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Anticancer treatments have significantly contributed to increasing cure rates of breast cancer in the last years; however, they can also lead to short- and long-term side effects, including gonadotoxicity, and compromised fertility in young women. Oncofertility is a crucial issue for young patients who have not yet completed their family planning at the time of cancer diagnosis. This review aims to cover all the latest available evidence in the field of oncofertility, including the gonadotoxicity of currently adopted anticancer therapies in the curative breast cancer setting, the available strategies for fertility preservation and the feasibility of achieving a pregnancy following anticancer treatment completion. Over the past years, a significant progress has been made in oncofertility care for young women with breast cancer. In the context of the currently available evidence, every young woman with newly diagnosed breast cancer should receive a proper and complete oncofertility counseling before starting any anticancer treatment to increase her chances of future pregnancies. [ABSTRACT FROM AUTHOR]

Takotsubo syndrome (TTS) is characterized by a transient left ventricular systolic dysfunction, burdened by significant acute and long-term mortality and morbidity. The prognosis of TTS, especially in the long-term, is influenced by both non-cardiovascular (non-CV) and CV comorbidities, among which cancer is one of the most common. The presence of a malignancy is proven to be associated with higher mortality in TTS. Moreover, a number of anticancer treatments has been reported to possibly cause TTS as a form of cardiotoxicity, even though clearcut associations are lacking. The aim of this narrative review is to sum up contemporary knowledge on the association of cancer and TTS, addressing unmet needs and practical implications. The importance of a close collaboration between cardiologists and oncologists is herein highlighted, both to allow an adequate management of the acute TTS phase, and to actively and safely return to the oncologic management once the acute setting is resolved.

Renal neoplasms are highlighted as one of the 10 most common types of cancer. Renal cell carcinoma (RCC) is the most common type of renal cancer, considered the seventh most common type of cancer in the Western world. The most frequently altered genes described as altered are VHL, PBRM1, SETD2, KDM5C, PTEN, BAP1, mTOR, TP53, TCEB1 (ELOC), SMARCA4, ARID1A, and PIK3CA. RCC therapies can be classified in three groups: monoclonal antibodies, tyrosine kinase inhibitors, and mTOR inhibitors. Besides, there are targeted agents to treat RCC. However, frequently patients present side effects and resistance. Even though many multidrug resistance mechanisms already have been reported to RCC, studies focused on revealing new biomarkers as well as more effective antitumor therapies with no or low side effects are very important. Some studies reported that natural products, such as honey, epigallocatechin-3-gallate (EGCG), curcumin, resveratrol, and englerin A showed antitumor activity against RCC. Moreover, nanoscience is another strategy to improve RCC treatment and reduce the side effects due to the improvement in pharmacokinetics and reduction of toxicities of chemotherapies. Taking this into account, we conducted a systemic review of recent research findings on RCC hallmarks, drug resistance, and adjuvant therapies. In conclusion, a range of studies reported that RCC is characterized by high incidence and increased mortality rates because of the development of resistance to standard therapies. Given the importance of improving RCC treatment and reducing adverse effects, nanoscience and natural products can be included in therapeutic strategies. [ABSTRACT FROM AUTHOR]

Simple Summary: Boron neutron capture therapy (BNCT) is an emerging anticancer treatment. The success of BNCT relies on the delivery of adequate quantities of 10B to tumor cells. Carboranes, polyhedral clusters containing boron, carbon and hydrogen atoms, are promising candidates as boron agents in BNCT. In this review, we provide an overview and state-of-the-art description of applications of carboranes for in vivo BNCT studies. We comprehensively report: (i) the different molecules used, (ii) their formulation and administration strategies, (iii) the tumor models investigated and (iv) qualitative and quantitative methodologies for carborane detection in in vivo experiments. Carboranes have emerged as one of the most promising boron agents in boron neutron capture therapy (BNCT). In this context, in vivo studies are particularly relevant, since they provide qualitative and quantitative information about the biodistribution of these molecules, which is of the utmost importance to determine the efficacy of BNCT, defining their localization and (bio)accumulation, as well as their pharmacokinetics and pharmacodynamics. First, we gathered a detailed list of the carboranes used for in vivo studies, considering the synthesis of carborane derivatives or the use of delivery system such as liposomes, micelles and nanoparticles. Then, the formulation employed and the cancer model used in each of these studies were identified. Finally, we examined the analytical aspects concerning carborane detection, identifying the main methodologies applied in the literature for ex vivo and in vivo analysis. The present work aims to identify the current strengths and weakness of the use of carboranes in BNCT, establishing the bottlenecks and the best strategies for future applications. [ABSTRACT FROM AUTHOR]

Chronic stress has a substantial influence on the tumor microenvironment (TME), leading to compromised effectiveness of anti-cancer therapies through diverse mechanisms. It disrupts vital functions of immune cells that play a critical role in anti-tumor immunity, such as the inhibition of dendritic cells (DCs) and lymphocytes, while simultaneously enhancing the activity of immune cells that support tumor growth, such as myeloid-derived suppressor cells and tumor-associated macrophages. Furthermore, chronic stress exerts a significant impact on crucial mechanisms within the TME, including angiogenesis, DNA repair, hypoxia, extracellular matrix deposition, and tumor metabolism. These alterations in the TME, induced by stress, result from the activation of the hypothalamic–pituitary–adrenal axis and sympathetic nervous system, in conjunction with epigenetic modifications. In conclusion, chronic stress significantly influences the TME and impedes the efficacy of anti-cancer treatments, underscoring the importance of targeting stress pathways to improve therapeutic results.

