Targeting monoamine oxidase A: a strategy for inhibiting tumor growth with both immune checkpoint inhibitors and immune modulators.

Monoamine oxidase A (MAOA) is a membrane-bound mitochondrial enzyme present in almost all vertebrate tissues that catalyzes the degradation of biogenic and dietary-derived monoamines. MAOA is known for regulating neurotransmitter metabolism and has been implicated in antitumor immune responses. In this review, we retrospect that MAOA inhibits the activities of various types of tumor-associated immune cells (such as CD8+ T cells and tumor-associated macrophages) by regulating their intracellular monoamines and metabolites. Developing novel MAOA inhibitor drugs and exploring multidrug combination strategies may enhance the efficacy of immune governance. Thus, MAOA may act as a novel immune checkpoint or immunomodulator by influencing the efficacy and effectiveness of immunotherapy. In conclusion, MAOA is a promising immune target that merits further in-depth exploration in preclinical and clinical settings.

Stochastic modeling of the mRNA life process: A generalized master equation.

The mRNA life cycle is a complex biochemical process, involving transcription initiation, elongation, termination, splicing, and degradation. Each of these molecular events is multistep and can create a memory. The effect of this molecular memory on gene expression is not clear, although there are many related yet scattered experimental reports. To address this important issue, we develop a general theoretical framework formulated as a master equation in the sense of queue theory, which can reduce to multiple previously studied gene models in limiting cases. This framework allows us to interpret experimental observations, extract kinetic parameters from experimental data, and identify how the mRNA kinetics vary under regulatory influences. Notably, it allows us to evaluate the influences of elongation processes on mature RNA distribution; e.g., we find that the non-exponential elongation time can induce the bimodal mRNA expression and there is an optimal elongation noise intensity such that the mature RNA noise achieves the lowest level. In a word, our framework can not only provide insight into complex mRNA life processes but also bridge a dialogue between theoretical studies and experimental data.

Combined pembrolizumab and bevacizumab therapy effectively inhibits non-small-cell lung cancer growth and prevents postoperative recurrence and metastasis in humanized mouse model.

Antibodies targeting the programmed cell death protein 1/programmed cell death ligand-1 (PD-1/PD-L1) pathway have dramatically changed the treatment landscape of advanced non-small cell lung cancer (NSCLC). However, combination approaches are required to extend this benefit beyond a subset of patients. In addition, it is of equal interest whether these combination therapy can be applied to neoadjuvant therapy of early-stage NSCLC. In this study, we hypothesized that combining immunotherapy with anti-angiogenic therapy may have a synergistic effect in local tumor control and neoadjuvant therapy. To this end, the effect of combination of bevacizumab and pembrolizumab in humanized mouse models was evaluated. Furthermore, we innovatively constructed a neoadjuvant mouse model that can simulate postoperative recurrence and metastasis of NSCLC to perform neoadjuvant study. Tumor growth and changes in the tumor vasculature, along with the frequency and phenotype of tumor-infiltrating lymphocytes, were examined. Additionally, in vivo imaging system (IVIS) was used to observe the effect of neoadjuvant therapy. Results showed that combination therapy could inhibited tumor growth by transforming tumor with low immunoreactivity into inflamed ('hot') tumor, as demonstrated by increased CD8+granzyme B+ cytotoxic T cell infiltration. Subsequent studies revealed that this process is mediated by vascular normalization and endothelial cell activation. IVIS results showed that neoadjuvant therapy can effectively prevent postoperative recurrence and metastasis. Taken together, these preclinical studies demonstrated that the combination of bevacizumab and pembrolizumab had a synergistic effect in both advanced tumor therapy and neoadjuvant setting and therefore provide a theoretical basis for translating this basic research into clinical applications.

Antibody-drug conjugates targeting CD248+ myofibroblasts effectively alleviate renal fibrosis in mice.

