Noninvasive prenatal screening and diagnosis of two fetuses with Williams syndrome in a cohort of 19,607 pregnancies.

BACKGROUND: This study aimed to evaluate the efficiency of noninvasive prenatal screening (NIPS) technology in screening for microdeletions in the 7q11.23 region. METHODS: 19,607 pregnant women underwent NIPS in our hospital. Maternal peripheral cell-free foetal DNA (cffDNA) was routinely screened for aneuploidy by cffDNA enrichment and simultaneously analyzed for pathogenic copy number variants (CNVs). The Williams syndrome (WS) 7q11.23 region was targeted in this study. Chromosomal microarray analysis (CMA) was used to verify the screen-positive samples. RESULTS: The mean concentration of cffDNA before and after enrichment increased from 9.44% to 19.32%, with a statistically significant difference. Two out of 19,607 samples tested for CNVs were found to have a heterozygous deletion at the 7q11.23 region, indicating a high risk for WS. CMA results confirmed the 1.5 megabase (Mb) deletions at the 7q11.23 region in amniotic fluid samples. One of the two WS foetuses had a small left ventricle by ultrasound screening, and the other did not have a significant cardiovascular abnormality phenotype. CONCLUSIONS: NIPS screening for Williams syndrome can be achieved by enriching cell-free foetal DNA and improving bioinformatic analysis algorithms.

PPIC-labeled CAFs: Key players in neoadjuvant chemotherapy resistance for gastric cancer.

BACKGROUND: Gastric cancer (GC) is the fourth leading cause of cancer deaths, with advanced cases having a median survival of less than one year. Neoadjuvant chemotherapy (NCT) is vital but faces drug resistance issues, partly due to cancer-associated fibroblasts (CAFs). Yet, specific CAF subpopulations contributing to resistance are poorly understood. METHODS: Differentially expressed genes (DEGs) between chemosensitive and resistant GC patients were identified using GEO2R. Single-cell sequencing (scRNA-seq) identified CAF-related genes. Immunohistochemistry verified key genes in NCT-treated GC samples, analyzing their correlation with tumor regression grade (TRG) and clinicopathological characteristics. RESULTS: PPIC as a gene highly expressed in CAFs was closely associated with NCT resistance in gastric cancer. Immunohistochemistry results revealed positivity for the expression of cyclophilin C (CypC), encoded by PPIC, in the 5-fluorouracil and cisplatin NCT resistant and -sensitive groups of gastric cancer patients at rates of 69.7 % (76/109) and 43.6 % (24/55), respectively (p < 0.001). The high expression of CypC in CAFs was positively correlated to tumor size (p = 0.025), T stage (p = 0.004), TNM stage (p = 0.004), and vascular invasion (p = 0.027). In cancer cells the expression of CypC was associated with OS (p = 0.026). However, in CAFs, CypC expression was not related to OS (p = 0.671). CONCLUSIONS: PPIC-labeled CAF subgroups are related to NCT resistance and poor prognosis in GC and they may cause drug resistance through signaling pathways such as glucose metabolism and extracellular matrix remodeling. However, the exact mechanism behind the involvement of PPIC-labeled CAF in drug resistance of GC requires further study.

Primary malignant melanoma of the gastroesophageal junction with KIT gene exon 11 mutation.

Mucosal melanoma (MM) represents an uncommon form of melanoma. Primary gastrointestinal tract (GIT) melanoma is even rarer. A 70-year-old male visited the Liaoning Cancer Hospital and Institute, China, due to upper abdominal discomfort for the past two months. His endoscopy revealed a prominent, 6-cm ulcerated neoplasm in the gastroesophageal junction (GEJ). Lesion endoscopic biopsy showed diffusely distributed tumour cells. He underwent subtotal gastrectomy with lymph node dissection (LND). Postoperative histopathology revealed a diffuse distribution of tumour cells with numerous tumourinfiltrating lymphocytes (TILs) and pigment granules. Immunohistochemical (IHC) results were positive for both S-100 and HMB-45. Molecular analysis showed KIT gene exon 11 mutations. Although the clinicians emphasised the necessity of systemic chemotherapy and immunotherapy with the patient and his family, the patient did not receive any adjuvant therapy and died 36 months after surgery. Primary malignant melanoma of GEJ should be considered in a differential diagnosis for gastrointestinal malignancies, especially after excluding the source of metastasis through a systemic examination.

