Review Open Access
Copyright ©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 21, 2023; 29(35): 5094-5103
Published online Sep 21, 2023. doi: 10.3748/wjg.v29.i35.5094
Developments and challenges in neoadjuvant therapy for locally advanced pancreatic cancer
Bo Zhou, Shi-Ran Zhang, Geng Chen, Ping Chen, Department of Hepatobiliary Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China
ORCID number: Bo Zhou (0000-0001-8376-3182); Geng Chen (0000-0002-1642-7098); Ping Chen (0000-0001-6575-8582).
Author contributions: Chen P contributed to the concept, design, and drafting of the article, and approved the final revision; Zhou B drafted the article; Zhang SR and Chen G revised the manuscript critically for intellectual content; all authors approved the version to be published.
Conflict-of-interest statement: All the authors report having no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Corresponding author: Ping Chen, MD, PhD, Professor, Surgeon, Department of Hepatobiliary Surgery, Daping Hospital, Army Medical University, No. 10 Changjiang Branch Road, Yuzhong District, Chongqing 400042, China.
Received: June 10, 2023
Peer-review started: June 10, 2023
First decision: July 10, 2023
Revised: July 19, 2023
Accepted: August 31, 2023
Article in press: August 31, 2023
Published online: September 21, 2023


Pancreatic ductal adenocarcinoma (PDAC) remains a significant public health challenge and is currently the fourth leading cause of cancer-related mortality in developed countries. Despite advances in cancer treatment, the 5-year survival rate for patients with PDAC remains less than 5%. In recent years, neoadjuvant therapy (NAT) has emerged as a promising treatment option for many cancer types, including locally advanced PDAC, with the potential to improve patient outcomes. To analyze the role of NAT in the setting of locally advanced PDAC over the past decade, a systematic literature search was conducted using PubMed and Web of Science. The results suggest that NAT may reduce the local mass size, promote tumor downstaging, and increase the likelihood of resection. These findings are supported by the latest evidence-based medical literature and the clinical experience of our center. Despite the potential benefits of NAT, there are still challenges that need to be addressed. One such challenge is the lack of consensus on the optimal timing and duration of NAT. Improved criteria for patient selection are needed to further identify PDAC patients likely to respond to NAT. In conclusion, NAT has emerged as a promising treatment option for locally advanced PDAC. However, further research is needed to optimize its use and to better understand the role of NAT in the management of this challenging disease. With continued advances in cancer treatment, there is hope of improving the outcomes of patients with PDAC in the future.

Key Words: Neoadjuvant therapy, Pancreatic ductal adenocarcinoma, Locally advanced pancreatic cancer, Chemoradiotherapy, Immunotherapy, Vaccine therapy

Core Tip: In recent years, neoadjuvant therapy (NAT) has emerged as a promising treatment option for many cancer types, including locally advanced pancreatic ductal adenocarcinoma, with the potential to improve patient outcomes. To analyze the role of NAT in the setting of locally advanced pancreatic ductal adenocarcinoma over the past decade, a systematic literature search was conducted using PubMed and Web of Science. Despite the potential benefits of NAT, there are still challenges that need to be addressed. Additionally, there is a need for better patient selection criteria to identify those who are most likely to benefit from this approach.


Pancreatic ductal adenocarcinoma (PDAC) is a malignancy with a poor prognosis, and it is currently the seventh leading cause of cancer-related death worldwide. The number of deaths from PDAC (466000) is almost equal to the number of new cases (496000) each year[1-3]. Experts predict that PDAC will surpass breast cancer as the third leading cause of cancer-related deaths by 2025 in 28 European countries[4]. The 5-year survival rate for patients with PDAC is less than 5%, and locally advanced pancreatic cancer (LAPC) accounts for one-third of all pancreatic cancer cases[5-7]. Unfortunately, approximately 60% of patients with LAPC present with metastatic disease and/or poor performance status, making them ineligible for surgery[8,9]. Despite improvements in diagnosis and treatment, clinical outcomes for these patients remain poor.