Myofibroblasts, or activated fibroblasts, play a critical role in the process of renal fibrosis. Targeting myofibroblasts to inhibit their activation or induce specific cell death has been considered to be an effective strategy to attenuate renal fibrosis. However, specific biomarkers for myofibroblasts are needed to ensure the efficacy of these strategies. Here, we verified that CD248 was mainly expressed in myofibroblasts in patients with chronic kidney disease, which was inversely correlated with renal function. The same result was also confirmed in renal fibrotic mice induced by unilateral ureteral obstruction and aristolochic acid nephropathy. By using an antibody-drug conjugate (ADC) named IgG78-DM1, in which maytansinoid (DM1) was linked to a fully human antibody IgG78 through an uncleavable SMCC linker, we demonstrated that it could effectively bind with and kill CD248+ fibroblasts in vitro and alleviate renal fibrosis in mice models. Besides, we confirmed that IgG78-DM1 had qualified biosafety in vivo. Our results confirmed that CD248 can be used as a specific marker for myofibroblasts, and specific killing of CD248+ myofibroblasts by IgG78-DM1 has excellent anti-fibrotic effect in renal fibrotic mice. Our study expanded the application of ADC and provided a novel strategy for the treatment of renal fibrosis.

Small Mitochondria-Targeting Fluorophore with Multifunctional Therapeutic Activities against Prostate Cancer via the HIF1α/OATPs Pathway.

Prostate cancer (PCa) is considered to be the most prevalent malignancy in males worldwide. Abiraterone is a 17α-hydroxylase/C17, 20-lyase (CYP17) inhibitor that has been approved for use in patients with prostate cancer. However, several negative aspects, such as drug resistance, toxicity, and lack of real-time monitoring of treatment responses, could appear with long-term use. Therefore, the development of anticancer agents with specific targeting to avoid side effects is imperative. Here, we used MHI-148, a type of heptamethine cyanine (HC) near-infrared fluorescence dye (NIRF), as a prototype structure to synthesize two theranostic agents, Abi-DZ-1 and Abi-783. The new compound Abi-DZ-1 retained the excellent photophysical characteristics and NIRF imaging property of MHI-148, and it could preferentially accumulate in prostate cancer cells but not in normal prostate epithelial cells via the HIF1α/organic anion-transporting polypeptides axis. NIRF imaging using Abi-DZ-1 selectively identified tumors in mice bearing PCa xenografts. Moreover, Abi-DZ-1 treatment significantly retarded the tumor growth in both a cell-derived xenograft model and a patient-derived tumor xenograft model. This finding demonstrated that Abi-DZ-1 may hold promise as a potential multifunctional theranostic agent for future tumor-targeted imaging and precision therapy. Constructing theranostic agents using the NIRF dye platform holds great promise in accurate therapy and intraoperative navigation.

PRMT5 regulates RNA m6A demethylation for doxorubicin sensitivity in breast cancer.

Cancer cells respond to various stressful conditions through the dynamic regulation of RNA m6A modification. Doxorubicin is a widely used chemotherapeutic drug that induces DNA damage. It is interesting to know whether cancer cells regulate the DNA damage response and doxorubicin sensitivity through RNA m6A modification. Here, we found that doxorubicin treatment significantly induced RNA m6A methylation in breast cancer cells in both a dose- and a time-dependent manner. However, protein arginine methyltransferase 5 (PRMT5) inhibited RNA m6A modification under doxorubicin treatment by enhancing the nuclear translocation of the RNA demethylase AlkB homolog 5 (ALKBH5), which was previously believed to be exclusively localized in the nucleus. Then, ALKBH5 removed the m6A methylation of BRCA1 for mRNA stabilization and further enhanced DNA repair competency to decrease doxorubicin efficacy in breast cancer cells. Importantly, we identified the approved drug tadalafil as a novel PRMT5 inhibitor that could decrease RNA m6A methylation and increase doxorubicin sensitivity in breast cancer. The strategy of targeting PRMT5 with tadalafil is a promising approach to promote breast cancer sensitivity to doxorubicin through RNA methylation regulation.

