• body composition
• chemotherapy toxicity
• exercise oncology
• paclitaxel
• pharmacokinetics
• physical activity

• (projectID: 13163). Stand up to Cancer

• Breast cancer
• Golgi
• Golgin-97
• Inflammatory cytokine
• MAPK signaling
• Metastasis

• Humans
• Animals
• Female
• Mice
• p38 Mitogen-Activated Protein Kinases/metabolism
• MAP Kinase Signaling System/drug effects
• Cell Line, Tumor
• Disease Progression
• Breast Neoplasms/pathology
• Breast Neoplasms/metabolism
• Zebrafish
• Cell Movement/drug effects
• Membrane Proteins/metabolism
• Membrane Proteins/genetics
• Golgi Matrix Proteins/metabolism
• Hyaluronoglucosaminidase

• breast cancer
• chemotherapy
• toxicity

• KotK_VUB/2022/13163/1 Kom op tege Kanker

• MCF-7
• MDA-MB-231
• THP-1
• co-culture
• escitalopram oxalate

• cancer
• drug resistance
• mechanisms
• microRNAs
• treatment strategies

• Anticancer
• Bioactive compounds
• Molecular mechanisms
• Paclitaxel

• Humans
• Paclitaxel/pharmacology
• Paclitaxel/chemistry
• Antineoplastic Agents/pharmacology
• Antineoplastic Agents/therapeutic use
• Neoplasms/drug therapy
• Plants

• bibliometric analysis
• biclustering analysis
• breast cancer
• endocrine therapy
• visualization

• Humans
• Female
• Research
• Bibliometrics
• China
• Databases, Factual
• Breast Neoplasms/drug therapy

• PD-L1
• breast cancer
• neoadjuvant therapy
• pathological response
• sTIL

• Humans
• Female
• Middle Aged
• Breast Neoplasms/drug therapy
• Breast Neoplasms/pathology
• Mastectomy
• Retrospective Studies
• Neoadjuvant Therapy
• Lymphocytes, Tumor-Infiltrating/pathology
• Indonesia
• Antineoplastic Combined Chemotherapy Protocols/therapeutic use

• breast cancer
• derivatives
• molecular targets
• natural products
• pathology

• Humans
• Female
• Biological Products/pharmacology
• Biological Products/therapeutic use
• Breast Neoplasms/pathology

• breast cancer
• metastasis
• nanotherapeutics

• ESA Canadian Cancer Society

• Cancer
• Chemotherapy
• Chemotherapy-induced peripheral neuropathy
• Peripheral Neuropathy
• Risk factors
• Severity
• Survivorship

Breast cancer is the most prevalent non-skin cancer diagnosed in females and developing novel therapeutic strategies to improve patient outcomes is crucial. The immune system plays an integral role in the body’s response to breast cancer and modulating this immune response through immunotherapy is a promising therapeutic option. Although immune checkpoint inhibitors were recently approved for the treatment of breast cancer patients, not all patients respond to immune checkpoint inhibitors as a monotherapy, highlighting the need to better understand the biology underlying patient response. Additionally, as radiotherapy is a critical component of breast cancer treatment, understanding the interplay of radiation and immune checkpoint inhibitors will be vital as recent studies suggest that combined therapies may induce synergistic effects in preclinical models of breast cancer. This review will discuss the mechanisms supporting combined approaches with radiotherapy and immune checkpoint inhibitors for the treatment of breast cancer. Moreover, this review will analyze the current clinical trials examining combined approaches of radiotherapy, immunotherapy, chemotherapy, and targeted therapy. Finally, this review will evaluate data regarding treatment tolerance and potential biomarkers for these emerging therapies aimed at improving breast cancer outcomes.

