Pancreatic Cancer Research beyond DNA Mutations

Hiromichi Sato; Kazuki Sasaki; Tomoaki Hara; Yoshiko Tsuji; Yasuko Arao; Chihiro Otsuka; Yumiko Hamano; Mirei Ogita; Shogo Kobayashi; Eric di Luccio; Takaaki Hirotsu; Yuichiro Doki; Hidetoshi Eguchi; Taroh Satoh; Shizuka Uchida; Hideshi Ishii

doi:10.3390/biom12101503

Pancreatic Cancer Research beyond DNA Mutations

Hiromichi Sato, Kazuki Sasaki, Tomoaki Hara, Yoshiko Tsuji, Yasuko Arao, Chihiro Otsuka, Yumiko Hamano, Mirei Ogita, Shogo Kobayashi, Eric di Luccio, Takaaki Hirotsu, Yuichiro Doki, Hidetoshi Eguchi, Taroh Satoh, Shizuka Uchida^*, Hideshi Ishii^*

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

5 Downloads (Pure)

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is caused by genetic mutations in four genes: KRAS proto-oncogene and GTPase (KRAS), tumor protein P53 (TP53), cyclin-dependent kinase inhibitor 2A (CDKN2A), and mothers against decapentaplegic homolog 4 (SMAD4), also called the big 4. The changes in tumors are very complex, making their characterization in the early stages challenging. Therefore, the development of innovative therapeutic approaches is desirable. The key to overcoming PDAC is diagnosing it in the early stages. Therefore, recent studies have investigated the multifaced characteristics of PDAC, which includes cancer cell metabolism, mesenchymal cells including cancer-associated fibroblasts and immune cells, and metagenomics, which extend to characterize various biomolecules including RNAs and volatile organic compounds. Various alterations in the KRAS-dependent as well as KRAS-independent pathways are involved in the refractoriness of PDAC. The optimal combination of these new technologies is expected to help treat intractable pancreatic cancer.

Original language	English
Article number	1503
Journal	Biomolecules
Volume	12
Issue number	10
ISSN	2218-273X
DOIs	https://doi.org/10.3390/biom12101503
Publication status	Published - Oct 2022

Keywords

Carcinoma, Pancreatic Ductal/metabolism
Cyclin-Dependent Kinases/metabolism
DNA/therapeutic use
Humans
Mutation
Pancreatic Neoplasms/metabolism
Proto-Oncogene Proteins p21(ras)/genetics
Tumor Suppressor Protein p53/metabolism
Volatile Organic Compounds
RNA
pancreatic ductal adenocarcinoma
sequencing
cancer metabolism
mutations

Access to Document

10.3390/biom12101503Licence: CC BY 4.0

Open Access articleFinal published version, 3.04 MBLicence: CC BY 4.0

Cite this

@article{a6f094fbedab445883b1b79e0b7fe599,

title = "Pancreatic Cancer Research beyond DNA Mutations",

abstract = "Pancreatic ductal adenocarcinoma (PDAC) is caused by genetic mutations in four genes: KRAS proto-oncogene and GTPase (KRAS), tumor protein P53 (TP53), cyclin-dependent kinase inhibitor 2A (CDKN2A), and mothers against decapentaplegic homolog 4 (SMAD4), also called the big 4. The changes in tumors are very complex, making their characterization in the early stages challenging. Therefore, the development of innovative therapeutic approaches is desirable. The key to overcoming PDAC is diagnosing it in the early stages. Therefore, recent studies have investigated the multifaced characteristics of PDAC, which includes cancer cell metabolism, mesenchymal cells including cancer-associated fibroblasts and immune cells, and metagenomics, which extend to characterize various biomolecules including RNAs and volatile organic compounds. Various alterations in the KRAS-dependent as well as KRAS-independent pathways are involved in the refractoriness of PDAC. The optimal combination of these new technologies is expected to help treat intractable pancreatic cancer.",

keywords = "Carcinoma, Pancreatic Ductal/metabolism, Cyclin-Dependent Kinases/metabolism, DNA/therapeutic use, Humans, Mutation, Pancreatic Neoplasms/metabolism, Proto-Oncogene Proteins p21(ras)/genetics, Tumor Suppressor Protein p53/metabolism, Volatile Organic Compounds, RNA, pancreatic ductal adenocarcinoma, sequencing, cancer metabolism, mutations",

