Medical humanistic literacy constitutes the spiritual foundation for the long-term development of healthcare undertakings， and serves as the internal driving force for every medical worker to stay true to their professional aspiration and abide by medical practice norms. At present， the medical industry has deeply integrated the cultivation of a correct understanding of performance with humanistic development， charting a path for practitioners to achieve career growth and value realization. As the recipient of the honorary title "Qilu Role Model of the Times"， Bai Xiaohui fulfilled the mission of medical practitioners throughout her life， consistently upholding the professional spirit of "respect life， heal the wounded and rescue the dying， be willing to dedicate oneself， and possess universal benevolence". She integrated her personal pursuit into the cause of national health， and interpreted the benevolence and responsibility of medical practitioners in the new era through practical actions and even her life. Her spiritual character embodies political awareness， professional competence and humanistic warmth， offering a vivid example for all medical workers to learn from.

In recent years， the clinical demand for fentanyl transdermal patches in the field of cancer pain has markedly increased. Nevertheless， prominent clinical problems persist， including inappropriate indication control， irregular dose titration and lagging management of adverse reactions. To address these issues， the Branch of Palliative Care， China International Exchange and Promotive Association for Medical and Health Care together with the Committee of Rehabilitation and Palliative Care， China Anti-Cancer Association organized a panel of specialists to revise the 2021 edition of Guidelines for the Rational Clinical Use of Fentanyl Transdermal Patches. Referring to the latest domestic and foreign literature and clinical research evidence， this guideline develops comprehensive and multi-dimensional recommendations covering core issues such as indication definition， preferred patient populations， dose conversion and titration， combination regimens for special types of cancer pain， adverse reaction intervention， drug interactions， safety management and patient education. This guideline intends to provide practical medication references for clinical practitioners， standardize the application of fentanyl transdermal patches in cancer pain management， and achieve the clinical goal of "standardized pain relief and comfortable anti-cancer treatment".

Objective To investigate the targeting relationships involving miR-331-3p，BCL6 and ITGA9， and to examine their effects on the proliferation， migration， invasion， and immune cell infiltration levels of adenoid cystic carcinoma （ACC） cells. Methods A dual-luciferase reporter assay was employed to verify the targeting relationships among miR-331-3p， BCL6， and ITGA9. The miR-331-3p mimic and cells transfected with pcDNA3.1-BCL6 plasmid were established using salivary adenoid cystic carcinoma-83 （SACC-83） tumor cells. Real-time quantitative PCR was used to detect the mRNA expression levels of miR-331-3p， BCL6， and ITGA9. Western blotting was performed to detect the protein relative expression levels of BCL6 and ITGA9. Cell proliferation was assessed using the CCK-8 assay. Cell migration and invasion were evaluated using scratch wound healing and Transwell assays， respectively. Furthermore， transfection models were established in ACC metastasis （ACC-M） cells using empty vector plasmids， ITGA9 and BCL6 overexpression plasmids， miRNA NC mimic， and miR-331-3p mimic. Western blotting was performed to detect the protein relative expression levels of BCL6 and ITGA9. Real-time quantitative PCR was used to detect the relative expression levels of chemokine genes secreted by tumor cells （CXCL9， CXCL10， and CXCL11）. Results The dual luciferase assay results indicated that miR-331-3p could specifically bind to BCL6. BCL6 could specifically bind to ITGA9. In SACC-83 cells， the relative expression levels of miR-331-3p were 1.01±0.16， 0.67±0.05， and 0.35±0.12 in the mimic+NC group， mimic+BCL6 group， and mimic NC+BCL6 group， respectively. The BCL6 mRNA relative expression levels were 1.01±0.21， 2.06±0.27， and 4.48±0.36， respectively， while the ITGA9 mRNA relative expression levels were 1.00±0.04， 0.55±0.07， and 0.35±0.17， respectively， with statistically significant differences （F=22.28， P=0.002； F=116.65， P<0.001； F=26.72， P=0.001）. The expression levels of miR-331-3p and ITGA9 decreased progressively， whereas BCL6 expression increased progressively in the above three groups （all P<0.05）. The ITGA9 protein relative expression levels in SACC-83 cells were 0.96±0.03， 0.87±0.02， and 0.67±0.05 in the mimic+NC group， mimic+BCL6 group， and mimic NC+BCL6 group， respectively. The BCL6 protein relative expression levels were 0.92±0.01， 1.13±0.02， and 1.72±0.02， respectively， with statistically significant differences （F=61.87， P<0.001； F=7.18， P=0.026）. The ITGA9 protein relative expression decreased progressively， while BCL6 protein relative expression increased progressively in the above three groups （all P<0.05）. The proliferation activities of SACC-83 cells were 100.00%±6.05%， 82.03%±2.47%， and 53.18%±5.47% in the mimic+NC group， mimic+BCL6 group， and mimic NC+BCL6 group， respectively. The apoptosis rates in these groups were 6.21%±0.23%， 15.31%±0.74%， and 27.47%±1.09%， respectively； migration rates were 54.17%±9.15%， 34.37%±5.84%， and 11.17%±5.25%， respectively； invasion rates were 52.33%±8.74%， 36.67%±4.73%， and 14.00%±2.00%， respectively， with statistically significant differences （F=69.15， P<0.001； F=572.93， P<0.001； F=28.66， P=0.001； F=32.56， P=0.001）. The proliferation activity， migration rate， and invasion rate of SACC-83 cells decreased progressively， while the apoptosis rate increased progressively in the above three groups （all P<0.05）. After ACC-M cells were transfected with the overexpression vectors of ITGA9 and miR-331-3p mimic， the mRNA relative expression levels of CXCL9， CXCL10， and CXCL11 all decreased （all P<0.05）； after transfection with BCL6 vectors respectively， the mRNA relative expression levels of CXCL9， CXCL10， and CXCL11 all increased （all P<0.05）. Conclusions miR-331-3p promotes ITGA9 expression by inhibiting BCL6. This regulation enhances the proliferation， migration， and invasion capabilities of ACC cells； reduces the infiltration of cytotoxic lymphocytes within the tumor； and thereby promotes tumor progression.