In 1992, Evans et al[10] first proposed the use of neoadjuvant therapy (NAT) for PDAC and found that patients treated with NAT had superior outcomes compared to those treated with postsurgical adjuvant therapy[11,12]. NAT is administered before surgery to reduce tumor mass, promote tumor downstaging, or eliminate early metastatic cells, thereby improving prognosis. In the last decade, the strategy of NAT followed by conversion surgery has been increasingly employed in the treatment of LAPC[13]. The goal of this review was to summarize and discuss research exploring the use of NAT for LAPC.


Pancreatic cancer is typically classified based on its resectability on preoperative imaging, according to guidelines such as the National Comprehensive Cancer Network 2022 edition, the Chinese guidelines for the Neoadjuvant Therapy of Pancreatic Cancer 2021 edition, and the International Association of Pancreatology[5,14,15]. LAPC is generally defined as local tumor growth with major involvement (> 180° circumferential) or true invasion of the superior mesenteric artery, celiac axis, or hepatic artery and/or involvement of the portal vein/superior mesenteric vein that prevents reconstruction[16]. Table 1 provides a summary of these criteria.

Table 1 Definitions of locally advanced pancreatic cancer by different groups.
NCCN[14]Head/uncinate process:Unreconstructible SMV/PV due to tumor involvement or occlusion (can be due to tumor or bland thrombus)
Solid tumor contact > 180° with the SMA or CA
Body and tail
Solid tumor contact of > 180° with the SMA or CA
Solid tumor contact with the CA and aortic involvement
IAP[15]Tumor contact/invasion of 180 or more degree CHABilateral narrowing/occlusion, exceeding the inferior border of the duodenum
Tumor contact/invasion showing tumor contact/invasion of the PHA and/or CA
CMA[5] HeadUnreconstructible SMV/PV due to tumor involvement or occlusion (can be due to tumor or bland thrombus). The tumor extensively involves the distal jejunal drainage branch of the superior mesenteric vein
Solid tumor contact of > 180° with the SMA or CA
Body and tail
Solid tumor contact of > 180° with the SMA or CA
Solid tumor contact with the CA and aortic involvement

LAPC, previously thought to be an incurable disease stage and an indication for palliative treatment, is now strongly considered a potentially curable disease. Gemcitabine (GEM)-based chemoradiotherapy is the standard treatment for LAPC, with a reported median survival of 24.2 mo and progression-free survival of 15 mo[17,18]. Polychemotherapy treatment with combined leucovorin calcium (folinic acid), fluorouracil, irinotecan hydrochloride, and oxaliplatin (FOLFIRINOX) and GEM + nab-paclitaxel is recommended[19].

In a database query of patients who received induction FOLFIRINOX for LAPC between 2010 and 2016, nearly 20% responded sufficiently to undergo resection, which improved overall survival compared to that of patients who did not undergo resection[20]. Another study enrolled 485 patients with at least three cycles of first-line chemotherapy with FOLFIRINOX or GEM plus nanoparticle albumin-bound paclitaxel (GA) between 2010 and 2017 and revealed that according to the Response Evaluation Criteria in Solid Tumors a partial response was more common among patients treated with FOLFIRINOX [27 of 140 patients (19%)] than among those treated with GA [8 of 140 patients (6%); P = 0.001]. In this cohort of patients, FOLFIRINOX was associated with higher rates of Response Evaluation Criteria in Solid Tumors-defined partial response and subsequent pancreatectomy than GA[21]. The different types of trials evaluating NAT for LAPC in recent years are summarized in Table 2[19,22-25].

Table 2 Summary of trials evaluating neoadjuvant therapy for locally advanced pancreatic cancer.
Type of study
Years of accrual
No. of patients
Primary endpoint
Key findings
NCT03652428[19]Phase 1; Phase 22019-20232412 mo after registration or until deathProton therapy with concurrent GEM + Nab-paclitaxelOngoing
NCT02578732[22]Phase 22016-202428Until progression, up to 5 yrFOLFOXOngoing
NCT04247165[23]Phase 1; Phase 22020-20242012 moDrug: GEM; Nab-paclitaxel; Nivolumab; IpilimumabOngoing
NCT02873598[24]Phase 1 2016-202115Up to 5 yrFOLFIRINOX or GEM/abraxane followed by SBRTNot yet publicly available
NCT02704143[25]Phase 2 2016-2020633 yrCombination of Cyberknife with S-1Promising efficacy