Advances in neuroendocrine prostate cancer research: From model construction to molecular network analyses.

Prostate cancer is the most common cancer among men and has a high incidence and associated mortality worldwide. It is an androgen-driven disease in which tumor growth is triggered via ligand-mediated signaling through the androgen receptor (AR). Recent evidence suggests that the widespread use of effective AR pathway inhibitors may increase the occurrence of neuroendocrine prostate cancer (NEPC), an aggressive and treatment-resistant AR-negative variant; however, mechanisms controlling NEPC development remain to be elucidated. Various preclinical models have recently been developed to investigate the mechanisms driving the NEPC differentiation. In the present study, we summarized strategies for the development of NEPC models and proposed a novel method for model evaluation, which will help in the timely and accurate identification of NEPC by virtue of its ability to recapitulate the heterogeneity of prostate cancer. Moreover, we discuss the origin and the mechanism of NEPC. The understanding of the regulatory network mediating neuroendocrine differentiation presented in this review could provide valuable insights into the identification of novel drug targets for NEPC as well as into the causes of antiandrogenic drug resistance.

Antibody-drug conjugates targeting CD248 inhibits liver fibrosis through specific killing on myofibroblasts.

BACKGROUND: Chronic liver injury induces pathological repair, resulting in fibrosis, during which hepatic stellate cells (HSCs) are activated and transform into myofibroblasts. CD248 is mainly expressed on myofibroblasts and was considered as a promising target to treat fibrosis. The primary aim of this study was to generate a CD248 specific antibody-drug conjugate (ADC) and evaluate its therapeutic efficacy for liver fibrosis and its safety in vivo. METHODS: CD248 expression was examined in patients with liver cirrhosis and in mice with CCl4-induced liver fibrosis. The ADC IgG78-DM1, which targets CD248, was prepared and its bioactivity on activated primary HSCs was studied. The anti-fibrotic effects of IgG78-DM1 on liver fibrosis were evaluated in CCl4-induced mice. The reproductive safety and biosafety of IgG78-DM1 were also evaluated in vivo. RESULTS: CD248 expression was upregulated in patients with liver cirrhosis and in CCl4-induced mice, and was mainly expressed on alpha smooth muscle actin (α-SMA)+ myofibroblasts. IgG78-DM1 was successfully generated, which could effectively bind with and kill CD248+ activated HSCs in vitro and inhibit liver fibrosis in vivo. In addition, IgG78-DM1 was demonstrated to have qualified biosafety and reproductive safety in vivo. CONCLUSIONS: Our study demonstrated that CD248 could be an ideal target for myofibroblasts in liver fibrosis, and CD248-targeting IgG78-DM1 had excellent anti-fibrotic effects in mice with liver fibrosis. Our study provided a novel strategy to treat liver fibrosis and expanded the application of ADCs beyond tumors.

Monoamine oxidase A drives neuroendocrine differentiation in prostate cancer.

Neuroendocrine transdifferentiation (NED) of prostate cancer (PCa) is the main cause of failure of androgen receptor inhibitor treatment. However, the molecular mechanisms underlying the development of NEPC, especially treatment-induced NEPC, remain unclear. Emerging evidence indicates that elevated monoamine oxidase A (MAOA) contribute to the proliferation, cell stemness, and bone metastasis in PCa. Here, we generated an enzalutamide-induced NED cell model to assess the role of MAOA during NED. Overall, MAOA expression was significantly increased upon Enz long-term exposure and was required for neuroendocrine marker expression. In particular, Enz was found to induce NED via the MAOA/mTOR/HIF-1α signaling axis. Further analyses revealed that the MAOA inhibitor clorgyline(CLG) may bring multiple benefits to CRPC patients, including better therapeutic effect and delays NED. These findings suggest that MAOA may be an important target for the development of anti-NED therapies, thereby providing a novel strategy for the combined application of CLG and AR inhibitors in the clinic.

