Survival Rates of Patients with Non-Small Cell Lung Cancer Depending on Lymph Node Metastasis: A Focus on Saliva.
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ABSTRACT:
SUBMITTER: Bel'skaya LV
PROVIDER: S-EPMC8161301 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundPathologic nodal stage is a key prognostic factor for patients with surgically resected lung cancer. We previously described the extent of missed intrapulmonary nodal metastasis in a cohort of patients treated at institutions in metropolitan Memphis, TN. With long-term follow-up, we now quantify the survival impact of missed nodal metastasis.MethodsWe conducted a prospective cohort study to evaluate inadvertently discarded lymph nodes in re-dissected remnant lung resection specimens from lung cancer patients. Retrieved material was histologically examined and classified as lymph nodes with and without metastasis. Survival information was obtained from hospital cancer registries. We plotted survival distributions with the use of the Kaplan-Meier method and evaluated them with proportional hazards models that controlled for important demographic and clinical factors.ResultsThe study included 110 patients who were 54% women and 69% white. Discarded lymph nodes with metastasis were found in 25 patients (23%). Patients with missed lymph node metastasis had an increased risk of death with an unadjusted hazard ratio of 2.0 (p = 0.06) and an adjusted hazard ratio of 1.4 (p = 0.45) compared with patients without missed lymph node metastasis. Patients with more than 2 missed lymph nodes with metastasis had 4.8 times the hazard of death (p = 0.0005) compared with patients without missed lymph node metastasis (adjusted hazard ratio 6.5, p = 0.0001).ConclusionsMetastasis to inadvertently discarded intrapulmonary lymph nodes from lung cancer resection specimens was associated with reduced survival. A more rigorous gross dissection protocol for lung cancer resection specimens may provide prognostically useful information.
| S-EPMC4958588 | biostudies-literature
Project description:BACKGROUND AND AIMS:EMR and endoscopic submucosal dissection (ESD) are widely accepted in Asia for treatment of early gastric cancer (EGC). Few studies have examined lymph node (LN) metastasis of EGC in Western populations. We sought to examine EGC and LN metastasis in a heterogeneous Western population. METHODS:Patients with surgically resected, histologically confirmed American Joint Committee on Cancer T1a gastric adenocarcinoma were identified in the Surveillance, Epidemiology, and End Results (SEER) database from 2002 to 2012. Patients were excluded if they had stage IV disease, had multiple primary cancers, or received neoadjuvant therapy. Rates of LN metastasis were calculated, and survival analyses were performed. RESULTS:Of 923 patients in the cohort, 72 (7.8%) had at least 1 positive LN on final pathology. When stratified by race, Asian/Pacific Islanders (APIs) demonstrated the lowest rate of LN metastases (n = 17/327, 5.2%), followed by Hispanics (n = 12/171, 7.0%), whites (n = 27/278, 9.7%), and blacks (n = 16/147, 10.9%). The highest rates of stage IA disease were observed in API (93.9%) and Hispanic (92.4%) patients, followed by white (89.9%) and black (87.1%) patients (P = .04). Survival analysis of T1a gastric cancer patients by race/ethnicity showed that 5-year overall survival was highest for API patients (API, 88%; Hispanic, 81%; black, 79%; and white, 77%; P < .01). CONCLUSIONS:The rate of LN metastasis in T1a gastric cancers in the United States is higher than the rates reported in Asia. Survival outcomes in T1a gastric cancers varied significantly by race, suggesting that definitive endoscopic treatment may not be appropriate for all patients in the United States.