Before the administration of chemotherapy, patients diagnosed with LAPC should undergo a thorough preliminary assessment of their performance status based on the Eastern Cooperative Oncology Group (ECOG) score[26]. In addition, it is imperative to evaluate nutritional status, symptom burden, and active comorbidities (with appropriate adjustments made for treatment as warranted) and to assess biliary tract patency while considering the need for diversion or stent placement. Geriatric assessment is recommended for patients who are aged 70 years and above[27]. For those patients exhibiting a good performance status (ECOG score between 0-1) along with good nutritional health, first-line chemotherapy is advised, similar to the approach for patients diagnosed with metastatic liver cancer. In contrast, for patients with higher ECOG scores, a GEM-based regimen is preferred due to its lower toxicity profile[28].

The use of stereotactic body radiation therapy (SBRT) with adjuvant chemotherapy in the treatment of LAPC has been a subject of interest among oncologists. While conventional fractionated radiation has been the standard approach, studies have explored the potential of SBRT in downstaging LAPC[29]. One recent study examined the efficacy of sequential SBRT following FOLFIRINOX chemotherapy in patients with stable but unresectable LAPC. The study authors reviewed medical records from 50 patients who were treated with induction FOLFIRINOX for a median of eight cycles, followed by SBRT. The median overall survival and progression-free survival were reported as 26.4 mo (95% confidence interval: 22.4-30.3) and 16.7 mo (95% confidence interval: 13.0-20.3), respectively[30]. While SBRT appears to have limited utility in the treatment of LAPC compared to conventional fractionated radiation, this study suggested that it may have a role in certain cases. A multidisciplinary approach should be considered when determining optimal treatment strategies for patients with LAPC who are not surgical candidates.

In addition to SBRT, Robert R. Wilson[31] first proposed particle therapy for the treatment of tumors in 1946. After more than 70 years of development, particle therapy has become another well-established tumor treatment method after surgery, chemotherapy, traditional radiotherapy, and immunotherapy[32]. Currently, particle radiotherapy, which includes proton and heavy ion radiotherapy, has been successfully applied to the treatment of cancer. C-ion and proton radiotherapy are the most commonly used types of particle radiotherapy in clinical practice and have higher accuracy and better cell killing effects, especially in high hypoxia areas and radiation-resistant cell cycle phases[33-35]. In addition, particle radiotherapy decreases the viability, proliferation, and migration of cancer cells[36-39]. Therefore, particle therapy is used to treat deeply penetrating and radiation-resistant tumors, especially pancreatic cancers.


Currently, the use of immunotherapy for LAPC is supported by limited data. A recent immune checkpoint inhibitor trial investigating anti-PD-L1 therapy in patients with LAPC failed to demonstrate efficacy due to the poor immunogenicity and immunosuppressive tumor microenvironment of pancreatic cancer[40,41]. However, a minority of patients have genetic mutations that may be targeted with specific interventions. Ongoing clinical trials targeting these mutations have led to discoveries[42,43].

Monoclonal antibodies (mAbs) have been an integral tool in cancer treatment for several decades. They possess the ability to directly kill cells through antibody-dependent cytotoxicity and other pathways and to regulate the immune microenvironment by blocking corresponding signaling pathways, reversing immunosuppression, and enhancing the activity of antitumor effector cells. Moreover, mAbs can even be utilized for the delivery of various therapeutic reagents (Table 3)[44-50].

Table 3 Monoclonal antibody-based therapies targeting non-immune cells for pancreatic ductal adenocarcinoma.
Type of study
Years of accrual
NCT01521325[44]Phase 12011-2013MesothelinMORAb-009
Patel et al[45]Preclinical study2013MUC-5ACNPC-1C
NCT03376659[46]Phase 1/Phase 22018-2023VEGFBevacizumab
NCT00614653[47]Phase 12008-2016VEGFBevacizumab
O'Sullivan et al[48]Preclinical study2017AnxA69E1
Smith et al[49]Phase 12008-2011DLL4Demcizumab
NCT02722954[50]Phase 12016-2017DLL4Demcizumab

Mesenchymal stem cells (MSCs) are present in some solid tumors, including PDAC, where they represent almost 100% of cells[51-54]. MSCs play a pivotal role in the development of PDAC. By attenuating MSC recruitment into tumors and inhibiting their tumor-supportive activities, therapeutic outcomes for cancer patients can be improved when MSCs are combined with other anticancer drugs, such as immunotherapy[51]. Numerous clinical studies are currently assessing MSC-based cell therapies[55,56].