• Advanced breast cancer
• HER2 positive
• hormone receptor
• metastatic breast cancer
• network meta-analysis
• subgroup analysis
• targeted therapies

To investigate the relationship between non-coding RNAs [especially circular RNAs (circRNAs)] and docetaxel resistance in breast cancer, and to find potential predictive biomarkers for taxane-containing therapies, we have performed transcriptome and microRNA (miRNA) sequencing for two established docetaxel-resistant breast cancer (DRBC) cell lines and their docetaxel-sensitive parental cell lines. Our analyses revealed differences between circRNA signatures in the docetaxel-resistant and -sensitive breast cancer cells, and discovered circRNAs generated by multidrug-resistance genes in taxane-resistant cancer cells. In DRBC cells, circABCB1 was identified and validated as a circRNA that is strongly up-regulated, whereas circEPHA3.1 and circEPHA3.2 are strongly down-regulated. Furthermore, we investigated the potential functions of these circRNAs by bioinformatics analysis, and miRNA analysis was performed to uncover potential interactions between circRNAs and miRNAs. Our data showed that circABCB1, circEPHA3.1 and circEPHA3.2 may sponge up eight significantly differentially expressed miRNAs that are associated with chemotherapy and contribute to docetaxel resistance via the PI3K-Akt and AGE-RAGE signaling pathways. We also integrated differential expression data of mRNA, long non-coding RNA, circRNA, and miRNA to gain a global profile of multi-level RNA changes in DRBC cells, and compared them with changes in DNA copy numbers in the same cell lines. We found that Chromosome 7 q21.12-q21.2 was a common region dominated by multi-level RNA overexpression and DNA amplification, indicating that overexpression of the RNA molecules transcribed from this region may result from DNA amplification during stepwise exposure to docetaxel. These findings may help to further our understanding of the mechanisms underlying docetaxel resistance in breast cancer.

• RNA sequencing
• breast cancer
• circRNA
• docetaxel resistance
• miRNA

• endocrine therapy
• hormone receptor
• meta-analysis
• metastatic breast cancer
• systematic review

• 2017EKMFTN_006 Italian Ministry of University and Research (MIUR)
• ESMO Fellowship 2020 - Translational European Society for Medical Oncology

Neurodegenerative disorders and cancer may appear unrelated illnesses. Yet, epidemiologic studies indicate an inverse correlation between their respective incidences for specific cancers. Possibly explaining these findings, increasing evidence indicates that common molecular pathways are involved, often in opposite manner, in the pathogenesis of both disease families. Genetic mutations in the MAPT gene encoding for TAU protein cause an inherited form of frontotemporal dementia, a neurodegenerative disorder, but also increase the risk of developing cancer. Assigning TAU at the interface between cancer and neurodegenerative disorders, two major aging-linked disease families, offers a possible clue for the epidemiological observation inversely correlating these human illnesses. In addition, the expression level of TAU is recognized as a prognostic marker for cancer, as well as a modifier of cancer resistance to chemotherapy. Because of its microtubule-binding properties, TAU may interfere with the mechanism of action of taxanes, a class of chemotherapeutic drugs designed to stabilize the microtubule network and impair cell division. Indeed, a low TAU expression is associated to a better response to taxanes. Although TAU main binding partners are microtubules, TAU is able to relocate to subcellular sites devoid of microtubules and is also able to bind to cancer-linked proteins, suggesting a role of TAU in modulating microtubule-independent cellular pathways associated to oncogenesis. This concept is strengthened by experimental evidence linking TAU to P53 signaling, DNA stability and protection, processes that protect against cancer. This review aims at collecting literature data supporting the association between TAU and cancer. We will first summarize the evidence linking neurodegenerative disorders and cancer, then published data supporting a role of TAU as a modifier of the efficacy of chemotherapies and of the oncogenic process. We will finish by addressing from a mechanistic point of view the role of TAU in de-regulating critical cancer pathways, including the interaction of TAU with cancer-associated proteins.