Circular RNA circNIPBL promotes NNK-induced DNA damage in bronchial epithelial cells via the base excision repair pathway.

Environmental chemical exposure often causes DNA damage, which leads to cellular dysfunction and the development of diseases. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a tobacco-specific carcinogen that is known to cause DNA damage, while remains unknown about the underlying mechanism. In this study, simulated doses of NNK exposure in smokers, ranging from 50 to 300 µM, were used to detect the DNA damage effects of NNK in two human bronchial epithelial cells, 16HBE and BEAS-2B. The comet assay revealed increased DNA damage in response to NNK treatment, as measured by increased Olive tail moment (OTM). NNK treatment also led to elevated foci formation and protein expression of γ-H2AX, a DNA damage sensor. Dysregulation of proliferation, cell cycle arrest and apoptosis, was also observed in NNK-treated cells. Furthermore, the most effective dose of NNK (300 µM) was used in subsequent mechanistic studies. A circular RNA circNIPBL was identified to be significantly up-regulated in NNK-treated cells, circNIPBL knockdown successfully alleviated NNK-induced DNA damage and reversed the cellular dysregulation, while circNIPBL overexpression had the opposite effect. Mechanistically, we identified an interaction between circNIPBL and PARP1, a critical enzyme of the base excision repair (BER) pathway. CircNIPBL silencing successfully alleviated the NNK-induced inhibition of BER pathway proteins, including PARP1, XRCC1, PCNA and FEN1, while overexpression of circNIPBL had the opposite effect. In summary, our study shows for the first time that circNIPBL promotes NNK-induced DNA damage and cellular dysfunction through the BER pathway. In addition, our findings reveal the crucial role of epigenetic regulation in carcinogen-induced genetic lesions and further our understanding of environmental carcinogenesis.

Queuing Models of Gene Expression: Analytical Distributions and Beyond.

Activation of a gene is a multistep biochemical process, involving recruitments of transcription factors and histone kinases as well as modification of histones. Many of these intermediate reaction steps would have been unspecified by experiments. Therefore, classical two-state models of gene expression established based on the memoryless (or Markovian) assumption would not well describe the reality in gene expression. Recent experimental data have indicated that the inactive phases of gene promoters are differently distributed, showing strong memory. Here, we use a nonexponential waiting-time distribution to model the complex activation process of a gene, and then analyze a queuing model of stochastic transcription. We successfully derive the analytical expression of the stationary mRNA distribution, which provides insight into the effect of molecular memory created by complex activating events on the mRNA expression. We find that the reduction in the waiting-time noise may result in the increase in the mRNA noise, contrary to the previous conclusion. Based on the derived distribution, we also develop a method to infer the waiting-time distribution from a known mRNA distribution. Data analysis on a realistic example verifies the validity of this method.

Multi-focused psychosocial residential rehabilitation interventions improve quality of life among cancer survivors: a community-based controlled trial.

BACKGROUND: Even though multi-focused psychosocial residence rehabilitation intervention (MPRRI) programs are widely implemented by the Shanghai Cancer Rehabilitation Club, these programs have not been rigorously evaluated. In this study, we evaluated the effects of a 21-day MPRRI program, on the quality of life (QoL) among cancer survivors. METHODS: A total of 388 cancer patients were enrolled to either receive the 21-day MPRRI (n = 129) intervention or a waiting-list comparison (WLC) intervention (n = 259). The intervention group was offered community-based 21-day MPRRI program, combining supportive-expressive group, cognitive-behavioral therapy, and Guolin Qigong. QoL was measured using the European Organization for Research and Treatment Quality of Life Version 3 Questionnaire. Multivariable linear models were used to compare changes in QoL values between the two groups. RESULTS: After adjustment for the QoL score and other covariates at baseline, there was no significant difference in global health status (mean = 3.8, 95% CI - 1.3-9.0, P = 0.14) between the two groups after 6 months intervention. While compared with the WLC group, the intervention group showed significant improvements in the QoL score (all P < 0.05); however, there were no clinically relevant changes in subscales including emotional functioning (ES = 0.58), cognitive functioning (ES = 0.53), pain (ES = 0.52), physical functioning (ES = 0.36), and insomnia (ES = 0.30). CONCLUSIONS: These preliminary results suggest the MPRRI program is both feasible and acceptable intervention for cancer survivors in community settings and is effective in significant improving QoL above.