Objective To analyze the concordance of Claudin18.2 expression with different antibody clone numbers in gastric adenocarcinoma tissues. Methods A total of 56 newly diagnosed cases of gastric adenocarcinoma （including oesophagogastric junction adenocarcinoma） who were tested using Claudin18.2 clone number EPR19202 at Cancer Hospital of Chinese Academy of Medical Sciences， Peking Union Medical College， Shenzhen Branch from December 2023 to September 2024 were selected as the research subjects. All patients were then tested with clone number 43-14A， and the positive detection rates of the two different clone number antibodies were compared. The intraclass correlation coefficient （ICC） and Cohen's Kappa coefficient were adopted to evaluate the consistency of the interpretation results of positive cell proportions with different intensities after staining with the two antibodies. Additionally， the Spearman correlation coefficient was employed to assess the correlation of expression levels detected by the two antibodies. Results The positive staining of Claudin18.2 detected by both antibodies EPR19202 and 43-14A was exhibited membranous staining in normal gastric mucosal epithelial cells and tumor cells. EPR19202 demonstrated brown to yellow-brown staining， while 43-14A showed brown to dark brown staining. Regarding the positive detection rate， there were 13 positive cases and 43 negative cases for EPR19202， resulting in a positive rate of 23.21%. For 43-14A， there were 24 positive cases and 32 negative cases， yielding a positive rate of 42.86%. The positive rate of 43-14A was significantly higher than that of EPR19202， indicating a statistically significant difference between the two positive rates （χ²=4.04， P=0.045）. The ICC assessment results showed that in the EPR19202 stained sections， the ICC values for the three physicians' interpretation of the percentages of moderately and strongly positive cells in this clone antibody stained sections were 0.87 and 0.78 respectively； in the 43-14A stained sections， the corresponding ICC values were 0.80 and 0.91， respectively. The complete consistency rate of the three physicians' interpretation of the positive/negative judgment of the two antibody stained sections was 84% to 93%， with a Cohen's Kappa value ranging from 0.56 to 0.86. According to the Landis & Koch standard， the consistency of the three physicians' interpretation reached a moderate to almost complete consistent level， and the consistency of 43-14A interpretation was better. The Spearman correlation analysis results showed that the two clone numbers were moderately to highly positively correlated in the proportion of moderately positive cells （r=0.49， P<0.001； r=0.60， P<0.001； r=0.65， P<0.001）， and moderately positively correlated in the proportion of strongly positive cells （r=0.41， P=0.002； r=0.51， P<0.001； r=0.49， P=0.001）， suggesting that there was a moderate correlation in their expression levels； the Cohen's Kappa value of the three physicians' joint interpretation was 0.57. Conclusions Both Claudin18.2 antibodies， EPR19202 and 43-14A， show accurate positive staining localization， making them suitable for detecting Claudin18.2 in gastric adenocarcinoma and related precancerous lesions. The two clones show moderate to high correlation in detection results， but certain discrepancies are observed in weakly positive and highly heterogeneous cases. Clone 43-14A demonstrates a higher positivity rate in gastric adenocarcinoma tissues and better consistency in physicians' interpretation.