• DNA protection
• TAU protein
• cancer
• neurodegeneration
• tauopathies

• breast cancer
• ovarian cancer
• prostate cancer
• taxane resistance

• RSG TBG - 133116 American Cancer Society
• NA Ralph W. and Grace M. Showalter Research Trust

• Cancer cells
• Cancer-associated fibroblast cells
• Gold nanoparticles
• Microtubules
• Normal fibroblast cells
• Retention
• Toxicity
• Uptake

• Natural Sciences and Engineering Research Council of Canada
• Canada Foundation for Innovation
• Canadian Network for Research and Innovation in Machining Technology, Natural Sciences and Engineering Research Council of Canada

Pertuzumab is a humanized anti-human epidermal growth factor receptor 2 (HER2) monoclonal antibody found in a Phase III clinical trial to significantly improve median survival in HER2 positive metastatic breast cancer (MBC) when used in combination with a taxane and Trastuzumab, and its clinical efficacy has transformed the therapeutic landscape of HER2-positive breast cancer. There are currently few reports on the pattern of use and value of Pertuzumab in real world settings. Our study describes the clinical efficacy and treatment costs of Pertuzumab in HER2-positive MBC treated in a tertiary cancer centre in Singapore in a predominantly Asian population.

To investigate the clinical efficacy and treatment costs of Pertuzumab in HER2-positive MBC in an Asian population in Singapore.

A retrospective study of 304 HER2-positive MBC patients seen at National Cancer Centre Singapore between 2011-2017 was conducted. Demographic and clinical data were extracted from electronic medical records. Clinical characteristics and billing data of patients who received Pertuzumab were compared with those who did not.

Thirty-one (62.0%) of the fifty (16.4%) patients who received Pertuzumab as first-line therapy. With a median follow-up of 21.5 mo, there was a statistically significant difference in the median overall survival between Pertuzumab and non-Pertuzumab groups [51.5 (95%CI: 35.8–60.0) vs 32.9 (95%CI: 28.1–37.5) mo; P = 0.0128]. Two (4.88%) patients in the Pertuzumab group experienced grade 3 (G3) cardiotoxicity. The median treatment cost incurred for total chemotherapy for the Pertuzumab group was 130456 Singapore Dollars compared to 34523 Singapore Dollars for the non-Pertuzumab group. The median percentage of total chemotherapy costs per patient in the Pertuzumab group spent on Pertuzumab was 50.3%.

This study shows that Pertuzumab use in the treatment of metastatic breast cancer is associated with a significantly better survival and a low incidence of serious cardiotoxicity. However, the proportionate cost of Pertuzumab therapy remains high and further cost-effectiveness studies should be conducted.

• Pertuzumab
• Chemotherapy
• Metastatic breast cancer
• Treatment cost

Cells experiencing delays in mitotic progression are prone to undergo apoptosis unless they can exit mitosis before proapoptotic factors reach a critical threshold. Microtubule targeting agents (MTAs) arrest cells in mitosis and induce apoptotic cell death engaging the BCL2 network. Degradation of the antiapoptotic BCL2 family member MCL-1 is considered to set the time until onset of apoptosis upon MTA treatment. MCL1 degradation involves its interaction with one of its key binding partners, the proapoptotic BH3-only protein NOXA. Here, we report that the mitochondria-associated E3-ligase MARCH5, best known for its role in mitochondrial quality control and regulation of components of the mitochondrial fission machinery, controls the levels of MCL1/NOXA protein complexes in steady state as well as during mitotic arrest. Inhibition of MARCH5 function sensitizes cancer cells to the proapoptotic effects of MTAs by the accumulation of NOXA and primes cancer cells that may undergo slippage to escape death in mitosis to cell death in the next G1 phase. We propose that inhibition of MARCH5 may be a suitable strategy to sensitize cancer cells to antimitotic drug treatment.

