Ovarian Cancer

Mechanistically, we demonstrated that TMEM158 positively regulates ABCG2 expression, which consequently contributes to drug resistance. In summary, we identified cfRNA TMEM158 as a potential diagnostic biomarker for ovarian cancer and elucidated the critical involvement of TMEM158-ABCG2 signaling axis in the development of doxorubicin resistance.

HRD genomic instability tests and multigene panel assessments serve as synergistic tools in EOC clinical settings, proving essential for identifying patients likely to benefit from PARPi therapy. These tools also enhance the detection of HRR and MMR gene variants, aiding in preventive care. Further investigations into the genetic profiles of HRD-negative tumors are crucial for advancing cancer risk management and developing novel therapeutic avenues.

Our study provides an example of implementation of molecular profiling in an academic pre-screening program. Further analysis will investigate treatment matching rates, drug access schemes, and their impact on treatment efficacy and survival.

This raises a possible nosological relationship between TSADUDT and SMARCA4/A2 deficient NSCLC. Increased understanding of the genetics, epigenetics, and mechanisms of oncogenesis in these poor prognostic tumors, which are often resistant to conventional treatment, opens a new horizon of therapy for the tumors.

These effects were similarly observed in OC mouse models treated with Tasquinimod. In conclusion, Tasquinimod can improve OC cells' sensitivity to DDP by down-regulating the HDAC4/p21 axis, offering insights into potential strategies for overcoming cisplatin resistance in OC.

Overall, our results provide insights into the role of TGF-β-mediated epigenetic regulation in ovarian cancer metastasis and underscore the therapeutic potential of targeting TGF-β signaling and its downstream effectors. Further research is needed to elucidate the underlying mechanisms and validate these therapeutic strategies.

Primary treatment strategies predominantly involve surgical intervention coupled with etoposide-cisplatin combination chemotherapy. In cases of recurrence, second-line chemotherapeutic agents including paclitaxel, irinotecan, and doxorubicin are commonly employed alongside localized radiotherapy. While specific genetic mutations remain elusive, emerging evidence suggests potential therapeutic effect involving mTOR inhibitors, PD-1 monoclonal antibodies, and antiangiogenic agents based on isolated case reports. The exploration of representative set of mutations will help for precise targeted therapies and remains a focal point of our ongoing research efforts.

Immune profiling shows reduced immunosuppressive regulatory T cells (Tregs) and M2 macrophages and improved CD8+ T cell/Treg ratios in LC knockout (LCKO) mice. Conversely, forced LC overexpression accelerates metastasis and increases the secretion of immunosuppressive chemokines, such as CCL22 and CCL5, highlighting the role of KRT14+ LCs in immune suppression and metastatic progression.

In a similar manner, a low-dose taxol treatment rescued mitotic errors in a high-grade serous ovarian carcinoma cell line OVKATE. Collectively, our results highlight the potential of targeting microtubule poleward flux to modify chromosome instability and provide insight into the mechanism through which low doses of taxol rescue certain mitotic errors in cancer cells.

A higher rate of P/LP variants is seen among Emirati patients at risk for hereditary breast and ovarian cancer syndrome compared with reports of similar patients from Western populations. Efforts to increase utilization and awareness of germline genetic testing are warranted among Emirati patients.

We emphasize the importance of long-term follow-up and real-world data coming from international registries to define the efficacy and safety of stopping PARPi at relapse at a pre-specified time. To this point, biomarkers able to identify the patients who will experience long-term remission with PARPi maintenance or develop early resistance are urgently needed to guide treatment decision and duration.

The findings of this study show that miR-34a-5p mediates GC apoptosis in PCOS by targeting LDHA and inhibiting glycolysis, suggesting its crucial role in PCOS pathophysiology, and offering potential therapeutic targets for improving follicular development and fertility outcomes in patients with PCOS. Further research is needed to explore the clinical implications of miR-34a-5p and its use as a biomarker for early diagnosis and prognosis of PCOS.

Yet emerging clinical and experimental evidence points to progestogens (endogenous progesterone or synthetic progesterone [progestin]) as the primary hormonal driver underlying seemingly estrogen-associated breast cancer risk...Estrogen HRT has shown an array of proven benefits, including ameliorating menopausal symptoms and improving bone health. Collective evidence thus suggests that estrogen HRT is likely to offer health benefits to perimenopausal or postmenopausal women, including breast cancer survivors, as well as young BRCA1/2 carriers with prophylactic oophorectomy for ovarian cancer prevention.