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Project description:Reactive oxygen species modulator 1 (romo1) causes cell hyperplasia and promotes cancer cell invasion. Based recent studies, the overexpression of romo1 is associated with lymphatic metastasis and poor prognosis in lung cancer. We aimed to evaluate associations between romo1 expression and lymph node metastasis in non-small cell lung cancer (NSCLC). Clinical data and pathological results were retrospectively reviewed for 98 subjects diagnosed with NSCLC and who underwent surgical biopsy between 1994 and 2009. A total 98 tumor specimens were analyzed. The romo1 H score was correlated with stage and was significantly higher in subjects with lymph node metastasis than in those without metastasis (173 vs 116; P < 0.05). The area (%) of grade 1 expression was significantly smaller (19.5 vs 37.0; P = 0.005) and the area of grade 3 expression was significantly larger (27.9 vs 6.00; P < 0.001) in subjects with lymph node metastasis than in those without metastasis. In stage I patients, disease free survival (DFS) (191 ± 18.8 vs. 75.6 ± 22.4 months, P = 0.004) was significantly longer in the low romo1 group than in the high romo1 group. A multivariate analysis showed a significant association between high romo1 expression and poor DFS (hazard ratio 5.59, 95 confidence interval, 1.54-20.3, P = 0.009). These findings support the prognostic value of romo1 in NSCLC, especially in stage I.
| S-EPMC7707601 | biostudies-literature
Project description:BackgroundSmall cell lung cancer (SCLC) is the most aggressive lung cancer subtype, with more than 70% of patients having metastatic disease and a poor prognosis. However, no integrated multi-omics analysis has been performed to explore novel differentially expressed genes (DEGs) or significantly mutated genes (SMGs) associated with lymph node metastasis (LNM) in SCLC.MethodsIn this study, whole-exome sequencing (WES) and RNA-sequencing were performed on tumor specimens to investigate the association between genomic and transcriptome alterations and LNM in SCLC patients with (N+, n=15) or without (N0, n=11) LNM.ResultsThe results of WES revealed that the most common mutations occurred in TTN (85%) and TP53 (81%). The SMGs, including ZNF521, CDH10, ZNF429, POLE, and FAM135B, were associated with LNM. Cosmic signature analysis showed that mutation signatures 2, 4, and 7 were associated with LNM. Meanwhile, DEGs, including MAGEA4, FOXI3, RXFP2, and TRHDE, were found to be associated with LNM. Furthermore, we found that the messenger RNA (mRNA) levels of RB1 (P=0.0087), AFF3 (P=0.058), TDG (P=0.05), and ANKRD28 (P=0.042) were significantly correlated with copy number variants (CNVs), and ANKRD28 expression was consistently lower in N+ tumors than in N0 tumors. Further validation in cBioPortal revealed a significant correlation between LNM and poor prognosis in SCLC (P=0.014), although there was no significant correlation between LNM and overall survival (OS) in our cohort (P=0.75).ConclusionsTo our knowledge, this is the first integrative genomics profiling of LNM in SCLC. Our findings are particularly important for early detection and the provision of reliable therapeutic targets.
| S-EPMC9989804 | biostudies-literature
Project description:Lymph nodes metastases are common in patients with lung cancer. Additionally, those patients are often at a higher risk for death from lung tumor than those with tumor-free lymph nodes. Somatic DNA alterations are key drivers of cancer, and copy number alterations (CNAs) are major types of DNA alteration that promote lung cancer progression. Here, we performed genome-wide DNA copy number analysis, and identified a novel lung-cancer-metastasis-related gene, EFNA4. The EFNA4 genome locus was significantly amplified, and EFNA4 mRNA expression was significantly up-regulated in lung cancer compared with normal lung tissue, and also in lung cancer with lymph node metastases compared with lung cancer without metastasis. EFNA4 encodes Ephrin A4, which is the ligand for Eph receptors. The function of EFNA4 in human lung cancer remains largely unknown. Through cell line experiments we showed that EFNA4 overexpression contributes to lung tumor cells growth, migration and adhesion. Conversely, EFNA4 knockdown or knockout led to the growth suppression of cells and tumor xenografts in mice. Lung cancer patients with EFNA4 overexpression have poor prognosis. Together, by elucidating a new layer of the role of EFNA4 in tumor proliferation and migration, our study demonstrates a better understanding of the function of the significantly amplified and overexpressed gene EFNA4 in lung tumor metastasis, and suggests EFNA4 as a potential target in metastatic lung cancer therapy.
