Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27638202
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Leveraging premalignant biology for immune-based cancer prevention
#MMPMID27638202
Spira A
; Disis ML
; Schiller JT
; Vilar E
; Rebbeck TR
; Bejar R
; Ideker T
; Arts J
; Yurgelun MB
; Mesirov JP
; Rao A
; Garber J
; Jaffee EM
; Lippman SM
Proc Natl Acad Sci U S A
2016[Sep]; 113
(39
): 10750-8
PMID27638202
show ga
Prevention is an essential component of cancer eradication. Next-generation
sequencing of cancer genomes and epigenomes has defined large numbers of driver
mutations and molecular subgroups, leading to therapeutic advances. By
comparison, there is a relative paucity of such knowledge in premalignant
neoplasia, which inherently limits the potential to develop precision prevention
strategies. Studies on the interplay between germ-line and somatic events have
elucidated genetic processes underlying premalignant progression and preventive
targets. Emerging data hint at the immune system's ability to intercept
premalignancy and prevent cancer. Genetically engineered mouse models have
identified mechanisms by which genetic drivers and other somatic alterations
recruit inflammatory cells and induce changes in normal cells to create and
interact with the premalignant tumor microenvironment to promote oncogenesis and
immune evasion. These studies are currently limited to only a few lesion types
and patients. In this Perspective, we advocate a large-scale collaborative effort
to systematically map the biology of premalignancy and the surrounding cellular
response. By bringing together scientists from diverse disciplines (e.g.,
biochemistry, omics, and computational biology; microbiology, immunology, and
medical genetics; engineering, imaging, and synthetic chemistry; and
implementation science), we can drive a concerted effort focused on cancer
vaccines to reprogram the immune response to prevent, detect, and reject
premalignancy. Lynch syndrome, clonal hematopoiesis, and cervical intraepithelial
neoplasia which also serve as models for inherited syndromes, blood, and viral
premalignancies, are ideal scenarios in which to launch this initiative.
|Germ Cells/metabolism
[MESH]
|Humans
[MESH]
|Immune System/pathology
[MESH]
|Models, Biological
[MESH]
|Neoplasm Proteins/metabolism
[MESH]
|Neoplasms/*immunology/*prevention & control
[MESH]
free
free
free
