Background Lung cancer is the second most commonly diagnosed cancer and ranks the first in mortality. Pathological lymph node status(pN) of lung cancer affects the treatment strategy after surgery while systematic lymph node dissection(SLND) is always unsatisfied. Methods We reviewed the clinicopathological features of 2,696 patients with LUAD and one single lesion ≤ 5 cm who underwent SLND in addition to lung resection at the Sun Yat-Sen University Cancer Center. The relationship between the pN status and all other clinicopathological features was assessed. All participants were stochastically divided into development and validation cohorts; the former was used to establish a logistic regression model based on selected factors from stepwise backward algorithm to predict pN status. C-statistics, accuracy, sensitivity, and specificity were calculated for both cohorts to test the model performance. Results Nerve tract infiltration (NTI), visceral pleural infiltration (PI), lymphovascular infiltration (LVI), right upper lobe (RUL), low differentiated component, tumor size, micropapillary component, lepidic component, and micropapillary predominance were included in the final model. Model performance in the development and validation cohorts was as follows: 0.861 (95% CI: 0.842–0.883) and 0.840 (95% CI: 0.804–0.876) for the C-statistics and 0.803 (95% CI: 0.784–0.821) and 0.785 (95% CI: 0.755–0.814) for accuracy, and 0.754 (95% CI: 0.706–0.798) and 0.686 (95% CI: 0.607–0.757) for sensitivity and 0.814 (95% CI: 0.794–0.833) and 0.811 (95% CI: 0.778–0.841) for specificity, respectively. Conclusion Our study showed an easy and credible tool with good performance in predicting pN in patients with LUAD with a single tumor ≤ 5.0 cm without SLND and it is valuable to adjust the treatment strategy.

The aim of this article was to explore the pathogenetic differences, as well as to provide a new way for the differential diagnosis of these two diseases by comparative analysis of CD(34)(+) cells numbers and their surface expression of granulocyte colony-stimulating factor receptor (G-CSFR) and granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR) in patients with aplastic anemia (AA) and myelodysplastic syndrome (MDS). Twenty-seven patients with AA, 45 patients with MDS, and 20 normal controls were enrolled in this study. The ratio of CD(34)(+) cells and their surface expression of G-CSFR and GM-CSFR were detected by flow cytometry (FCM). The ratio of CD(34)(+) cells in BMMNC of AA, MDS patients and controls were 0.2438 +/- 0.1129%, 2.1677 +/- 1.1345% and 1.0792 +/- 0.3221%, respectively. Compared with normal controls as well as MDS patients, the ratio of CD(34)(+) cells in BMMNC of AA was significantly reduced (P < 0.05). The ratio of CD(34)(+) cells in MDS was significantly elevated than controls (P < 0.05). The ratio of CD(34)(+) cells in BMMNC of MDS-RA and MDS-RAEB patients were 1.2821 +/- 0.4658% and 3.7729 +/- 2.3360%, respectively. Compared with normal controls and MDS-RA patients, the ratio of CD(34)(+) cells in MDS-RAEB was significantly elevated (P < 0.05). The ratio of CD(34)(+) cells in MDS-RA was significantly elevated than AA patients (P < 0.05). The surface expression of G-CSFR on CD(34)(+) cells of AA, MDS patients and controls were 34.402 +/- 21.8357%, 26.376 +/- 15.2895% and 21.443 +/- 7.4465%, respectively. The surface expression of G-CSFR on CD(34)(+) cells of MDS-RA and MDS-RAEB patients were 22.788 +/- 14.7628% and 30.682 +/- 15.5346%. The surface expression of GM-CSFR on CD(34)(+) cells of AA, MDS patients and controls were 6.5961 +/- 4.4322%, 18.2737 +/- 10.9841% and 4.2753 +/- 2.6249%, respectively. Compared with AA and controls, the expression of GM-CSFR in MDS patients was significantly elevated (P < 0.05). The surface expression of GM-CSFR on CD(34)(+) cells of MDS-RA and MDS-RAEB patients were 16.1625 +/- 6.9487% and 22.1003 +/- 14.2983%. In AA patients, the ratio of CD(34)(+) cells in BMMNC less than 0.1% accounts for 75% (6/8) SAA patients, compared with 10.55% (2/19) in CAA (P < 0.05). The detection of CD(34)(+) cells and their surface expression of granulocyte (macrophage) colony-stimulating factor receptors G (M)-CSFR in AA and MDS are helpful in the differential diagnosis or prognosis of these two disorders.