• Breast cancer survivors
• Cardio-oncology
• Chemotherapy cardiotoxicity

• erythrocyte
• erythropoiesis
• microtubule
• microtubule-targeted agent
• nuclear extrusion

Cancer immune therapy has recently shown tremendous promise to combat many different cancers. The microtubule is a well-defined and very effective cancer therapeutic target. Interestingly, several lines of evidence now suggest that microtubules are intimately connected to the body’s immune responses. This raises the possibility that the combination of microtubule inhibitors and immune therapy can be a highly effective option for cancer treatments. However, our understanding on this potentially important aspect is still very limited, due in part to the multifaceted nature of microtubule functions. Microtubules are not only involved in maintaining cell morphology, but also a variety of cellular processes, including the movement of secretory vesicles and organelles, intracellular macromolecular assembly, signaling pathways, and cell division. Microtubule inhibitors may be subdivided into two classes: Anti-depolymerization agents such as the taxane family, and anti-polymerization agents such as colchicine and vinka alkaloids. These two different classes may have different effects on immune cell subtypes. Anti-depolymerization agents can not only induce NK cells, but also appear to inhibit T regulatory (Treg) cells. However, different inhibitors may have different functions even among the same class. For example, the doxetaxel anti-depolymerization agent up-regulates cytotoxic T cells, while paclitaxel down-regulates them. Certain anti-polymerization agents such as colchicine appear to down-regulate most immune cell types, while inducing dendritic cell maturation and increasing M1 macrophage population. In contrast, the vinblastine anti-polymerization agent activates many of these cell types, albeit down-regulating Treg cells. In this review, we focus on the various effects of tubulin inhibitors on the activities of the body’s immune system, in the hope of paving the way to develop an effective cancer therapy by combining tubulin-targeting anticancer agents and immune therapy.

• cell cycle dysregulation
• chemotherapeutics
• cytokines
• immune cells
• immune therapy
• microtubule inhibitors

Breast cancer is the second most common malignancy, worldwide. Treatment decisions are based on tumor stage, histological subtype, and receptor expression and include combinations of surgery, radiotherapy, and systemic treatment. These, together with earlier diagnosis, have resulted in increased survival. However, initial treatment efficacy cannot be guaranteed upfront, and these treatments may come with (long-term) serious adverse effects, negatively affecting a patient's quality of life. Gene expression-based tests can accurately estimate the risk of recurrence in early stage breast cancers. Disease recurrence correlates with treatment resistance, creating a major need to resensitize tumors to treatment. Notch signaling is frequently deregulated in cancer and is involved in treatment resistance. Preclinical research has already identified many combinatory therapeutic options where Notch involvement enhances the effectiveness of radiotherapy, chemotherapy or targeted therapies for breast cancer. However, the benefit of targeting Notch has remained clinically inconclusive. In this review, we summarize the current knowledge on targeting the Notch pathway to enhance current treatments for breast cancer and to combat treatment resistance. Furthermore, we propose mechanisms to further exploit Notch-based therapeutics in the treatment of breast cancer.

• Notch
• breast cancer
• personalized precision treatment
• resensitisation
• treatment resistance

• anticancer properties
• natural compounds
• substances from marin

• Animals
• Antineoplastic Agents/chemistry
• Antineoplastic Agents/pharmacology
• Aquatic Organisms/chemistry
• Biological Products/chemistry
• Biological Products/pharmacology
• Humans
• Plants/chemistry

Some chemotherapy drugs can damage the nerves and cause peripheral neuropathy which is accompanied by severe neuropathic pain or gait impairment. The purpose of this study was to assess the feasibility and the safety of acupuncture for the treatment of peripheral neuropathy following chemotherapy in Korean breast cancer patients.

This study was a prospective single-arm observational study using before and after measurements in breast cancer patients presenting with taxane-induced peripheral neuropathy.

This study was performed at East-West Medical Center at Daegu Catholic University Hospital, Daegu, South Korea.

Acupuncture was administered 3 times a week for 4 consecutive weeks, for 25 ± 5 minutes at each session.

The primary outcome measure was severity of CIPN using the Neuropathic Pain Symptom Inventory (NPSI) assessed by a self-administered questionnaire and Nerve Conduction Study (NCS) of extremities. The secondary outcome measure was quality of life (QoL) assessed by a self-administered questionnaire using the 36-Item Short From Health Survey (SF-36).

