Oncotarget

BUFFALO, NY- November 15, 2023 – A new #editorial paper was #published in Oncotarget's Volume 14 on March 31, 2023, entitled, “Obesity paradox and lung cancer, metformin-based therapeutic opportunity?”

In their recent editorial, researchers Pedro Barrios-Bernal, Norma Hernández-Pedro, Luis Lara-Mejía, and Oscar Arrieta from Instituto Nacional de Cancerología discuss obesity, diabetes and lung cancer. Obesity is a complex multifactorial disease with detrimental effects on health. This disease induces a proinflammatory state, innate and adaptative immune system dysfunction, and immune exhaustion, which in conjunction promote cancer growth.

Although obesity and type 2 diabetes mellitus (T2DM) have been associated with lung cancer (LC) development, several confounding factors, such as chronic inflammation, high insulin levels, microbiome, as well as the oncogenic potential of growth and sexual hormones, have introduced uncertainty and avoid the fully recognition of this relationship [1, 2]. Thus, therapies that can bring potential therapeutic effects to both comorbidities are being tested globally and their effect on cancer cells.

“Altogether, there is a strong relationship between high BMI and increase survival in different LC stages and in combination with some anticancer therapies. Metformin has been shown to be a metabolism modifier that may adapt signaling pathways and immune sensitivity in tumor microenvironment.”

DOI - https://doi.org/10.18632/oncotarget.28432

Correspondence to - Oscar Arrieta - [email protected]

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28432

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, obesity, lung cancer, metformin, tyrosine-kinase inhibitors, BMI, EGFR, obesity paradox

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget

Facebook - https://www.facebook.com/Oncotarget/

X - https://twitter.com/oncotarget

Instagram - https://www.instagram.com/oncotargetjrnl/

YouTube - https://www.youtube.com/@OncotargetJournal

LinkedIn - https://www.linkedin.com/company/oncotarget

Pinterest - https://www.pinterest.com/oncotarget/

Reddit - https://www.reddit.com/user/Oncotarget/

Media Contact

18009220957

BUFFALO, NY- November 13, 2023 – A new #editorial perspective was #published in Oncotarget's Volume 14 on March 11, 2023, entitled, “C/EBPβ cooperates with MYB to maintain the oncogenic program of AML cells.”

In this new paper, researcher Karl-Heinz Klempnauer from Westfälische-Wilhelms-Universität discusses recent studies on the role of transcription factor MYB in acute myeloid leukemia (AML). MYB has been identified as a key regulator of a transcriptional program for self-renewal of AML cells.

The MYB gene initially attracted attention as the progenitor of a retrovirally-transduced oncogene that induces a myeloid leukemia in chicken [1–4]. MYB encodes a transcription factor with essential roles in the development of the hematopoietic system [5] and the proliferation and differentiation of hematopoietic progenitor cells [6]. Subsequent work identified MYB also as a crucial player in the development and maintenance of leukemia in humans.

“Recent work summarized here has now highlighted the CCAAT-box/enhancer binding protein beta (C/EBPβ) as an essential factor and potential therapeutic target that cooperates with MYB and coactivator p300 in the maintenance of the leukemic cells.”

DOI - https://doi.org/10.18632/oncotarget.28377

Correspondence to - Karl-Heinz Klempnauer - [email protected]

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28377

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, MYB, C/EBPbeta, p300, GFI1, AML

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget

Facebook - https://www.facebook.com/Oncotarget/

X - https://twitter.com/oncotarget

Instagram - https://www.instagram.com/oncotargetjrnl/

YouTube - https://www.youtube.com/@OncotargetJournal

LinkedIn - https://www.linkedin.com/company/oncotarget

Pinterest - https://www.pinterest.com/oncotarget/

Reddit - https://www.reddit.com/user/Oncotarget/

Media Contact

18009220957

BUFFALO, NY- November 8, 2023 – A new editorial #paper was #published in Oncotarget's Volume 14 on March 31, 2023, entitled, “Impact of SHP2 tyrosine phosphorylation on the development of acquired resistance to allosteric SHP2 inhibitors.”

The SH2 domain-containing tyrosine phosphatase 2 (SHP2) is a ubiquitously expressed non-receptor protein tyrosine phosphatase, encoded by the PTPN11 gene. It is positively regulated by upstream receptor tyrosine kinases (RTKs) to activate downstream the RAS-ERK pathway.