Mucin 1 (MUC1) is overexpressed in approximately 90% of PDAC cells[57-60]. A study demonstrated that an antibody similar to the anti-MUC1 antibody GP1.4 could inhibit the proliferation and migration of cancer cells[61]. Additionally, Muc1-c, an isoform of MUC1 with the ability to cross membranes and inhibit tumor growth, could be used as a carrier for cytotoxins in the future[62].

The overexpression of vascular endothelial growth factor mRNA is a common feature in most human tumors and is strongly associated with increased invasiveness, vascular density, metastasis, recurrence, and a poor prognosis[63]. The approval of bevacizumab, a mAb that targets vascular endothelial growth factor, has paved the way for the development of other inhibitors targeting this pathway[64,65].

Annexin A6 (AnxA6) is the largest member of the conserved annexin family of proteins and is known for its modular domain organization and interactions with a variety of proteins and lipids[66,67]. Elevated levels of AnxA6 have been documented during the progression of pancreatic cancer[48,68,69]. In a recent study, O'Sullivan et al[48] isolated a novel anti-AnxA6 antibody, 9E1, and demonstrated its ability to reduce the invasion capacity of pancreatic cancer cells.

The Notch signaling pathway plays a vital role in the development of embryonic and tissue homeostasis, and it has been implicated in various malignancies. One of the key ligands in mammals is Delta-like ligand 4, which contributes significantly to cancer progression[70]. Demcizumab, a humanized anti-Delta-like ligand 4 antibody, has shown potential for reversing chemotherapy resistance when used in combination with paclitaxel and GEM. However, a recent study showed that while the combination was safe, it did not improve efficacy[71].

Radioimmunotherapy is emerging as a significant treatment option for patients with PDAC[72]. Recent studies have identified CD147 and B7-H3 as potential targets for radioimmunotherapy and have demonstrated the highly promising therapeutic effects of such treatments for PDAC[73,74].

Vaccine therapy for LAPC

Owing to the intertumoral and intratumoral heterogeneity of pancreatic cancer, immunotherapy, targeted therapy, and other promising treatments have been extensively tested in preclinical studies and clinical trials. However, almost all strategies have shown little significant advantage over conventional chemotherapy against pancreatic cancer, and this issue is often compounded by prevalent therapeutic resistance[75,76]. Cancer vaccines have emerged as a promising therapeutic approach for pancreatic cancer because of their multiple targets, small nonspecific effects, wide therapeutic windows, low toxicity, and induction of lasting immune memory. In particular, mRNA-based vaccines possess numerous advantages over conventional vaccines in terms of factors including efficiency, safety, increased developmental potential, and low production costs. They have facilitated significant technological and conceptual progress in personalized and precise treatment. Hence, they represent a potential choice for novel therapies for pancreatic cancer[77,78].

Cancer gene and signaling pathway therapy for LAPC

Recent evidence has revealed that numerous genes and signaling pathways play critical roles in the pathogenesis and progression of PDAC and thus could be potential valuable therapeutic targets[79,80].

Molecular pathways

Activating mutations of KRAS and the phosphoinositide 3 kinase/AKT/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway are frequently observed in PDAC and are associated with a poor prognosis[80,81]. In addition, numerous receptor tyrosine kinases have been implicated in the development and progression of PDAC, including tropomyosin receptor kinase, epidermal growth factor receptor, insulin-like growth factor receptor, fibroblast growth factor receptor, vascular epidermal growth factor receptor, platelet-derived growth factor receptor, and others[79,82-84].