Alleviating Pyroptosis of Intestinal Epithelial Cells to Restore Mucosal Integrity in Ulcerative Colitis by Targeting Delivery of 4-Octyl-Itaconate.

Current therapies primarily targeting inflammation often fail to address the root relationship between intestinal mucosal integrity and the resulting dysregulated cell death and ensuing inflammation in ulcerative colitis (UC). First, UC tissues from human and mice models in this article both emphasize the crucial role of Gasdermin E (GSDME)-mediated pyroptosis in intestinal epithelial cells (IECs) as it contributes to colitis by releasing proinflammatory cytokines, thereby compromising the intestinal barrier. Then, 4-octyl-itaconate (4-OI), exhibiting potential for anti-inflammatory activity in inhibiting pyroptosis, was encapsulated by butyrate-modified liposome (4-OI/BLipo) to target delivery for IECs. In brief, 4-OI/BLipo exhibited preferential accumulation in inflamed colonic epithelium, attributed to over 95% of butyrate being produced and absorbed in the colon. As expected, epithelium barriers were restored significantly by alleviating GSDME-mediated pyroptosis in colitis. Accordingly, the permeability of IECs was restored, and the resulting inflammation, mucosal epithelium, and balance of gut flora were reprogrammed, which offers a hopeful approach to the effective management of UC.

Role of pathological tumor regression grade of lymph node metastasis following neoadjuvant chemotherapy in locally advanced gastric cancer.

AIMS: To confirm whether the pathological response of lymph node metastasis (LNM) to neoadjuvant chemotherapy (NCT) can predict the prognosis of patients with gastric cancer (GC). METHODS: A total of 979 patients with locally advanced GC were included. χ2 test was used to analyze the relationship between LNM TRG and clinicopathological factors. Cox proportional hazards model was used to analyze the relationship between LNM TRG, clinicopathological factors, and overall survival (OS). RESULTS: A total of 21,162 lymph nodes were evaluated, with 237 patients (35.4%) in the response group and 433 patients (64.6%) in the non-response group. The non-responsive group was strongly associated with higher ypT, ypN, ypTNM, primary tumor (PT) TRG (all p < 0.001), positive cancer nodules (p = 0.001), and more distant LNM location (p < 0.001). Patients with the same PT TRG but different LNM TRG had different prognosis. There was no difference in OS between the responding and non-responding groups of LNM at location 2, 3, and M. YpN, tumor location, and LNM location were independent prognostic factors. CONCLUSIONS: The combination of LNM TRG and PT TRG could better predict patient prognosis. Lymph node dissection should be routinely performed after NCT to provide the reference of radical resection.

Clinical features, polysomnography, and genetics association study of restless legs syndrome in clinic based Chinese patients: A multicenter observational study.

STUDY OBJECTIVES: To systemically describe the clinical features, polysomnography (PSG) finding, laboratory tests and single-nucleotide polymorphisms (SNPs) in a clinic based Chinese primary restless legs syndrome (RLS) population. METHODS: This observational study, conducted from January 2020 to October 2021 across 22 sleep labs in China, recruited 771 patients diagnosed with RLS following the 2014 RLSSG criteria. Clinical data, PSG testing, and laboratory examination and SNPs of patients with RLS were collected. A total of 32 SNPs in 24 loci were replicated using the Asian Screening Array chip, employing data from the Han Chinese Genomes Initiative as controls. RESULTS: In this study with 771 RLS patients, 645 had primary RLS, and 617 has DNA available for SNP study. Among the 645 primary RLS, 59.7% were women. 33% had a family history of RLS, with stronger familial influence in early-onset cases. Clinical evaluations showed 10.4% had discomfort in body parts other than legs. PSG showed that 57.1% of RLS patients had periodic leg movement index (PLMI) of >5/h and 39.1% had PLMI >15/h, respectively; 73.8% of RLS patients had an Apnea-Hypopnea Index (AHI) > 5/h, and 45.3% had an AHI >15/h. The laboratory examinations revealed serum ferritin levels <75 ng/ml in 31.6%, and transferrin saturation (TSAT) of <45% in 88.7% of RLS patients. Seven new SNPs in 5 genes showed a significant allelic association with Chinese primary RLS, with one previously reported (BTBD9) and four new findings (TOX3, PRMT6, DCDC2C, NOS1). CONCLUSIONS: Chinese RLS patients has specific characters in many aspects. A high family history with RLS not only indicates strong genetic influence, but also reminds us to consider the familial effect in the epidemiological study. Newly developed sequencing technique with large samples remains to be done.