Acupuncture significantly reduced the severity of CIPN assessed by NPSI score. Four weeks after the last treatment, the symptoms were not aggravated. According to NCS, 42.9% of participants showed improvement of sensory neuropathy. At the end of the treatment, SF-36 scores were significantly increased for variables including physical functioning, role limitations due to physical health problems, social functioning, and general health perceptions compared to those of baseline measurement.

Acupuncture improved symptoms of CIPN and QoL in Korean women suffering from peripheral neuropathy after chemotherapy using taxane for breast cancer. The effects of acupuncture lasted for at least 1 month after the treatment.

• CDK4/6 inhibitor
• PLK4
• TTK
• breast cancer
• drug resistance

• chemoresistance
• combination cancer therapy
• magnetic core−shell nanoparticles
• microRNA therapeutics
• targeted delivery

• Doxorubicin
• Drug Delivery Systems
• Drug Resistance, Neoplasm
• Humans
• Magnetic Resonance Imaging
• Magnetics
• Magnetite Nanoparticles
• MicroRNAs
• Neoplasms

• Adrenal Cortex Hormones/adverse effects
• Bisphosphonate-Associated Osteonecrosis of the Jaw/etiology
• Bone Density Conservation Agents/adverse effects
• Diphosphonates
• Drug Interactions
• Female
• Humans
• Italy
• Male
• Neoplasms/drug therapy
• Osteonecrosis
• Retrospective Studies
• Taxoids/adverse effects

Drug-induced reticulate hyperpigmentation is uncommon. Including the patient described in this report, chemotherapy-associated reticulate hyperpigmentation has only been described in ten individuals. This paper describes the features of a woman with recurrent and metastatic breast cancer who developed paclitaxel-induced reticulate hyperpigmentation and reviews the characteristics of other oncology patients who developed reticulate hyperpigmentation from their antineoplastic treatment. A 55-year-old Taiwanese woman who developed reticulate hyperpigmentation on her abdomen, back and extremities after receiving her initial treatment for metastatic breast cancer with paclitaxel is described. The hyperpigmentation became darker with each subsequent administration of paclitaxel. The drug was discontinued after five courses and the pigment faded within two months. PubMed was searched with the key words: Breast, cancer, chemotherapy, hyperpigmentation, neoplasm, reticulate, tumor, paclitaxel, taxol. The papers generated by the search, and their references, were reviewed. Chemotherapy-induced reticulate hyperpigmentation has been described in four men and six women. Bleomycin, cytoxan, 5-fluorouracil, idarubacin, and paclitaxel caused the hyperpigmentation. The hyperpigmentation faded in 83% of the patients between two to six months after the associated antineoplastic agent was discontinued. In conclusion, chemotherapy-induced reticulate hyperpigmentation is a rare reaction that may occur during treatment with various antineoplastic agents. The hyperpigmentation fades in most individuals once the treatment is discontinued. Therefore, cancer treatment with the associated drug can be continued in patients who experience this cutaneous adverse event.

• Breast
• Cancer
• Chemotherapy
• Hyperpigmentation
• Neoplasm
• Reticulate
• Tumor
• Paclitaxel
• Taxol

• breast cancer
• dasatinib
• drug resistance
• paclitaxel

• metastatic breast cancer
• nab-paclitaxel
• taxanes

In pre-clinical studies, the anti-tumor activity of T-DM1 was enhanced when combined with taxanes or pertuzumab. This phase 1b/2a study evaluated the safety/tolerability of T-DM1 + paclitaxel ± pertuzumab in HER2-positive advanced breast cancer.

In phase 1b (n = 60), a 3 + 3 dose-escalation approach was used to determine the maximum tolerated dose (MTD) of T-DM1 + paclitaxel ± pertuzumab. The primary objective of phase 2a was feasibility, with 44 patients randomized to T-DM1 + paclitaxel ± pertuzumab at the MTD identified in phase 1b.