Tumor suppressor genes

Tumor suppressor genes play a vital role in regulating cell growth by preventing severe metastasis; in tumors, these genes can be altered via mutation or chromosomal rearrangement. In PDAC, several tumor suppressor genes, including cyclin-dependent kinase inhibitor p16, p53, and suppressor of mothers against decapentaplegic protein 4, are frequently mutated[80,82].

DNA repair factors

Studies have revealed that PDAC ranks as the third most common cancer associated with mutations in the BReast CAncer gene and mismatch repair genes, following breast and ovarian cancers[85-87]. Novel combination therapies evaluating immune therapies and targeted agents are being tested for patients with PDAC linked to impaired DNA damage repair[88,89].

Epithelial-mesenchymal transition

Epithelial-mesenchymal transition is a critical process in which epithelial cells acquire mesenchymal features[90,91]. In the context of PDAC, epithelial-mesenchymal transition has been associated with tumor initiation, invasion, metastasis, and resistance to therapy[92].

Cancer stem cells

Cancer stem cells (CSCs) play a critical role in tumor initiation, progression, and therapeutic resistance. In PDAC, CSCs express cell surface markers such as CD24, CD44, CD133, epithelial-specific antigen, c-Met, C-X-C motif chemokine receptor 4, and aldehyde dehydrogenase[93]. CSCs have been shown to protect tumor cells from the cytotoxic effects of chemotherapy drugs and are associated with advanced tumor recurrence. However, the mechanisms underlying CSC-mediated drug resistance remain unclear.


Evaluation of treatment response and prediction of resectability after NAT remains a challenge for patients with LAPC. Pathological assessment of response after surgical resection remains the gold standard, but this approach is limited by its invasiveness[94,95]. Multidetector computed tomography is the most commonly used imaging modality to evaluate the response of LAPC after NAT. Its advantages over other techniques include higher spatial resolution and multiplanar reconstruction capabilities[96]. Other imaging modalities, such as endoscopic ultrasound, diffusion-weighted imaging, positron emission tomography, and perfusion computerized tomography, show significant potential to become powerful tools for assessing tumor resectability and predicting survival after NAT[97]. Tumor markers are also commonly used as evaluation indicators, with carbohydrate antigen 19-9 being the only biomarker currently recommended by the National Comprehensive Cancer Network guidelines for assessing NAT response. Other promising indicators being studied include circulating tumor cells, circulating tumor DNA, and microRNAs, among others[96].


LAPC remains a challenging disease, despite significant progress made in its treatment over the past decade. Notably, immunotherapy has shown remarkable improvements in the management of LAPC. Across all fields of pancreatic cancer research, substantial advancements have been achieved. Basic research has significantly improved the understanding of this disease. Moreover, the advent of advanced DNA and RNA sequencing technologies has enabled The Cancer Genome Atlas consortium to study both the whole genome and transcriptomes of human tumors, thereby facilitating the identification of driver mutations and transcriptional programs implicated in carcinogenesis. These efforts are poised to accelerate the application of precision medicine strategies[98-100]. Administration of NAT for the treatment of LAPC can provide important benefits, although more in-depth studies are needed. Therefore, a multidisciplinary team comprising surgeons, oncologists, radiation oncologists, and radiologists is essential for the optimal treatment of LAPC. The most urgent issues to address include identifying patients who are most suitable for NAT and evaluating treatment effects in a timely and accurate manner to achieve more precise and effective treatments for patients with LAPC.


Provenance and peer review: Invited article; Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Gastroenterology and hepatology

Country/Territory of origin: China

Peer-review report’s scientific quality classification

Grade A (Excellent): 0

Grade B (Very good): B

Grade C (Good): C

Grade D (Fair): 0

Grade E (Poor): 0

P-Reviewer: Nagaya M, Japan; Shalaby MN, Egypt S-Editor: Yan JP L-Editor: Filipodia P-Editor: Cai YX

