma. Tumors recurred in distinct manners that were dependent on IDH mutation status and attributable to changes in histological feature composition, somatic alterations, and microenvironment interactions. Hypermutation and acquired CDKN2A deletions were associated with an increase in proliferating neoplastic cells at recurrence in both glioma subtypes, reflecting active tumor growth. IDH-wild-type tumors were more invasive at recurrence, and their neoplastic cells exhibited increased expression of neuronal signaling programs that reflected a possible role for neuronal interactions in promoting glioma progression. Mesenchymal transition was associated with the presence of a myeloid cell state defined by specific ligand-receptor interactions with neoplastic cells. Collectively, these recurrence-associated phenotypes represent potential targets to alter disease progression.

Details

Database :
OAIster
Journal :
Cell; vol 185, iss 12, 2184-2199.e16; 0092-8674
Notes :
application/pdf, Cell vol 185, iss 12, 2184-2199.e16 0092-8674
Publication Type :
Electronic Resource
Accession number :
edsoai.on1391573121
Document Type :
Electronic Resource