基于应激系统理论的护理干预在颅内肿瘤切除术患者中的应用效果

目的探讨基于应激系统理论的护理干预在颅内肿瘤切除术患者中的应用效果。方法选取2016年5月至2020年5月间郑州市第一人民医院收治的行颅内肿瘤切除术的60例患者为研究对象,采用随机数表法分为对照组和观察组,每组30例。对照组患者围术期给予常规护理,观察组患者在对照组的基础上给予基于应激系统理论的护理干预措施,比较两组患者的入睡时间、睡眠时间、觉醒次数、成人心理弹性量表(RSA)评分、皮质醇(Cor)、去甲肾上腺素(NE)和肾上腺素(E)水平及护理满意度。结果护理前,两组患者入睡时间、睡眠时间和觉醒次数比较,差异无统计学意义(P>0.05),护理后,两组患者入睡时间和觉醒次数均升高,睡眠时间均缩短,但观察组均优于对照组,差异均有统计学意义(均P <0.05);护理前,两组患者RSA评分比较,差异无统计学意义(P>0.05),护理后两组患者RSA评分均升高,且观察组高于对照组,差异均有统计学意义(均P <0.05)。护理前,两组患者Cor、NE和E水平比较,差异无统计学意义(P> 0.05),护理后,两组患者上述指标均升高,但观察组均低于对照组,差异均有统计学意义(均P <0.05)。观察组患者护理满意度为96.7%,高于对照组的73.3%,差异无统计学意义(P <0.05)。结论基于应激系统理论的护理干预可显著改善颅内肿瘤切除术患者的心理、生理应激反应和睡眠质量,患者的护理满意度较高,值得临床借鉴。     

营养支持对降低ICU肿瘤重症患者呼吸机相关性肺炎的临床效果

目的探讨营养支持对降低ICU肿瘤重症患者呼吸机相关性肺炎的临床效果。方法选取2018年6月至2019年9月间四川电子科技大学医学院附属肿瘤医院收治的90例行气管插管机械通气治疗的肿瘤重症患者,采用随机数字表法分为观察组47例和对照组43例。观察组患者采用早期肠内外营养支持,对照组患者采用常规营养支持,比较两组患者呼吸机相关性肺炎(VAP)发生率、住院时间、机械通气时间及21d致死率;比较两组患者入ICU第1天及治疗14d后淋巴细胞计数、血红蛋白、血清总蛋白及血清白蛋白水平。结果诊疗后,观察组患者淋巴细胞计数、血红蛋白、白蛋白及总蛋白水平均增加,且均大于对照组,对照组患者淋巴细胞计数升高,血红蛋白、白蛋白及总蛋白水平均下降,差异均有统计学意义(均P <0.05)。观察组患者VAP发病率、住院时间、机械通气时长与21天致死率均低于对照组,差异均有统计学意义(均P <0.05)。结论早期营养支持对降低ICU肿瘤重症患者VAP发病率效果较好,且可有效改善机体状况及预后。     

原发不明颈部转移癌的诊治

原发不明的颈部转移性癌（CCUP）占所有头颈部恶性肿瘤的3%~5%。随着PET-CT、分子病理学、内镜等辅助检查的发展和放疗技术的进步,这类疾病的诊治水平逐渐提高。手术和放射治疗是CCUP最主要的治疗方式。但因CCUP发病率较低、异质性大,目前仍缺少前瞻性临床试验数据,在治疗方面存在很多争议,本文就近年CCUP的诊疗进展做一综述。     

Ⅳ期NSCLC原发肿瘤三维放射治疗失败模式分析

目的 探讨Ⅳ期NSCLC原发肿瘤三维放疗联合药物一线治疗的失败模式特点及放疗相关因素的影响。方法 选择2003年3月至2020年7月708例初诊Ⅳ期NSCLC患者,χ²检验失败模式单因素分析;Kaplan‐Meier法并log‐rank检验、Cox回归模型多因素生存分析。结果 708例首次失败发生率71.2%,≤6个月、>6~12个月、>12~24个月、>24个月的治疗失败发生率分别为22.7%、28.8%、13.3%、6.4%,中位生存期分别为7.2、13.4、22.2、37.6个月,差异有统计学意义（χ²=226.013,P<0.001）。复发失败发生率为21.3%,寡转移和非寡转移的复发失败发生率差异无统计学意义。转移失败发生率为66.3%,从高到低依次为脑>骨>肺>胸膜腔>肝>远处淋巴结>肾上腺>其他部位,约1/2病例发生新增转移器官,约1/3病例发生原转移器官进展。转移状态、治疗失败发生时间、病理类型、性别、综合治疗强度是预后的独立影响因素。结论 Ⅳ期NSCLC原发肿瘤放疗的失败模式与一线药物治疗不同,局部失败显著降低,转移失败为主,脑转移发生率最高,治疗失败发生时间越晚,OS期越长。寡转移、女性、非鳞癌、治疗失败发生时间晚、4~6个周期化疗同期放疗剂量≥63 Gy是延长生存的独立预后因子。     

