Citations

The NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Lung Cancer Screening provide criteria for selecting individuals for screening and offer recommendations for evaluating and managing lung nodules detected during initial and subsequent annual screening. These NCCN Guidelines Insights focus on recent updates to the NCCN Guidelines for Lung Cancer Screening.

Background/Objectives: Little information has been published on patients diagnosed with brain metastasis secondary to lung cancer. Correlating outcome patterns (hospice care, lost to follow-up, death before hospice care or treatment) and specific characteristics of treated and untreated patients may identify subsets of patients who may benefit from treatment. Methods: We evaluated data from the Kentucky Cancer Registry and identified 284 cases who were diagnosed with brain metastasis secondary to non-small cell lung cancer (NSCLC) between 1 August 2016, and 31 December 2019. We evaluated type and timing of treatment received, as well as focused on those patients who did not receive treatment. For those patients who did not receive treatment, various characteristics that may have impacted their decision or ability to undergo follow-up were also evaluated. This included social history, disease burden, as well as oncology treatment timelines. Lastly, due to the high smoking rate in Kentucky, we conducted an analysis of patient tobacco use. Results: Our results show that 61 cases (21.8%) never received treatment for lung cancer with brain metastasis. Further analysis of the non-treated cases demonstrated that 19 cases (31.1%) never met with an oncology team while in the hospital or after discharge; 14 of the 61 cases (23.0%) were too sick to receive treatment and died prior to having the option of treatment; and 47 of the 61 cases (77.0%) may have had the option of treatment but declined. Conclusions: Historically, patients with brain metastases have faced poor prognoses and limited treatment options. However, advancements in systemic chemoimmunotherapy and targeted therapies have introduced new treatment possibilities, offering improved symptom control and the potential for prolonged survival. This analysis is crucial for identifying potential barriers to care, optimizing resource allocation, and guiding future research.

Objective The aim of this study was to determine whether pollutants such as fire smoke–related particulate matter <2.5 μm (PM 2.5 ) are associated with incident rheumatoid arthritis (RA) and RA‐associated interstitial lung disease (RA‐ILD). Methods This patient–control study used Veterans Affairs (VA) data from October 1, 2009, to December 31, 2018. We identified patients with incident RA and RA‐ILD using validated algorithms, matching each patient to ≤10 controls on age, sex, and VA enrollment year. We obtained pollutants including fire smoke PM 2.5 , carbon monoxide, nitrogen oxides (NOx), ozone, overall PM 2.5 , PM 10 , and sulfur dioxide (SO 2 ) at least one year before the index date. We fit conditional logistic regression models to estimate adjusted odds ratios (aORs) with 95% confidence intervals (CIs) for incident RA and RA‐ILD, adjusted for confounders. Results We identified 9,701 patients with incident RA (mean age 65 years, 86% male), including 531 patients with RA‐ILD (mean age 69 years, 91% male), and 68,852 matched controls. Fire smoke PM 2.5 was not associated with RA (aOR 1.07, 95% CI 0.92–1.23) but was associated with RA‐ILD (aOR 1.98, 95% CI 1.08–3.62, per 1 μg/m 3 ). Increased levels of NOx were associated with RA (aOR 1.16, 95% CI 1.06–1.27, highest vs lowest quartile). The highest quartiles of ozone (aOR 1.19, 95% CI 1.06–1.34) and PM 10 (aOR 1.25, 95% CI 1.10–1.43) were associated with seronegative RA. Carbon monoxide, overall PM 2.5 , and SO 2 were not, or negatively, associated with RA and RA‐ILD. Conclusion Increased fire smoke PM 2.5 was associated with RA‐ILD, whereas NOx, ozone, and PM 10 were associated with RA risk. Thus, air pollution may increase the risk of RA and RA‐ILD. image

Abstract Background In the United States, a growing number of lung transplants are performed each year, necessitating an increased number of general and transplant pulmonologists skilled in the care of these complex patients. However, pulmonary and critical care medicine (PCCM) fellowships across the country do not universally have dedicated lung transplantation curricula, and there is scarce literature in this area. We describe the generation of a content outline for curriculum development created through modified electronic Delphi methodology. Objective To identify “must know” topics in lung transplantation for a graduating PCCM fellows. Methods We developed expert consensus on “must know” lung transplant topics and subtopics (“items”) for a graduating fellow through three survey rounds from July 2023 to October 2023. Thirty-three panelists were asked to rank author-provided items as “must know,” “nice to know,” or “not necessary to know” and to generate new items in round 1 to be submitted for ranking in subsequent rounds. “Must know consensus” was defined as ≥50% must know responses. Results Survey response and completion rates across rounds were 58–70% and 96–100%, respectively. In round 1, panelists were provided eight topics and 30 subtopics for initial ranking. Panelists generated 82 new items in this round, of which 19 were included in round 2 for ranking after author review, together with one item from round 1 that required reranking. From round 2, only two items required reranking, and these items comprised round 3. Seven topics were identified as “must know”: transplant immunology, evaluation of a lung transplant candidate, surgical and peri/postoperative management, rejection, immunosuppression, infections, and other complications, together with 36 subtopics. Conclusion Self-identified lung transplantation experts obtained consensus on seven “must know” topics and 36 subtopics in lung transplantation for graduating PCCM fellows. The findings serve as a starting point for future curriculum development.

