Asia-Pacific journal of clinical oncology最新文献

Introduction: Hypersensitivity reactions (HSRs), an unpredictable and sometimes harmful reaction, may hamper the effectiveness of chemotherapy and lead to the need for drug switching. The recall of ranitidine from the drug market due to the N-nitrosodimethylamine production necessitates the identification of a proper alternative for the prevention of HSRs. Our study aimed to evaluate the efficacy of oral famotidine in the prevention of HSRs in patients who received chemotherapy agents, particularly platinum-based and taxanes.

Methods: A total of 426 patients who were treated with platinum-based agents or taxanes as part of their regimen were divided into two groups. The famotidine group, including 213 patients, received the standard premedication along with an oral dose of 40 mg famotidine the night before and 1 h prior to the chemotherapy session. The control group, also including 213 patients, received only the standard premedication without famotidine.

Results: Based on the results of this study, six patients in the control group experienced HSRs with a range of varying severities. No HSRs were observed by any of the patients in the famotidine group (p-value = 0.022).

Conclusion: Administration of oral famotidine is beneficial in preventing chemotherapy-induced HSRs.

Clinical trial registration: It was also registered with the Iran Clinical Trial Centre under code IRCT20160310026998N13.

Aim: Smoking is a chronic relapsing condition that is under-reported in oncology settings. People who report current smoking (CS) and those who report recently quitting smoking (RQ) should receive cessation support when they are diagnosed with cancer. The study aimed to identify whether differences exist in the smoking cessation support given to CS and RQ in oncology and what advice is given regarding the benefits of cessation.

Method: A survey exploring smoking cessation practices was completed by oncology clinicians (medical, nursing, and allied health) at nine cancer centers in Australia. Data were analyzed using mixed-effects ordinal regression modeling.

Results: Across the 177 clinicians completing the survey, the reported provision of smoking cessation care was significantly higher for CS than for RQ in relation to asking about smoking status (odds ratio [OR] 3.03, p = 0.001), advice on the benefits of quitting (OR 2.86, p = 0.001), and advice to call the Quitline (OR 5.08, p < 0.001). Exploratory analyses indicated doctors and nurse specialists were four times more likely to report referring CS to a Quitline compared to RQ (OR 4.38, p = 0.001; OR 4.29, 95%, p = 0.005, respectively). The cessation benefits that clinicians most often cited to their patients was that quitting "can reduce the chance of developing treatment complications and side effects".

Conclusion: The relative lack of smoking cessation care provided to RQ in oncology suggests that the high risk of smoking relapse is not well-recognized. Greater awareness and training are needed regarding advising RQ about the survival-specific benefits of continuing to not smoke, offering referrals, and offering follow-up support.

Shortening treatment time with moderately hypofractionated radiotherapy benefits patients by reducing inconvenience and costs, but its use in the definitive treatment of unresectable Stage 3 non-small cell lung cancer is controversial due to lack of level one evidence and toxicity concerns. Pivotal systemic therapy trials utilize conventionally fractionated chemoradiation at 2 Gy per fraction given over 6 weeks. In practice, 4 weeks of chemoradiation at 2.75 Gy per fraction is sometimes employed to reduce the treatment burden for selected patients, especially those who are older or have comorbidities. It is uncertain if the two fractionation regimens are similar in biologically effectiveness, especially with varying systemic therapy. This systematic review aimed to collate the survival and toxicity outcomes for 4 weeks of moderately hypofractionated chemoradiation, using > 50 -60 Gy in 20 fractions. Eight studies met the eligibility criteria; seven studies were from a database search of MEDLINE, EMBASE, Cochrane Library, and Web of Science and one study was added later. Two studies were prospective randomized trials and six were retrospective cohort studies. No study included immunotherapy. The historical evidence has been limited, but emerging data is promising, especially when compared to outcomes of standard chemoradiation. Thus, further investigation of this strategy is justified.