Canadian Consensus for Biomarker Testing and Treatment of TRK Fusion Cancer in Pediatric Patients

Neurotrophic tyrosine receptor kinase gene fusions (NTRK) are oncogenic drivers present at a low frequency in most tumour types (<5%), and at a higher frequency (>80%) in a small number of rare tumours (e.g., infantile fibrosarcoma [IFS]) and considered mutually exclusive with other common oncogenic drivers. Health Canada recently approved two tyrosine receptor kinase (TRK) inhibitors, larotrectinib (for adults and children) and entrectinib (for adults), for the treatment of solid tumours harbouring NTRK gene fusions. In Phase I/II trials, these TRK inhibitors have demonstrated promising overall response rates and tolerability in patients with TRK fusion cancer who have exhausted other treatment options. In these studies, children appear to have similar responses and tolerability to adults. In this report, we provide a Canadian consensus on when and how to test for NTRK gene fusions and when to consider treatment with a TRK inhibitor for pediatric patients with solid tumours. We focus on three pediatric tumour types: non-rhabdomyosarcoma soft tissue sarcoma/unspecified spindle cell tumours including IFS, differentiated thyroid carcinoma, and glioma. We also propose a tumour-agnostic consensus based on the probability of the tumour harbouring an NTRK gene fusion. For children with locally advanced or metastatic TRK fusion cancer who have either failed upfront therapy or lack satisfactory treatment options, TRK inhibitor therapy should be considered.     

Urate Nephropathy from Tumor Lysis Syndrome in an Undiagnosed Case of Prostate Cancer

Prostate cancer can masquerade as just normocytic anemia and thrombocytopenia, thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), or tumor lysis syndrome (TLS). We are reporting an intriguing case of metastatic prostate cancer which remained undiagnosed until the patient showed signs of tumor lysis syndrome (TLS), leading to urate nephropathy requiring urgent hemodialysis. Tumor lysis syndrome is an oncological emergency but an exceedingly rare complication in non-hematological malignancies, including prostate cancer. It is challenging to recognize features of TLS in a case such as this with an unknown diagnosis. In the case of an established diagnosis of malignancy, however, checking baseline renal function, uric acid, lactate dehydrogenase (LDH), potassium, and phosphate to monitor for TLS as well as considering urate lowering therapy can help prevent adverse outcomes.     

Signal-transducing innate receptors in tumor immunity

The signal-transducing innate receptors represent classes of pattern recognition receptors (PRRs) that play crucial roles in the first line of the host defense against infections by the recognition of pathogen-derived molecules. Because of their poorly discriminative nature compared with antigen receptors of the adaptive immune system, they also recognize endogenous molecules and evoke immune responses without infection, resulting in the regulation of tumor immunity. Therefore, PRRs may be promising targets for effective cancer immunotherapy, either by activating or inhibiting them. Here, we summarize our current knowledge of signal-transducing PRRs in the regulation of tumor immunity.     

Clonal dynamics of circulating tumor DNA during immune checkpoint blockade therapy for melanoma

Assessment of treatment efficacy of immune checkpoint inhibitors in melanoma patients is difficult as the response to these therapies varies among patients or lesions. The clonal evolution of cancer during immune checkpoint blockade therapy could cause treatment resistance. We investigated the potential of liquid biopsy in monitoring the mutational profiles of metastatic melanoma during immunotherapy. Plasma samples collected from 21 Japanese metastatic melanoma patients before immune checkpoint blockade therapy were subjected to whole-exome sequencing (WES). Furthermore, 14 Japanese patients with melanoma were enrolled for longitudinal analysis of circulating tumor DNA (ctDNA). Plasma samples were collected prospectively before and during therapy and sequenced. WES of the pretreatment plasma from Japanese melanoma patients showed detectable ctDNA levels with wide ranges of variant allele frequencies within a sample, suggesting clonal and subclonal mutations in ctDNA. In targeted sequencing using longitudinal samples, ctDNA levels correlated with increased tumor size, while ctDNA content immediately decreased after a surge in a patient exhibiting pseudo-progression, suggesting the potential of ctDNA analysis in discriminating between pseudo- and true progression. Mutant ctDNA levels showed different patterns within the clinical course of specific patients, suggesting that these mutations were derived from different tumor clones with distinct therapeutic responses. During further investigation, WES of plasma samples from 1 patient showed marked differences in the mutational profiles of ctDNA, including expansive tumor evolution during an acute exacerbation. Immunotherapy may induce characteristic clonal evolutions of tumors; longitudinal analysis of ctDNA has the potential of determining these tumor evolution patterns and therapeutic responses.