To investigate the mechanism of Qitu Erzhi Decoction(QTEZ) in ameliorating chemotherapy-induced myelosuppression and the focus of its decomposed formulae on the effects of hematopoietic cells of the three lineages, respectively. Ultra performance liquid chromatography-quadrupole time-of-flight tandem mass spectrometry(UPLC-Q-TOF-MS) was used to identify the components of QTEZ intestinal absorption liquid and obtain the target sites, which were intersected with chemotherapy-induced myelosuppression targets collected from several databases, including OMIM, and an interaction network was established based on network pharmacology for Gene Ontology(GO) functional analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway analysis. Hematopoietic stem cells of mice were taken after intraperitoneal injection of 5-fluorouracil for myelosuppression modeling and randomly divided into the model group, Qitu Erzhi group, Astragali Radix-Angelicae Sinensis Radix group, Ligustri Lucidi Fructus-Ecliptae Herba group, Psoraleae Fructus-Cuscutae Semen group, and positive drug group, which were given the corresponding traditional Chinese medicine intestinal absorption liquid and the positive drug granulocyte colony-stimulating factor, respectively. The normal hematopoietic stem cells were taken as the control group and were given the intervention of normal saline. The proliferation of hematopoietic progenitor cells of three lineages was observed by flow cytometry, and the cell cycle and colony formation assay were observed. Western blot was used to verify the effect of QTEZ on the pathway proteins including phosphoinositide 3-kinase(PI3K), phosphorylated PI3K(p-PI3K), protein kinase B(AKT), and phosphorylated AKT(p-AKT). RT-qPCR and Western blot were used to detect the effects of QTEZ on cell cycle-related targets such as CDK inhibitor 1(P21), cyclin D1(CCND1), and cyclin-dependent kinase 4(CDK4). The results showed that a total of 158 components were identified by QTEZ, and 375 component and disease intersecting targets were obtained, 21 core components and 40 core targets were obtained after constructing the network, and GO and KEGG enrichment showed signaling pathways such as PI3K/AKT. QTEZ and its decomposed formulae could promote the 5-fluorouracil-blocked cell cycle to resume operation, and all of them had different degrees of restoration effects on the set of colonies, among which QTEZ had the best restoration effect, and the Astragali Radix-Angelicae Sinensis Radix group had a focused effect on colony forming unit-erythrocyte. Western blot results indicated that there was no significant difference in the expression levels of pathway proteins among the groups. RT-qPCR and Western blot results showed that QTEZ could down-regulate P21 and up-regulate the protein and mRNA expression of CDK4 and CCND1. In conclusion, QTEZ and its decomposed formulas can exert a protective effect on hematopoietic stem cells with 5-fluorouracil-induced myelosuppression by promoting the normal operation of the cell cycle and colony formation, and the mechanism may be related to the down-regulation of the cell cycle-related targets of P21 and the up-regulation of CDK4 and CCND1. In addition, Astragali Radix-Angelicae Sinensis Radix can have a targeted protective effect on erythrocytes.

Antineoplastic drugs have clear health hazards to the human body. In recent years, the scale of use of antineoplastic drugs had continued to expand, and the occupational exposure risk of medical personnel had also increased, which had attracted widespread attention. Taking effective measures to prevent occupational exposure can protect the health of medical personnel. This article reviewed the laws, regulations, guidelines, and industry guidance documents on occupational exposure prevention and control of antineoplastic drugs issued by relevant departments and associations in China. It summarized the scientific management experience of antineoplastic drugs in China, with the aim of reducing the occupational exposure risk of antineoplastic drugs in the future, and assisting the healthy development of China's medical and health industry.