In this new editorial, researchers Giulia Franciosa and Jesper V. Olsen from the University of Copenhagen discuss potential leukemia therapies that effectively prevent adaptive resistance. Acute myeloid leukemia (AML) is a bone marrow malignancy characterized by a blockage of differentiation and an uncontrolled proliferation of myeloid hematopoietic progenitor cells. The internal tandem duplication (ITD) in the juxtamembrane domain of the RTK FLT3 is an oncogenic driver mutation that leads to constitutive activation of its tyrosine kinase activity. Consequently, FLT3 inhibitors that block its tyrosine kinase activity represent the targeted treatment option for patients with FLT3-ITD AML, often administrated in combination with induction chemotherapy.

“Nevertheless, the short duration of remission urges the development of novel combinatorial therapies for FLT3-ITD AML.”

Since 2016, several potent and selective allosteric, noncovalent SHP2 inhibitors have been developed and tested in clinical trials for solid tumors. A recent study reported the effectiveness of short-term treatment with the allosteric SHP2 inhibitor SHP099 as a single agent in clinically relevant mouse models of Flt3-ITD AML. This observation was in contrast with published data showing that allosteric SHP2 inhibition is only effective as combination treatment with inhibitors of other nodes of the RAS-ERK pathway. In a research article published by Pfeiffer et al., the Olsen’s lab at University of Copenhagen showed that two commercial FLT3-ITDpositive AML cell lines (MV-4-11 and MOLM-13) developed adaptive resistance after prolonged treatment in vitro with the allosteric SHP2 inhibitor SHP099.

“All in all, the findings by Pfeiffer et al. suggest that combined inhibition of SHP2 and mutated RTKs are effective in preventing adaptive resistance, but also highlight the need for development of more potent and effective SHP2 inhibitors and combination therapies for clinical applications.”

DOI - https://doi.org/10.18632/oncotarget.28392

Correspondence to - Giulia Franciosa - [email protected]

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28392

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, SHP2, PTPN11, tyrosine, phosphorylation

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget

Facebook - https://www.facebook.com/Oncotarget/

X - https://twitter.com/oncotarget

Instagram - https://www.instagram.com/oncotargetjrnl/

YouTube - https://www.youtube.com/@OncotargetJournal

LinkedIn - https://www.linkedin.com/company/oncotarget

Pinterest - https://www.pinterest.com/oncotarget/

Reddit - https://www.reddit.com/user/Oncotarget/

Media Contact

18009220957

BUFFALO, NY- November 6, 2023 – A new #editorial paper was #published in Oncotarget's Volume 14 on October 31, 2023, entitled, “The uncharted role of HER2 mutant alleles in breast cancer.”

Somatic HER2 mutations are a novel class of therapeutic targets across different cancer types. Treatment with the tyrosine kinase inhibitor (TKI) neratinib as a single agent continues to be evaluated in HER2-mutant metastatic disease. However, responses are heterogeneous, with frequent early progression.

In this new editorial, researchers Rashi Kalra, Bora Lim, Matthew J. Ellis, and Shyam M. Kavuri from Baylor College of Medicine discuss the under-explored effects of individual HER2 mutant alleles on therapeutic response, a role for HER2 mutation in metastatic propensity, and differences in patient outcomes in ER+ invasive lobular carcinoma (ILC) versus invasive ductal carcinoma (IDC). The preclinical efficacy of additional agents is also discussed, particularly the pan-HER inhibitor poziotinib.

“In summary, preclinical findings described above support clinical investigation of poziotinib in a subset of ER + mBC harboring HER2 somatic mutations and suggest further studies to evaluate poziotinib as a therapeutic agent in additional tumor types.”

DOI - https://doi.org/10.18632/oncotarget.28489

Correspondence to - Shyam M. Kavuri - [email protected]

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28489

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, metastasis, poziotinib, HER2, neratinib, invasive lobular breast carcinoma

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget

Facebook - https://www.facebook.com/Oncotarget/

X - https://twitter.com/oncotarget

Instagram - https://www.instagram.com/oncotargetjrnl/

YouTube - https://www.youtube.com/@OncotargetJournal

LinkedIn - https://www.linkedin.com/company/oncotarget

Pinterest - https://www.pinterest.com/oncotarget/

Reddit - https://www.reddit.com/user/Oncotarget/

Media Contact

18009220957

Extrahepatic biliary cancer is a specific type of biliary cancer that occurs outside the liver. It is considered rare, quite serious and often symptomless until later stages. The average age at diagnosis is 72. Extrahepatic biliary cancer typically involves the bile ducts, which carry bile from the liver and gallbladder to the small intestine. It can also involve the gallbladder, which plays a role in the digestion of fats by storing, concentrating and releasing bile as needed.

