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Biomedicines
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Advances in Targeting Genomics and the Tumor Immune System to...
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Advances in Targeting Genomics and the Tumor Immune System to Treat Gastrointestinal Cancers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 2345

Special Issue Editor

Prof. Dr. Jeeyun Lee

E-Mail Website
Guest Editor
Division of Hematology/Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul 135-710, Republic of Korea
Interests: gastric cancer; colorectal cancer; sarcoma; melanoma

Special Issue Information

Dear Colleagues,

Although mortality rates have declined in recent years, the majority of cancers are still difficult to treat and the medical need for better cancer treatments is evident. The current anticancer armamentarium includes many active agents that are applied across tumor types. Globally, next-generation sequencing is widely available for oncology patients. However, the clinical implication of genomic aberrations needs to be defined in detail, especially in gastrointestinal oncology area. With the launch of various molecularly targeted agents and immunotargeted agents, subsets of patients with specific genomic aberrations need to be actively discussed and shared within the community. In light of this, we invite research and review papers related to any area of NGS analysis and clinical implications (i.e., genomic aberrations and treatment response, genomic aberrations and prediction of immunotherapy response, survival, new targets, etc.). We also welcome NGS-based clinical trials in GI oncology and preclinical papers to support further clinical research developments.

We hope that this Special Issue reflects the exciting era that we are living in with respect to the field of clinical genomics oncology, its applications in gastrointestinal cancer treatment, and the targeting of the tumor immune system.

Prof. Dr. Jeeyun Lee
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • genomics
  • precision oncology
  • next-generation sequencing
  • gastrointestinal cancer
  • tumor

Published Papers (2 papers)

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Research

12 pages, 2622 KiB  
Article
Prevalence of RAF1 Aberrations in Metastatic Cancer Patients: Real-World Data
by Sung Hee Lim, Jaeyun Jung, Jung Young Hong, Seung Tae Kim, Se Hoon Park, Joon Oh Park, Kyoung-Mee Kim and Jeeyun Lee
Biomedicines 2023, 11(12), 3264; https://doi.org/10.3390/biomedicines11123264 - 9 Dec 2023
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Abstract
Purpose: Therapeutic targeting of RAF1 is a promising cancer treatment, but the relationship between clinical features and RAF1 aberrations in terms of the MAPK signaling pathway is poorly understood in various solid tumors. Methods: Between October 2019 and June 2023 at Samsung Medical [...] Read more.
Purpose: Therapeutic targeting of RAF1 is a promising cancer treatment, but the relationship between clinical features and RAF1 aberrations in terms of the MAPK signaling pathway is poorly understood in various solid tumors. Methods: Between October 2019 and June 2023 at Samsung Medical Center, 3895 patients with metastatic solid cancers underwent next-generation sequencing (NGS) using TruSight Oncology 500 (TSO500) assays as routine clinical practice. We surveyed the incidence of RAF1 aberrations including mutations (single-nucleotide variants [SNVs]), amplifications (copy number variation), and fusions. Results: Among the 3895 metastatic cancer patients, 77 (2.0%) exhibited RAF1 aberrations. Of these 77 patients, 44 (1.1%) had RAF1 mutations (SNV), 25 (0.6%) had RAF1 amplifications, and 10 (0.3%) had RAF1 fusions. Among the 10 patients with RAF1 fusions, concurrent RAF1 amplifications and RAF1 mutations were detected in one patient each. The most common tumor types were bladder cancer (11.5%), followed by ampulla of Vater (AoV) cancer (5.3%), melanoma (3.0%), gallbladder (GB) cancer (2.6%), and gastric (2.3%) cancer. Microsatellite instability high (MSI-H) tumors were observed in five of 76 patients (6.6%) with RAF1 aberrations, while MSI-H tumors were found in only 2.1% of patients with wild-type RAF1 cancers (p < 0.0001). Conclusion: We demonstrated that approximately 2.0% of patients with metastatic solid cancers have RAF1 aberrations according to NGS of tumor specimens. Full article
(This article belongs to the Special Issue Advances in Targeting Genomics and the Tumor Immune System to Treat Gastrointestinal Cancers)
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11 pages, 10530 KiB  
Article
Clinical Implication of Concurrent Amplification of MET and FGFR2 in Metastatic Gastric Cancer
by Seonggyu Byeon, Jaeyun Jung, Seung Tae Kim, Kyoung-Mee Kim and Jeeyun Lee
Biomedicines 2023, 11(12), 3172; https://doi.org/10.3390/biomedicines11123172 - 28 Nov 2023
Viewed by 1025
Abstract
Background: c-mesenchymal epithelial transition factor receptor (c-MET) and fibroblast growth factor receptor 2 (FGFR2) amplification have been identified as factors associated with advanced stage and poor prognosis in gastric cancer (GC). While they are typically considered mutually exclusive, concurrent amplifications have been reported [...] Read more.
Background: c-mesenchymal epithelial transition factor receptor (c-MET) and fibroblast growth factor receptor 2 (FGFR2) amplification have been identified as factors associated with advanced stage and poor prognosis in gastric cancer (GC). While they are typically considered mutually exclusive, concurrent amplifications have been reported in a small subset of GC patients. Methods: in this retrospective study, we analyzed the clinical outcomes of GC patients with MET and FGFR2 amplification using the next-generation sequencing (NGS) database cohort at Samsung Medical Center, which included a total of 2119 patients between October 2019 and April 2021. Results: Of 2119 cancer patients surveyed, the number of GC patients was 614 (29.0%). Out of 614 GC patients, 39 (6.4%) had FGFR2 amplification alone, 22 (3.6%) had MET amplification, and 2 GC patients (0.3%) had concurrent FGFR2 and MET amplification. Two patients with concurrent FGFR2 and MET amplification did not respond to first-line chemotherapy. These two patients had significantly shorter overall survival (3.6 months) compared to patients with FGFR2 or MET amplification alone (13.6 months and 8.4 months, respectively) (p = 0.004). Lastly, we tested the existence of FGFR2 and MET in tumor specimens from different organ sites. Initially, the NGS was tested in a primary tumor specimen from stomach cancer, where the MET copy number was 14.1 and the FGFR2 copy number was 5.3. We confirmed that both MET and FGFR2 were highly amplified in the primary tumor using FISH (MET–CEP7 ratio = 5 and FGFR2–CEP7 ratio = 3). However, although the MET copy number was normal in peritoneal seeding using FISH, FGFR2 remained amplified using FISH (FGFR2–CEP7 ratio = 7) with high FGFR2 protein overexpression. Hence, there was intra-patient molecular heterogeneity. Conclusions: our findings suggest that concurrent amplification of FGFR2 and MET in GC patients is associated with clinical aggressiveness and may contribute to non-responsiveness to chemotherapy or targeted therapy. Full article
(This article belongs to the Special Issue Advances in Targeting Genomics and the Tumor Immune System to Treat Gastrointestinal Cancers)
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