The characteristics of patients who had never received anticancer treatments at admission of an acute supportive palliative care unit (ASPCU) have never been explored. From a consecutive sample of 422 advanced cancer patients, 62 patients with no previous anticancer therapy were selected and compared with a random sample of patients who had received anticancer treatments. Age, gender, primary tumor, Karnofsky status, characteristics of admission, the level of education, economic status, awareness of disease, the presence of cachexia, and comorbidities and palliative prognostic score, symptom intensity, opioid drugs used at admission, reasons for admission to APSCU were recorded in both groups. At time of discharge, ESAS and analgesic drugs used were recorded again. Discharge modalities were also recorded. One month after the end of recruitment period (the last patient enrollment), a follow-up was performed by phone contacts with relatives to assess survival at three months after discharge. Patients without previous anticancer therapy (14.7%) were mainly admitted to ASPCU for a low Karnofsky level and high symptom burden, often waiting for or needing a histological diagnosis to make a decision for the next therapeutic steps. This group of patients were older (P <0.0005), more frequently males (P =0.007), and had more comorbidities (P <0.0005) in comparison with treated patients. Twenty-four per cent of these patients started chemotherapy subsequently. Treatment-naive patients had a higher level of symptom burden, which was less responsive to a comprehensive palliative and more frequently died within three months in comparison with treated patients. Treatment-naive patients showed a higher level of symptom burden, which was less responsive to a comprehensive palliative treatment. In addition they more frequently died within three months in comparison with treated patients. [ABSTRACT FROM AUTHOR]

Anticancer therapies and regenerative medicine are being developed to destroy tumor cells, as well as remodel, replace, and support injured organs and tissues. Nowadays, a suitable three-dimensional structure of the scaffold and the type of cells used are crucial for creating bio-inspired organs and tissues. The materials used in medicine are made of non-degradable and degradable biomaterials and can serve as drug carriers. Developing flexible and properly targeted drug carrier systems is crucial for tissue engineering, regenerative medicine, and novel cancer treatment strategies. This review is focused on presenting innovative biomaterials, i.e., electrospun nanofibers, 3D-printed scaffolds, and hydrogels as a novel approach for anticancer treatments which are still under development and awaiting thorough optimization. [ABSTRACT FROM AUTHOR]

Cyclic fasting or calorie-restricted, low-carbohydrate, low-protein diets, collectively referred to as fasting-mimicking diets (FMDs), demonstrated additive or synergistic antitumour effects when combined with chemotherapy, targeted therapies, or immunotherapy in several preclinical in vivo models, including murine models of breast cancer, lung cancer, and colorectal cancer. However, no data on the antitumour efficacy of cyclic FMD in patients with cancer have been published so far. Here, we aim at reporting on patients with advanced cancer achieving complete and long-lasting tumour remissions with cyclic FMD in combination with standard anticancer therapies in the context of the phase Ib NCT03340935 trial. The NCT03340935 trial enrolled 101 patients with different tumour types, and it showed that a severely calorie-restricted FMD regimen is safe and feasible in patients with cancer receiving concomitant standard-of-care antineoplastic therapies. In addition, cyclic FMD resulted in positive metabolic and immunologic modifications, thus recapitulating the biological effects that in preclinical models were found to mediate the antitumour effects of fasting/FMD. Of the 101 patients enrolled in the NCT03340935 trial, we identified five patients with advanced, poor prognosis solid neoplasms (n = 1: extensive stage small cell lung cancer; n = 1: metastatic pancreatic adenocarcinoma; n = 1: metastatic colorectal cancer; n = 2: metastatic triple-negative breast cancer), who achieved complete and long-lasting tumour responses when treated with a combination of cyclic FMD and standard systemic treatments in the context of the NCT03340935 trial. These excellent responses prompt the initiation of clinical trials to investigate cyclic FMD in combination with standard antitumour therapies in specific clinical contexts. • In the NCT03340935 trial, patients received cyclic FMD plus with standard therapies. • One patient with ES SCLC achieved CR (40 Mo.) with FMD plus pembrolizumab. • One patient with mPDAC achieved CR (52 Mo.) with FMD plus abraxane–gemcitabine. • One patient with mKRASmut CRC achieved CR (42 Mo.) with FMD plus XELIRI–bevacizumab. • Two mTNBC patients achieved CR (36 Mo., 25 Mo.) with FMD plus CBDCA + gemcitabine. [ABSTRACT FROM AUTHOR]

