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BackgroundThe diagnosis of cancer can motivate patients to change their dietary habits. Evidence on changes in dietary intake before and after breast cancer diagnosis in Chinese women has been limited.Patients and methodsIn an ongoing prospective cohort study which involved 1,462 Chinese women with early-stage breast cancer, validated food frequency questionnaire was used to assess prediagnostic dietary intake (using questionnaire to recall dietary intake before diagnosis, which completed at baseline, ie, 0–12 months after diagnosis) and postdiagnostic dietary intake at 18-month and 36-month follow-ups after diagnosis. This study quantitatively compared dietary intake across three time points before and after breast cancer diagnosis.ResultsBreast cancer patients significantly and continuously increased vegetables and fruits consumption, from 4.54 servings/day at prediagnosis to 5.19 and 5.59 servings/day at 18-month and 36-month follow-ups postdiagnosis, respectively (each compared to baseline, P<0.001). At 18-month follow-up postdiagnosis, the intake of whole grains, refined grains, eggs, and nuts increased significantly (P<0.001, each). Conversely, the consumption of red meat (P<0.001), processed meat (P<0.001), poultry (P<0.001), dairy products (P<0.001), soy foods (P=0.024), sugar drinks (P<0.001), and coffee (P<0.001) decreased significantly. Compared with prediagnosis diet, the assessment at 36-month follow-up postdiagnosis observed similar dietary changes. The magnitude of changes between two postdiagnosis dietary assessments was much smaller than comparisons made between each of these time points with that of prediagnosis intakes. Postdiagnosis changes in dietary intake occurred in parallel with changes in macronutrients, vitamins, and minerals.ConclusionChinese breast cancer patients reported significant and long-term changes in dietary intake after cancer diagnosis, which was in line with current dietary recommendation. The present findings suggested that a cancer diagnosis might be a stimulus for patients to take up health-protective changes; health care professionals should consider this as a window of opportunity to educate patients on healthy lifestyle. Further follow-up of this cohort would enable clinicians to determine whether such dietary changes could improve long-term outcomes.

Preoperative chemotherapy is a promising strategy for the treatment of esophageal squamous cell carcinoma (ESCC). Acquired resistance to chemotherapy is a major obstacle in improving patient prognosis. Cancer-associated fibroblasts (CAFs) are the primary components of the tumor microenvironment and play a crucial role in tumor development; these cells are also potential therapeutic targets for cancer. Using protein arrays, we identified a key secreted cytokine, PAI-1, from CAFs pretreated with cisplatin that was induced after DNA damage of CAFs. The PAI-1 in the tumor microenvironment promoted tumor growth and attenuated the effects of cisplatin treatment. Extracellular PAI-1 activated the AKT and ERK1/2 signaling pathways and inhibited caspase-3 activity and reactive oxygen species accumulation. Tiplaxtinin as a PAI-1 inhibitor could play synergistic effects with cisplatin in vitro and in vivo. In clinical samples, ESCC patients with high expression of PAI-1 in CAFs presented a significantly worse progression-free survival. Taken together, our results showed that PAI-1 secreted from cisplatin-activated CAFs promoted tumor growth and reduced the effects of cisplatin in a paracrine manner, establishing a preclinical rationale to target this cytokine to further improve the clinical response of esophageal squamous cell carcinoma.

Understanding interactions between tumor and the host immune system holds great promise to uncover biomarkers for targeted therapies and clinical outcomes. However, systematical analysis of immune signatures in esophageal squamous cell carcinoma (ESCC) remains largely unstudied. In this study, immune signatures containing 708 immune related genes were curated from mRNA microarray data with tumor and paired normal tissues from 119 ESCC patients. Differential expression and survival analysis were performed with validations from Human Protein Atlas and an independent cohort of 110 ESCC patients by immunohistochemistry staining. We identified a total of 186 significantly dysregulated genes in ESCC, including downregulated genes SPINK5, IL1RN and upregulated genes SPP1 and PLAU, which were further confirmed in Human Protein Atlas data. Moreover, nine immune related genes (ABL1, ATF2, ATG5, C6, CD38, HMGB1, ICOSLG, IL12RB2 and PLAU) were significantly associated with patients' overall survival, among which, prognostic model was built including three independent factors ABL1, CD38 and ICOSLG. Validation by immunohistochemistry staining suggested that combination with tumor infiltrated CD4+ and CD8+ T lymphocytes would yield higher performance in distinguishing cases as high or low risk of unfavorable prognosis. In summary, we profiled the immune status in ESCC and established predictive and prognostic factors for ESCC, which could reflect immune disorders within tumor microenvironments and independently distinguish patients with a high risk of reduced survival, providing novel predictive and therapeutic targets for ESCC patients in the future.