This study successfully identified MX1 as being negatively associated with AD and ovarian cancer and assessed the potential drug compounds that bind most closely to it. Our findings provide important rationale and candidate targets for the development of novel therapeutic strategies for AD and ovarian cancer.

This review will focus on some new developments including criteria and ancillary tests that may help to improve interobserver reproducibility at clinically important thresholds. These issues include proposals for a separate terminology of teratoma-associated ovarian mucinous neoplasms, the role of TP53 immunohistochemistry in distinction of crowded mucinous borderline tumors and expansile mucinous carcinomas as well as the assignment of the infiltrative pattern of invasion, which recently has been validated as important prognostic factor even in low stage mucinous ovarian carcinoma.

Positive β-catenin expression significantly correlated with tumor grade in serous ovarian carcinoma. Most low-grade serous carcinoma cases exhibited membranous β-catenin expression, whereas high-grade serous carcinoma cases predominantly displayed cytoplasmic staining. Therapeutic strategies aimed at inhibiting β-catenin signaling could provide a novel approach to improving outcomes for patients with high-grade ovarian cancer.

Stronger immunostaining of some cytokines in endometriomas compared to ovarian cancer reflects an inflammatory and immune response that could be future targets for new discoveries about the infiltrative behavior of endometriosis.

Virtually all PSROC participants in the SOLO2/ENGOT-Ov21 experienced one or more AE whilst on placebo. Furthermore, study investigators attributed one quarter of AEs to be related to placebo therapy and dose alterations and treatment changes were made based on these AE. Further work is needed to improve measurement and categorization of AEs in trials of maintenance therapy in PSROC.

Considering the in-vitro cytotoxic activity and apoptotic gene expressions of thymoquinone, an important treatment agent, since it is a promising agent for the future of cancer treatment, more comprehensive studies may pave the way for its clinical use.

In both Pt/PARPi-sensitive and -resistant cells, USP1/PARP1 combined blockade enhances replicative stress, DNA damage, and cell death. Our work dissected the biological interaction between USP1 and PARP1 and recommended this axis as a promising and powerful therapeutic choice for not only sensitive but also chemoresistant patients with ovarian cancer irrespective of their HR status.

If the NLRP3 inflammasome is to be exploited as a therapeutic target, further laboratory-based investigation is required to determine its role in cancer. Furthermore, its relationship with clinically important characteristics such as histopathological subtype may be of key significance in developing targeted therapies towards specific cohorts of patients.

Ovarian NET localizations without teratomous components have a molecular profile analogous to midgut NET metastases. For these patients, a thorough review of imaging should be performed to identify a possible undetected midgut NET and a corresponding follow-up strategy may be recommended.

ALKBH5 hinders FOXP2-mediated transcriptional repression of CEP55 to promote the malignant progression of OC via cell cycle and EMT.

The biomarker analysis revealed a clear association between elevated LLT1 expression and an immunosuppressive TME in patient cohorts from TCGA and clinical databases. Therefore, this study provides a foundation for utilizing LLT1 as a potential target to improve clinical responses in ICI non-responsive patients with upregulated LLT1.

The present study demonstrated that AHSG, derived from cancer cells, exerts a negative regulatory effect on OC cell motility, migration, and metastasis. These findings suggest that AHSG is a potential candidate for OC treatment.

This review will help to elucidate the roles of RLIP76 and VEGF in tumor and corpus luteum angiogenesis, tumorigenesis, and the specific regulation of RLIP76 and VEGF. Thus, we reviewed the potential role of RLIP76 and VEGF in the angiogenesis of the tumor and corpus luteum in the tumor and ovarian microenvironment.

Diagnostic laparoscopy could be considered before debulking surgery, to assess resectability of disease and to avoid a futile exploratory laparotomy. HIPEC after cytoreductive surgery (CRS) remains controversial, with possible survival benefit for KTs of gastric origin, particularly when peritoneal dissemination is present but the PCI is low.