1.  Sung H, Ferlay J, Siegel RL, Laversanne M, Soerjomataram I, Jemal A, Bray F. Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries. CA Cancer J Clin. 2021;71:209-249.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27258]  [Cited by in F6Publishing: 19062]  [Article Influence: 9531.0]  [Reference Citation Analysis (7)]
2.  Park W, Chawla A, O'Reilly EM. Pancreatic Cancer: A Review. JAMA. 2021;326:851-862.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 256]  [Cited by in F6Publishing: 148]  [Article Influence: 74.0]  [Reference Citation Analysis (0)]
3.  Wood LD, Canto MI, Jaffee EM, Simeone DM. Pancreatic Cancer: Pathogenesis, Screening, Diagnosis, and Treatment. Gastroenterology. 2022;163:386-402.e1.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 17]  [Article Influence: 17.0]  [Reference Citation Analysis (0)]
4.  Ferlay J, Partensky C, Bray F. More deaths from pancreatic cancer than breast cancer in the EU by 2017. Acta Oncol. 2016;55:1158-1160.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 197]  [Cited by in F6Publishing: 170]  [Article Influence: 24.3]  [Reference Citation Analysis (0)]
5.  Study Group of Pancreatic Surgery in China Society of Surgery of Chinese Medical Association; Pancreatic Disease Committee of China Research Hospital Association. [The guideline for neoadjuvant therapy of pancreatic cancer in China (2020 edition)]. Zhonghua Wai Ke Za Zhi. 2020;58:657-667.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 1]  [Reference Citation Analysis (0)]
6.  Ducreux M, Cuhna AS, Caramella C, Hollebecque A, Burtin P, Goéré D, Seufferlein T, Haustermans K, Van Laethem JL, Conroy T, Arnold D; ESMO Guidelines Committee. Cancer of the pancreas: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol. 2015;26 Suppl 5:v56-v68.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 667]  [Cited by in F6Publishing: 725]  [Article Influence: 90.6]  [Reference Citation Analysis (0)]
7.  Neoptolemos JP, Kleeff J, Michl P, Costello E, Greenhalf W, Palmer DH. Therapeutic developments in pancreatic cancer: current and future perspectives. Nat Rev Gastroenterol Hepatol. 2018;15:333-348.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 506]  [Cited by in F6Publishing: 506]  [Article Influence: 101.2]  [Reference Citation Analysis (0)]
8.  Strobel O, Neoptolemos J, Jäger D, Büchler MW. Optimizing the outcomes of pancreatic cancer surgery. Nat Rev Clin Oncol. 2019;16:11-26.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 304]  [Cited by in F6Publishing: 337]  [Article Influence: 84.3]  [Reference Citation Analysis (0)]
9.  Mizrahi JD, Surana R, Valle JW, Shroff RT. Pancreatic cancer. Lancet. 2020;395:2008-2020.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 869]  [Cited by in F6Publishing: 696]  [Article Influence: 232.0]  [Reference Citation Analysis (0)]
10.  Evans DB, Rich TA, Byrd DR, Cleary KR, Connelly JH, Levin B, Charnsangavej C, Fenoglio CJ, Ames FC. Preoperative chemoradiation and pancreaticoduodenectomy for adenocarcinoma of the pancreas. Arch Surg. 1992;127:1335-1339.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 539]  [Cited by in F6Publishing: 566]  [Article Influence: 18.3]  [Reference Citation Analysis (0)]
11.  Springfeld C, Ferrone CR, Katz MHG, Philip PA, Hong TS, Hackert T, Büchler MW, Neoptolemos J. Neoadjuvant therapy for pancreatic cancer. Nat Rev Clin Oncol. 2023;20:318-337.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
12.  Wang C, Tan G, Zhang J, Fan B, Chen Y, Chen D, Yang L, Chen X, Duan Q, Maimaiti F, Du J, Lin Z, Gu J, Luo H. Neoadjuvant Therapy for Pancreatic Ductal Adenocarcinoma: Where Do We Go? Front Oncol. 2022;12:828223.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
