Evidence map›Paper›PMID 34949655›Full record

ArticleCancer genomics & proteomics

Extent and Instability of Trimethylation of Histone H3 Lysine Increases With Degree of Malignancy and Methionine Addiction.

Jun Yamamoto, Yusuke Aoki, Sachiko Inubushi, Qinghong Han, Kazuyuki Hamada, Yoshihiko Tashiro, Kentaro Miyake, Ryusei Matsuyama, Michael Bouvet, Steven G Clarke and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 49 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Jun YamamotoAntiCancer Inc., San Diego, CA, U.S.A.; all@anticancer.com.
Yusuke AokiAntiCancer Inc., San Diego, CA, U.S.A.
Sachiko InubushiAntiCancer Inc., San Diego, CA, U.S.A.
Qinghong HanAntiCancer Inc., San Diego, CA, U.S.A.
Kazuyuki HamadaAntiCancer Inc., San Diego, CA, U.S.A.
Yoshihiko TashiroAntiCancer Inc., San Diego, CA, U.S.A.
Kentaro MiyakeDepartment of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Ryusei MatsuyamaDepartment of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Michael BouvetDepartment of Surgery, University of California, San Diego, La Jolla, CA, U.S.A.
Steven G ClarkeDepartment of Chemistry and Biochemistry, University of California, Los Angeles, CA, U.S.A.
Itaru EndoDepartment of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan; endoit@yokohama-cu.ac.jp.
Robert M HoffmanAntiCancer Inc., San Diego, CA, U.S.A.; jun.ymmt.1014@gmail.com.
AntiCancer (United States) · USYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimMethionine addiction is a fundamental and general hallmark of cancer, termed the Hoffman effect. Methionine addiction is due to excessive use of and dependence on methionine by cancer cells. In the present report, we correlated the extent of methionine addiction and degree of malignancy with the amount and stability of methylated histone H3 lysine marks. MATERIALS AND

methodsWe established low- and high-malignancy variants from a parental human pancreatic-cancer cell line and compared their sensitivity to methionine restriction and histone H3 lysine methylation status.

resultsA low-malignancy, low-methionine-addiction revertant of the parental pancreatic-cancer cell line had less methylated H3K9me3 and was less sensitive to methionine restriction effected by recombinant methioninase (rMETase) than the parental cell line. A high-malignancy variant of the pancreatic cancer cell line had increased methylated H3K9me3 and was more sensitive to methionine restriction by rMETase with regard to inhibition of proliferation and to instability of histone H3 lysine methylation than the parental cell line. Orthotopic malignancy in nude mice was reduced in the low-methionine-addiction revertant and greater in the high-malignancy variant than in the parental cell line.

conclusionThe present study indicates that the degree of malignancy is linked to the extent of methionine addiction and the level and instability of trimethylation of histone H3, suggesting these phenomena are linked as a fundamental basis of oncogenic transformation.

Indexed as

AnimalsCarbon-Sulfur LyasesCell Line, TumorCell Transformation, NeoplasticHistone CodeHistonesHumansLysineMethionineMethylationMicePancreatic NeoplasmsRecombinant ProteinsTumor BurdenXenograft Model Antitumor AssaysCarbon-Sulfur LyasesHistonesL-methionine gamma-lyaseLysineMethionineRecombinant Proteinshigh-methionine addiction variantshistone H3 lysinelow-methionine-addiction revertantmalignancyMethionine addictionmethionine dependencemethionine restrictionovermethylationtransmethylation

Identifiers

PMID34949655
PMCPMC8717956
OpenAlexW4200389065

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.