| S-EPMC9454565 | biostudies-literature
Project description:Lung adenocarcinoma (LUAD) occupies major causes of tumor death. Identifying potential prognostic risk genes is crucial to predict the overall survival of patients with LUAD. In this study, we constructed and proved an 11-gene risk signature. This prognostic signature divided LUAD patients into low- and high-risk groups. The model outperformed in prognostic accuracy at varying follow-up times (AUC for 3 years: 0.699, 5 years: 0.713, and 7 years: 0.716). Two GEO datasets also indicate the great accuracy of the risk signature (AUC = 782 and 771, respectively). Multivariate analysis identified 4 independent risk factors including stage N (HR 1.320, 95% CI 1.102-1.581, P = 0.003), stage T (HR 3.159, 95% CI 1.920-3.959, P < 0.001), tumor status (HR 5.688, 95% CI 3.883-8.334, P < 0.001), and the 11-gene risk model (HR 2.823, 95% CI 1.928-4.133, P < 0.001). The performance of the nomogram was good in the TCGA database (AUC = 0.806, 0.798, and 0.818 for 3-, 5- and 7-year survival). The subgroup analysis in different age, gender, tumor status, clinical stage, and recurrence stratifications indicated that the accuracy was high in different subgroups (all P < 0.05). Briefly, our work established an 11-gene risk model and a nomogram merging the model with clinicopathological characteristics to facilitate individual prediction of LUAD patients for clinicians.
| S-EPMC10133305 | biostudies-literature
Project description:BackgroundLung adenocarcinoma (LUAD) patients experiencing lymph node metastasis (LNM) always exhibit poor clinical outcomes. A biomarker or gene signature that could predict survival in these patients would have a substantial clinical impact, allowing for earlier detection of mortality risk and for individualized therapy.MethodsWith the aim to identify a novel mRNA signature associated with overall survival, we analysed LUAD patients with LNM extracted from The Cancer Genome Atlas (TCGA). LASSO Cox regression was applied to build the prediction model. An external cohort was applied to validate the prediction model.ResultsWe identified a 4-gene signature that could effectively stratify a high-risk subset of these patients, and time-dependent receiver operating characteristic (tROC) analysis indicated that the signature had a powerful predictive ability. Gene Set Enrichment Analysis (GSEA) showed that the high-risk subset was mainly associated with important cancer-related hallmarks. Moreover, a predictive nomogram was established based on the signature integrated with clinicopathological features. Lastly, the signature was validated by an external cohort from Gene Expression Omnibus (GEO).ConclusionIn summary, we developed a robust mRNA signature as an independent factor to effectively classify LUAD patients with LNM into low- and high-risk groups, which might provide a basis for personalized treatments for these patients.
| S-EPMC6469135 | biostudies-literature
Project description:Lymph nodes are important peripheral immune organs in which numerous important immune responses occur. During the process of lymphatic metastasis, lymph nodes are also sites through which tumor cells must pass. Therefore, it is essential to develop a drug delivery system that can specifically transfer immunostimulatory medicine into lymph nodes to block lymphatic metastasis. Here, we developed a nucleic acid drug delivery system containing cationic agarose (C-agarose) and CpG oligodeoxynucleotides. C-agarose has a high affinity for Siglec-1 on the surface of lymph node sinus macrophages, which have a high specificity for targeting lymph nodes. Subcutaneous implantation of C-agarose+CpG gel caused the accumulation of CpG in the lymph node sinus macrophages and generated antitumor immune responses in the lymph node. C-agarose+CpG gel treatment decreased the metastasis size in the tumor-draining lymph node (TDLN) and lung metastatic nodules and suppressed tumor growth in both a mouse 4T1 breast cancer model and a B16F10 melanoma model. On this basis, this study proposes a nonsurgical invasive lymph node targeting immunotherapy concept that may provide a new approach for antitumor metastasis.
