Monoallelic IDH1 R132H mutation mediates glioma cell response to anti-cancer therapies via induction of senescence

2021 ◽  
pp. molcanres.0284.2021
Author(s):  
Daqian Zhan ◽  
Ding Ma ◽  
Shuang Wei ◽  
Bachchu Lal ◽  
Yi Fu ◽  
...  
Keyword(s):  
Cell Response ◽  
Glioma Cell ◽  
Cancer Therapies ◽  
Idh1 R132h ◽  
Anti Cancer ◽  
R132h Mutation

ANTICANCER EFFECT OF UVARIA GENUS

2014 ◽  
pp. 98-101
Author(s):  
Thi Bich Hien Le ◽  
Viet Duc Ho ◽  
Thi Hoai Nguyen
Keyword(s):  
Biological Activities ◽  
Current Trend ◽  
Healthcare Systems ◽  
Chemical Compositions ◽  
Cancer Therapies ◽  
Pharmacological Effects ◽  
Anticancer Effect ◽  
Anti Cancer ◽  
Tropical Areas ◽  
Cancer Activity

Nowadays, cancer treatment has been a big challenge to healthcare systems. Most of clinical anti-cancer therapies are toxic and cause adverse effects to human body. Therefore, current trend in science is seeking and screening of natural compounds which possess antineoplastic activities to utilize in treatment. Uvaria L. - Annonaceae includes approximately 175 species spreading over tropical areas of Asia, Australia, Africa and America. Studies on chemical compositions and pharmacological effects of Uvaria showed that several compound classes in this genus such as alkaloid, flavonoid, cyclohexen derivaties, acetogenin, steroid, terpenoid, etc. indicate considerable biological activities, for example anti-tumor, anti-cancer, antibacterial, antifungal, antioxidant, etc. Specifically, anti-cancer activity of fractions of extract and pure isolated compounds stands out for cytotoxicity against many cancer cell lines. This study provides an overview of anti-cancer activity of Uvaria and suggests a potential for further studies on seeking and developing novel anti-cancer compounds. Key words: Anti-cancer, Uvaria.

Potential of Mesenchymal Stem Cells in Anti-Cancer Therapies

2020 ◽  
Vol 15 (6) ◽  
pp. 482-491 ◽  
Author(s):  
Milena Kostadinova ◽  
Milena Mourdjeva
Keyword(s):  
Cancer Cells ◽  
Small Population ◽  
Tumor Formation ◽  
Bioactive Molecules ◽  
Cancer Therapies ◽  
New Methods ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
Blocking Mechanisms

Mesenchymal stem/stromal cells (MSCs) are localized throughout the adult body as a small population in the stroma of the tissue concerned. In injury, tissue damage, or tumor formation, they are activated and leave their niche to migrate to the site of injury, where they release a plethora of growth factors, cytokines, and other bioactive molecules. With the accumulation of data about the interaction between MSCs and tumor cells, the dualistic role of MSCs remains unclear. However, a large number of studies have demonstrated the natural anti-tumor properties inherent in MSCs, so this is the basis for intensive research for new methods using MSCs as a tool to suppress cancer cell development. This review focuses specifically on advanced approaches in modifying MSCs to become a powerful, precision- targeted tool for killing cancer cells, but not normal healthy cells. Suppression of tumor growth by MSCs can be accomplished by inducing apoptosis or cell cycle arrest, suppressing tumor angiogenesis, or blocking mechanisms mediating metastasis. In addition, the chemosensitivity of cancer cells may be increased so that the dose of the chemotherapeutic agent used could be significantly reduced.