One of the main genetic factors that contribute to biliary cancer is the mutation of Kras, a gene that regulates cell growth and division. Mutated Kras can cause cells to grow uncontrollably and form tumors. Another important genetic factor is the mutation of p53, a gene that normally acts as a guardian of the genome and triggers cell death or repair when DNA damage occurs. Mutated p53 can impair this function and allow cells to survive and accumulate more mutations.

“[...] the exact role of p53 in the development of extrahepatic biliary cancer remains elusive.”

In a new editorial paper, researchers Munemasa Nagao, Kenta Mizukoshi, Shinnosuke Nakayama, Mio Namikawa, Yukiko Hiramatsu, Takahisa Maruno, Yuki Nakanishi, Tatsuaki Tsuruyama, Akihisa Fukuda, and Hiroshi Seno from Kyoto University Graduate School of Medicine discussed their recent study exploring the role of p53 in preventing the development of extrahepatic biliary cancer. On March 31, 2023, their editorial was published in Oncotarget, entitled, "p53 protects against formation of extrahepatic biliary precancerous lesions in the context of oncogenic Kras."

Full blog - https://www.oncotarget.org/2023/11/02/p53s-protective-role-in-extrahepatic-biliary-precancerous-lesions/

Paper DOI - https://doi.org/10.18632/oncotarget.28380

Correspondence to - Akihisa Fukuda - [email protected]

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28380

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, BilIN, ICPN, biliary cancer, Kras, p53

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget

Facebook - https://www.facebook.com/Oncotarget/

X - https://twitter.com/oncotarget

Instagram - https://www.instagram.com/oncotargetjrnl/

YouTube - https://www.youtube.com/@OncotargetJournal

LinkedIn - https://www.linkedin.com/company/oncotarget

Pinterest - https://www.pinterest.com/oncotarget/

Reddit - https://www.reddit.com/user/Oncotarget/

Media Contact

18009220957

BUFFALO, NY- November 1, 2023 – A new research paper was published in Oncotarget's Volume 14 on October 31, 2023, entitled, “FAAH inhibition ameliorates breast cancer in a murine model.”

Breast cancer is the leading cancer among females worldwide. Disease outcome depends on the hormonal status of the cancer and whether or not it is metastatic, but there is a need for more efficacious therapeutic strategies where first line treatment fails. In this new study, researchers Mallika Tripathy, Amy Bui, Jared Henderson, Jeffrey Sun, Christian Rutan Woods, Soumya Somani, Thao Doan, Anto Sam Crosslee Louis Sam Titus, and Chandra Mohan from the University of Houston’s Department Biomedical Engineering examined Fatty Acid Amide Hydrolase (FAAH) inhibition and endocannabinoids as therapeutic alternatives.

“This study explores the functional relevance and therapeutic potential of FAAH inhibition combined with the proapoptotic activity of exogenous endocannabinoids on breast cancer survival.”

FAAH is an integral membrane enzyme that hydrolyzes endocannabinoids, rendering them inactive, and FAAH inhibition is predicted to increase cancer cell death. To test this, breast cancer cells were probed for FAAH expression using Western blot analysis, treated with FAAH inhibitors, exogenous endocannabinoids, and combinations of the two treatments, and assessed for viability. High levels of FAAH were observed in different breast cancer cell lines.

FAAH inhibition was more effective than exogenous endocannabinoid treatment, and the combination of FAAH inhibitors and endocannabinoids was the most effective in inducing apoptosis of breast cancer cells in vitro. In addition, in vivo FAAH inhibition reduced breast cancer growth in immunodeficient mice. Further research exploring the therapeutic potential and impact of FAAH expression on cancer cells is warranted.

“FAAH inhibition is a promising approach, and tremendous progress has been made in the field to validate this mechanism as an alternative to chemotherapy.”

DOI - https://doi.org/10.18632/oncotarget.28534

Correspondence to - Chandra Mohan - [email protected]

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28534

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, FAAH, breast cancer, cancer therapy, apoptosis

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget

Facebook - https://www.facebook.com/Oncotarget/

X - https://twitter.com/oncotarget

Instagram - https://www.instagram.com/oncotargetjrnl/

YouTube - https://www.youtube.com/@OncotargetJournal

LinkedIn - https://www.linkedin.com/company/oncotarget

Pinterest - https://www.pinterest.com/oncotarget/

Reddit - https://www.reddit.com/user/Oncotarget/

Media Contact

18009220957

BUFFALO, NY- October 30, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on March 24, 2023, entitled, “Neutrophil PAD4: how does it function in cancer beyond promoting NETosis?”