Background The prevalence and impact of right ventricular dysfunction (RVD) in degenerative mitral regurgitation (DMR) is unknown. We aimed to determine whether RVD assessed by echocardiography in routine clinical practice is independently associated with mortality in patients with DMR. Methods and Results We used data from the MIDA‐Q (Mitral Regurgitation International DAtabase‐Quantitative) registry, which included patients with isolated DMR due to mitral valve prolapse from January 2003 to January 2020 from 5 tertiary centers across North America, Europe, and the Middle East. A cohort of 2917 (mean age: 66 years, 70.8% male patients, follow‐up: 5.2 [3.3–8.3] years) consecutive patients with severe DMR was included and long‐term mortality was analyzed. RVD, identified in 426 (14.6%) patients, was associated with reduced 8‐year survival (55%±3% versus 77%±1%; P <0.001), overall and in all subgroups of patients, even after comprehensive adjustment including left ventricular dilatation and dysfunction, DMR severity, pulmonary pressures, and surgery (adjusted hazard ratio, 1.44 [95% CI, 1.17–1.77]; P <0.001). This excess mortality was observed under medical management (adjusted hazard ratio, 1.57 [95% CI, 1.20–2.05]; P =0.001) and after surgical correction of mitral regurgitation (adjusted hazard ratio, 1.45 [95% CI, 1.02–2.05]; P =0.039). Patients with RVD undergoing surgery within 3 months of diagnosis experienced a better 8‐year survival (73%±4% versus 43%±4%; P <0.001), even after adjustment (adjusted hazard ratio, 0.44 [95% CI, 0.29–0.67]; P <0.001) despite an increase of 1‐month postoperative mortality (7.1% versus 0.5% for patients without RVD; P <0.001). Conclusions RVD is observed in 14.6% of severe DMR and exhibits a powerful and independent association with excess mortality partially attenuated by mitral surgery. Therefore, assessment of right ventricular systolic function should be included in routine DMR evaluation and in the clinical decision‐making process.

Background/Objectives: Lung cancer is a devastating disease with the highest mortality rate among cancer types. Over 60% of non-small cell lung cancer (NSCLC) patients, accounting for 87% of lung cancer diagnoses, require radiation therapy. Rapid treatment initiation significantly increases the patient’s survival rate and reduces the mortality rate. Accurate tumor segmentation is a critical step in diagnosing and treating NSCLC. Manual segmentation is time- and labor-consuming and causes delays in treatment initiation. Although many lung nodule detection methods, including deep learning-based models, have been proposed. Most of these methods still have a long-standing problem of high false positives (FPs). Methods: Here, we developed an electronic health record (EHR)-guided lung tumor auto-segmentation called EXACT-Net (EHR-enhanced eXACtitude in Tumor segmentation), where the extracted information from EHRs using a pre-trained large language model (LLM) was used to remove the FPs and keep the TP nodules only. Results: The auto-segmentation model was trained on NSCLC patients’ computed tomography (CT), and the pre-trained LLM was used with the zero-shot learning approach. Our approach resulted in a 250% boost in successful nodule detection using the data from ten NSCLC patients treated in our institution. Conclusions: We demonstrated that combining vision-language information in EXACT-Net multi-modal AI framework greatly enhances the performance of vision only models, paving the road to multimodal AI framework for medical image processing.

Abstract Idiopathic pulmonary fibrosis (IPF) is characterized by the sustained activation of interstitial fibroblasts leading to excessive collagen deposition and progressive organ failure. Epigenetic and metabolic abnormalities have been shown to contribute to the persistent activated state of scar-forming fibroblasts. However, how epigenetic changes regulate fibroblast metabolic responses to promote fibroblast activation and progressive fibrosis remains largely unknown. Here, we show that the epigenetic regulator CBX5 (chromobox protein homolog 5) is critical to the transition of quiescent fibroblasts to activated collagen-producing fibroblasts in response to bleomycin-induced lung injury. Loss of mesenchymal CBX5 attenuated fibrosis development, and this effect was accompanied by the downregulation of pathogenic fibroblast genes, including Cthrc1, Col1a1, and Spp1, and by the upregulation of metabolic genes with antifibrotic activity such as Ppara and Pparg. Single-cell RNA sequencing and immunohistochemistry analyses revealed that CBX5 expression was enriched in pathogenic fibroblasts and fibroblastic foci of IPF lungs. Bulk RNA-sequencing analysis combined with metabolic assessments demonstrated that CBX5 silencing in IPF fibroblasts potently inhibited transforming growth factor–stimulated glycolysis while enhancing AMPK signaling and mitochondrial metabolism. Finally, interruption of the CBX5 pathway in IPF fibroblasts in vitro and in IPF lung explants ex vivo synergistically potentiated the activation of metformin-induced AMP-activated protein kinase activation and inhibited collagen secretion. Collectively, our findings identify CBX5 as an epigenetic regulator linking metabolic maladaptation to the persistent activated state of lung fibroblasts during IPF progression.