Triple-negative breast cancer (TNBC) is the most malignant subtype of breast cancer (BC), characterized by limited treatment options and poor clinical outcomes. Aberrant FGFR signaling has been implicated in TNBC; however, the therapeutic potential of targeting FGFRs for TNBC treatment remains unclear. This study investigated the anti-cancer activity of the selective pan-FGFR inhibitor Erdafitinib and its underlying mechanisms using both in vitro and in vivo models. The results demonstrated that Erdafitinib suppressed TNBC tumorigenicity by promoting FGFR1/4 degradation, generating reactive oxygen species (ROS), inducing DNA damage, and ultimately triggering cell death. Mechanistic analyses revealed that Erdafitinib facilitated FGFR1/4 degradation through ubiquitination, enhanced interaction between TRIM25 and FGFR1/4, and subsequent lysosomal degradation. Furthermore, RNA-seq data from the TCGA and GEO databases, along with paired tumor tissues from TNBC patients, indicated that FGFR4 was significantly upregulated in TNBC. Notably, co-knockdown of FGFR1 and FGFR4 induced cytotoxicity in MDA-MB-231 cells, highlighting the therapeutic relevance of FGFR1/4 degradation by Erdafitinib in TNBC. These findings provide novel insights into the mechanisms underlying the anti-cancer efficacy of Erdafitinib, supporting its potential as a promising therapeutic agent for TNBC.

As a zinc-containing family of endopeptidases, matrix metalloproteinases (MMPs) are not only the main hydrolytic enzymes for the degradation of extracellular matrix and basement membrane, but also the main protein family involved in tumor metastasis. In addition to playing a key role in normal physiological processes, previous studies have shown that MMPs are also important in tumorigenesis and development, including but not limited to promoting epithelial-mesenchymal transformation, angiogenesis, and inducing the expression of adhesion molecules. Therefore, as a potential diagnostic marker and therapeutic target, the relationship between MMPs and carcinogenesis and metastasis has also been widely studied. As the most frequent intraocular malignant tumor in adults, uveal melanoma (UM) poses a great threat to patients' visual acuity and lives. MMPs contribute to UM progression by promoting extracellular matrix degradation, tumor microenvironment remodeling, and metastasis. Clinical and bioinformatic studies have identified MMPs as both prognostic biomarkers and potential therapeutic targets in UM, supported by their association with tumor characteristics, immune-related phenotypes, and the expression of endogenous inhibitors like TIMPs. This article comprehensively reviews the expression profiles and clinical significance of MMPs in UM, highlighting their roles in tumor progression, metastasis, and potential as therapeutic targets.

Kidney cancer is a highly prevalent malignancy, consistently ranking among the top ten cancers affecting both men and women, and its mortality has been increasing globally. Renal cell carcinoma is the most common type and has a tendency to metastasize, with a predilection for spreading to other organs. While the adrenal gland is located adjacent to the kidney, metastasis of renal cell carcinoma to the adrenal gland is considered rare compared with other sites such as the lungs, liver, and bones. In addition, the occurrence of metastasis to the contralateral adrenal gland is an exceedingly rare phenomenon.

Many factors, including environmental and genetic variables, contribute to Colorectal Cancer (CRC) risk. The genetic components of risk can be divided into monogenic and polygenic factors. Just as monogenic factors can increase risk for more than one condition, polygenic factors may also underlie multiple phenotypes, including behavioral traits. In order to understand the biology of CRC risk better, it is important to understand the shared polygenic genetic architecture contributing to CRC risk and other phenotypes, including CRC associated risk factors.

Long non-coding RNAs (lncRNAs) play crucial roles in cancer pathogenesis, including colorectal cancer (CRC). Distinct lncRNA transcripts from the same gene show diverse regulatory roles in cancer. The MIR100HG, a lncRNA gene characterized by multiple transcript variants, has been implicated in promoting CRC oncogenesis. However, the specific functions of individual MIR100HG transcripts in tumorigenesis remain unclear.

The performance of FFPE tissue-derived DNA on the MethylationEpicV1.0 array can be unpredictable as the protocol only has two quality checks; checkpoint 1 for DNA quantity and checkpoint 2 for DNA quality assessment. We sought to incorporate a third, previously developed bisulfite conversion quality check prior to processing 255 FFPE tissue derived DNA samples.

The PEGASUS trial was the first study to evaluate and demonstrate the benefits of 68Ga-perfusion PET/CT in the lung stereotactic body radiotherapy (SBRT) planning process in preserving functional lung volumes while respecting target volume coverage and doses to other organs at risk. Here we report the prespecified exploratory endpoint of SBRT on health-related quality of life (HRQoL).

Nabothian cysts are benign cervical lesions commonly observed in women of reproductive age, typically ranging from 2 to 10 mm in diameter and often asymptomatic. These cysts arise from the obstruction of cervical mucous glands, a phenomenon frequently linked to childbirth, minor trauma, or chronic cervicitis. While small Nabothian cysts are usually incidental findings, giant Nabothian cysts-those exceeding 4 cm-are rare and can present diagnostic and therapeutic challenges. Their size and appearance may mimic malignant entities such as adenoma malignum, necessitating advanced imaging and histopathological evaluation. Although their association with infertility remains controversial, some evidence suggests that large cysts might interfere with fertility by obstructing the cervical canal or altering mucus production, which is critical for sperm transport. This report examines a rare case of giant Nabothian cysts in the context of assisted reproductive technology, highlighting their management and potential implications for infertility treatment.