| S-EPMC6529739 | biostudies-literature
Project description:BackgroundThis study aimed to assess the correlation of katanin P60 expression with clinical characteristics and survival profiles of surgical non-small cell lung cancer (NSCLC) patients.MethodsTwo hundred and sixty-five primary NSCLC patients treated by surgical resection were retrospectively viewed. The expression of katanin P60 in the tumor specimen was detected by the immunohistochemical (IHC) staining assay. Preoperative clinical data were collected from patients' medical records, and survival data were extracted from follow-up records.ResultsThere were 127 (47.9%) and 138 (52.1%) patients with katanin P60-low expression and -high expression, respectively; in addition, patients presenting katanin P60-high+, -high++, and -high+++ expression were 62 (23.4%), 63 (23.8%), and 13 (4.9%), respectively. Katanin P60 expression was correlated with lymph node (LYN) metastasis and advanced TNM stage but not pathological grade, tumor size, carcinoembryonic antigen (CEA) level or other non-tumor features in NSCLC patients. Regarding survival profiles, disease-free survival (DFS) and overall survival (OS) were both the lowest in katanin P60-high+++ expression patients, followed with katanin P60-high++ patients, katanin P60-high+ patients, and the highest in katanin P60-low expression patients. Further analysis illustrated that katanin P60-high expression was an independent predictive factor for unfavorable DFS and OS in NSCLC patients.ConclusionsKatanin P60 presents potential as a biomarker for lymph node metastasis and prognosis in NSCLC patients.
| S-EPMC7339556 | biostudies-literature
Project description:BackgroundLymph node metastasis (LNM) is a major factor contributing to the high mortality rate of ovarian cancer, making the treatment of this disease challenging. However, the molecular mechanism underlying LNM in ovarian cancer is still not well understood, posing a significant obstacle to overcome.ResultsThrough data mining from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, we have identified MEOX1 as a specific gene associated with LNM in ovarian cancer. The expression of MEOX1 was found to be relatively high in serous ovarian adenocarcinoma, and its higher expression were associated with increased tumor grade and poorer clinical prognosis for ovarian cancer patients. Bioinformatics analysis revealed that MEOX1 exhibited the highest mRNA levels among all cancer types in ovarian cancer tissues and cell lines. Furthermore, gene set enrichment analysis (GSEA) and pathway analysis demonstrated that MEOX1 was involved in various LNM-related biological activities, such as lymphangiogenesis, lymphatic vessel formation during metastasis, epithelial-mesenchymal transition (EMT), G2/M checkpoint, degradation of extracellular matrix, and collagen formation. Additionally, the expression of MEOX1 was positively correlated with the expression of numerous prolymphangiogenic factors in ovarian cancer. To validate our findings, we conducted experiments using clinical tissue specimens and cell lines, which confirmed that MEOX1 was highly expressed in high-grade serous ovarian cancer (HGSOC) tissues and various ovarian cancer cell lines (A2780, SKOV3, HO8910, and OVCAR5) compared to normal ovarian tissues and normal ovarian epithelial cell line IOSE-80, respectively. Notably, we observed a higher protein level of MEOX1 in tumor tissues of LNM-positive HGSOC compared to LNM-negative HGSOC. Moreover, our fundamental experiments demonstrated that suppression of MEOX1 led to inhibitory effects on ovarian cancer cell proliferation and EMT, while overexpression of MEOX1 enhanced the proliferation and EMT capacities of ovarian cancer cells.ConclusionsThe results of our study indicate that MEOX1 plays a role in the lymph node metastasis of ovarian cancer by regulating multiple biological activities, including the proliferation and EMT of ovarian cancer, lymphangiogenesis, and ECM remodeling. Our findings suggest that MEOX1 could serve as a potential biomarker for the diagnosis and treatment of ovarian cancer with LNM.
| S-EPMC10938838 | biostudies-literature