Lipid Metabolism-Related Gene Signature Predicts Prognosis and Indicates Immune Microenvironment Infiltration in Advanced Gastric Cancer.

Objective: Abnormal lipid metabolism is known to influence the malignant behavior of gastric cancer. However, the underlying mechanism remains elusive. In this study, we comprehensively analyzed the biological significance of genes involved in lipid metabolism in advanced gastric cancer (AGC). Methods: We obtained gene expression profiles from The Cancer Genome Atlas (TCGA) database for early and advanced gastric cancer samples and performed differential expression analysis to identify specific lipid metabolism-related genes in AGC. We then used consensus cluster analysis to classify AGC patients into molecular subtypes based on lipid metabolism and constructed a diagnostic model using least absolute shrinkage and selection operator- (LASSO-) Cox regression analysis and Gene Set Enrichment Analysis (GSEA). We evaluated the discriminative ability and clinical significance of the model using the Kaplan-Meier (KM) curve, ROC curve, DCA curve, and nomogram. We also estimated immune levels based on immune microenvironment expression, immune checkpoints, and immune cell infiltration and obtained hub genes by weighted gene co-expression network analysis (WGCNA) of differential genes from the two molecular subtypes. Results: We identified 6 lipid metabolism genes that were associated with the prognosis of AGC and used consistent clustering to classify AGC patients into two subgroups with significantly different overall survival and immune microenvironment. Our risk model successfully classified patients in the training and validation sets into high-risk and low-risk groups. The high-risk score predicted poor prognosis and indicated low degree of immune infiltration. Subgroup analysis showed that the risk model was an independent predictor of prognosis in AGC. Furthermore, our results indicated that most chemotherapeutic agents are more effective for AGC patients in the low-risk group than in the high-risk group, and risk scores for AGC are strongly correlated with drug sensitivity. Finally, we performed qRT-PCR experiments to verify the relevant results. Conclusion: Our findings suggest that lipid metabolism-related genes play an important role in predicting the prognosis of AGC and regulating immune invasion. These results have important implications for the development of targeted therapies for AGC patients.

Orthogonal LoxPsym sites allow multiplexed site-specific recombination in prokaryotic and eukaryotic hosts.

Site-specific recombinases such as the Cre-LoxP system are routinely used for genome engineering in both prokaryotes and eukaryotes. Importantly, recombinases complement the CRISPR-Cas toolbox and provide the additional benefit of high-efficiency DNA editing without generating toxic DNA double-strand breaks, allowing multiple recombination events at the same time. However, only a handful of independent, orthogonal recombination systems are available, limiting their use in more complex applications that require multiple specific recombination events, such as metabolic engineering and genetic circuits. To address this shortcoming, we develop 63 symmetrical LoxP variants and test 1192 pairwise combinations to determine their cross-reactivity and specificity upon Cre activation. Ultimately, we establish a set of 16 orthogonal LoxPsym variants and demonstrate their use for multiplexed genome engineering in both prokaryotes (E. coli) and eukaryotes (S. cerevisiae and Z. mays). Together, this work yields a significant expansion of the Cre-LoxP toolbox for genome editing, metabolic engineering and other controlled recombination events, and provides insights into the Cre-LoxP recombination process.

Authenticity identification of high - Temperature Daqu Baijiu through multi-channel visual array sensor of organic dyes combined with smart phone App.

High - temperature Daqu Baijiu faces a challenge from illegal adulteration of high-grade Baijiu bottles with low-grade Baijiu, affecting its quality and value. This study developed a rapid identification method for high temperature Daqu Baijiu with the same aroma type using a four-channel visual array sensor and detection of color changes caused by competition coordination with Zn2+ and color-changing organic dyes. The array sensor demonstrated high stability and repeatability in targeting flavor components and achieved 97.78 % or more accuracy combined with DD-SIMCA model in detecting adulteration across the Baijiu with same aroma type. The results of GC-MS and Quantum Chemical Calculation showed that esters, acids, and pyrazines played a crucial role. The smart phone App could quickly identify the authenticity of Baijiu with accuracy achieved 93 %. This research provides a foundation for rapid and reliable assessment of Baijiu quality and authenticity, enabling the industry to combat fraudulent practices effectively.

Scientific Problem Solving and Brain Symmetry Index: An exploratory EEG study.