13.  Gemenetzis G, Groot VP, Blair AB, Laheru DA, Zheng L, Narang AK, Fishman EK, Hruban RH, Yu J, Burkhart RA, Cameron JL, Weiss MJ, Wolfgang CL, He J. Survival in Locally Advanced Pancreatic Cancer After Neoadjuvant Therapy and Surgical Resection. Ann Surg. 2019;270:340-347.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 167]  [Cited by in F6Publishing: 189]  [Article Influence: 63.0]  [Reference Citation Analysis (0)]
14.  Tempero MA, Malafa MP, Al-Hawary M, Behrman SW, Benson AB, Cardin DB, Chiorean EG, Chung V, Czito B, Del Chiaro M, Dillhoff M, Donahue TR, Dotan E, Ferrone CR, Fountzilas C, Hardacre J, Hawkins WG, Klute K, Ko AH, Kunstman JW, LoConte N, Lowy AM, Moravek C, Nakakura EK, Narang AK, Obando J, Polanco PM, Reddy S, Reyngold M, Scaife C, Shen J, Vollmer C, Wolff RA, Wolpin BM, Lynn B, George GV. Pancreatic Adenocarcinoma, Version 2.2021, NCCN Clinical Practice Guidelines in Oncology. J Natl Compr Canc Netw. 2021;19:439-457.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 160]  [Cited by in F6Publishing: 192]  [Article Influence: 96.0]  [Reference Citation Analysis (0)]
15.  Isaji S, Mizuno S, Windsor JA, Bassi C, Fernández-Del Castillo C, Hackert T, Hayasaki A, Katz MHG, Kim SW, Kishiwada M, Kitagawa H, Michalski CW, Wolfgang CL. International consensus on definition and criteria of borderline resectable pancreatic ductal adenocarcinoma 2017. Pancreatology. 2018;18:2-11.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 294]  [Cited by in F6Publishing: 286]  [Article Influence: 57.2]  [Reference Citation Analysis (0)]
16.  Kwon W, Thomas A, Kluger MD. Irreversible electroporation of locally advanced pancreatic cancer. Semin Oncol. 2021;48:84-94.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 3]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
17.  Von Hoff DD, Ervin T, Arena FP, Chiorean EG, Infante J, Moore M, Seay T, Tjulandin SA, Ma WW, Saleh MN, Harris M, Reni M, Dowden S, Laheru D, Bahary N, Ramanathan RK, Tabernero J, Hidalgo M, Goldstein D, Van Cutsem E, Wei X, Iglesias J, Renschler MF. Increased survival in pancreatic cancer with nab-paclitaxel plus gemcitabine. N Engl J Med. 2013;369:1691-1703.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4035]  [Cited by in F6Publishing: 4059]  [Article Influence: 405.9]  [Reference Citation Analysis (0)]
18.  Mizusawa J, Fukutomi A, Katayama H, Ishii H, Ioka T, Okusaka T, Ueno H, Ueno M, Ikeda M, Mizuno N, Ozaka M, Fukuda H, Furuse J; Hepatobiliary and Pancreatic Oncology Group of the Japan Clinical Oncology Group. Protocol digest of randomized phase II study of modified FOLFIRINOX versus gemcitabine plus nab-paclitaxel combination therapy for locally advanced pancreatic cancer: Japan clinical oncology group study (JCOG1407). Pancreatology. 2018;18:841-845.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 14]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
19.  Department of Radiation Oncology, University of Maryland, Baltimore.   Phase I Nab-Paclitaxel Plus Gemcitabine With Proton Therapy for Locally Advanced Pancreatic Cancer (LAPC). [accessed 2023 Apr 25]. In: [Internet]. Bethesda (MD): U.S. National Library of Medicine. Available from: Identifier: NCT03652428.  [PubMed]  [DOI]  [Cited in This Article: ]
20.  McIntyre CA, Cohen NA, Goldman DA, Gonen M, Sadot E, O'Reilly EM, Varghese AM, Yu KH, Balachandran VP, Soares KC, D'Angelica MI, Drebin JA, Kingham TP, Allen PJ, Wei AC, Jarnagin WR. Induction FOLFIRINOX for patients with locally unresectable pancreatic ductal adenocarcinoma. J Surg Oncol. 2022;125:425-436.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 2]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]