Objective To investigate the correlation， clinical relevance， and underlying molecular mechanisms associated with the expression of caudal type homeobox transcription factor 2 （CDX2） and the cancer stem cell （CSC） markers CD133 and CD44 in colorectal cancer （CRC）. Methods A total of 72 CRC patients who underwent surgical treatment at Luoyang Central Hospital from January 2016 to January 2018 were selected as the study subjects. The expression levels of CDX2， CD133， and CD44 in cancer tissues and normal tissues were compared； the clinical pathological characteristics and prognosis of patients with different CDX2， CD133， and CD44 expression were analyzed； univariate and multivariate Cox proportional hazards regression models were used to analyze prognostic factors； Pearson's chi-square test and Phi correlation analysis was used to test the correlation of expression between CDX2 and CD133， CD44. CDX2 in SW480 cells was silenced or overexpressed by lentivirus transfection； cell proliferation ability was detected by colony formation assay； migration ability was detected by scratch assay； invasion ability was detected by Transwell invasion assay； and the effect of CDX2 expression on CD133 and CD44 expression was analyzed by Western blotting. Results High expression of CDX2 accounted for 48.61% （35/72）， while low expression accounted for 51.39% （37/72）； both CD133 and CD44 showed high expression in 31.94% （23/72） of cases. There were statistically significant differences in T stage （χ²=6.18， P=0.013）， N stage （χ²=6.95， P=0.008）， and TNM stage （χ²=4.81， P=0.028） between patients with high and low CDX2 expression. In patients with high expression of both CD133 and CD44 compared to those with other expression patterns， there were also statistically significant differences in T stage （χ²=4.25， P=0.039）， N stage （χ²=5.91， P=0.015）， and TNM stage （χ²=5.13， P=0.024）. Multivariate analysis showed that low CDX2 expression was an independent risk factor simultaneously affecting recurrence free survival （RFS） and overall survival （OS） in CRC patients （RFS： HR=2.61， 95%CI： 1.18-5.77， P=0.018； OS： HR=2.69， 95%CI： 1.23-5.89， P=0.014）. Survival analysis showed that the 4-year RFS rates for CRC patients with low and high CDX2 expression were 32.07% and 85.53%， respectively， with a statistically significant difference （χ²=49.63， P<0.001）； the 4-year OS rates for CRC patients with low and high CDX2 expression were 21.62% and 82.86%， respectively， with a statistically significant difference （χ²=51.38， P<0.001）. The results of Pearson's chi-square test and Phi correlation analysis showed that the expression of CDX2 was significantly negatively correlated with CD133 （φ=-0.33， χ²=8.05， P=0.005）， CD44 （φ=-0.31， χ²=6.71， P=0.010） and CD133 combined with CD44 （φ=-0.49， χ²=17.12， P<0.001）. In CRC SW480 cells， the relative expression levels of CD133 in the blank control group， CDX2-silenced group， and CDX2-overexpressing group were 0.60±0.05， 0.93±0.05， and 0.42±0.06， respectively， and the relative expression levels of CD44 were 0.50±0.03， 0.77±0.08， and 0.35±0.03， respectively， with statistically significant differences （F=63.88， P<0.001； F=52.90， P<0.001）. Compared with the blank control group， the expression of CD133 and CD44 was significantly increased in the CDX2-silenced cells， while it was significantly decreased in the CDX2-overexpressing cells （all P<0.05）. Additionally， the expression levels of CD133 and CD44 in the CDX2-silenced cells were significantly higher than those in the CDX2-overexpressing cells （both P<0.05）. The numbers of cell clones in the blank control group， CDX2-silenced group， and CDX2-overexpressing group were 86.67±10.69， 206.00±17.52， and 44.33±6.51， respectively； the cell migration rates were 0.30±0.02， 0.51±0.03， and 0.22±0.03， respectively； and the numbers of invasive cells were 150.33±16.65， 312.67±28.29， and 65.67±12.22， respectively， with statistically significant differences （F=136.42， P<0.001； F=82.21， P<0.001； F=115.56， P<0.001）. Compared with the blank control group， the proliferation， migration， and invasion abilities of cells in the CDX2-silenced group were significantly enhanced （all P<0.05）， while those in the CDX2-overexpressing group were significantly reduced （all P<0.05）. The proliferation， migration， and invasion abilities of cells in the CDX2-silenced group were significantly stronger than those in the CDX2-overexpressing group （all P<0.05）. Conclusions Low CDX2 expression is an independent risk factor for poor prognosis in CRC， and CDX2 can serve as a prognostic marker for CRC. CDX2 expression is negatively correlated with the CSC markers CD133 and CD44. Silencing CDX2 significantly enhances the proliferative, migratory, and invasive capacities of SW480 cells, concomitant with upregulated expression of CD133 and CD44.