Expansion of pathologically activated immune suppressive myeloid cells called myeloid-derived suppressor cells (MDSC) is one of the hallmarks of cancer. In most tumor types, MDSC are represented primarily by pathologically activated neutrophils (PMN-MDSC). In this new editorial, researchers Laura Garcia-Gerique and Yulia Nefedova from the Wistar Institute discussed their team’s recent study identifying a novel mechanism by which neutrophil PAD4 promotes cancer progression.

“Using several transplantable and genetically engineered mouse models, we demonstrated that tumor growth was accompanied by significantly elevated enzymatic activity of neutrophil PAD4 [10]. To further clarify the role of PAD4 in tumor progression, we utilized PAD4fl/fl MRP8Cre mice with targeted deletion of PAD4 in myeloid cells, primarily neutrophils.”

PMN-MDSC originate in the bone marrow and migrate to various sites including tumor tissues and premetastatic niches. These cells have a relatively short lifespan (less than 48 hours) and, therefore, are continually replaced from the bone marrow. Tumor-infiltrating PMN-MDSC possess a potent suppressive activity as they are able to inhibit both antigen-specific immune responses of T cells and non-specific anti-CD3/CD28-stimulated responses. As a result, a highly immunosuppressive environment is created in tumors, which prevents their rejection via immunological mechanisms.

In addition, PMN-MDSC employ non-immunological mechanisms to facilitate tumor progression, including angiogenesis, remodeling of extracellular matrix, and production of cytokines. In patients with solid tumors, levels of MDSC in circulation and tumor tissues have been positively associated with a poor response to the therapy in many types of cancer and represent an independent indicator of poor outcomes. However, many of the details about how PMN-MDSC support cancer progression, and thus approaches for therapeutically targeting these cells, remain enigmatic.

“Taken together, our study identified a new mechanism responsible for transcriptional regulation of neutrophil migration and a new mechanism by which neutrophil PAD4 is contributing to tumor progression. PAD4 inhibitors are in development and may enter early phase clinical trials in the future.”

DOI - https://doi.org/10.18632/oncotarget.28369

Correspondence to - Yulia Nefedova - [email protected]

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28369

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, PAD4, PMN-MDSC, neutrophils, neutrophil migration

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget

Facebook - https://www.facebook.com/Oncotarget/

X - https://twitter.com/oncotarget

Instagram - https://www.instagram.com/oncotargetjrnl/

YouTube - https://www.youtube.com/@OncotargetJournal

LinkedIn - https://www.linkedin.com/company/oncotarget

Pinterest - https://www.pinterest.com/oncotarget/

Reddit - https://www.reddit.com/user/Oncotarget/

Media Contact

18009220957

BUFFALO, NY- October 25, 2023 – A new editorial perspective was published in Oncotarget's Volume 14 on March 24, 2023, entitled, “Genetic modifiers of p53: opportunities for breast cancer therapies.”

Each day our cells encounter a wide range of genomic damage and the p53 protein arbitrates decisions of cell cycle arrest to allow repair of DNA or promote elimination of cells with malignant potential through apoptosis. In this new editorial perspective, researchers Prabin Dhangada Majhi, Aman Sharma and D. Joseph Jerry from the University of Massachusetts, Pioneer Valley Life Sciences Institute and Rays of Hope Center for Breast Cancer Research discuss TP53 mutations.

The prevalence of TP53 mutations in nearly all tumors emphasizes its role as a formidable barrier that must be breached to allow oncogenic transformation. Inherited mutations in TP53 are also the primary genetic lesions found in Li-Fraumeni Syndrome (LFS), a familial cancer predisposition characterized by tumors in many tissues. However, tissues are not all equally vulnerable to disruptions in p53 function.

Among women with inherited mutations in TP53, breast cancer is by far the most common tumor (Figure 1). Somatic mutations in TP53 are also prevalent in sporadic breast cancers, especially in the triple-negative subtype. The proportion rises to nearly 50% of breast cancers that exhibit impaired function of the p53 pathway based on gene expression signatures as a surrogate biomarker of p53 activity. Therefore, the breast epithelium appears to be uniquely sensitive to alterations in p53 function.

“Genomewide association studies (GWAS) have identified over 300 polymorphisms that contribute to breast cancer risk [38–41]. These provide a rich resource of candidate polymorphisms that may modify the consequences of mutations in TP53.”