Introduction: Despite the increased demand for medical cannabis (MC), MASCC guidelines state that there is insufficient evidence of its efficacy and safety. Although research has explored medical professionals' perceptions of MC, there is to our knowledge minimal research exploring patients' perceptions, particularly in an Australian cancer setting.

Methods: A survey of Australian cancer patients attending oncology outpatient clinics was performed. Patients were ≥ 18 years and had a confirmed diagnosis of cancer (solid or hematological).

Results: A total of 413 patients were approached between April 2019 and March 2020 out of which 82% (350) consented to participate. A total of 19% (67/350) were using MC. Despite being used for symptom control, such as pain (61%), and, in some cases for perceived anticancer activity (12% to cure, and 16% to slow the cancer), only a minority of users believed that the evidence was of high quality for these indications (28% for physical benefits and 29% for anticancer activity). Nonusers were even more skeptical of the evidence for these indications (17% and 11%, respectively). Only a minority of patients (31% of users and 8% of nonusers) accessed information on MC from clinicians. Most instead relied on resources such as TV, friends, family, social media, and websites.

Conclusion: This study demonstrates current real-world cancer patients' perceptions on the evidence for MC, the sources of information used to shape their health beliefs, and compares users to nonusers. The results highlight the need for treating teams to combat potential misinformation that patients may be accessing about MC and provide information on treatments with stronger evidence.

Some patients with metastatic castration-resistant prostate cancer (mCRPC) possess germline or acquired defects in the DNA damage repair (DDR) genes BRCA1 and BRCA2. Tumors with BRCA mutations exhibit sensitivity to poly-ADP ribose polymerase inhibitors (PARPi) such as olaparib and rucaparib. As a result, molecular diagnostic testing to identify patients with BRCA mutations eligible for the PARPi therapy has become an integral component of managing patients with mCRPC. There are practical challenges in the current molecular testing pathway in Australia that can compromise testing success. Testing success is often contingent on quality of tissue handling and laboratory processing techniques to minimize DNA degradation and suboptimal sequencing data quality. Greater adoption of best testing practices in Australia can be facilitated with education and greater awareness of expert recommendations. Here, we provide expert recommendations on how to optimize BRCA molecular diagnostic testing in patients with mCRPC. Optimization and standardization of molecular diagnostic testing will support health care providers and institutes in establishing more efficient testing pathways, enabling access to targeted therapies such as PARPi, and improving patient outcomes.

Aim: Manatū Hauora, the Ministry of Health of New Zealand (NZ), published minimum standards for molecular testing of colorectal cancers (CRCs) in June 2018. These included mismatch repair (MMR) testing at diagnosis and BRAFV600E mutation analysis on newly diagnosed stage IV CRCs. This study aimed to determine the proportion of patients with CRC in the South Island of NZ with metastatic deficient mismatch repair (dMMR) CRC, the proportion of metastatic CRCs and dMMR CRCs that have a BRAFV600E mutation, and audit testing for BRAF mutations and appropriate referral to genetics services.

Methods: People from the South Island with histologically diagnosed colorectal adenocarcinoma between July 1, 2018, and June 30, 2019, were identified by the National Cancer Registry. Data points extracted from the electronic medical record included staging, MMR status, BRAF mutation testing, and genetics referral.

Results: A total of 845 patients met the inclusion criteria; 166 of 845 (19.6%) had dMMR CRC, and of these 130 (78%) had BRAF mutation, 256 patients developed metastatic disease by data cut-off, 20 (7.8%) had dMMR, and 41 (22.2%) had BRAF mutation. When indicated, 275 of 330 (83.3%) were tested for BRAF mutation and 32 of 45 (71.1%) referred to genetics. Compared with other populations, South Island CRC patients had higher rates of dMMR and BRAF mutation.