Background: To compare the efficacy and safety of monthly administrations of gonadotropin releasing hormone (GnRH) agonists LY01005 and Zoladex® in Chinese patients with premenopausal breast cancer. Methods: From October 2020 to November 2021, 188 premenopausal breast cancer patients were enrolled in 34 hospitals and randomized 1:1 to receive either LY01005 or Zoladex® every 28 days for a total of three injections. All patients concomitantly received oral tamoxifen (TAM). The primary efficacy endpoint was cumulative probability of maintaining menopausal level [oestradiol (E2) ≤30 pg/ml] from day 29 to day 85. The second efficacy endpoint included changes in E2, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) compared with the baseline. Pharmacokinetics (PK), pharmacodynamics (PD), and safety were analyzed. The study also evaluated the pharmacokinetic and pharmacodynamic characteristics of LY01005. Results: A total of 188 patients were randomised and 187 patients received either LY01005 or Zoladex®. Cumulative probabilities of maintaining menopausal level (E2≤30 pg/ml) from day 29 to day 85 were 93.1% for LY01005 and 86.3% for Zoladex®. The between-group difference was 6.8% (95% CI: -2.3%, 15.9%) and primary efficacy in the LY01005 group was not inferior to that in the Zoladex® group. Changes in E2, LH, and FSH levels compared with the baseline were equivalent between the two groups (E2: 89.34% to 90.23% vs. 82.11% to 85.02%; LH: 88.89% to 95.52% vs. 89.70% to 97.02%; FSH: 75.36% to 80.85% vs.73.07% to 80.24%, respectively). After three consecutive doses of LY01005, the LH and FSH levels of the subjects showed a transient increase after the first dose, reached a peak on the second day and then started to decrease. The LH and FSH reached a lower level and remained at or below that level until the 85th day. Both treatments were well-tolerated. Conclusion: LY01005 is as effective as Zoladex® in suppressing E2 to menopausal levels in Chinese patients with premenopausal breast cancer, with a similar safety profile.

Objective: To investigate whether F.nucleatum affects the chemotherapy resistance of colorectal cancer by regulating ABC subfamily G subtype 2 (ABCG2), in view of the fact that the correlation between the two has not been reported. Methods: Oxaliplatin was used to interfere with colorectal cancer cells and co-cultured with F.nucleatum to establish a chemotherapy-induced model of microbial infection. Calcein AM/PI cell staining, trypan blue staining, and cell counting kit 8 (CCK-8) method were used to detect cell activity. Real-time fluorescence quantitative polymerase chain reaction and western blot were used to detect ABCG2 mRNA and protein expression levels in colorectal cancer cells. The target gene was knocked down by constructing shRNA plasmids. The HCT-116 cell F.nucleatum infection model was constructed and transcriptome sequencing and Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene ontology (GO) analyses were performed to determine the differential gene expression enrichment pathways. Genistein (GST) was used as an E-cadherin blocker, and triclabendazole sulfoxide (TCBZSO) was used as an ABCG2 blocker. Immunofluorescence was used to detect E-cadherin and β-catenin protein expressions and intracellular localization levels. The subcutaneous xenograft model of nude mice was constructed in vivo, and the expression level of ABCG2 protein in tissues was detected by immunohistochemical staining. Results: CCK-8 results showed that F. nucleatum+oxaliplatin group [HT-29, (92.26±1.66)%; HCT-116, (82.13±1.84)%] cell relative survival rate was higher than that of oxaliplatin group [HT-29, (79.64±3.72)%; HCT-116, (67.56±2.96)%; P＜0.001]. The relative survival rate of oxaliplatin and F. nucleatum co-culture group with ABCG2-knockdown HCT-116 cells [(61.44±1.48)%] was lower than that of F. nucleatum and oxaliplatin co-cultured with HCT-116 cells [(69.29±4.45)%, P=0.015]. GO enrichment analysis showed that HCT-116 cells co-cultured with F.nucleatum were significantly enriched in "β-catenin binding", "cadherin binding" and "regulation of Wnt signaling pathway". RT-qPCR results showed that the relative expression of ABCG2 mRNA in F.nucleatum + genistein group was significantly lower than that in F.nucleatum group (P＜0.001). The results in vivo showed that the tumor weight in the F.n+L-OHP+TCBZSO group [(0.12±0.02)g] was lower than that in the F.n+L-OHP group [(0.33±0.05)g, P＜0.001]. Immunohistochemistry suggested that the promotion of ABCG2 protein expression by F. nucleatum was blocked after TCBZSO intervention. Conclusion:F. nucleatum up-regulates ABCG2 expression through E-cadherin/β-catenin signaling pathway to promote colorectal cancer resistance to oxaliplatin.