DOI - https://doi.org/10.18632/oncotarget.28387

Correspondence to - D. Joseph Jerry - [email protected]

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28387

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, p53, Li-Fraumeni syndrome, genetic modifiers, breast cancer, DNA repair

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget

Facebook - https://www.facebook.com/Oncotarget/

X - https://twitter.com/oncotarget

Instagram - https://www.instagram.com/oncotargetjrnl/

YouTube - https://www.youtube.com/@OncotargetJournal

LinkedIn - https://www.linkedin.com/company/oncotarget

Pinterest - https://www.pinterest.com/oncotarget/

Reddit - https://www.reddit.com/user/Oncotarget/

Media Contact

18009220957

BUFFALO, NY- October 23, 2023 – A new research paper was published in Oncotarget's Volume 14 on October 19, 2023, entitled, “Apoptotic cells may drive cell death in hair follicles during their regression cycle.”

Intravital microscopy in live mice has shown that the elimination of epithelial cells during hair follicle regression involves supra-basal cell differentiation and basal cell apoptosis through synergistic action of TGF-β (transforming growth factor) and mesenchymal-epithelial interactions. In this process the basal epithelial cells are not internally committed to death and the mesenchymal dermal papilla (DP) plays an essential role in death induction. Given that DP cells are not necessary for completion of the cycle, only for its initiation, it is still an open question as to the mechanism that leads to the propagation of apoptosis towards the regenerative stem cell population.

In their new study, researchers Bradley D. Keister, Kailin R. Mesa and Krastan B. Blagoev from the National Science Foundation, The Jane Coffin Childs Memorial Fund for Medical Research, Yale School of Medicine, Johns Hopkins University, Bulgarian Academy of Sciences, and Sorbonne Université performed a quantitative analysis of the length of hair follicles to investigate their regression cycle.

“In this paper we introduced a mathematical model of the hair follicle regression cycle that postulates that the regression is initiated by the dermal papilla, but that this signal affects only the cells adjacent to it.”

The data are consistent with a propagation mechanism driven by apoptotic cells inducing apoptosis in their neighboring cells. The observation that the apoptosis slows down as the apoptotic front approaches the stem cells at the end of the follicle is consistent with a gradient of a pro-survival signal sent by these stem cells. An experiment that can falsify this mechanism is proposed.

“In conclusion, hair follicle regression may be governed by cell-cell induced programmed cell death, which slows down as the stem cell compartment is approached and does not affect the stem cell compartment from which the growth phase is initiated. The class of models introduced here can be used to describe the renewal kinetics of other stem cell niches like the intestinal stem cell niche [18].”

DOI - https://doi.org/10.18632/oncotarget.28529

Correspondence to - Krastan B. Blagoev - [email protected]

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28529

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, hair follicle, stem cells, regression cycle, mathematical model, analysis

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget

Facebook - https://www.facebook.com/Oncotarget/

X - https://twitter.com/oncotarget

Instagram - https://www.instagram.com/oncotargetjrnl/

YouTube - https://www.youtube.com/@OncotargetJournal

LinkedIn - https://www.linkedin.com/company/oncotarget

Pinterest - https://www.pinterest.com/oncotarget/

Reddit - https://www.reddit.com/user/Oncotarget/

Media Contact

18009220957

Hepatocellular carcinoma (HCC) is the most common type of liver cancer. It is particularly challenging to treat because HCC is often diagnosed in late stage and resistant to chemotherapy and radiation. However, advancements in targeted therapies and immunotherapies have opened new avenues for the treatment of this aggressive disease.

In a new editorial paper, researchers Sawako Suzuki, Divya Venkatesh, Tomoaki Tanaka, and Carol Prives from Columbia University highlight the role of a metabolic enzyme known as glutamine synthase 2 (GLS2) in regulating ferroptosis in HCC. Ferroptosis is a form of cell death that involves iron-dependent accumulation of lipid peroxides. On October 19, 2023, their editorial was published in Oncotarget, entitled, “GLS2 shapes ferroptosis in hepatocellular carcinoma.”

Full blog - https://www.oncotarget.org/2023/10/19/how-a-metabolic-enzyme-can-trigger-cell-death-in-liver-cancer-cells/

Paper DOI - https://doi.org/10.18632/oncotarget.28526

Correspondence to - Carol Prives - [email protected]

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28526

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

Keywords - cancer, ferroptosis, hepatocellular carcinoma, GLS2, p53, tumor suppression

About Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:

SoundCloud - https://soundcloud.com/oncotarget

Facebook - https://www.facebook.com/Oncotarget/

X - https://twitter.com/oncotarget

Instagram - https://www.instagram.com/oncotargetjrnl/

YouTube - https://www.youtube.com/@OncotargetJournal

LinkedIn - https://www.linkedin.com/company/oncotarget

Pinterest - https://www.pinterest.com/oncotarget/

Reddit - https://www.reddit.com/user/Oncotarget/

Media Contact

18009220957