Conclusion: Less than 10% of patients (n = 20) had metastatic dMMR CRC. These patients could be considered candidates for immune checkpoint inhibitor therapy, a small number that would not significantly burden the NZ health system if funded. The vast majority of dMMR CRC was sporadic. Rates of testing could be improved.

Aim: Breast cancer (BC) is the most frequently diagnosed malignancy worldwide, necessitating continued research into its molecular mechanisms. Circular RNAs (circRNAs) are increasingly recognized for their role in various cancers, including BC. This study explores the role of circRNA kinesin family member 4A (circKIF4A) in BC progression and its underlying molecular mechanisms.

Methods: BC cell lines were cultured, and circKIF4A expression was knocked down. Cell viability, proliferation, migration, and invasion were assessed using the Cell Counting Kit-8, colony formation assay, and Transwell assays. The expression of circKIF4A, miR-874-3p, and glycerophosphodiester phosphodiesterase domain-containing 5 (GDPD5) was quantified using qRT-PCR and Western blot analysis. Subcellular fractionation was performed to localize circKIF4A within the cell. The interactions between circKIF4A and miR-874-3p, as well as between miR-874-3p and GDPD5, were evaluated using RNA pull-down and dual-luciferase assays. Rescue experiments were conducted with miR-874-3p inhibition or GDPD5 overexpression to confirm the mechanistic pathway.

Results: circKIF4A was found to be upregulated in BC cells. Its knockdown significantly inhibited cell proliferation, migration, and invasion. circKIF4A acts as a sponge for miR-874-3p, reducing its expression. miR-874-3p targets and suppresses GDPD5, a key regulator in BC cell growth. Silencing miR-874-3p or overexpressing GDPD5 reversed the tumor-suppressive effects of circKIF4A knockdown.

Conclusion: circKIF4A promotes BC cell proliferation and invasiveness by regulating the miR-874-3p/GDPD5 axis. These findings highlight a potential therapeutic target in BC and contribute to the understanding of circRNA involvement in cancer progression.

Purpose: Our study aims to evaluate the characteristics of serum soluble PD-1 (sPD-1) and soluble PD-L1 (sPD-L1) levels and their correlations with immune status and prognosis in advanced lung cancer patients.

Methods: Patients diagnosed with advanced lung cancer based on histology or cytology in Peking University People's Hospital from July 2020 to November 2021 were enrolled. Clinicopathological data were recorded and analyzed. Treatment efficacy was evaluated according to RESIST 1.1 criteria. The serum levels of sPD-L1 and sPD-1 were detected by enzyme-linked immunosorbent assay (ELISA). Lymphocyte subsets were measured by flow cytometry to evaluate the immune status of the patients.

Results: A total of 65 patients with advanced lung cancer were enrolled. sPD-L1 level in lung cancer patients (15.67 ± 11.09 pg/mL, p = 0.001) was significantly higher than those in healthy controls (5.21 ± 4.46 pg/mL). sPD-1 level did not show a significant difference between patients with lung cancer and healthy controls. sPD-L1 level in patients with progressive disease (PD) was significantly higher than those with partial response (PR) (20.94 ± 8.91 vs. 13.14 ± 12.66 pg/mL, p = 0.033). In treatment-naïve patients, sPD-L1 level was negatively correlated with the lymphocyte ratio (correlation coefficient = -0.452, p = 0.014). Kaplan-Meier survival analysis showed that patients with low sPD-L1 level had a significantly longer progression-free survival (PFS) (10.4 vs. 5.7 months, p = 0.023). However, sPD-1 level did not correlate with lymphocyte subsets or prognosis in overall patients with lung cancer. Subgroup analysis showed that prolonged PFS in patients with low sPD-L1 level was exclusively shown in the NSCLC subgroup, not in the SCLC subgroup. In the subgroups of patients who subsequently received immunotherapy, low sPD-L1 level was correlated with longer PFS in the overall patients and NSCLC patients, and low sPD-1 level was correlated with longer PFS exclusively in NSCLC patients.