Gastric cancer remains a leading cause of cancer-related mortality worldwide, characterized by poor prognosis due to its aggressive nature and high metastatic potential. While the E2-conjugating enzyme UBE2I (UBC9), essential for SUMOylation, has been implicated in various cancers, its precise role in gastric cancer remains poorly understood. In the study, we demonstrate significant UBC9 overexpression in gastric cancer tissues, which correlates with poor clinical outcomes. Functional analyses revealed that UBC9 knockdown significantly suppressed gastric cancer cell proliferation, migration, and invasion in vitro and in vivo, whereas UBC9 overexpression enhanced these malignant phenotypes. Through integrated transcriptomic and proteomic analyses, we identified ATF2 (Activating Transcription Factor 2) as a crucial downstream effector of UBC9-mediated oncogenic signaling. The mechanistic relationship between these factors was confirmed as ATF2 knockdown substantially attenuated the oncogenic effects of UBC9 overexpression. This newly identified UBC9-ATF2 regulatory axis promotes gastric cancer progression by enhancing cellular proliferation and metastatic potential. Our findings establish UBC9 and ATF2 as promising prognostic biomarkers and potential therapeutic targets, suggesting that intervention in the UBC9-ATF2 axis may provide novel therapeutic strategies for inhibiting gastric cancer progression and improving patient outcomes.

Cardiac calcified amorphous tumors (CATs) represent rare, nonneoplastic intraluminal heart masses, with limited case reports in existing literature. Asymptomatic cases localized in the right atrium are particularly unusual.

Our earlier work reported the association of inflammatory biomarker with a reduced breast cancer chemotherapy relative dose intensity (RDI) resulting in an unfavourable survival outcome. This current study aimed to assess the prognostic role of inflammatory biomarkers in patients with breast cancer, particularly Interleukin-8 (IL-8).

Aberrant cell adhesion signaling is known to either accelerate or inhibit cancer progression, but the underlying molecular basis has yet to be established. The immunoglobulin superfamily 11 (IgSF11) functions as a cell adhesion protein and is overexpressed in several types of cancer, including high-grade glioma. However, it remains unknown whether and how IgSF11 stimulates malignant phenotypes.

To quantitatively analyse the contrast-enhanced ultrasound (CEUS) parameters of endometrial lesions and explore the differences in CEUS parameters between benign and malignant endometrial lesions.

This study aimed to assess the clinical outcomes and prognostic factors of patients with synchronous head and neck squamous cell carcinoma (HNSCC) and esophageal squamous cell carcinoma (ESCC) who underwent simultaneous concurrent chemoradiotherapy (CCRT) and esophagectomy.

Sorafenib, a ferroptosis agonist, is a first-line treatment for advanced hepatocellular carcinoma (HCC). However, its clinical efficacy is limited due to drug resistance, resulting in modest improvements in patient survival. Hence, the present study has been designed to identify critical molecular targets associated with sorafenib resistance and investigate the potential inhibitors in overcoming this therapeutic challenge.

Acquired resistance is unavoidable in lung adenocarcinoma (LUAD) treated with osimertinib, however, the underlying mechanisms remain largely unknown. Here, we report that the long non-coding RNA (lncRNA) APCDD1L-AS1 is upregulated in osimertinib-resistant LUAD tissues and cells and is associated with short survival of osimertinib-resistant LUAD patients. Our data showed that APCDD1L-AS1 upregulation is an independent risk factor for overall survival in patients with osimertinib-resistant LUAD. APCDD1L-AS1 knockdown enhanced osimertinib sensitivity both in vitro and in vivo, whereas APCDD1L-AS1 overexpression promoted osimertinib resistance. Mechanistically, APCDD1L-AS1 accelerates the tricarboxylic acid (TCA) cycle by forming complexes and maintaining the stability of dihydrolipoamide S-succinyltransferase (DLST), which inhibits the ubiquitination and degradation of DLST. Moreover, we demonstrate that hypoxia-inducible factor (HIF)-1α transcriptionally activates APCDD1L-AS1 by binding to the APCDD1L-AS1 promoter region under hypoxic conditions. Overall, our data confirm that APCDD1L-AS1 is upregulated by hypoxia-induced HIF-1α, which drives the TCA cycle by stabilising DLST to further promote osimertinib resistance in LUAD. Our findings provide new insights into the role of HIF-1α/APCDD1L-AS1/DLST axis-related reprogramming of hypoxia and the TCA balance in conferring osimertinib resistance in LUAD and confirm the therapeutic potential for targeting the APCDD1L-AS1.

To evaluate the clinical efficacy of evidence-based Enhanced Recovery After Surgery (ERAS) nursing protocols in patients undergoing robotic-assisted partial nephrectomy using the Da Vinci system.

To explore the clinical data and CT findings associated with outcomes prognosis of patients with sarcomatoid non-small cell lung cancer (s-NSCLC).

The incidence of local recurrence remains noteworthy among lung cancer patients treated with stereotactic body radiation therapy (SBRT). The aim of the study is to identify the risk factors and develop a nomogram for local control (LC) prediction.

Effective management of patients undergoing treatment with lutetium-177 labeled DOTA-ibandronic acid (177Lu-DOTA-IBA) necessitates the identification of radiological response biomarkers that can mitigate disease progression and facilitate patient stratification for subsequent treatment decisions. This study aims to evaluate the metabolic tumor volume (MTV) as a quantitative measure of radiological response in bone metastases using gallium-68 labeled DOTA-ibandronic acid (68Ga-DOTA-IBA) PET/CT.