Abstract Background At intensive care unit (ICU) admission, the issue about prognosis of critically ill cancer patients is of clinical interest, especially after ICU discharge. Our objective was to assess the factors associated with 3- and 6-month survival of ICU cancer survivors. Methods Based on the French OutcomeRea™ database, we included solid cancer patients discharged alive, between December 2005 and November 2013, from the medical ICU of the university hospital in Grenoble, France. Patient characteristics and outcome at 3 and 6 months following ICU discharge were extracted from available database. Results Of the 361 cancer patients with unscheduled admissions, 253 (70%) were discharged alive from ICU. The main primary cancer sites were digestive (31%) and thoracic (26%). The 3- and 6-month mortality rates were 33 and 41%, respectively. Factors independently associated with 6-month mortality included ECOG performance status (ECOG-PS) of 3–4 (OR,3.74; 95%CI: 1.67–8.37), metastatic disease (OR,2.56; 95%CI: 1.34–4.90), admission for cancer progression (OR,2.31; 95%CI: 1.14–4.68), SAPS II of 45 to 58 (OR,4.19; 95%CI: 1.76–9.97), and treatment limitation decision at ICU admission (OR,4.00; 95%CI: 1.64–9.77). Interestingly, previous cancer chemotherapy prior to ICU admission was independently associated with lower 3-month mortality (OR, 0.38; 95%CI: 0.19–0.75). Among patients with an ECOG-PS 0–1 at admission, 70% (n = 66) and 61% (n = 57) displayed an ECOG-PS 0–2 at 3- and 6-months, respectively. At 3 months, 74 (55%) patients received anticancer treatment, 13 (8%) were given exclusive palliative care. Conclusions Factors associated with 6-month mortality are almost the same as those known to be associated with ICU mortality. We highlight that most patients recovered an ECOG-PS of 0–2 at 3 and 6 months, in particular those with a good ECOG-PS at ICU admission and could benefit from an anticancer treatment following ICU discharge.

Cancer treatment is associated with various side effects of antitumor agents, which increase the morbidity and mortality of these patients. Cardiovascular complications are considered to be one of the most important side effect of the anticancer drugs. The antitumor drugs that express cardiovascular effects include anthracyclines, tyrosine kinase inhibitors, taxanes, fluoropyrimidines, alkylating agents, vascular endothelial growth factor inhibitors, immune checkpoint inhibitors, proteasome inhibitors and human epidermal growth receptor type 2 antibodies. The spectrum of cardiovascular effects of anticancer drugs is broad and include, among others, heart failure, arrhythmias such as atrial fibrillation and ventricular tachyarrhythmias, hypertension (systemic or pulmonary), cardiomyopathy, myocarditis, valve disease, pericardial disease, vascular events (arterial thrombosis, venous thromboembolism) and myocardial ischemia (acute coronary syndrome, angina). The molecular mechanisms by which anti-cancer therapies lead to cardiotoxicity are diverse and vary according to the specific type of agent used. They include oxidative stress, topoisomerase 2-β inhibition in cardiomyocytes, inflammation, endothelial dysfunction, apoptosis, disruption of Ca2+ homeostasis, mitochondrial dysfunction, DNA damage, increase in various circulating microRNAs levels, alterations in the function of voltage-gated potassium channels. The management of cardiovascular complications in cancer patients is a new challenge for oncologists and cardiologists. Thus the cardio-oncology field has developed the last decade in order to precisely predict and efficiently treat the cancer treatment-related cardiovascular diseases. • Cardiovascular complications are considered to be one of the most important side effect of the anticancer drugs. • Anticancer treatments can cause cardiovascular complication with various underlying molecular mechanisms. • The management of the cardiovascular complications in cancer patients is a new challenge for oncologists and cardiologists. [ABSTRACT FROM AUTHOR]

Abstract Background Long non-coding RNA PTPRG antisense RNA 1 (PTPRG-AS1) deregulation has been reported in various human malignancies and identified as an important modulator of cancer development. Few reports have focused on the detailed role of PTPRG-AS1 in epithelial ovarian cancer (EOC) and its underlying mechanism. This study aimed to determine the physiological function of PTPRG-AS1 in EOC. A series of experiments were also performed to identify the mechanisms through which PTPRG-AS1 exerts its function in EOC. Methods Reverse transcription-quantitative polymerase chain reaction was used to determine PTPRG-AS1 expression in EOC tissues and cell lines. PTPRG-AS1 was silenced in EOC cells and studied with respect to cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo. The putative miRNAs that target PTPRG-AS1 were predicted using bioinformatics analysis and further confirmed in luciferase reporter and RNA immunoprecipitation assays. Results Our data verified the upregulation of PTPRG-AS1 in EOC tissues and cell lines. High PTPRG-AS1 expression was associated with shorter overall survival in patients with EOC. Functionally, EOC cell proliferation, migration, invasion in vitro, and tumor growth in vivo were suppressed by PTPRG-AS1 silencing. In contrast, cell apoptosis was promoted by loss of PTPRG-AS1. Regarding the mechanism, PTPRG-AS1 could serve as a competing endogenous RNA in EOC cells by decoying microRNA-545-3p (miR-545-3p), thereby elevating histone deacetylase 4 (HDAC4) expression. Furthermore, rescue experiments revealed that PTPRG-AS1 knockdown-mediated effects on EOC cells were, in part, counteracted by the inhibition of miR-545-3p or restoration of HDAC4. Conclusions PTPRG-AS1 functioned as an oncogenic lncRNA that aggravated the malignancy of EOC through the miR-545-3p/HDAC4 ceRNA network. Thus, targeting the PTPRG-AS1/miR-545-3p/HDAC4 pathway may be a novel strategy for EOC anticancer therapy.