Kinase Inhibitors Targeting Anti-angiogenesis as Anti-cancer Therapies

2012 ◽  
Vol 1 (4) ◽  
pp. 335-346 ◽  
Author(s):  
Jing Liu ◽  
Feiyang Liu ◽  
David L. Waller ◽  
Junfeng Wang ◽  
Qingsong Liu
Keyword(s):  
Kinase Inhibitors ◽  
Cancer Therapies ◽  
Anti Cancer

scholarly journals AB0080 A SYSTEM-LEVEL APPROACH IDENTIFIES A CRITICAL REGULATOR OF CHONDROSARCOMA PROGRESSION

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1340.3-1340
Author(s):  
H. Kim ◽  
Y. Cho ◽  
J. H. Kim
Keyword(s):  
Histological Grade ◽  
System Level ◽  
Clinical Approach ◽  
Cancer Therapies ◽  
Functional Roles ◽  
Network Analyses ◽  
Molecular Events ◽  
Anti Cancer ◽  
Tumor Growth And Metastasis ◽  
Chemotherapy Agents

Background:Chondrosarcomas are cartilaginous tumors that constitute one-third of skeletal system cancers. Chondrosarcomas are capable of transitioning to highly metastatic and treatment-refractory states, resulting in significant patient mortality. However, the molecular events accompanying this behavior remain unknown.Objectives:We aimed to uncover the molecular pathway underlying such tumor progression that confers a higher malignancy to chondrosarcoma.Methods:We conducted unsupervised gene co-expression network analyses using transcriptomes of patients with chondrosarcoma and extracted a characteristic transcription network underlying chondrosarcoma malignancy. By implementing a system-level upstream analysis of this gene network, we identified the transcriptional factor as a key regulator governing chondrosarcoma progression. We unraveled the functional roles of the identified factor in promoting tumor growth and metastasis of chondrosarcomas in the context of their unique microenvironments.Results:By conducting system-level upstream analysis, we identified a factor as a transcriptional regulator that governs the malignancy gene module. The identified factor was upregulated in chondrosarcoma biopsies associated with a high histological grade and conferred chondrosarcoma cells invasiveness and tumor-initiating capacity. In an orthotopic xenograft mouse model, the identified factor modulated local outgrowth and pulmonary metastasis of chondrosarcoma. Pharmacological inhibition of the identified factor in conjunction with the chemotherapy agents such as cisplatin or doxorubicin synergistically enhanced chondrosarcoma cell apoptosis and abolished malignant phenotypes of chondrosarcoma in mice.Conclusion:Our study provides a proof of concept evidence that inhibiting the identified factor suppresses progression of chondrosarcoma and improves the efficacy of chemotherapy in cellular and pre-clinical levels. Taken together, we believe that our findings provide novel molecular insights for the development of new anti-cancer therapies to target chondrosarcomas.References:[1]Gelderblom H, et al. The clinical approach towards chondrosarcoma. Oncologist 13, 320-329 (2008)Disclosure of Interests:None declared

scholarly journals ECG Scoring for the Evaluation of Therapy-Naïve Cancer Patients to Predict Cardiotoxicity

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1197
Author(s):  
Julia Pohl ◽  
Raluca-Ileana Mincu ◽  
Simone M. Mrotzek ◽  
Reza Wakili ◽  
Amir A. Mahabadi ◽  
...  
Keyword(s):  
High Risk ◽  
Cancer Patients ◽  
Left Ventricular ◽  
Cardiac Biomarkers ◽  
Cancer Therapies ◽  
University Hospitals ◽  
Anti Cancer ◽  
Risk Patients ◽  
Qrs Duration ◽  
Ecg Score

Objective: To evaluate a new electrocardiographic (ECG) score reflecting domains of electrical and structural alterations in therapy-naïve cancer patients to assess their risk of cardiotoxicity. Methods: We performed a retrospective analysis of 134 therapy-naïve consecutive cancer patients in our two university hospitals concerning four ECG score parameters: Contiguous Q-waves, markers of left ventricular (LV) hypertrophy, QRS duration and JTc prolongation. Cardiotoxicity was assessed after a short-term follow-up (up to 12 months). Results: Of all the patients (n = 25), 19% reached 0 points, 50% (n = 67) reached 1 point, 25% (n = 33) reached 2 points, 5% (n = 7) reached 3 points and 0.7% reached 4 or 5 points (n = 1 respectively). The incidence of cardiotoxicity (n = 28 [21%]) increased with the ECG score, with 0 points at 0%, 1 point 7.5%, 2 points 55%, 3 points 71% and ≥3 points 50%. In the ROC (Receiver operating curves) analysis, the best cut-off for predicting cardiotoxicity was an ECG score of ≥2 points (sensitivity 82%, specificity 82%, AUC 0.84, 95% CI 0.77–0.92, p < 0.0001) which was then defined as a high-risk score. High-risk patients did not differ concerning their age, LV ejection fraction, classical cardiovascular risk factors or cardiac biomarkers compared to those with a low-risk ECG score. Conclusion: ECG scoring prior to the start of anti-cancer therapies may help to identify therapy-naïve cancer patients at a higher risk for the development of cardiotoxicity.