Scientific problem solving has recently attracted fixation in the field of cognitive neuroscience and science education. Until now, there is very little evidence on the brain dynamics of scientific problem-solving processes. In this study, we were interested in exploring whether Brain Symmetry Index (BSI) would be an EEG index to reveal neural information. The present EEG study used two levels of complexity physics problems to research the neural mechanism of problem solving. Results indicated that relatively greater BSI found during difficult problem solving on the prefrontal theta and beta band. However, smaller BSI on the occipital alpha was found when solving difficult problems. There was no significant relationship between BSI and self-effort evaluation. The current study proposes an EEG index - BSI to reflect underlying brain functional characteristic.

Correlation of clinicopathological and prognostic characteristics between endometriosis-associated and primary ovarian cancer.

BACKGROUND: The main aim of this study was to establish the clinicopathological and prognostic correlations between endometriosis-associated and non-endometriosis-associated primary ovarian cancer, with a view to providing a reference guide for revision of diagnostic criteria for malignant transformation of endometriosis. METHODS: Clinicopathological and follow-up data of 174 patients with clear cell and endometrial ovarian cancer were retrospectively extracted. Cases were divided into endometriosis-associated and non-endometriosis-associated primary ovarian cancer for comparative analysis of clinicopathological characteristics and prognosis. RESULTS: Average age and post-menopausal rate in the endometriosis-associated ovarian cancer group were lower relative to the primary ovarian cancer group (P < 0.05). Body mass index, age at menopause, operation history, dysmenorrhea, complications, tumor size, tumor side, ascites, CA125, HE4, CA19.9, stage, differentiation, expression of ER, PR, P53, P16, Ki67, MMR, HNF-1ß and Napsin A were not significantly different between the groups (P > 0.05). Furthermore, rates of resistance to platinum chemotherapy, relapse, progression-free survival and overall survival were comparable between the two groups (P > 0.05). CONCLUSION: Endometriosis-associated and primary ovarian cancers of the same pathological type are speculated to be homologous in terms of origin from malignant transformation of endometriosis. It may therefore be necessary to revise the diagnostic criteria for ovarian endometriosis malignancy.

Soil microbiota plays a key regulatory role in the outbreak of tobacco root rot.

Introduction: Root rot caused by the fungal pathogen Fusarium sp. poses significant challenges to tobacco cultivation in China, leading to major economic setbacks. The interplay between this pathogen and the wider soil microbial community remains poorly understood. Methods: High-throughput sequencing technology was utilized to evaluate soil prokaryotic, fungal, and protistan communities. We compared microbial communities in infected soils to those in healthy soils from the same field. Additionally, the influence of pH on the microbial communities was assessed. Results: Infected soils displayed elevated levels of soil nutrients but diminished observed richness across prokaryotic, fungal, and protistan groups. The pathogenic fungi Fusarium solani f sp. eumartii's abundance was notably increased in infected soils. Infection with F. solani significantly altered the soil's microbial community structure and interactions, manifested as a decrease in network scale and the number of keystone species. An evaluation of prokaryotes' role in F. solani's invasion revealed an increased number of connecting nodes in infected soils. Additionally, relationships between predatory protists and fungi were augmented, whereas predation on F. solani declined. Discussion: The study underscores the significance of comprehending the interactions among soil microorganisms and brings to light the susceptibility of soil microbial communities to pathogen invasion. It offers insights into the multifaceted relationships and potential vulnerabilities within the soil ecosystem in the context of Fusarium sp. invasion.

TEAD4 antagonizes cellular senescence by remodeling chromatin accessibility at enhancer regions.

Dramatic alterations in epigenetic landscapes are known to impact genome accessibility and transcription. Extensive evidence demonstrates that senescent cells undergo significant changes in chromatin structure; however, the mechanisms underlying the crosstalk between epigenetic parameters and gene expression profiles have not been fully elucidated. In the present study, we delineate the genome-wide redistribution of accessible chromatin regions that lead to broad transcriptome effects during senescence. We report that distinct senescence-activated accessibility regions (SAAs) are always distributed in H3K27ac-occupied enhancer regions, where they are responsible for elevated flanking senescence-associated secretory phenotype (SASP) expression and aberrant cellular signaling relevant to SASP secretion. Mechanistically, a single transcription factor, TEAD4, moves away from H3K27ac-labled SAAs to allow for prominent chromatin accessibility reconstruction during senescence. The enhanced SAAs signal driven by TEAD4 suppression subsequently induces a robust increase in the expression of adjacent SASP genes and the secretion of downstream factors, which contribute to the progression of senescence. Our findings illustrate a dynamic landscape of chromatin accessibility following senescence entry, and further reveal an insightful function for TEAD4 in regulating the broad chromatin state that modulates the overall transcriptional program of SASP genes.