Background: Most lung cancers are diagnosed at an advanced stage and therefore have a poor prognosis. One major challenge is to choose the most adapted sampling technique to obtain a rapid pathological diagnosis so as to start treatment as early as possible. A growing number of techniques have been developed in recent years. This study sought to assess the diagnostic efficiency of each, along with the respective duration of the diagnostic pathways., Methods: This retrospective, bicentric, observational study enrolled patients with inoperable lung cancer (stage III or IV) diagnosed in 2018-2019. Diagnostic efficiency was assessed based on the different examinations performed to achieve a precise diagnosis (pathology, immunohistochemistry, and/or molecular biology). The time between the first medical contact and treatment initiation was also assessed., Results: Overall, 625 patients were included (median age 67 years; men 67 %; adenocarcinoma 55 %). The most frequent examinations were bronchial endoscopy (n = 469, 75 %), followed by metastasis biopsy (n = 137, 21.9 %) and guided transthoracic core-needle biopsy (TCNB) (n = 116, 18.6 %). 372 patients had only one procedure (59.5 %), mainly bronchial endoscopy (n = 217, 34.7 %) and metastasis biopsy (n = 71, 11 %). The most efficient examination was thoracic surgery (surgical pleural biopsy, (n = 32, 100 %); mediastinoscopy (n = 26, 96.3 %); surgical pulmonary biopsy (n = 14, 93.3 %). The second most efficient examination was metastasis biopsy (n = 126, 94 %) followed by guided TCNB (n = 108, 93.1 %). The median time from first medical contact to first examination was 4 days (interquartile range 25 %-75 % 1-8). The median time from first medical contact to pathological result was 17 days (10-34). The median time from first medical contact to treatment start was 48 days (30-69)., Conclusions: In order to make an accurate and rapid diagnosis of lung cancer, it is crucial to choose the most appropriate technique. Bronchial endoscopy remains the first-line examination for central lesions, as it is efficient and easily accessible. Guided TCNB and metastasis biopsy are the preferred techniques for peripheral lesions. The choice of the diagnostic technique should be part of a multidisciplinary approach and a dedicated pathway to optimize initial management., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Rapid development of anticancer treatments in recent years has greatly improved prognosis of cancer patients. However, with extension of survival time of cancer patients, various short-term and long-term side effects brought about by anticancer treatments, especially cardiotoxicity, have become increasingly prominent. Nonetheless, at present, there is few diagnostic methods with extremely high sensitivity and specificity to detect and accurately predict whether patients with anticancer treatment will experience cardiovascular complications. Inflammation, fibrosis and oxidative stress are considered to be important mechanisms involved in cardiotoxicity anticancer treatments. The cardiovascular biomarkers having the ability to predict and detect cardiovascular dysfunction earlier than clinical symptoms as well as left ventricular ejection fraction monitored by echocardiography, are of great value to timely treatment adjustment and prognosis evaluation. Cardiac troponin T/I and brain natriuretic peptide/N-terminal prohormone of brain natriuretic peptide have been routinely used in clinical practice to monitor cardiotoxicity, and some new biomarkers such as soluble suppression of tumorigenecity-2, myeloperoxidase, growth differentiation factor-15, galectin-3, endothelin-1, have potential in this area. In the future, larger-scale experimental studies are needed to provide sufficient evidences, and how to detect them quickly and at low cost is also a problem to be dealed with. [ABSTRACT FROM AUTHOR]

Long intergenic non-protein coding RNA 1124 (LINC01124) has been identified as an important regulator of non-small-cell lung cancer. However, the expression and detailed role of LINC01124 in hepatocellular carcinoma (HCC) remain unestablished to date. Therefore, this study aimed to elucidate the role of LINC01124 in the aggressiveness of HCC cells and identify the underlying regulatory mechanism. Quantitative reverse transcriptase-polymerase chain reaction was performed to measure the expression of LINC01124 in HCC. Cell Counting Kit-8 assay, Transwell cell migration and invasion assays, and a xenograft tumor model were used to investigate the function of LINC01124 in HCC cells, and bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and rescue experiments were used to elucidate the underlying mechanisms. Herein, LINC01124 overexpression was confirmed in HCC tissues as well as cell lines. Further, the downregulation of LINC01124 decreased HCC cell proliferation, migration, and invasion in vitro, whereas the upregulation of LINC01124 triggered the opposite results. Additionally, LINC01124 ablation impaired tumor growth in vivo. Mechanistic analyses revealed that LINC01124 functions as a competing endogenous RNA to sponge microRNA-1247-5p (miR-1247-5p) in HCC cells. Moreover, forkhead box O3 (FOXO3) was identified as a direct target of miR-1247-5p. FOXO3 was positively regulated by LINC01124 in HCC cells through the sequestration of miR-1247-5p. Finally, rescue assays revealed that the inhibition of miR-1247-5p or overexpression of FOXO3 reversed the effects of LINC01124 silencing on the HCC cell malignant phenotype. In summary, LINC01124 plays a tumor-promoting role in HCC by regulating the miR-1247-5p--FOXO3 axis. The LINC01124--miR-1247-5p--FOXO3 pathway may provide a foundation for the identification of alternative therapies for HCC. [ABSTRACT FROM AUTHOR]