Conclusion: Serum sPD-L1 level was higher in patients with advanced lung cancer than healthy individuals, which was negatively correlated with the proportion of lymphocytes and prognosis. Serum sPD-1 level did not show significant difference between patients with lung cancer and healthy individuals, which showed no correlation with lymphocyte subsets and the prognosis of overall patients, except NSCLC patients receiving immunotherapy.

Aim: The response rates to immune checkpoint inhibitors (ICI) remain low (13%-20%) in metastatic head and neck cancer patients, indicating an urgent need to better understand factors predictive of response to these agents. This study explored the impact of smoking status, marijuana use, and alcohol consumption on treatment outcomes in recurrent-metastatic (R/M) head and neck squamous cell carcinoma (HNSCC) patients treated with ICI.

Methods: A retrospective analysis was performed on 201 R/M HNSCC patients treated with ICI between January 15th 2016 and April 9th 2020 at a single institution.

Results: Gender: 154 male (77%), 47 female (23%). Median age 61 (IQR: 55-68). ICI drug: pembrolizumab 100 (50%), nivolumab 91 (45%), nivolumab + ipilimumab 10 (5%). Line of therapy: first: 98 (49%), second and beyond: 103 (51%). Tumor site: oropharynx 84 (42%), oral cavity 45 (22%), larynx 26 (13%), other sites 46 (23%). p16 tumor status: negative 132 (66%), positive 69 (34%). Smoking status: former 111 (55%), never 54 (27%), current 36 (18%), median pack-year 18 (IQR: 0-37). Alcohol use: yes 110 (55%), no 91 (54%). Marijuana use: yes 47 (23%), no 154 (77%). Overall response rate: 36 (18%). Median OS: 12 months (95% CI: 9.4-14.8). Tobacco: former (HR: 0.75, 95% CI: 0.50, 1.11), current (HR: 0.58, 95% CI: 0.33, 1.02). Marijuana: yes (HR: 0.93, 95% CI: 0.58, 1.49). Alcohol: yes (HR: 1.04, 95% CI: 0.72, 1.49).

Conclusion: In our cohort, smoking status, marijuana use, and alcohol consumption did not have a statistically significant impact on OS in patients with R/M HNSCC treated with ICI.

Introduction: The role of afatinib in the first-line treatment of EGFR-mutant advanced non-small cell lung cancer (NSCLC) patients has been proven through clinical trials and real-world studies. However, additional data on the effectiveness of afatinib in patients with brain metastases are lacking.

Methods: EGFR-mutant NSCLC patients with brain metastases were retrospectively reviewed across nine cancer centers in Vietnam from April 1, 2018 to June 1, 2022. The primary endpoints included central nervous system progression-free survival (CNS-PFS) and overall survival (OS). The secondary endpoints were the objective response rate (ORR) and CNS-ORR.

Results: Among 87 enrolled patients, 21.8%, 17.2%, and 60.9% received whole-brain radiation, gamma knife, and no locoregional therapy, respectively. With a median follow-up of 32.2 months for CNS-PFS and 35.3 months for OS, the median CNS-PFS and OS were 17.9 and 29.9 months, respectively. In multivariate analysis, patients receiving whole-brain radiation had significantly shorter CNS-PFS than those untreated with local therapy (16.1 vs. 22.6 months, p = 0.019), but not translating to an inferior OS. Furthermore, both the CNS-PFS and OS of patients with uncommon mutations were significantly worse than those of patients with Del19 (11.3 vs. 24.2 months, p = 0.013 and 17.7 vs. 34.0 months, p = 0.003, respectively). Univariate and multivariate analyses showed that a lower afatinib starting dose did not significantly affect CNS-PFS or OS. The CNS-ORR and ORR were 77.4% and 71.3%, respectively.

Conclusion: In our real-world study, afatinib showed encouraging effectiveness in Vietnamese patients with EGFR-mutant NSCLC and brain metastases at baseline.