Moxibustion therapy is an important traditional non-pharmacological treatment in traditional medicine for improving chemotherapy-induced bone marrow suppression. By reviewing recent studies on moxibustion intervention for chemotherapy-induced bone marrow suppression, this article summarized and analyzed the current research status. In clinical studies, moxibustion therapy that tonifies the spleen, nourishes the kidneys, warms yang, and nourishes blood has been verified to be effective for chemotherapy-induced bone marrow suppression, but the efficacy may vary among individuals receiving different chemotherapy regimens. Experimental studies have shown that moxibustion therapy primarily improves chemotherapy-induced bone marrow suppression by repairing bone marrow tissue structure, increasing the amounts of hematopoietic stem cells, improving bone marrow hematopoietic microenvironment, repairing bone marrow cell DNA, and regulating signaling pathways such as Notch, Wnt, phosphatidylinositol 3-kinase/protein kinase B/ mammalian target protein of rapamycin and other signaling pathways. Future research can further systematically reveal the mechanisms of moxibustion therapy, such as alleviating hematopoietic stem cell aging induced by chemotherapy, regulating miRNAs to improve bone marrow suppression, and investigate the sensitivity of patients with bone marrow suppression caused by different chemotherapy regimens to moxibustion therapy, in order to complete and standardize the application protocols of moxibustion.

To investigate the biological activity and antitumor effect of pegylated recombinant human interleukin 2 (PEG-rhIL-2) obtained by site-specific conjugation of polyethylene glycol (PEG) with non-natural amino acids, and to explore its antitumor mechanism.

Immune checkpoints include a series of receptor-ligand pairs that play a key role in the proliferation, activation, and immune regulatory responses of immune cells. Although immune checkpoint inhibitors (ICIs), such as programmed death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) have achieved good therapeutic effects in clinical practice, some patients still experience ineffective treatment and immune resistance. A large amount of evidence has shown that immune checkpoint proteins are related to cell metabolism during immune regulation. On the one hand, immune checkpoints connect to alter the metabolic reprogramming of tumor cells to compete for nutrients required by immune cells. On the other hand, immune checkpoints regulate the metabolic pathways of immune cells, such as phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) to affect the activation of immune cells. Based on a review of the literature, this article reviews the mechanisms by which PD-1, CTLA-4, T cell immunoreceptor with Ig and ITIM domains (TIGIT), T cell immunoglobulin and mucin domain-containing protein 3 (TIM-3), cluster of differentiation 47 (CD47), and indoleamine 2,3-dioxygenase 1 (IDO1) regulate cell metabolic reprogramming, and looks forward to whether targeting the ligand-receptor pairs of immune checkpoints in a "dual regulation" manner and inhibiting metabolic pathways can effectively solve the problem of tumor immune resistance.
.

Taxanes are essential chemotherapy agents for breast cancer treatment. However, patients frequently experience chemotherapy-induced peripheral neuropathy (CIPN) during their course of treatment. Cryotherapy is a non-pharmacological approach that has been explored for its potential effects on preventing or improving CIPN. However, although several studies have reported on the effects of cryotherapy, no comprehensive review has been conducted to confirm its benefits.

Checkpoint inhibitor pneumonitis (CIP) is a rare type of immune-related adverse reaction, that can seriously affect the subsequent anti-tumor immunotherapy and even lead to respiratory failure or death. However, if identified and diagnosed early, and treated promptly and appropriately, most patients have a good prognosis, and some may be eligible for subsequent immune rechallenge. In order to standardize diagnosis and treatment of patients with CIP and improve their prognosis, the Department of Pulmonary and Critical Care Medicine of Peking Union Medical College Hospital initiated and developed the consensus, which was discussed and reached a consensus by experts from the Oncology Respiratory Disease Committee of China Anti-Cancer Association, Lung Cancer Group of Thoracic Society of Chinese Medical Association and Beijing Cancer Prevention and Treatment Research Association. The consensus formed 18 expert recommendations on the risk factors, clinical characteristics, diagnostic evaluation measures, diagnostic criteria, differential diagnosis, treatment strategies and rehabilitation plans of CIP for clinicians' reference.