LncRNA MACC1-AS1 associates with DDX5 to modulate MACC1 transcription in breast cancer cells.

MACC1 is a master oncogene involved in multiple aspects of cancer metastasis in a broad variety of tumors. However, the molecular mechanism by which MACC1 transcription is regulated remains unclear. Here, we show that in breast cancer cells, lncRNA MACC1-AS1 serves as a cis-factor to up-regulate MACC1 transcription and this regulation increases the cell proliferation potential. Mechanistically, MACC1-AS1 forms a complex with DEAD-Box helicase 5 (DDX5) and simultaneously interacts with the distal region of the MACC1 promoter. The interaction allows its associated DDX5 to spatially contact the MACC1 core promoter and shift from MACC1-AS1 to the core promoter. Moreover, binding of DDX5 to the core promoter results in local recruitment of the transcription factor SP-1, thus enhancing MACC1 transcription. Our findings reveal a molecular mechanism by which MACC1-AS1 cis-regulates MACC1 transcription by interacting with the distal promoter region and delivering DDX5 to the core-promoter of the gene.

Potential mechanisms of cancer-associated fibroblasts in therapeutic resistance.

Despite continuous improvements in research and new cancer therapeutics, the goal of eradicating cancer remains elusive because of drug resistance. For a long time, drug resistance research has been focused on tumor cells themselves; however, recent studies have found that the tumor microenvironment also plays an important role in inducing drug resistance. Cancer-associated fibroblasts (CAFs) are a main component of the tumor microenvironment. They cross-talk with cancer cells to support their survival in the presence of anticancer drugs. This review summarizes the current knowledge of the role of CAFs in tumor drug resistance. An in-depth understanding of the mechanisms underlying the cross-talk between CAFs and cancer cells and insight into the importance of CAFs in drug resistance can guide the development of new anticancer strategies.

Single-cell transcriptome analysis reveals dynamic changes of the preclinical A549 cancer models, and the mechanism of dacomitinib.

The in vitro A549 cells, and A549 xenografts in nude mouse, were two commonly used models for anti-cancer drug discovery. However, the biological and molecular characteristics of these two classic models, and also the dynamic transcriptome changes after dacomitinib exposure remains elusive. We performed single-cell RNA sequencing to define the transcriptome profile at single-cell resolution, and processed tumor samples for bulk RNA and protein analysis to validate the differently expressed genes. Transcriptome profiling revealed that the in vitro A549 cells are heterogeneous. The minimal subpopulation of the in vitro A549 cells, which were characterized by the signature of response to unfolded protein, became the overriding subpopulation of the xenografts. The EGFR non-activating A549 cells were resistant to dacomitinib in vitro, while A549 xenografts were comparatively sensitive as EGFR-activating HCC827 xenografts. Dacomitinib inhibited MAPK signaling pathway, and increased the immune response in the A549 xenografts. A phagocytosis checkpoint stanniocalcin-1 (STC1) was significantly inhibited in dacomitinib-treated xenografts. So here our study gives the first insight of the heterogeneity of the two classic models, and the translational potential of dacomitinib being used into a broader patient population rather than EGFR common activating mutation.

A novel 3D-fluorescence sensing strategy based on HN-chitosan polymer probe for rapid identification and quantification of potential adulteration in saffron.

Saffron is a candidate for various kinds of fraud to make huge profits. The present study proposed an efficient three-dimensional (3D) fluorescence sensing strategy based on hydrophilic hydrazine-naphthalimide functionalized chitosan (HN-chitosan) polymer probe for rapid identification and quantification of potential adulteration in saffron. The amino functional group in the HN-chitosan probe reacted specifically with the Oxygen-containing group of active ingredients in saffron, amplifying the signal difference between saffron and the adulterants, which was comprehensively characterized by 3D fluorescence. Four advanced chemometrics methods were applied for the classification of saffron and adulterated saffron, and good performance were obtained in both training and prediction sets. Furthermore, the PLS regression model was applied to the prediction of adulteration level in saffron and showed satisfactory accuracy. This strategy provides a new solution for rapid identification and quantification of potential adulteration in saffron, which contributes to the healthy development of its industry.

