Search

BackgroundThe prevalence of venous thromboembolism (VTE) is high in patients with cancer and can often present as the first symptom of malignancy. Cancer-associated VTE is one of the most important risk factors contributing to cancer mortality, making its prevention and treatment critical for patients with lung cancer.MethodsWe systematically searched for observational studies that estimated the prevalence of VTE in patients with lung cancer. A comprehensive search of electronic databases, including PubMed, EMBASE and Cochrane Library, was systematically conducted from database inception through January 21, 2022. The qualities of included studies were assessed in three domains, including patient selection, comparison, and results. Random effects meta-analyses of the prevalence of VTE in lung cancer were conducted using the metaprop procedure. Chi-square test and I2 value were used to evaluate study heterogeneity.ResultsThirty-five studies involving 742,156 patients were considered eligible for this study. The pooled prevalence of VTE among patients with lung cancer was 5% (95% CI: 0.043–0.056, P = 0.000). The regional prevalence of VTE was 7% (95% CI: 0.06–0.08; I2 = 99.2%) in North America, 8% (95% CI: 0.06–0.10; I2 = 97.6%) in Asia, 6% (95% CI: 0.04–0.09; I2 = 95.9%) in Europe and 11% (95% CI: 0.07–0.15) in Australasia.ConclusionsThe prevalence of lung cancer-related VTE is high and region-specific. These results of this review emphasize the importance of understanding the incidence of lung cancer-related VTE and provide argue for VTE screening of patients with lung cancer.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/, identifier PROSPERO (CRD42022306400).

BackgroundUndifferentiated small round-cell sarcomas (uSRCSs) are a subgroup of sarcomas that are difficult to diagnose. Some uSRCSs have specific gene re-arrangements, but others do not. Currently, there is no specific treatments for advanced uSRCSs, and its treatment is largely based on general experience with sarcomas, which includes chemotherapy, targeted therapy, and immunotherapy. In this article, we report a patient with uSRCS who responded to treatment with anti-VEGF inhibitor surufatinib and anti-PD-1 inhibitor camrelizumab after progression on first-line chemotherapy, second-line anlotinib combined with immunotherapy, and third-line chemotherapy.Case descriptionIn July 2020, a 37-year-old female patient was diagnosed with advanced uSRCS. Results for the Ewing sarcoma RNA binding protein 1 and Wilms tumor suppressor (EWSR1/WT1) fusion gene were negative. The patient was also negative with BCOR (BCL6 co-repressor) and CIC (capicua transcriptional repressor) fusion gene. The next-generation sequencing results revealed point mutations on Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Beta (PIK3CB), Transcription Factor Binding To IGHM Enhancer 3 (TFE3), Mucin 16 (MUC16), and AXL (Axl, also called UFO, ARK, and Tyro7, is part of a family of receptor tyrosine kinases). The patient received 4 cycles of the Ifosfamide and epirubicin hydrochloride regimen, and her best objective response was stable disease. On November 3, 2020, a computed tomography (CT) scan revealed progressive disease (PD). Two cycles of camrelizumab (a programmed death-1 inhibitor) plus anlotinib (an anti- vascular endothelial growth factor drug) were administered, but PD was again observed. Thus, a regimen of gemcitabine plus docetaxel was adopted. Unfortunately, the disease progressed once again after two cycles of the treatment. On February 4, 2021, the patient began to receive targeted therapy with surufatinib combined with camrelizumab. A CT scan showed that the tumor achieved a partial response. As of April 2023, the patient had a progression-free survival time of 26 months.ConclusionsSurufatinib in combination with camrelizumab could be effective in the treatment of advanced uSRCSs.