In Silico Discovery of a Small Molecule Suppressing Lung Carcinoma A549 Cells Proliferation and Inducing Autophagy via mTOR Pathway Inhibition.

Mammalian target of rapamycin (mTOR) kinase is vital to the regulation of cell growth and proliferation, and it has been taken as a promising target to develop cancer therapies. By reference to the crystal structure of mTOR-PP242, we explored to discover potential ATP-competitive inhibitors of mTOR. Through the integrated use of multiple in silico screenings, the tremendous amount of compounds from the SPECS database were finally reduced to 30. After several rounds of convincing biological tests in A549 cells, the newfound C-4 was identified as a potential ATP-competitive inhibitor of mTOR. Besides A549 cell proliferation suppression caused by C-4, autophagy was also determined through autophagosome observation and autophagy flux detection in C-4 treated A549 cells. We demonstrated that C-4 could inhibit cell growth and proliferation, and this inhibition may be associated with autophagy.

The Application of Heptamethine Cyanine Dye DZ-1 and Indocyanine Green for Imaging and Targeting in Xenograft Models of Hepatocellular Carcinoma.

Near infrared fluorescence (NIRF) imaging has strong potential for widespread use in noninvasive tumor imaging. Indocyanine green (ICG) is the only Food and Drug Administration (FDA) -approved NIRF dye for clinical diagnosis; however, it is unstable and poorly targets tumors. DZ-1 is a novel heptamethine cyanine NIRF dye, suitable for imaging and tumor targeting. Here, we compared the fluorescence intensity and metabolism of DZ-1 and ICG. Additionally, we assayed their specificities and abilities to target tumor cells, using cultured hepatocellular carcinoma (HCC) cell lines, a nude mouse subcutaneous xenograft model of liver cancer, and a rabbit orthotopic transplantation model. We found that DZ-1 accumulates in tumor tissue and specifically recognizes HCC in subcutaneous and orthotopic models. The NIRF intensity of DZ-1 was one order of magnitude stronger than that of ICG, and DZ-1 showed excellent intraoperative tumor targeting in the rabbit model. Importantly, ICG accumulated at tumor sites, as well as in the liver and kidney. Furthermore, DZ-1 analog-gemcitabine conjugate (NIRG) exhibited similar tumor-specific targeting and imaging properties, including inhibition of tumor growth, in HCC patient-derived xenograft (PDX) mice. DZ-1 and NIRG demonstrated superior tumor-targeting specificity, compared to ICG. We show that DZ-1 is an effective molecular probe for specific imaging, targeting, and therapy in HCC.

Post-transcriptional regulation tends to attenuate the mRNA noise and to increase the mRNA gain.

Post-transcriptional regulation is ubiquitous in prokaryotic and eukaryotic cells, but how it impacts gene expression remains to be fully explored. Here, we analyze a simple gene model in which we assume that mRNAs are produced in a constitutive manner but are regulated post-transcriptionally by a decapping enzyme that switches between the active state and the inactive state. We derive the analytical mRNA distribution governed by a chemical master equation, which can be well used to analyze the mechanism of how post-transcription regulation influences the mRNA expression level including the mRNA noise. We demonstrate that the mean mRNA level in the stochastic case is always higher than that in the deterministic case due to the stochastic effect of the enzyme, but the size of the increased part depends mainly on the switching rates between two enzyme states. More interesting is that we find that in contrast to transcriptional regulation, post-transcriptional regulation tends to attenuate noise in mRNA. Our results provide insight into the role of post-transcriptional regulation in controlling the transcriptional noise.