scholarly journals IDH1 Non-Canonical Mutations and Survival in Patients with Glioma

Diagnostics ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 342 ◽  
Author(s):  
Enrico Franceschi ◽  
Dario De Biase ◽  
Vincenzo Di Nunno ◽  
Annalisa Pession ◽  
Alicia Tosoni ◽  
...  
Keyword(s):  
Idh1 Mutation ◽  
Who Grade ◽  
Tissue Samples ◽  
1P19q Codeletion ◽  
Idh1 R132h ◽  
Rare Mutations ◽  
Grade Ii ◽  
Idh1 Mutations ◽  
R132h Mutation ◽  
Generation Sequencing

Background: Non-canonical mutations of the isocitrate dehydrogenase (IDH) genes have been described in about 20–25% and 5–12% of patients with WHO grade II and III gliomas, respectively. To date, the prognostic value of these rare mutations is still a topic of debate. Methods: We selected patients with WHO grade II and III gliomas and IDH1 mutations with available tissue samples for next-generation sequencing. The clinical outcomes and baseline behaviors of patients with canonical IDH1 R132H and non-canonical IDH1 mutations were compared. Results: We evaluated 433 patients harboring IDH1 mutations. Three hundred and ninety patients (90.1%) had a canonical IDH1 R132H mutation while 43 patients (9.9%) had a non-canonical IDH1 mutation. Compared to those with the IDH1 canonical mutation, patients with non-canonical mutations were younger (p < 0.001) and less frequently presented the 1p19q codeletion (p = 0.017). Multivariate analysis confirmed that the extension of surgery (p = 0.003), the presence of the 1p19q codeletion (p = 0.001), and the presence of a non-canonical mutation (p = 0.041) were variables correlated with improved overall survival. Conclusion: the presence of non-canonical IDH1 mutations could be associated with improved survival among patients with IDH1 mutated grade II–III glioma.

scholarly journals Determining lines of therapy in patients with solid cancers: a proposed new systematic and comprehensive framework

2021 ◽  
Author(s):  
Kamal S. Saini ◽  
Chris Twelves
Keyword(s):  
Cancer Therapies ◽  
Clinical Progression ◽  
Curative Intent ◽  
Palliative Intent ◽  
Solid Malignancies ◽  
Anti Cancer ◽  
Progression Of Disease ◽  
Uniform Manner ◽  
Comprehensive Framework ◽  
Key Terms

AbstractThe complexity of neoplasia and its treatment are a challenge to the formulation of general criteria that are applicable across solid cancers. Determining the number of prior lines of therapy (LoT) is critically important for optimising future treatment, conducting medication audits, and assessing eligibility for clinical trial enrolment. Currently, however, no accepted set of criteria or definitions exists to enumerate LoT. In this article, we seek to open a dialogue to address this challenge by proposing a systematic and comprehensive framework to determine LoT uniformly across solid malignancies. First, key terms, including LoT and ‘clinical progression of disease’ are defined. Next, we clarify which therapies should be assigned a LoT, and why. Finally, we propose reporting LoT in a novel and standardised format as LoT N (CLoT + PLoT), where CLoT is the number of systemic anti-cancer therapies (SACT) administered with curative intent and/or in the early setting, PLoT is the number of SACT given with palliative intent and/or in the advanced setting, and N is the sum of CLoT and PLoT. As a next step, the cancer research community should develop and adopt standardised guidelines for enumerating LoT in a uniform manner.

Sign in / Sign up

Export Citation Format

Share Document