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State-of-the-Art Molecular Oncology in Japan
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State-of-the-Art Molecular Oncology in Japan

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 9043

Special Issue Editor

Dr. Yosuke Minami

E-Mail Website
Guest Editor
National Cancer Center Hospital East, Kashiwa 277-8577, Chiba, Japan
Interests: leukemia; molecular target therapy; precision medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recently, whole exome sequencing for cancer has been performed by a next-generation sequencer, and the era of precision medicine has arrived also in Japan. It is important to detect actionable mutations relevant to treatment decision-making, and the treatment strategies for cancer have undergone drastic changes with the rapid development of new molecular targeted drugs.

To update current status of molecular and translational oncology studies of different cancers, we set up this Special Issue to collect high-quality papers from Japanese scholars in molecular oncology field. Especially, we will show the cutting edge progress regarding molecular targeted therapies and the promising clinical strategies in cancer especially for leukemia. Please note that the special issue is focused on molecular research, so the pure clinical research will not be accepted. But clinical submissions with biomolecular experiments are welcomed. All original research and review articles are welcomed in this Special Issue.

Dr. Yosuke Minami
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • molecular oncology
  • precision medicine
  • molecular targeted therapy
  • blood cancer
  • drug resistance
  • leukemia

Published Papers (3 papers)

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Research

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18 pages, 3533 KiB  
Article
The Rationale for the Dual-Targeting Therapy for RSK2 and AKT in Multiple Myeloma
by Reiko Isa, Mano Horinaka, Taku Tsukamoto, Kentaro Mizuhara, Yuto Fujibayashi, Yoko Taminishi-Katsuragawa, Haruya Okamoto, Shusuke Yasuda, Yuka Kawaji-Kanayama, Yayoi Matsumura-Kimoto, Shinsuke Mizutani, Yuji Shimura, Masafumi Taniwaki, Toshiyuki Sakai and Junya Kuroda
Int. J. Mol. Sci. 2022, 23(6), 2919; https://doi.org/10.3390/ijms23062919 - 08 Mar 2022
Cited by 2 | Viewed by 3061
Abstract
Multiple myeloma (MM) is characterized by remarkable cytogenetic/molecular heterogeneity among patients and intraclonal diversity even in a single patient. We previously demonstrated that PDPK1, the master kinase of series of AGC kinases, is universally active in MM, and plays pivotal roles in cell [...] Read more.
Multiple myeloma (MM) is characterized by remarkable cytogenetic/molecular heterogeneity among patients and intraclonal diversity even in a single patient. We previously demonstrated that PDPK1, the master kinase of series of AGC kinases, is universally active in MM, and plays pivotal roles in cell proliferation and cell survival of myeloma cells regardless of the profiles of cytogenetic and genetic abnormalities. This study investigated the therapeutic efficacy and mechanism of action of dual blockade of two major PDPK1 substrates, RSK2 and AKT, in MM. The combinatory treatment of BI-D1870, an inhibitor for N-terminal kinase domain (NTKD) of RSK2, and ipatasertib, an inhibitor for AKT, showed the additive to synergistic anti-tumor effect on human MM-derived cell lines (HMCLs) with active RSK2-NTKD and AKT, by enhancing apoptotic induction with BIM and BID activation. Moreover, the dual blockade of RSK2 and AKT exerted robust molecular effects on critical gene sets associated with myeloma pathophysiologies, such as those with MYC, mTOR, STK33, ribosomal biogenesis, or cell-extrinsic stimuli of soluble factors, in HMCLs. These results provide the biological and molecular rationales for the dual-targeting strategy for RSK2 and AKT, which may overcome the therapeutic difficulty due to cytogenetic/molecular heterogeneity in MM. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Japan)
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Review

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13 pages, 1252 KiB  
Review
Genetic Landscape of Chronic Myeloid Leukemia and a Novel Targeted Drug for Overcoming Resistance
by Ryo Yoshimaru and Yosuke Minami
Int. J. Mol. Sci. 2023, 24(18), 13806; https://doi.org/10.3390/ijms241813806 - 07 Sep 2023
Cited by 1 | Viewed by 1517
Abstract
Tyrosine kinase inhibitors (TKIs) exemplify the success of molecular targeted therapy for chronic myeloid leukemia (CML). However, some patients do not respond to TKI therapy. Mutations in the kinase domain of BCR::ABL1 are the most extensively studied mechanism of TKI resistance in CML, [...] Read more.
Tyrosine kinase inhibitors (TKIs) exemplify the success of molecular targeted therapy for chronic myeloid leukemia (CML). However, some patients do not respond to TKI therapy. Mutations in the kinase domain of BCR::ABL1 are the most extensively studied mechanism of TKI resistance in CML, but BCR::ABL1-independent mechanisms are involved in some cases. There are two known types of mechanisms that contribute to resistance: mutations in known cancer-related genes; and Philadelphia-associated rearrangements, a novel mechanism of genomic heterogeneity that occurs at the time of the Philadelphia chromosome formation. Most chronic-phase and accelerated-phase CML patients who were treated with the third-generation TKI for drug resistance harbored one or more cancer gene mutations. Cancer gene mutations and additional chromosomal abnormalities were found to be independently associated with progression-free survival. The novel agent asciminib specifically inhibits the ABL myristoyl pocket (STAMP) and shows better efficacy and less toxicity than other TKIs due to its high target specificity. In the future, pooled analyses of various studies should address whether additional genetic analyses could guide risk-adapted therapy and lead to a final cure for CML. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Japan)
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16 pages, 1322 KiB  
Review
Emerging Targeted Therapy for Specific Genomic Abnormalities in Acute Myeloid Leukemia
by Sung-Gi Chi and Yosuke Minami
Int. J. Mol. Sci. 2022, 23(4), 2362; https://doi.org/10.3390/ijms23042362 - 21 Feb 2022
Cited by 6 | Viewed by 3939
Abstract
We describe recent updates of existing molecular-targeting agents and emerging novel gene-specific strategies. FLT3 and IDH inhibitors are being tested in combination with conventional chemotherapy for both medically fit patients and patients who are ineligible for intensive therapy. FLT3 inhibitors combined with non-cytotoxic [...] Read more.
We describe recent updates of existing molecular-targeting agents and emerging novel gene-specific strategies. FLT3 and IDH inhibitors are being tested in combination with conventional chemotherapy for both medically fit patients and patients who are ineligible for intensive therapy. FLT3 inhibitors combined with non-cytotoxic agents, such as BCL-2 inhibitors, have potential therapeutic applicability. The menin-MLL complex pathway is an emerging therapeutic target. The pathway accounts for the leukemogenesis in AML with MLL-rearrangement, NPM1 mutation, and NUP98 fusion genes. Potent menin-MLL inhibitors have demonstrated promising anti-leukemic effects in preclinical studies. The downstream signaling molecule SYK represents an additional target. However, the TP53 mutation continues to remain a challenge. While the p53 stabilizer APR-246 in combination with azacitidine failed to show superiority compared to azacitidine monotherapy in a phase 3 trial, next-generation p53 stabilizers are now under development. Among a number of non-canonical approaches to TP53-mutated AML, the anti-CD47 antibody magrolimab in combination with azacitidine showed promising results in a phase 1b trial. Further, the efficacy was somewhat better in patients with the TP53 mutation. Although clinical evidence has not been accumulated sufficiently, targeting activating KIT mutations and RAS pathway-related molecules can be a future therapeutic strategy. Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Japan)
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