Additionally, we discuss current preventive measures for BRCA1/2 mutation carriers and targeted treatment options based on the concept of synthetic lethality. Finally, we explore the challenges of acquired therapy resistance and discuss potential alternative avenues for targeting BRCA1/2 mutant tumors.

CD1a expression affected the recurrence and prognosis of OV and is closely related to various immune cell levels.

Pre-emptive treatment with antiemetics are required to manage early-phase NINV during niraparib maintenance therapy in patients with risk factors. Additional larger studies are needed to confirm these findings and to develop optimal preventive strategies for NINV.

Dysregulation of Trp metabolism in ovarian cancer tissue samples, as well as the upregulation of kynurenine expression levels in the plasma of patients with ovarian cancer, were demonstrated to be unfavorable prognostic factors for the progression-free survival of patients with ovarian cancer. The present study demonstrated that the dysregulation of Trp metabolism could potentially be used as a diagnostic biomarker for ovarian cancer, as well as the potential of targeting SLC7A5 for immunotherapeutic management of patients with ovarian cancer in the future.

The observed differences in efficacy between various angiogenesis inhibitors highlight the importance of personalized treatment approaches. Further research is warranted to explore the long-term benefits of these combination strategies and refine them to obtain optimal patient outcomes.

These results indicate marked heterogeneity of expression of metabolism-associated markers in ovarian cancer; however, there was a lack of association with clinical benefit after chemotherapy/anti-vascular endothelial growth factor treatment. Notwithstanding the lack of prognostic value, knowledge of the pattern of expression of these biomarkers in tumors can be useful for patient stratification purposes when new drugs targeting these metabolic pathways will be tested.

The prevalence and spectrum of BRCAm in OC patients from Yunnan Province are different from those in other groups. BRCA status testing is advised for all OC patients, particularly those with a family history of HBOC.

The pharmacokinetics and biodistribution results revealed a significant enhancement in the delivery of rapamycin to tumors by rapamycin PFC nanoparticles, which, in turn, led to a significant reduction in ovarian tumor growth. Therefore, rapamycin PFC nanoparticles have the potential to be clinically beneficial in cisplatin-treated ovarian cancer patients.

Silencing the expression of ATG7 or BECN1, two autophagy genes, rescued the migratory phenotype of the NKX3-2-silenced ovarian cancer cells. Taken together, these data reveal the mechanism by which the LPA-NKX3-2 axis promotes the invasiveness of ovarian cancer cells and supports the possibility of targeting NKX3-2 to reduce the migratory capacity of cancer cells in response to a permissive microenvironment.

Our study shows that GBC is potentially a clinically and molecularly different entity, with specific epidemiological, clinical, and histological features, as well as a distinctive altered immune state and genetic signature. Nevertheless, further studies are needed to better understand the biology of GBC and to identify new targets against which develop new, more effective, targeted therapies.

Zolbetuximab, a monoclonal antibody targeting claudin 18.2, showed a survival benefit in first line metastatic treatment in patients with claudin 18.2 positive gastric and gastro-oesophageal junction adénocarcinoma, in two phase III studies. CAR T-cells specifically targeting this protein have also shown promising efficacy from the second line of treatment. Considering the probable impact of the expression status of claudin 18.2 in future treatment algorithms, this review aims to present the pathophysiology underlying the targeting of claudin 18.2, summarize state of the art results of anti-claudin 18.2 therapies and discuss future challenges for the management of patients with claudin 18.2 positive gastric and gastro-oesophageal junction adenocarcinoma.

We discuss how these factors may lead to the underutilization of genetic testing in North America and throughout the world and discuss alternative models of genetic healthcare delivery. We have invited leaders in cancer genetic from around the world to tell us what they think are the barriers to testing in their host countries.

In conclusion, the obtained data reveal the potential antiproliferative, apoptotic, and anti-invasive effects of our original ThCND-AgNP molecule in ovarian cancer. While these results need further confirmation through more detailed experiments, they will provide insights for future studies.

These markers may offer a significant lead time over imaging, potentially enabling earlier intervention. Further research is needed to validate these findings.

The mapping of SRE-rich intervals in minigenes is a valuable approach for the identification of spliceogenic variants that outperforms any prediction software. Indeed, 12 spliceogenic SRE-variants were identified in the critical intervals.