author = "Hiromichi Sato and Kazuki Sasaki and Tomoaki Hara and Yoshiko Tsuji and Yasuko Arao and Chihiro Otsuka and Yumiko Hamano and Mirei Ogita and Shogo Kobayashi and {di Luccio}, Eric and Takaaki Hirotsu and Yuichiro Doki and Hidetoshi Eguchi and Taroh Satoh and Shizuka Uchida and Hideshi Ishii",

year = "2022",

month = oct,

doi = "10.3390/biom12101503",

language = "English",

volume = "12",

journal = "Biomolecules",

issn = "2218-273X",

publisher = "MDPI",

number = "10",

}

TY - JOUR

T1 - Pancreatic Cancer Research beyond DNA Mutations

AU - Sato, Hiromichi

AU - Sasaki, Kazuki

AU - Hara, Tomoaki

AU - Tsuji, Yoshiko

AU - Arao, Yasuko

AU - Otsuka, Chihiro

AU - Hamano, Yumiko

AU - Ogita, Mirei

AU - Kobayashi, Shogo

AU - di Luccio, Eric

AU - Hirotsu, Takaaki

AU - Doki, Yuichiro

AU - Eguchi, Hidetoshi

AU - Satoh, Taroh

AU - Uchida, Shizuka

AU - Ishii, Hideshi

PY - 2022/10

Y1 - 2022/10

N2 - Pancreatic ductal adenocarcinoma (PDAC) is caused by genetic mutations in four genes: KRAS proto-oncogene and GTPase (KRAS), tumor protein P53 (TP53), cyclin-dependent kinase inhibitor 2A (CDKN2A), and mothers against decapentaplegic homolog 4 (SMAD4), also called the big 4. The changes in tumors are very complex, making their characterization in the early stages challenging. Therefore, the development of innovative therapeutic approaches is desirable. The key to overcoming PDAC is diagnosing it in the early stages. Therefore, recent studies have investigated the multifaced characteristics of PDAC, which includes cancer cell metabolism, mesenchymal cells including cancer-associated fibroblasts and immune cells, and metagenomics, which extend to characterize various biomolecules including RNAs and volatile organic compounds. Various alterations in the KRAS-dependent as well as KRAS-independent pathways are involved in the refractoriness of PDAC. The optimal combination of these new technologies is expected to help treat intractable pancreatic cancer.

AB - Pancreatic ductal adenocarcinoma (PDAC) is caused by genetic mutations in four genes: KRAS proto-oncogene and GTPase (KRAS), tumor protein P53 (TP53), cyclin-dependent kinase inhibitor 2A (CDKN2A), and mothers against decapentaplegic homolog 4 (SMAD4), also called the big 4. The changes in tumors are very complex, making their characterization in the early stages challenging. Therefore, the development of innovative therapeutic approaches is desirable. The key to overcoming PDAC is diagnosing it in the early stages. Therefore, recent studies have investigated the multifaced characteristics of PDAC, which includes cancer cell metabolism, mesenchymal cells including cancer-associated fibroblasts and immune cells, and metagenomics, which extend to characterize various biomolecules including RNAs and volatile organic compounds. Various alterations in the KRAS-dependent as well as KRAS-independent pathways are involved in the refractoriness of PDAC. The optimal combination of these new technologies is expected to help treat intractable pancreatic cancer.

KW - Carcinoma, Pancreatic Ductal/metabolism

KW - Cyclin-Dependent Kinases/metabolism

KW - DNA/therapeutic use

KW - Humans

KW - Mutation

KW - Pancreatic Neoplasms/metabolism

KW - Proto-Oncogene Proteins p21(ras)/genetics

KW - Tumor Suppressor Protein p53/metabolism

KW - Volatile Organic Compounds

KW - RNA

KW - pancreatic ductal adenocarcinoma

KW - sequencing

KW - cancer metabolism

KW - mutations

UR - http://www.scopus.com/inward/record.url?scp=85140433095&partnerID=8YFLogxK

U2 - 10.3390/biom12101503

DO - 10.3390/biom12101503

M3 - Review article

C2 - 36291712

VL - 12

JO - Biomolecules

JF - Biomolecules

SN - 2218-273X

IS - 10

M1 - 1503

ER -

Pancreatic Cancer Research beyond DNA Mutations

Abstract

Keywords

Access to Document

Other files and links

Fingerprint

Cite this