The MTD was T-DM1 3.6 mg/kg every three weeks (q3w) or 2.4 mg/kg weekly + paclitaxel 80 mg/m² weekly ± pertuzumab 840 mg loading dose followed by 420 mg q3w. Phase 2a patients had received a median of 5.0 (range: 0–10) prior therapies for advanced cancer. In phase 2a, 51.2 % received ≥12 paclitaxel doses within 15 weeks, and 14.0 % received 12 paclitaxel doses by week 12. Common all-grade adverse events (AEs) were peripheral neuropathy (90.9 %) and fatigue (79.5 %). A total of 77.3 % experienced grade ≥3 AEs, most commonly neutropenia (25.0 %) and peripheral neuropathy (18.2 %). Among the 42 phase 2a patients with measurable disease, the objective response rate (ORR) was 50.0 % (95 % confidence interval (CI) 34.6–65.4); the clinical benefit rate (CBR) was 56.8 % (95 % CI 41.6–71.0). No pharmacokinetic interactions were observed between T-DM1 and paclitaxel.

This regimen showed clinical activity. Although there is potential for paclitaxel to be added to T-DM1 ± pertuzumab, peripheral neuropathy was common in this heavily pretreated population.

ClinicalTrials.gov NCT00951665. Registered August 3, 2009.

The online version of this article (doi:10.1186/s13058-016-0691-7) contains supplementary material, which is available to authorized users.

• Breast neoplasms
• Chemistry
• Disease-free survival
• Paclitaxel
• Pharmaceutical

• Adult
• Aged
• Albumins/administration & dosage
• Albumins/therapeutic use
• Antineoplastic Agents/administration & dosage
• Antineoplastic Agents/therapeutic use
• Breast Neoplasms/drug therapy
• Female
• Humans
• Injections
• Middle Aged
• Neoplasm Metastasis
• Paclitaxel/administration & dosage
• Paclitaxel/therapeutic use
• Survival Analysis
• Treatment Outcome
• Young Adult

Microtubules (MTs) are components of the cytoskeleton made up of polymerized alpha and beta tubulin dimers. MT structure and function must be maintained throughout the cell cycle to ensure proper execution of mitosis and cellular homeostasis. The protein tyrosine phosphatase, PTPN13, localizes to distinct compartments during mitosis and cytokinesis. We have previously demonstrated that the HPV16 E6 oncoprotein binds PTPN13 and leads to its degradation. Thus, we speculated that HPV infection may affect cellular proliferation by altering the localization of a PTPN13 phosphatase substrate, EphrinB1, during mitosis. Here we report that EphrinB1 co-localizes with MTs during all phases of the cell cycle. Specifically, a cleaved, unphosphorylated EphrinB1 fragment directly binds tubulin, while its phosphorylated form lacks MT binding capacity. These findings suggest that EphrinB1 is a novel microtubule associated protein (MAP). Importantly, we show that in the context of HPV16 E6 expression, EphrinB1 affects taxane response in vitro. We speculate that this reflects PTPN13's modulation of EphrinB1 phosphorylation and suggest that EphrinB1 is an important contributor to taxane sensitivity/resistance phenotypes in epithelial cancers. Thus, HPV infection or functional mutations of PTPN13 in non-viral cancers may predict taxane sensitivity.

There is a deep need to improve the care of metastatic breast cancer (MBC) patients, since even today it remains an incurable disease. Taxanes are considered the most effective cytotoxic drugs for the treatment of MBC, both in monotherapy and in combined schedules, but the need for synthetic solvents contributes to the severe toxicities and may have a negative impact on the efficacy. Nanoparticle albumin-bound paclitaxel (Nab-paclitaxel) is a colloidal suspension of paclitaxel and human serum albumin initially developed to avoid the toxicities associated with conventional taxanes.

The aim of this prospective, single-center open-label, noncomparative study was to evaluate the efficacy and safety of nab-paclitaxel in MBC patients pretreated with taxanes. The patients were treated with nab-paclitaxel as a single agent, 260 mg/m² on day 1 of each 3-week cycle or 125 mg/m² weekly. The primary endpoint was the overall response rate (ORR). Secondary objectives were duration of response, clinical benefit rate, progression-free survival (PFS), overall survival, and safety.