Mycobacterium tuberculosis Secreted Proteins As Potential Biomarkers for the Diagnosis of Active Tuberculosis and Latent Tuberculosis Infection.

BACKGROUND: The detection of Mycobacterium tuberculosis (Mtb) specific human antibodies has been an important diagnostic aid in the diagnosis of tuberculosis (TB) cases with smear-negative sputum samples, especially for the screening of high-risk population. This study focused on the analysis and comparison of the four potential Mtb-secreted proteins (ESAT6, CFP10, Ag85B, Hsp16.3) and the fusion protein Ag85B-Hsp16.3 as new markers in the serodiagnosis between active TB and latent TB infection (LTBI). METHODS: These five recombinant proteins were produced and used in optimized ELISA to detect IgG serum antibodies against the four secreted proteins. The capacity of identifying infection was evaluated either in active TB patients or LTBI individuals, which was compared with the control groups consisting of hospitalized non-TB individuals. RESULTS: The results showed that Ag85B-Hsp16.3/ESAT6 and Hsp16.3/ESAT6 were the best-associated antigens for serology diagnosis of the active TB and LTBI individuals because of their specificity, sensitivity, YI values, and positive rates, respectively. ELISA test demonstrated that 41.67% (25/60) of blood donors respond to Ag85B-Hsp16.3/ESAT6. The consistency of this positive respond with clinical diagnosis almost reached 84% (21/25). CONCLUSION: Thus, a combined test of multiple Mtb-secreted proteins Ag85B, Hsp16.3, and ESAT6 may be the ascendant preliminary screening antigens for active TB or LTBI patients.

Defining biological networks for noise buffering and signaling sensitivity using approximate Bayesian computation.

Reliable information processing in cells requires high sensitivity to changes in the input signal but low sensitivity to random fluctuations in the transmitted signal. There are often many alternative biological circuits qualifying for this biological function. Distinguishing theses biological models and finding the most suitable one are essential, as such model ranking, by experimental evidence, will help to judge the support of the working hypotheses forming each model. Here, we employ the approximate Bayesian computation (ABC) method based on sequential Monte Carlo (SMC) to search for biological circuits that can maintain signaling sensitivity while minimizing noise propagation, focusing on cases where the noise is characterized by rapid fluctuations. By systematically analyzing three-component circuits, we rank these biological circuits and identify three-basic-biological-motif buffering noise while maintaining sensitivity to long-term changes in input signals. We discuss in detail a particular implementation in control of nutrient homeostasis in yeast. The principal component analysis of the posterior provides insight into the nature of the reaction between nodes.

[Associations between physical exercise and quality of life in breast cancer patients].

OBJECTIVE: To investigate the associations between physical exercise and quality of life in breast cancer patients. METHODS: A cross-sectional study was conducted among 3 344 community breast cancer patients between April and July 2013 in Shanghai, China. Data were collected using a questionnaire, including socio-demographic situation, cancer survival and health behaviors, and scores of EORTC QLQ-C30 Simplified Chinese version and FACT-G Simplified Chinese version. RESULTS: Among a total of 3 344 breast cancer patients, the patients doing exercise reported significantly higher EORTC physical functioning scores, role functioning scores, emotional functioning scores, global health scores, and FACT-G physical well-being scores, social well-being scores, emotional well-being scores, functional well-being scores, and FACT-G total scores than the patients who didn't take exercise (P < 0.05, P(Adjusted)<0.05) . Breast cancer patients who did exercise more than or equal to 5 times/week reported significantly higher EORTC role functioning scores, cognitive functioning scores, emotional functioning scores, global health scores and FACT-G physical well-being scores, functional well-being scores, and FACT-G total scores than patients who did exercise less than 5 times/week (P < 0.05, P(Adjusted)<0.05 ). CONCLUSIONS: There are active associations between physical exercise and quality of life in breast cancer patients. Engagement in physical exercise is beneficial to breast cancer patients with long-term survival.