Objective To investigate the efficacy and safety of nab-paclitaxel combined with bevacizumab in the treatment of platinum-resistant recurrent ovarian cancer. Methods A total of 71 patients with platinum-resistant recurrent ovarian cancer admitted to Qilu Hospital of Shandong University from June 2022 to June 2025 were enrolled. All patients received ≥3 cycles of nab-paclitaxel combined with bevacizumab. Efficacy and safety were evaluated after treatment. Survival outcomes were estimated using the Kaplan-Meier method and compared via log-rank tests. Results The mean number of treatment cycles of 5.63±1.37. The ORR was 50.70%（36/71）. The DCR was 81.69% （58/71）. The DCR in patients with time interval from last platinum-based chemotherapy to recurrence ≤3 months was significantly lower than that in patients with a time interval of >3 months and ≤6 months [72.97% （27/37） vs. 91.18% （31/34）； χ²=3.93， P=0.048]. After 4 cycles of treatment， patients with a carbohydrate antigen 125 （CA125） decrease of ≥50% had an ORR of 66.67% （30/45） and a DCR of 91.11% （41/45）， both higher than those with a decrease of <50% [26.67% （4/15） and 60.00% （9/15）， respectively； χ²=7.33， P=0.007； χ²=7.84， P=0.005]. Patients without prior bevacizumab treatment had higher ORR [70.37% （19/27）] and DCR [96.3% （26/27）] than those who had previously received bevacizumab [38.64% （17/44） and 72.73% （32/44）， respectively； χ²=6.74， P=0.009； χ²=6.21， P=0.013]. Survival analysis showed that the median progression-free survival （PFS） of the 71 patients was 7.0 months. The median PFS for patients with a time from last platinum-based chemotherapy to recurrence of > 3 months and ≤ 6 months （9.0 months） showed a trend of prolongation compared to those with ≤ 3 months （6.0 months）， but there was no statistically significant difference （χ²=3.82， P=0.051）.The most common adverse events were neurotoxicity [57.75% （41/71）]， proteinuria [46.48% （33/71）]， and nausea/vomiting [46.48% （33/71）]， predominantly grade 1-2. The main grade 3-4 adverse reaction was neutropenia [15.49% （11/71）]. Conclusions Nab-paclitaxel combined with bevacizumab shows promising efficacy and good tolerability in the treatment of platinum-resistant recurrent ovarian cancer.

Lung cancer ranks among the top malignancies in terms of both incidence and mortality rates. The liver is a common site of distant metastasis， which is closely associated with the poor prognosis. In recent years， immune checkpoint inhibitors （ICIs） have achieved significant breakthroughs in the treatment of advanced lung cancer. Patients with liver metastasis can also benefit from ICI therapy. However， compared to the overall population， the presence of liver metastasis remains an independent prognostic factor for poor efficacy of immunotherapy. Based on recent research， summarizing the impact of liver metastasis on the efficacy of immunotherapy for lung cancer， the underlying mechanisms， and future research directions may provide certain reference basis for formulating comprehensive treatment strategies for lung cancer patients with liver metastasis.

Platinum resistance is the leading cause of treatment failure in advanced ovarian cancer. Iron metabolic reprogramming has emerged as a new focus in drug resistance research， with nuclear receptor coactivator 4 （NCOA4）-mediated ferritinophagy being a core pathway. Based on the latest evidence， a "shield and sword" dual model of NCOA4 is proposed： during the drug resistance formation period， NCOA4 supplies iron via the IRP2-NCOA4 axis to support RRM2-mediated DNA repair， acting as a protective "shield"； under specific interventions， its overactivation elevates the labile iron pool， exceeds antioxidant thresholds， and triggers ferroptosis， turning into a lethal "sword." Accordingly， a "sequential" strategy is proposed—first inhibiting the "shield" to sensitize chemotherapy， then activating the "sword" to eliminate the drug-resistant cells—offering a new direction for reversing platinum resistance.

Peripheral T-cell lymphoma （PTCL） is a heterogeneous group of malignant tumors originating from post-thymic mature T cells and natural killer cells， encompassing multiple subtypes， almost all of which exhibit high aggressiveness. Currently， the first-line treatment for PTCL patients still follows the therapeutic regimen for aggressive B-cell lymphoma， but the efficacy duration is short and the adverse effects are severe， with an overall 5-year survival rate of only approximately 30%， indicating a poor prognosis. In recent years， with the advancement of molecular genetics and epigenetics， novel targeted drugs have emerged continuously and demonstrated good efficacy and safety profile in various clinical studies. Combination therapies of new drugs are expected to overcome the efficacy limitations of monotherapy. To explore and summarize the latest research progress and clinical prospects of targeted therapy for PTCL， which can provide a basis for clinical decision-making of targeted therapy for PTCL.