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Cells
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Advances in Cancer Genomics
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Advances in Cancer Genomics

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (15 April 2023) | Viewed by 7609

Special Issue Editors

Prof. Dr. San Ming Wang

E-Mail Website
Guest Editor
Cancer Centre and Institute of Translational Medicine, Faculty of Health Sciences, University of Macau, Macau, China
Interests: cancer genomics and genetics; hereditary cancer; bioinformatics; oncogenic predisposition in the Asian population
Prof. Dr. Edwin Chong Wing Cheung

E-Mail Website
Guest Editor
Cancer Centre, Centre of Precision Medicine Research & Training, Faculty of Health Sciences, University of Macau, Macau, China
Interests: nuclear hormone; cancers; genomics
Dr. Ningyi Shao

E-Mail Website
Guest Editor
Department of Biomedical Sciences, Faculty of Health Sciences, University of Macau, Taipa, Macau, China
Interests: human development and diseases; genome; transcriptome; epigenome

Special Issue Information

Dear Colleagues,

Cancer is a genetic disease. One of the major aims of the Human Genome Project is to reveal the genetic basis of cancer. The rapid development and wide application of next-generation sequencing technologies and bioinformatics tools have greatly accelerated the progress of cancer genomic studies. The knowledge derived from our progress enhances our deeper understanding of the genetic basis of cancer, and translates into clinical applications for cancer diagnosis, treatment, and prevention. This Special Issue will provide a forum to reflect on the latest progress in the field, including, but not limited to, the topics of oncogenic evolution, cancer susceptibility genes, oncogene and tumor suppressors, cancer susceptibility, mutations, ethnic-specific cancer susceptibility, population screening, clinical applications, etc.. Submissions can be either original reports or reviews that summarize the progress in a specific topic.

We look forward to your contributions.

Prof. Dr. San Ming Wang
Prof. Dr. Edwin Chong Wing Cheung
Dr. Ningyi Shao
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • cancer genomics and genetics
  • bioinformatics
  • oncogenic variation
  • oncogenic evolution
  • diagnostic markers

Published Papers (3 papers)