Background: At intensive care unit (ICU) admission, the issue about prognosis of critically ill cancer patients is of clinical interest, especially after ICU discharge. Our objective was to assess the factors associated with 3- and 6-month survival of ICU cancer survivors.Methods: Based on the French OutcomeRea™ database, we included solid cancer patients discharged alive, between December 2005 and November 2013, from the medical ICU of the university hospital in Grenoble, France. Patient characteristics and outcome at 3 and 6 months following ICU discharge were extracted from available database.Results: Of the 361 cancer patients with unscheduled admissions, 253 (70%) were discharged alive from ICU. The main primary cancer sites were digestive (31%) and thoracic (26%). The 3- and 6-month mortality rates were 33 and 41%, respectively. Factors independently associated with 6-month mortality included ECOG performance status (ECOG-PS) of 3-4 (OR,3.74; 95%CI: 1.67-8.37), metastatic disease (OR,2.56; 95%CI: 1.34-4.90), admission for cancer progression (OR,2.31; 95%CI: 1.14-4.68), SAPS II of 45 to 58 (OR,4.19; 95%CI: 1.76-9.97), and treatment limitation decision at ICU admission (OR,4.00; 95%CI: 1.64-9.77). Interestingly, previous cancer chemotherapy prior to ICU admission was independently associated with lower 3-month mortality (OR, 0.38; 95%CI: 0.19-0.75). Among patients with an ECOG-PS 0-1 at admission, 70% (n = 66) and 61% (n = 57) displayed an ECOG-PS 0-2 at 3- and 6-months, respectively. At 3 months, 74 (55%) patients received anticancer treatment, 13 (8%) were given exclusive palliative care.Conclusions: Factors associated with 6-month mortality are almost the same as those known to be associated with ICU mortality. We highlight that most patients recovered an ECOG-PS of 0-2 at 3 and 6 months, in particular those with a good ECOG-PS at ICU admission and could benefit from an anticancer treatment following ICU discharge. [ABSTRACT FROM AUTHOR]

Background: Generalizability of registrative clinical trials to real-world clinical practice is influenced by comparability of patients in the two settings. We compared characteristics of cancer patients in registrative trials with real-world clinical practice in Italy., Methods: Data on age, sex and performance status (PS) were derived from web-based monitoring registries developed by Italian Medicines Agency (AIFA) and corresponding registrative trials reported in the European Public Assessment Reports (EPAR) of European Medicines Agency (EMA). Weighted means were calculated in registries and trials and differences were described. Multivariate analysis was performed using Principal Component Analysis and Cluster Analysis., Findings: From January, 2013 to April, 2023, 419,461 unique pairs of patients and therapeutic indications were recorded in 129 AIFA registries. Within 140 related trials, 87,452 patients had been enrolled. Median age and rate of elderly (≥65 years old) patients were higher in monitoring registries than in clinical trials [mean difference of median age 5.3 years, p < 0.001; mean difference of elderly rate 17.17% (95% CI 1.06, 1.48)]. Overall, rate of female patients was not different between registries and trials [mean difference -0.55% (95% CI -1.06, -0.05)]. Mean rate of patients with deteriorated PS was low both in trials (3.1%) and in registries (4.3%) with a mean difference of 1.27% (95% CI 1.06, 1.48). Two clusters were identified with multivariate analysis: one including more registries (higher median age and elderly rate, lower female rate, higher rate of deteriorated patients), the other more trials (lower median age and elderly rate, higher female rate, lower rate of deteriorated patients)., Interpretation: This study supports that cancer patients enrolled in trials do only partially represent those who have been treated in Italy in clinical practice. Inclusiveness of registrative trials should be increased to ensure generalizability of results to real-world population., Funding: Partially supported by Italian Ministry of Health., Competing Interests: SC declares: support for attending meetings and/or travel from Novartis and Roche; payment for participation on advisory board from EliLilly and AstraZeneca; leadership in scientific society: President of AIOM 2021–2023. MCP declares: institutional grants or contracts from Bayer, AstraZeneca, Roche; payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events from Astellas, Pfizer, Ipsen, AstraZeneca; support for attending meetings and/or travel from Menarini. MDM declares: institutional grants or contracts from Tesaro/GSK, Beigene, Exelixis, MSD, Pfizer and Roche; fees for consulting or participation in advisory board from AstraZeneca, Boehringer Ingelheim, Janssen, Merck Sharp & Dohme, Novartis, Pfizer, Roche, GlaxoSmithKline, Amgen, Merck, Takeda. FP declares: institutional grants or contracts from Roche, Bayer, AstraZeneca, Pfizer, Incyte, Tesaro/GSK, Merck; consulting fees from Bayer, Pierre Fabre, Astra Zeneca, Incyte, Ipsen, Clovis, Astellas, Sanofi, Roche, Pfizer; leadership in scientific society: President of AIOM 2023–2025. All the other Authors declare no potential conflict of interest., (© 2024 The Author(s).)