Objective: To evaluate the efficacy and safety of venetoclax in combination with multidrug chemotherapy in patients with newly diagnosed acute leukemia of ambiguous lineage (ALAL) . Methods: A retrospective analysis of clinical data was performed on patients with newly diagnosed ALAL who were hospitalized at Jiangsu Provincial People's Hospital from June 2021 to July 2024. Of the 13 patients who received initial induction therapy with venetoclax combined with multidrug chemotherapy, 8 received VAA+P regimen, and 5 received V+IA regimen. Patients with FLT3 mutation were treated with FLT3 inhibitor, and Ph(+) patients received an additional tyrosine kinase inhibitor. Overall survival (OS), disease-free survival (DFS), and adverse events were analyzed. Results: According to the World Health Organization 5th edition of the classification of hematolymphoid tumors, the immunophenotypes were T/myeloid mixed-phenotype acute leukemia (MPAL) (n=4), B/myeloid MPAL (n=7), and ALAL- not otherwise specified (n=2). Of the seven patients with B/myeloid MPAL, four were Ph(+) and belonged to the group with specific gene abnormalities of ALAL. Three patients had FLT3 mutation (one with FLT3-TKD mutation and two with FLT3-ITD mutation). Prior to the second course of consolidation therapy, the efficacy of venetoclax induction therapy was evaluated, and a complete response rate of 100% was achieved in 13 patients. In the subsequent consolidation therapy phase, one patient discontinued treatment and was lost to follow-up; nine patients underwent allogeneic hematopoietic stem cell transplantation, four of whom died due to posttransplant complications and five achieved DFS. Of the three patients (≥70 years old) who received consolidation therapy as before, two achieved DFS and one died due to central nervous system leukemia. The median OS time was not reached in 13 patients; the 75th percentile survival time was 12.0 months, with a 12-month cumulative survival rate of 64.5%. The median DFS time was not reached in all patients; the 75th percentile DFS time was 8.2 months, with a 12-month cumulative DFS rate of 67.1%. All patients experienced grade 3 or 4 hematologic toxicity, including neutropenia and thrombocytopenia, during and after induction therapy. All patients recovered hematopoietic function after the initial induction therapy, with no fatal hemorrhage, tumor lysis syndrome, neurological adverse events, or grade 3 or higher organ toxicity, excluding preexisting conditions. Conclusion: Venetoclax in combination with multidrug chemotherapy was effective and associated with tolerable adverse reactions in patients with newly diagnosed ALAL.

Lung cancer is the leading cause of cancer-related deaths worldwide, characterized by high incidence and mortality rates. The primary reasons for treatment failure in lung cancer patients are tumor invasion and drug resistance, particularly resistance to chemotherapeutic agents and epidermal growth factor receptor (EGFR) mutant targeted therapy, which considerably undermine the therapeutic outcomes for those with advanced lung cancer. Epithelial-mesenchymal transition (EMT) serves as a crucial biological process closely associated with physiological or pathological processes such as tissue embryogenesis, organogenesis, wound repair, and tumor invasion. Numerous studies have indicated that EMT, mediated through various signaling pathways, plays a pivotal role in the initiation, progression, and metastasis of lung cancer, while it is also closely associated with drug resistance in lung cancer cells. Therefore, research focusing on the molecular mechanisms and pathophysiology related to EMT can contribute to reversing drug resistance in drug treatment for lung cancer, thereby improving prognosis. This article reviews the progress in research on EMT in the invasion, metastasis, and drug resistance of lung cancer based on relevant domestic and international literature.

Myelosuppression is a common hematological side effect of oncological treatment, mainly including neutropenia, thrombocytopenia and anemia. Due to the delay in its clinical manifestation, a well-established out-of-hospital management system can help clinicians better prevent and manage the myelosuppression associated with oncology treatment and ensure the effectiveness and safety of antitumor therapy. This consensus focuses on a detailed compilation and summary of the definition and grading of myelosuppression associated with oncological treatment, the principles of out-of-hospital management, the management process and management methods, develops a risk stratification assessment table for oncology treatment-related myelosuppression, and puts forward 8 recommendations based on the risk stratification, which is aimed at providing medical workers with a reference plan for the out-of-hospital management of myelosuppression associated with oncological treatment.

Immune checkpoint inhibitor (ICI) has been widely used in lung cancer patients. While ICI treatment improves the overall survival of patients, it can also lead to a series of immune-related adverse events (irAE). Severe irAE should be treated with glucocorticoids and biological agents. Opportunistic infections should be highly vigilant during the treatment of glucocorticoids and biological agents. We report a patient with locally advanced non-small cell lung cancer who developed severe ICI-related colitis after chemotherapy combined with immunotherapy. The patient developed hematogenous disseminated Mycobacterium tuberculosis infection and pulmonary aspergillosis during the treatment with glucocorticoids and biological agents (infliximab). The purpose of this study is to draw the attention of clinicians to opportunistic infections when dealing with irAE.