Recruitment of transcription factor ETS1 to activated accessible regions promotes the transcriptional program of cilia genes.

Defects in cilia genes, which are critical for cilia formation and function, can cause complicated ciliopathy syndromes involving multiple organs and tissues; however, the underlying regulatory mechanisms of the networks of cilia genes in ciliopathies remain enigmatic. Herein, we have uncovered the genome-wide redistribution of accessible chromatin regions and extensive alterations of expression of cilia genes during Ellis-van Creveld syndrome (EVC) ciliopathy pathogenesis. Mechanistically, the distinct EVC ciliopathy-activated accessible regions (CAAs) are shown to positively regulate robust changes in flanking cilia genes, which are a key requirement for cilia transcription in response to developmental signals. Moreover, a single transcription factor, ETS1, can be recruited to CAAs, leading to prominent chromatin accessibility reconstruction in EVC ciliopathy patients. In zebrafish, the collapse of CAAs driven by ets1 suppression subsequently causes defective cilia proteins, resulting in body curvature and pericardial oedema. Our results depict a dynamic landscape of chromatin accessibility in EVC ciliopathy patients, and uncover an insightful role for ETS1 in controlling the global transcriptional program of cilia genes by reprogramming the widespread chromatin state.

FAP, CD10, and GPR77-labeled CAFs cause neoadjuvant chemotherapy resistance by inducing EMT and CSC in gastric cancer.

OBJECTIVE: A significant proportion of patients can not benefit from neoadjuvant chemotherapy (NCT) due to drug resistance. Cancer-associated fibroblasts (CAFs) influence many biological behaviours of tumors, including chemo-resistance. This study aims to explore whether CAFs expressing FAP, CD10, and GPR77 affect the efficacy of NCT and the prognosis of patients with gastric cancer, and its mechanism. METHODS: One hundred seventy-one patients with locally progressive gastric adenocarcinoma who had undergone NCT and radical surgery were collected. Immunohistochemistry was used to detect the expression of FAP, CD10, and GPR77 in CAFs; the EMT markers (N-cadherin, Snail1, and Twist1) and the CSC markers (ALDH1, CD44, and LGR5) in gastric cancer cells. The χ2 test was used to analyze the relationship between the expression of CAF, EMT, and CSC markers and the clinicopathological factors, as well as the relationship between CAF markers and EMT, and CSC markers. Logistic regression and Cox risk regression were used to analyze the relationship between the expression of CAF, EMT, and CSC markers and TRG grading and OS; Kaplan-Meier analysis was used for survival analysis and plotting the curves. RESULTS: The expression of CAF markers FAP, CD10, and GPR77 was closely associated with that of EMT markers; FAP and CD10 were closely related to CSC markers. In the univariate analysis of pathological response, CAF markers (FAP, CD10, GPR77), EMT markers (N-cadherin, Snail1, Twist1), and CSC markers (ALDH1, LGR5, CD44), were all closely associated with pathological response (all p < 0.05). Only Twist1 was an independent factor affecting pathological response in multifactorial analysis (p = 0.001). In a univariate analysis of OS, expression of FAP and CD10 in CAF, as well as expression of EMT biomarkers (N-cadherin, Snail1), were significant factors influencing patient prognosis (all p < 0.05). Multifactorial analysis revealed N-cadherin (p = 0.032) and Snail1 (p = 0.028), as independent prognostic factors affecting OS. CONCLUSION: FAP, CD10, and GPR77 labeled CAF subgroup may lead to NCT resistance and poor prognosis by inducing EMT and CSC of gastric cancer cells in locally advanced gastric cancer patients.

What is new in cancer-associated fibroblast biomarkers?

The tumor microenvironment is one of the important drivers of tumor development. Cancer-associated fibroblasts (CAFs) are a major component of the tumor stroma and actively participate in tumor development, invasion, metastasis, drug resistance, and other biological behaviors. CAFs are a highly heterogeneous group of cells, a reflection of the diversity of their origin, biomarkers, and functions. The diversity of CAF origin determines the complexity of CAF biomarkers, and CAF subpopulations expressing different biomarkers may play contrasting roles in tumor progression. In this review, we provide an overview of these emerging CAF biomarkers and the biological functions that they suggest, which may give a better understanding of the relationship between CAFs and tumor cells and be of great significance for breakthroughs in precision targeted therapy for tumors. Video Abstract.