[Associations between vegetables and fruit intake and quality of life in breast cancer patients].

OBJECTIVE: To investigate the associations between vegetables and fruit intake and quality of life in breast cancer patients. METHODS: A total of 3 344 community breast cancer patients were selected through cluster sampling method between April and July 2013, in Shanghai, China. Data were collected using a questionnaire, which included socio-demographic situation, cancer survival and health behaviors(i.e. vegetables or fruit intake, exercise), European Organization for Research and Treatment (EORTC) QLQ-C30 Simplified Chinese version(3rd edition) and Functional Assessment of Cancer Therapy scale (FACT-G) Simplified Chinese version(4th edition) were used to evaluate the quality of life. Crude quality of life scores were compared between groups. Multiple linear models were used to calculate and compare adjusted means of quality of life between groups, controlling relevant factors. RESULTS: After adjusting relevant factors, breast cancer patients who ate more than 250 g vegetables reported higher EORTC physical functioning scores, cognitive functioning scores, emotional functioning scores, global health scores than patients who ate equal or less than 250 g vegetables(respectively (80.79 ± 0.85) vs (79.34 ± 0.82), (80.07 ± 1.03) vs (77.84 ± 0.99), (84.17 ± 0.95) vs (82.76 ± 0.92), (65.75 ± 1.50) vs (62.92 ± 1.45)), t values respectively were 2.76, 3.54, 2.40, 3.17, all P values were <0.05; and breast cancer patients who ate more than 250 g vegetables reported higher FACT-G social well-being scores, function well-being scores, FACT-G total scores than patients who ate equal or less than 250 g vegetables (respectively (17.92 ± 0.40) vs (17.31 ± 0.39), (14.86 ± 0.42) vs (14.34 ± 0.40), (74.78 ± 1.01) vs (73.05 ± 0.97)), t values respectively were 2.49, 2.05, 2.90, all P values were <0.05. After adjusting relevant factors, breast cancer patients who ate fruit everyday reported higher EORTC physical functioning scores, role functioning scores, cognitive functioning scores, emotional functioning scores, social functioning scores, global health scores than patients who didn't eat fruit everyday (respectively (80.40 ± 0.82) vs (79.22 ± 0.87), (89.81 ± 1.00) vs (88.06 ± 1.05), (79.78 ± 0.99) vs (77.11 ± 1.04), (84.43 ± 0.92) vs (81.56 ± 0.97), (77.95 ± 1.25) vs (75.56 ± 1.31), (65.48 ± 1.44) vs (61.74 ± 1.51)), t values respectively were 2.15, 2.64, 4.07, 4.71, 2.89, 4.02, all P values were <0.05; and breast cancer patients who ate fruit everyday reported higher FACT-G physical well-being scores, social well-being scores, emotional well-being scores, functional well-being scores, FACT-G total scores than patients who didn't eat fruit everyday(respectively (23.35 ± 0.26) vs (22.85 ± 0.28), (17.91 ± 0.39) vs (16.98 ± 0.41), (18.59 ± 0.22) vs (18.18 ± 0.23), (14.79 ± 0.40) vs (14.17 ± 0.42), (74.71 ± 0.97) vs (72.17 ± 1.02)), t values respectively were 2.92, 3.65, 2.91, 2.35, 4.05 , all P values were <0.05. CONCLUSION: There are active associations between vegetables / fruit intake and quality of life in breast cancer patients. Proper diet may help improve quality of life in breast cancer patients.