A total of 42 patients (median age 48 years, median Eastern Cooperative Oncology Group performance status 0, triple-negative MBC 19%, all pretreated with a taxane-based therapy, mainly in advanced disease) were enrolled in the study. The ORR was 23.8%, including one complete response (2.4%) and nine partial responses (21.4%); the disease control rate was 50%. The median duration of response was 7.2 months. After a median follow-up of 9 months, the median PFS was 4.6 months. ORR and PFS were similar irrespective of the previous chemotherapy lines, metastatic sites, and biomolecular expression. Nab-paclitaxel was well tolerated, and the most frequent treatment-related toxicities were mild to moderate (grades 1–2).

This real-life study shows that nab-paclitaxel has a significant antitumor activity and a manageable safety profile in patients pretreated with taxanes and experiencing a treatment failure after at least one line of chemotherapy.

• anthracyclines
• metastatic breast cancer
• nab-paclitaxel

• BCSC, breast cancer stem cells
• CDK
• CDK, cyclin dependent kinase
• CDKi, cyclin dependent kinase inhibitor
• CK, cytokeratin
• EGFR, epidermal growth factor receptor
• EMT, epithelial-mesenchymal transition
• ER, estrogen receptor
• HER2, human epidermal growth factor receptor 2
• PR, progesterone receptor
• Pin1, peptidyl-prolyl cis-trans isomerase NIMA-interacting 1
• Smad3
• TNBC, triple negative breast cancer
• cyclin
• paclitaxel
• triple negative breast cancer

• metastatic breast cancer
• nab-paclitaxel
• quality of life
• taxanes

The genus Corylus is an important woody species in Northeast China. Its products, hazelnuts, constitute one of the most important raw materials for the pastry and chocolate industry. However, limited genetic research has focused on Corylus because of the lack of genomic resources. The advent of high-throughput sequencing technologies provides a turning point for Corylus research. In the present study, we performed de novo transcriptome sequencing for the first time to produce a comprehensive database for the Corylus heterophylla Fisch floral buds.

The C. heterophylla Fisch floral buds transcriptome was sequenced using the Illumina paired-end sequencing technology. We produced 28,930,890 raw reads and assembled them into 82,684 contigs. A total of 40,941 unigenes were identified, among which 30,549 were annotated in the NCBI Non-redundant (Nr) protein database and 18,581 were annotated in the Swiss-Prot database. Of these annotated unigenes, 25,311 and 10,514 unigenes were assigned to gene ontology (GO) categories and clusters of orthologous groups (COG), respectively. We could map 17,207 unigenes onto 128 pathways using the Kyoto Encyclopedia of Genes and Genomes Pathway (KEGG) database. Additionally, based on the transcriptome, we constructed a candidate cold tolerance gene set of C. heterophylla Fisch floral buds. The expression patterns of selected genes during four stages of cold acclimation suggested that these genes might be involved in different cold responsive stages in C. heterophylla Fisch floral buds.

The transcriptome of C. heterophylla Fisch floral buds was deep sequenced, de novo assembled, and annotated, providing abundant data to better understand the C. heterophylla Fisch floral buds transcriptome. Candidate genes potentially involved in cold tolerance were identified, providing a material basis for future molecular mechanism analysis of C. heterophylla Fisch floral buds tolerant to cold stress.

• Adaptation, Physiological/genetics
• China
• Cold Temperature
• Corylus/genetics
• Gene Expression Profiling
• Gene Expression Regulation, Plant
• Genes, Plant
• High-Throughput Nucleotide Sequencing
• Inflorescence/genetics
• Microsatellite Repeats
• Molecular Sequence Annotation
• Sequence Analysis, DNA
• Transcriptome

• Corylus/genetics
• Corylus/metabolism
• Gene Expression Regulation, Plant
• Paclitaxel/metabolism
• Transcriptome/genetics