In the real world, the plasma drug concentration range of Icotinib treated with epidermal growth factor receptor (EGFR) gene mutant non-small cell lung cancer (NSCLC) is not yet clear, and there may be a correlation between drug concentration and its efficacy, as well as adverse reactions. This study conducted therapeutic drug monitoring (TDM) of Icotinib. The aim of this study was to analyze the drug exposure of Icotinib in targeted therapy for NSCLC, and to investigate the relationship between Icotinib drug concentration and its efficacy and safety.

Chemotherapy-induced anemia (CIA) is one of the most common complications in cancer patients. If CIA treatment is not effective, it will affect the normal implementation of chemotherapy regimens, and reduce the quality of life of patients and shorten clinical survival. At present, CIA has serious shortcomings in treatment rate and unsatisfactory therapeutic effect. It is often forced to reduce the dose of chemotherapy or delay chemotherapy due to anemia that cannot be rapidly and effectively treated in clinical practice. These problems are mainly related to factors such as complex etiology of the disease, late timing of clinical intervention, and certain limitations in existing treatment options. Therefore, disease management needs to further strengthen the concept of early diagnosis and early treatment to avoid the increased clinical burden due to the severity of anemia. Meanwhile, with the in-depth understanding of the mechanism of anemia, new drug research and development based on the comprehensive regulatory mechanism of hypoxia-inducible factor (HIF) has begun in clinical practice. A phase Ⅲ clinical study of Roxostat in the treatment of chemotherapy-induced anemia in patients with non-medullary malignancies was presented at the European Society of Medical Oncology (ESMO) conference in 2023. This hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI) drug is an oral preparation, which has shown good efficacy and safety in the study, and has superior compliance compared with recombinant human erythropoietin-α (rHuEPO-α). Starting from the re-understanding of the mechanism of CIA, this review analyzes the current diagnosis and treatment dilemmas of CIA, puts forward suggestions in combination with the "Guildlines of Chinese Society of Clinical Oncology (CSCO) clinical practice in tumor-related anemia (2024)", and introduces and looks forward to HIF-PHI, a new therapeutic drug in the future.

Stevens-Johnson syndrome (SJS) and toxic epidermalnecrolysis (TEN) are acute, severe and fatal diseases involving the skin and mucous membranes, most commonly caused by pharmaceutical factors. These include various sensitizing antibiotics, non-steroidal anti-inflammatory drugs and so on. Immune-associated Stevens-Johnson syndrome/toxic epidermolysis caused by programmed death-1 (PD-1) inhibitors has not been reported. On April 11, 2024, a male patient with primary bronchial lung cancer (right lung squamous cell carcinoma T3N3M1b ⅣA phase driver gene KRAS G12S PD-L1 negative, PS 0 score) was admitted to the department of respiratory and critical care medicine of Bishan hospital affiliated to Chongqing medical university. On March 25, 2024, the patient underwent the 3rd cycle of anti-tumor therapy "Tirellizumab 200 mg+albumin paclitaxel 400 mg+carboplatin 450 mg", and on April 9, 2024, Stevens-Johnson syndrome and toxic epidermolysis occurred, and the epidermolysis area reached more than 95%. After permanent discontinuation of immunosuppressants, anti-infection, hormone, nutritional support, immunoglobulin and other comprehensive treatment, the patient was eventually cured and successfully discharged.

Lung cancer is one of the most malignant tumor, representing a significant threat to human health. In China, its mortality rate is the highest among all malignant tumors. The occurrence of drug resistance has resulted in unfavourable prognosis for patients with lung cancer, and overcoming drug resistance is a significant challenge that needs to be addressed. Nano-drug delivery technology has been an important approach to overcome drug resistance in lung cancer. Targeting to the mechanisms of drug resistance, by enabling the combined delivery of drugs, increasing the efficiency of drug delivery and improving the targeting and safety of drugs, nano-drug delivery technology offers a novel approach to tackling drug resistance in lung cancer. This paper describes the current status of lung cancer treatment, mechanisms of drug resistance, strategies to overcome drug resistance, and the application of nanotechnology in the diagnosis and treatment of lung cancer. In addition, it summarizes the recent research progress on the application of nano-drug delivery technology to overcome drug resistance in lung cancer. Finally, the current prospects and challenges of nano-drug delivery technology are discussed.
.