Context Omega-3 (n-3) polyunsaturated fatty acids (PUFAs), especially docosahexaenoic acid and eicosapentaenoic acid, demonstrate possible beneficial effects as adjuvants in cancer treatment. One mechanism seems to be related to alterations in the redox status of cancer cells. Such alterations are thought to act in synergy with conventional anticancer agents. Objective This review examines published data on the effects of cotreatment with anticancer agents and n-3 PUFAS on oxidative stress parameters to determine whether any patterns of oxidative stress alterations can be identified. Data Sources A systematic search of MEDLINE (via PubMed) was conducted to identify articles published in English, Spanish, or Portuguese until November 2017. Study Selection The following inclusion criteria were applied: (1) individuals or animals with cancer or malignant cell lines supplemented with some source of n-3 PUFAs; (2) concomitant use of anticancer treatment; and (3) evaluation of oxidative stress–related variables. Data Extraction A standardized outline was used to extract the following data: study type, supplement used, type of cells, tumor or patient characteristics, study design, anticancer treatment used, and oxidative stress-related outcomes. Results After the literature search and screening of 1563 citations, 28 studies were included for data extraction and evaluation: 16 in vitro studies (2 of which also used in vivo studies), 8 animal studies, and 4 human studies (3 clinical trials and 1 case series). In most in vitro and animal studies, intervention groups receiving cotreatment with n-3 PUFAs showed enhanced lipid peroxidation and cytotoxicity compared with groups receiving anticancer treatment alone. Eleven of the 12 studies that investigated the effect of vitamin E on the sensitivity of cancer cells to the oxidative stress caused by n-3 PUFAs showed that vitamin E abolished the positive effects of cotreatment. Conclusions Alterations in oxidative stress caused by cotreatment with anticancer agents and n-3 PUFAs can exert positive effects on the efficacy of conventional treatment. This seems to occur in most cells and tumors tested thus far, but not all. Identifying tumors that are sensitive to these oxidative effects may provide support for the rational use of n-3 PUFAs as an adjuvant treatment in specific types of cancer. [ABSTRACT FROM AUTHOR]

Introduction Li-Fraumeni syndrome (LFS), due to TP53 germline mutations, is characterised by a remarkably high incidence of multiple primary cancers (MPCs), and the key role of p53 in response to DNA damage questions the contribution of anticancer treatments to MPCs development. Materials and methods We first evaluated genotoxicity of X-rays and different classes of conventional chemotherapies, thanks to genotoxicity assays, based on the measurement of transcriptional response to DNA damage and performed in murine splenocytes, either exposed ex vivo or extracted from exposed mice. We then exposed a total of 208 Trp53 Δ / Δ, wt/ Δ or wt/wt mice to clinical doses of X-rays or genotoxic or non-genotoxic chemotherapies. Tumour development was monitored using whole-body magnetic resonance imaging and pathological examination at death. Results: X-rays and conventional chemotherapies, except mitotic spindle poisons, were found to be genotoxic in both p53 genotoxicity assays. Exposition to X-rays and the topoisomerase inhibitor etoposide, analysed as genotoxic anticancer treatment, drastically increase the tumour development risk in Trp53 Δ / Δ and wt/ Δ mice (hazard ration [HR] = 4.4, 95% confidence interval [CI] [2.2–8.8], p < 0.001*** and HR = 4.7, 95% CI [2.4–9.3], p < 0.001***, respectively). In contrast, exposure to the non-genotoxic mitotic spindle poison, docetaxel, had no impact on tumour development. Conclusions This study shows that radiotherapy and genotoxic chemotherapies significantly increase the risk of tumour development in a LFS mice model. These results strongly support the contribution of genotoxic anticancer treatments to MPC development in LFS patients. Therefore, to reduce the risk of MPCs in germline TP53 mutation carriers, radiotherapy should be avoided whenever possible, surgical treatment prioritised, and non-genotoxic treatments considered. [ABSTRACT FROM AUTHOR]