PurposeThis study aimed to develop and validate a clinicopathological model to predict pathological complete response (pCR) to neoadjuvant chemotherapy (NAC) in breast cancer patients and identify key prognostic factors.MethodsThis retrospective study analyzed data from 279 breast cancer patients who received NAC at Zhejiang Provincial People’s Hospital from 2011 to 2021. Additionally, an external validation dataset, comprising 50 patients from Lanxi People’s Hospital and Second Affiliated Hospital, Zhejiang University School of Medicine from 2022 to 2023 was utilized for model verification. A multivariate logistic regression model was established incorporating clinical, ultrasound features, circulating tumor cells (CTCs), and pathology variables at baseline and post-NAC. Model performance for predicting pCR was evaluated. Prognostic factors were identified using survival analysis.ResultsIn the 279 patients enrolled, a pathologic complete response (pCR) rate of 27.96% (78 out of 279) was achieved. The predictive model incorporated independent predictors such as stromal tumor-infiltrating lymphocyte (sTIL) levels, Ki-67 expression, molecular subtype, and ultrasound echo features. The model demonstrated strong predictive accuracy for pCR (C-statistics/AUC 0.874), especially in human epidermal growth factor receptor 2 (HER2)-enriched (C-statistics/AUC 0.878) and triple-negative (C-statistics/AUC 0.870) subtypes, and the model performed well in external validation data set (C-statistics/AUC 0.836). Incorporating circulating tumor cell (CTC) changes post-NAC and tumor size changes further improved predictive performance (C-statistics/AUC 0.945) in the CTC detection subgroup. Key prognostic factors included tumor size >5cm, lymph node metastasis, sTIL levels, estrogen receptor (ER) status and pCR. Despite varied pCR rates, overall prognosis after standard systemic therapy was consistent across molecular subtypes.ConclusionThe developed predictive model showcases robust performance in forecasting pCR in NAC-treated breast cancer patients, marking a step toward more personalized therapeutic strategies in breast cancer.

ObjectiveThis study aims to evaluate the value of contrast-enhanced ultrasound (CEUS), shear wave elastography (SWE), and their combined use in the differentiation of American College of Radiology (ACR) thyroid imaging reporting and data system (TI-RADS) 4 and 5 category thyroid nodules coexisting with Hashimoto’s thyroiditis (HT).Materials and methodsA total of 133 pathologically confirmed ACR TI-RADS 4 and 5 category nodules coexisting with HT in 113 patients were included; CEUS and SWE were performed for all nodules. The sensitivity, specificity, negative predictive value (NPV), positive predictive value (PPV), accuracy, and the area under the receiver operating characteristic curve (AUC) of the SWE, CEUS, and the combined use of both for the differentiation of benign and malignant nodules were compared, respectively.ResultsUsing CEUS alone, the sensitivity, specificity, PPV, NPV, and accuracy were 89.2%, 66.0%, 81.3%, 78.6%, and 80.5%, respectively. Using SWE alone, Emax was superior to Emin, Emean, and Eratio for the differentiation of benign and malignant nodules with the best cutoff Emax >46.8 kPa, which had sensitivity of 65.1%, specificity of 90.0%, PPV of 91.5%, NPV of 60.8%, and accuracy of 74.4%, respectively. Compared with the diagnostic performance of qualitative CEUS or/and quantitative SWE, the combination of CEUS and SWE had the best sensitivity, accuracy, and AUC; the sensitivity, specificity, PPV, NPV, accuracy, and AUC were 94.0%, 66.0%, 82.1%, 86.8%, 83.5%, and 0.80 (95% confidence interval: 0.713, 0.886), respectively.ConclusionIn conclusion, CEUS and SWE were useful for the differentiation of benign and malignant ACR TI-RADS 4 and 5 category thyroid nodules coexisting with HT. The combination of CEUS and SWE could improve the sensitivity and accuracy compared with using CEUS or SWE alone. It could be a non-invasive, reliable, and useful method to differentiate benign from malignant ACR TI-RADS 4 and 5 category thyroid nodules coexisting with HT.