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Research

14 pages, 2561 KiB  
Article
Increased Radiation Sensitivity in Patients with Phelan-McDermid Syndrome
by Sarah Jesse, Lukas Kuhlmann, Laura S. Hildebrand, Henriette Magelssen, Martina Schmaus, Beate Timmermann, Stephanie Andres, Rainer Fietkau and Luitpold V. Distel
Cells 2023, 12(5), 820; https://doi.org/10.3390/cells12050820 - 6 Mar 2023
Viewed by 1554
Abstract
Phelan-McDermid syndrome is an inherited global developmental disorder commonly associated with autism spectrum disorder. Due to a significantly increased radiosensitivity, measured before the start of radiotherapy of a rhabdoid tumor in a child with Phelan-McDermid syndrome, the question arose whether other patients with [...] Read more.
Phelan-McDermid syndrome is an inherited global developmental disorder commonly associated with autism spectrum disorder. Due to a significantly increased radiosensitivity, measured before the start of radiotherapy of a rhabdoid tumor in a child with Phelan-McDermid syndrome, the question arose whether other patients with this syndrome also have increased radiosensitivity. For this purpose, the radiation sensitivity of blood lymphocytes after irradiation with 2Gray was examined using the G0 three-color fluorescence in situ hybridization assay in a cohort of 20 patients with Phelan-McDermid syndrome from blood samples. The results were compared to healthy volunteers, breast cancer patients and rectal cancer patients. Independent of age and gender, all but two patients with Phelan-McDermid syndrome showed significantly increased radiosensitivity, with an average of 0.653 breaks per metaphase. These results correlated neither with the individual genetic findings nor with the individual clinical course, nor with the respective clinical severity of the disease. In our pilot study, we saw a significantly increased radiosensitivity in lymphocytes from patients with Phelan-McDermid syndrome, so pronounced that a dose reduction would be recommended if radiotherapy had to be performed. Ultimately, the question arises as to the interpretation of these data. There does not appear to be an increased risk of tumors in these patients, since tumors are rare overall. The question, therefore, arose as to whether our results could possibly be the basis for processes, such as aging/preaging, or, in this context, neurodegeneration. There are no data on this so far, but this issue should be pursued in further fundamentally based studies in order to better understand the pathophysiology of the syndrome. Full article
(This article belongs to the Special Issue Advances in Cancer Genomics)
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14 pages, 3656 KiB  
Article
The BRCAness Landscape of Cancer
by Maoni Guo and San Ming Wang
Cells 2022, 11(23), 3877; https://doi.org/10.3390/cells11233877 - 1 Dec 2022
Cited by 6 | Viewed by 3323
Abstract
BRCAness refers to the damaged homologous recombination (HR) function due to the defects in HR-involved non-BRCA1/2 genes. BRCAness is the important marker for the use of synthetic lethal-based PARP inhibitor therapy in breast and ovarian cancer treatment. The success provides an opportunity [...] Read more.
BRCAness refers to the damaged homologous recombination (HR) function due to the defects in HR-involved non-BRCA1/2 genes. BRCAness is the important marker for the use of synthetic lethal-based PARP inhibitor therapy in breast and ovarian cancer treatment. The success provides an opportunity of applying PARP inhibitor therapy to treat other cancer types with BRCAness features. However, systematic knowledge is lack for BRCAness in different cancer types beyond breast and ovarian cancer. We performed a comprehensive characterization for 40 BRCAness-related genes in 33 cancer types with over 10,000 cancer cases, including pathogenic variation, homozygotic deletion, promoter hypermethylation, gene expression, and clinical correlation of BRCAness in each cancer type. Using BRCA1/BRCA2 mutated breast and ovarian cancer as the control, we observed that BRCAness is widely present in multiple cancer types. Based on the sum of the BRCAneass features in each cancer type, we identified the following 21 cancer types as the potential targets for PARPi therapy: adrenocortical carcinoma, bladder urothelial carcinoma, brain lower grade glioma, colon adenocarcinoma, esophageal carcinoma, head and neck squamous carcinoma, kidney chromophobe, kidney renal clear cell carcinoma, kidney renal papillary cell carcinoma, liver hepatocellular carcinoma, lung adenocarcinoma, lung squamous cell carcinoma, mesothelioma, rectum adenocarcinoma, pancreatic adenocarcinoma, prostate adenocarcinoma, sarcoma, skin cutaneous melanoma, stomach adenocarcinoma, uterine carcinosarcoma, and uterine corpus endometrial carcinoma. Full article
(This article belongs to the Special Issue Advances in Cancer Genomics)
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12 pages, 1610 KiB  
Article
Prevalence and Prognostic Relevance of Homologous Recombination Repair Gene Mutations in Uterine Serous Carcinoma
by Lin Dong, Tingting Wang, Ning Li, Hongwen Yao, Jianming Ying, Lingying Wu and Guangwen Yuan
Cells 2022, 11(22), 3563; https://doi.org/10.3390/cells11223563 - 11 Nov 2022
Cited by 3 | Viewed by 1657
Abstract
Uterine serous carcinoma (USC) is a rare but aggressive subtype of endometrial cancer lacking efficacious treatments. USC bears molecular and pathological resemblance to high-grade serous ovarian cancer, for which mutations in homologous recombination repair (HRR) genes have been associated with better treatment outcomes [...] Read more.
Uterine serous carcinoma (USC) is a rare but aggressive subtype of endometrial cancer lacking efficacious treatments. USC bears molecular and pathological resemblance to high-grade serous ovarian cancer, for which mutations in homologous recombination repair (HRR) genes have been associated with better treatment outcomes with platinum-based chemotherapy and poly-ADP ribose polymerase 1/2 inhibitors (PARPi). We aimed to investigate the prevalence of tumor HRR (tHRR) gene mutations and its potential prognostic value in USC patients. Sixty consecutive USC patients with available tumor tissue samples and complete follow-up records were included. Tumor mutations in relevant HRR genes were identified using next-generation sequencing and correlated with the progress-free survival (PFS) and disease-specific survival (DSS) of the patients. Among the 60 patients’ USC, 22 (36.7%) carried tumor HRR gene mutations (tHRRmt), with ATM, BRCA1, and BRCA2 being the most frequently mutated genes. Survival analysis showed similar PFS (HR, 0.500; 95% CI, 0.203–1.232; p = 0.132), but significantly longer DSS in the tHRRmt patients than in the HRR gene wild-type (tHRRwt) patients (HR, 0.176; 95% CI, 0.050–0.626; p = 0.007). In FIGO stage III and IV patients, the tHRRmt group also displayed longer DSS than the tHRRwt group (p = 0.008). Notably, USC patients with abnormal p53 in our cohort, both PFS and DSS were significantly longer in the tHRRmt group over the tHRRwt group (p = 0.040 and p = 0.008, respectively). The HRR gene mutations are highly prevalent in USC and may be related to better clinical outcomes as a prognostic marker. Further study is needed to confirm whether tHRRmt patients may benefit from treatments targeting homologous recombination such as platinum and PARPi. Full article
(This article belongs to the Special Issue Advances in Cancer Genomics)
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