Introduction: Anticancer treatments such as aggressive chemotherapy and radiotherapy have deleterious gonadotoxic side effects and are considered the most common causes of pathological and iatrogenic fertility loss in women. Areas covered: In order to preserve fertility of young women and girls with cancer, several established, experimental, and debatable options can be offered in the emerging field of oncofertility. This article reviews the effects of anticancer treatments on female fertility and discusses the current challenges and future directions of fertility preservation options that can be offered to the female patients with cancer. Expert commentary: Although promising, several medical, economic, social and legal barriers face oncofertility practice around the globe especially in underserved areas. To overcome such barriers, more effective solutions should be provided to spread awareness and enhance communication between patients, oncologists and gynecologists. Early referral by oncologists before initiation of chemotherapy and radiotherapy is an important key factor for success in female fertility preservation strategies. [ABSTRACT FROM AUTHOR]

Anticancer treatments induce vulvovaginal complications that alter the quality of life and sexuality of patients. New technologies, such as photobiomodulation, could address this problem, for which few effective therapeutic solutions exist. The objective of this study was to describe the characteristics of patients seeking treatment and to observe the effects of photobiomodulation. This is a prospective cohort of patients treated for cancer, in failure of first-line medical treatment, managed at the University Hospital of Nîmes. The history, symptoms and impact of the disorders on their quality of life were collected. At follow-up, improvement was assessed using the PGI-I and FSFI questionnaires. Twenty-eight patients were treated. They were all menopausal, half of them after anticancer treatments [chemotherapy (78%), radiotherapy (36%), hormone therapy (36%)]. The main symptom reported was vaginal dryness (72%). Seventy-one percent of patients (n=20) felt that their daily life was affected≥8/10. All patients had sexual dysfunction. Twenty-two patients received at least 6 sessions of photobiomodulation. Seventy-two percent (n=18) of patients felt better or much better after treatment (PGI-I≤2). The median improvement estimated by the patients was 65% (Q1=50%; Q3=72.5%). There was also a significant clinical improvement. No serious adverse events were reported. Due to the small number of patients in a heterogeneous population with no control group, we cannot extrapolate our results. However, the objective was to assess the status of these pathologies and the contribution of photobiomodulation in patients who have failed first-line treatment; and these results are encouraging., (Copyright © 2023 Société Française du Cancer. Published by Elsevier Masson SAS. All rights reserved.)

The article focuses on the mutation detected on 22 samples of glioblastoma (GBM) which affects the codon 132 of the isocitrate dehydrogenase 1 gene (IDH1) in chromosome locus 2q33. It mentions that detecting IDH1 mutations can help diagnose and treat patients with glioma. It adds that the development of a therapeutic method to control the activity of IDH1 can help make wild type (wt) IDH1 tumor cells become sensitive to the cytotoxic impacts of radio and chemotherapy to enhance patient outcome.

Long intergenic non-protein coding RNA 1124 (LINC01124) has been identified as an important regulator of non-small-cell lung cancer. However, the expression and detailed role of LINC01124 in hepatocellular carcinoma (HCC) remain unestablished to date. Therefore, this study aimed to elucidate the role of LINC01124 in the aggressiveness of HCC cells and identify the underlying regulatory mechanism. Quantitative reverse transcriptase-polymerase chain reaction was performed to measure the expression of LINC01124 in HCC. Cell Counting Kit-8 assay, Transwell cell migration and invasion assays, and a xenograft tumor model were used to investigate the function of LINC01124 in HCC cells, and bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and rescue experiments were used to elucidate the underlying mechanisms. Herein, LINC01124 overexpression was confirmed in HCC tissues as well as cell lines. Further, the downregulation of LINC01124 decreased HCC cell proliferation, migration, and invasion in vitro , whereas the upregulation of LINC01124 triggered the opposite results. Additionally, LINC01124 ablation impaired tumor growth in vivo . Mechanistic analyses revealed that LINC01124 functions as a competing endogenous RNA to sponge microRNA-1247-5p (miR-1247-5p) in HCC cells. Moreover, forkhead box O3 (FOXO3) was identified as a direct target of miR-1247-5p. FOXO3 was positively regulated by LINC01124 in HCC cells through the sequestration of miR-1247-5p. Finally, rescue assays revealed that the inhibition of miR-1247-5p or overexpression of FOXO3 reversed the effects of LINC01124 silencing on the HCC cell malignant phenotype. In summary, LINC01124 plays a tumor-promoting role in HCC by regulating the miR-1247-5p-FOXO3 axis. The LINC01124-miR-1247-5p-FOXO3 pathway may provide a foundation for the identification of alternative therapies for HCC., Competing Interests: The authors declare that they have no conflicts of interest to report regarding the present study., (© 2022 Sun et al.)