E3 ubiquitin ligases (E3s), the second most common cancer-related functional protein family, play vital roles in multiple tumors. However, their importance in prognosis and immunotherapy of lung adenocarcinoma (LUAD) is not clear. First, utilizing the data from The Cancer Genome Atlas (TCGA), we comprehensively assessed the expression profile and immunological association of 13 E3s in LUAD patients. Consequently, MARCH1 was considered a candidate for further study. Second, several algorithms were applied to assess the correlation between MARCH1 and immunological characteristics in the LUAD tumor microenvironment. Third, an immune risk score (IRS) was developed to predict the prognosis. Finally, the immunological relationship of MARCH1 in pan-cancer was also estimated. We found that E3s were disordered in LUAD. Among them, MARCH1 was positively correlated with most immunological characteristics, indicating that MARCH1 designed an inflamed TME in LUAD. Coincidently, LUAD with low MARCH1 expression had a poor prognosis and was not sensitive to immune checkpoint blockers. In addition, the IRS could accurately predict the prognosis. In pan-cancer, MARCH1 was also positively correlated with most immunological characteristics. In conclusion, MARCH1 could be a novel and promising biomarker for immune status and effectiveness of immunotherapy for LUAD patients.

BackgroundCongenital medulloblastoma is very rare, and many cases involve germline mutations that can lead to inherited syndromes. Here, we first report two brothers with congenital medulloblastoma who were diagnosed with Gorlin-Goltz syndrome caused by SUFU mutation.Clinical presentationMedulloblastoma was detected in two brothers at 2 and 3 months of age, with very similar imaging features. Genetic testing revealed that both children and their mother carried SUFU gene germline mutations, and both brothers were diagnosed with Gorlin-Goltz syndrome.ConclusionGorlin-Goltz syndrome-associated congenital medulloblastoma with SUFU germline mutation is very rare. Pathological types mostly involve desmoplastic/nodular or extensive nodularity; chemotherapy is the main treatment, and studies revealing prognostic data are scarce.

Long non-coding RNA LINC00152 (cytoskeleton regulator, or LINC00152) is an 828-bp lncRNA located on chromosome 2p11.2. LINC00152 was originally discovered during research on hepatocarcinogenesis and has since been regarded as a crucial oncogene that regulates gene expression in many cancer types. LINC00152 is aberrantly expressed in various cancers, including gastric, breast, ovarian, colorectal, hepatocellular, and lung cancer, and glioma. Several studies have indicated that LINC00152 is correlated with cell proliferation, apoptosis, migration, invasion, cell cycle, epithelial-mesenchymal transition (EMT), chemotherapy and radiotherapy resistance, and tumor growth and metastasis. High LINC00152 expression in most tumors is significantly associated with poor patient prognosis. Mechanistic analysis has demonstrated that LINC00152 can serve as a competing endogenous RNA (ceRNA) by sponging miRNA, regulating the abundance of the protein encoded by a particular gene, or modulating gene expression at the epigenetic level. LINC00152 can serve as a diagnostic or prognostic biomarker, as well as a therapeutic target for most cancer types. In the present review, we discuss the roles and mechanisms of LINC00152 in human cancer, focusing on its functions in chemotherapy and radiotherapy resistance.

The long non-coding RNA (lncRNA) PVT1 was first found to activate variant translocations in the plasmacytoma of mice. Human lncPVT1 is located on chromosome 8q24.21, at the same locus as the well-known MYC oncogene. LncPVT1 has been found to promote the progression of various malignancies. Chemoresistance and radioresistance seriously affect tumor treatment efficacy and are associated with the dysregulation of physiological processes in cancer cells, including apoptosis, autophagy, stemness (for cancer stem cells, CSC), hypoxia, epithelial–mesenchymal transition (EMT), and DNA damage repair. Previous studies have also implicated lncPVT1 in the regulation of these physiological mechanisms. In recent years, lncPVT1 was found to modulate chemoresistance and radioresistance in some cancers. In this review, we discuss the mechanisms of lncPVT1-mediated regulation of cellular chemoresistance and radioresistance. Due to its high expression in malignant tumors and sensitization effect in chemotherapy and radiotherapy, lncPVT1 is expected to become an effective antitumor target and chemotherapy and radiotherapy sensitizer, which requires further study.