Background: Depression is a common psychiatric problem in the elderly and oncology patients. In elderly people with cancer, depression has a peculiar phenomenology. It has a significant impact on the quality of life. Moreover, it is associated with poor adherence to treatments, increased risk of suicide, and mortality. Nevertheless, the topic of depression in elderly people with cancer remains unexplored., Objective: The main goal of this article is to review the literature from the past 20 years on the relationships between depression, cancer, and aging., Methods: The methods followed the Prisma model for eligibility of studies. The articles in which the keywords "depression", "cancer", " elderly, aging, or geriatric" were present, either in the text or in the abstract, were selected. 8.056 articles, by matching the keywords "depression and elderly and cancer," were identified. Only 532 papers met the eligibility criteria of search limits and selection process. Out of 532 papers, 467 were considered irrelevant, leaving 65 relevant studies. Out of 65 suitable studies, 39 (60.0%) met our quality criteria and were included., Results: The risk factors associated with depression in elderly people with cancer can be divided into 4 groups: 1) tumor-related; 2) anticancer treatment-related; 3) patients-related; 4) number and type of comorbidity. The main obstacles in diagnosing depression in elderly patients with cancer are the overlap of the symptoms of cancer and side effects of treatment with the symptoms of depression but also the different ways of reporting depressive symptoms of elderly people and the different clinical types of depression. There is a lack of data regarding validated scales to assess depression in geriatric patients with cancer. Any mental illness, specifically co-occurring anxiety and depression, increases the risk of diagnosis delay and anticancer treatment adherence. Cancer and the diagnosis of mental disorders prior to cancer diagnosis correlate with an increased risk for suicide. A non-pharmacological therapeutic approach, pharmacological treatment and/or a combination of both can be used to treat elderly patients with cancer, but a detailed analysis of comorbidities and the assessment of polypharmacy is mandatory in order to avoid potential side-effects and interactions between antidepressants and the other drugs taken by the patients., Conclusion: Future research should be conducted with the aim of developing a modified and adapted assessment method for the diagnosis and treatment of depression in elderly people with cancer in order to improve their clinical outcomes and quality of life., (© 2021 Massa et al.)

There is a need for new, safer, and more effective agents to treat cancer. Cytostatics that have transition metals at their core have attracted renewed interest from scientists. Researchers are attempting to use chemotherapeutics, such as cisplatin, in combination therapy (i.e., in order to enhance their effectiveness). Moreover, studies are being carried out to modify molecules, by developing them into multinuclear structures, linking different compounds to commonly used drugs, or encapsulating them in nanoparticles to improve pharmacokinetic parameters, and increase the selectivity of these drugs. Therefore, we attempted to organize recent drug findings that contain palladium and platinum atoms in their structures. [ABSTRACT FROM AUTHOR]

Background: Long non-coding RNA PTPRG antisense RNA 1 (PTPRG-AS1) deregulation has been reported in various human malignancies and identified as an important modulator of cancer development. Few reports have focused on the detailed role of PTPRG-AS1 in epithelial ovarian cancer (EOC) and its underlying mechanism. This study aimed to determine the physiological function of PTPRG-AS1 in EOC. A series of experiments were also performed to identify the mechanisms through which PTPRG-AS1 exerts its function in EOC. Methods: Reverse transcription-quantitative polymerase chain reaction was used to determine PTPRG-AS1 expression in EOC tissues and cell lines. PTPRG-AS1 was silenced in EOC cells and studied with respect to cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo. The putative miRNAs that target PTPRG-AS1 were predicted using bioinformatics analysis and further confirmed in luciferase reporter and RNA immunoprecipitation assays. Results: Our data verified the upregulation of PTPRG-AS1 in EOC tissues and cell lines. High PTPRG-AS1 expression was associated with shorter overall survival in patients with EOC. Functionally, EOC cell proliferation, migration, invasion in vitro, and tumor growth in vivo were suppressed by PTPRG-AS1 silencing. In contrast, cell apoptosis was promoted by loss of PTPRG-AS1. Regarding the mechanism, PTPRG-AS1 could serve as a competing endogenous RNA in EOC cells by decoying microRNA-545-3p (miR-545-3p), thereby elevating histone deacetylase 4 (HDAC4) expression. Furthermore, rescue experiments revealed that PTPRG-AS1 knockdown-mediated effects on EOC cells were, in part, counteracted by the inhibition of miR-545-3p or restoration of HDAC4. Conclusions: PTPRG-AS1 functioned as an oncogenic lncRNA that aggravated the malignancy of EOC through the miR-545-3p/HDAC4 ceRNA network. Thus, targeting the PTPRG-AS1/miR-545-3p/HDAC4 pathway may be a novel strategy for EOC anticancer therapy. [ABSTRACT FROM AUTHOR]

Competing Interests: V. Sibaud déclare avoir des liens ponctuels avec Amgen, BMS, Boehringer Ingelheim, MSD, Novartis, Pierre Fabre et Roche.

Cancer therapy is mainly based on different combinations of surgery, radiotherapy, and chemotherapy. Additionally, targeted therapies (designed to disrupt specific tumor hallmarks, such as angiogenesis, metabolism, proliferation, invasiveness, and immune evasion), hormonotherapy, immunotherapy, and interventional techniques have emerged as alternative oncologic treatments. Conventional imaging techniques and current response criteria do not always provide the necessary information regarding therapy success particularly to targeted therapies. In this setting, MR imaging offers an attractive combination of anatomic, physiologic, and molecular information, which may surpass these limitations, and is being increasingly used for therapy response assessment., (Copyright © 2016 Elsevier Inc. All rights reserved.)