The standard third-line treatment of metastatic colorectal cancer (mCRC) includes the small-molecule anti-vascular drugs (Regofenib and Fruquintinib) and the chemotherapy drug trifluridine and tipiracil hydrochloride (TAS-102). There is no standard treatment for mCRC if the third-line treatment failed. Therefore, it is a pressing need to develop new therapeutic approaches to improve the survival of patients who developed drug resistance to the third-line treatment. In this study, we report a case of mCRC with RAS/BRAF wild-type, who was successfully treated using cetuximab in combination with fruquintinib after resistance to chemotherapy, bevacizumab, cetuximab and regorafenib. This patient responded to this combination regimen. Then, we discuss the mechanisms of action of this combination. Furthermore, we introduce the clinical trials on the combination regimens of anti-EGFR with anti-vascular monoclonal antibodies. Finally, we discuss the clinical explorations of using combination of anti-EGFR with small-molecule anti-VEGF drugs and their potential benefits. The clinical effects of small-molecule anti-vascular drugs in combination with anti-EGFR in the treatment of CRC warrant further explored.

The long noncoding RNA (lncRNA) LINC00152, also known as CYTOR, displays aberrant expression in various cancers. However, its clinical value and functional mechanisms in breast cancer remain insufficiently understood. Our study found that LINC00152 is significantly upregulated in breast cancer, and that it acts as an indicator of poor survival prognosis. Further studies revealed that LINC00152 knockdown suppresses cell proliferation and tumorigenicity in vitro and in vivo. Mechanistic analyses demonstrated that LINC00152 directly binds to KLF5 protein and increases KLF5 stability. Moreover, LINC00152 is also a KLF5-responsive lncRNA, and KLF5 activates LINC00152 transcription by directly binding to its promoter. Our study suggests that LINC00152 promotes tumor progression by interacting with KLF5. LINC00152 may be a valuable prognostic predictor for breast cancer, and the positive feedback loop of LINC00152-KLF5 could be a therapeutic target in pharmacological strategies.

E3 ubiquitin ligases (E3s), the second most common cancer-related functional protein family, play vital roles in multiple tumors. However, their importance in prognosis and immunotherapy of lung adenocarcinoma (LUAD) is not clear. First, utilizing the data from The Cancer Genome Atlas (TCGA), we comprehensively assessed the expression profile and immunological association of 13 E3s in LUAD patients. Consequently, MARCH1 was considered a candidate for further study. Second, several algorithms were applied to assess the correlation between MARCH1 and immunological characteristics in the LUAD tumor microenvironment. Third, an immune risk score (IRS) was developed to predict the prognosis. Finally, the immunological relationship of MARCH1 in pan-cancer was also estimated. We found that E3s were disordered in LUAD. Among them, MARCH1 was positively correlated with most immunological characteristics, indicating that MARCH1 designed an inflamed TME in LUAD. Coincidently, LUAD with low MARCH1 expression had a poor prognosis and was not sensitive to immune checkpoint blockers. In addition, the IRS could accurately predict the prognosis. In pan-cancer, MARCH1 was also positively correlated with most immunological characteristics. In conclusion, MARCH1 could be a novel and promising biomarker for immune status and effectiveness of immunotherapy for LUAD patients. [ABSTRACT FROM AUTHOR]

Background: Congenital medulloblastoma is very rare, and many cases involve germline mutations that can lead to inherited syndromes. Here, we first report two brothers with congenital medulloblastoma who were diagnosed with Gorlin-Goltz syndrome caused by SUFU mutation. Clinical presentation: Medulloblastoma was detected in two brothers at 2 and 3 months of age, with very similar imaging features. Genetic testing revealed that both children and their mother carried SUFU gene germline mutations, and both brothers were diagnosed with Gorlin-Goltz syndrome. Conclusion: Gorlin-Goltz syndrome-associated congenital medulloblastoma with SUFU germline mutation is very rare. Pathological types mostly involve desmoplastic/nodular or extensive nodularity; chemotherapy is the main treatment, and studies revealing prognostic data are scarce. [ABSTRACT FROM AUTHOR]