21.  Perri G, Prakash L, Qiao W, Varadhachary GR, Wolff R, Fogelman D, Overman M, Pant S, Javle M, Koay EJ, Herman J, Kim M, Ikoma N, Tzeng CW, Lee JE, Katz MHG. Response and Survival Associated With First-line FOLFIRINOX vs Gemcitabine and nab-Paclitaxel Chemotherapy for Localized Pancreatic Ductal Adenocarcinoma. JAMA Surg. 2020;155:832-839.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 55]  [Cited by in F6Publishing: 59]  [Article Influence: 29.5]  [Reference Citation Analysis (0)]
22.  Brown University  FOLFOX-A For Locally Advanced Pancreatic Cancer: A Phase II Brown University Oncology Research Group Trial. [accessed 2023 Apr 25]. In: [Internet]. Bethesda (MD): U.S. National Library of Medicine. Available from: Identifier: NCT02578732.  [PubMed]  [DOI]  [Cited in This Article: ]
23.  Chen I  Nivolumab, Ipilimumab and Chemoradiation in Pancreatic Cancer. [accessed 2023 Apr 25]. In: [Internet]. Bethesda (MD): U.S. National Library of Medicine. Available from: Identifier: NCT04247165.  [PubMed]  [DOI]  [Cited in This Article: ]
24.  University of Colorado, Denver.   A Dose Escalation Trial of SBRT After Induction Chemotherapy for Locally Advanced Pancreatic Cancer. [accessed 2023 Apr 25]. In: [Internet]. Bethesda (MD): U.S. National Library of Medicine. Available from: Identifier: NCT02873598.  [PubMed]  [DOI]  [Cited in This Article: ]
25.  Zhu X, Cao Y, Lu M, Zhao X, Jiang L, Ye Y, Ju X, Zhang H. Stereotactic body radiation therapy with sequential S-1 for patients with locally advanced pancreatic cancer and poor performance status: An open-label, single-arm, phase 2 trial. Radiother Oncol. 2021;162:178-184.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
26.  Stein SM, James ES, Deng Y, Cong X, Kortmansky JS, Li J, Staugaard C, Indukala D, Boustani AM, Patel V, Cha CH, Salem RR, Chang B, Hochster HS, Lacy J. Final analysis of a phase II study of modified FOLFIRINOX in locally advanced and metastatic pancreatic cancer. Br J Cancer. 2016;114:737-743.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 119]  [Cited by in F6Publishing: 129]  [Article Influence: 18.4]  [Reference Citation Analysis (0)]
27.  Tempero MA, Malafa MP, Al-Hawary M, Asbun H, Bain A, Behrman SW, Benson AB 3rd, Binder E, Cardin DB, Cha C, Chiorean EG, Chung V, Czito B, Dillhoff M, Dotan E, Ferrone CR, Hardacre J, Hawkins WG, Herman J, Ko AH, Komanduri S, Koong A, LoConte N, Lowy AM, Moravek C, Nakakura EK, O'Reilly EM, Obando J, Reddy S, Scaife C, Thayer S, Weekes CD, Wolff RA, Wolpin BM, Burns J, Darlow S. Pancreatic Adenocarcinoma, Version 2.2017, NCCN Clinical Practice Guidelines in Oncology. J Natl Compr Canc Netw. 2017;15:1028-1061.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 556]  [Cited by in F6Publishing: 614]  [Article Influence: 122.8]  [Reference Citation Analysis (0)]
28.  Suker M, Beumer BR, Sadot E, Marthey L, Faris JE, Mellon EA, El-Rayes BF, Wang-Gillam A, Lacy J, Hosein PJ, Moorcraft SY, Conroy T, Hohla F, Allen P, Taieb J, Hong TS, Shridhar R, Chau I, van Eijck CH, Koerkamp BG. FOLFIRINOX for locally advanced pancreatic cancer: a systematic review and patient-level meta-analysis. Lancet Oncol. 2016;17:801-810.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 528]  [Cited by in F6Publishing: 566]  [Article Influence: 80.9]  [Reference Citation Analysis (0)]
29.  Barros AG, Pulido CF, Machado M, Brito MJ, Couto N, Sousa O, Melo SA, Mansinho H. Treatment optimization of locally advanced and metastatic pancreatic cancer (Review). Int J Oncol. 2021;59.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 2]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
30.  Jung JH, Song C, Jung IH, Ahn J, Kim B, Jung K, Lee JC, Kim J, Hwang JH. Induction FOLFIRINOX followed by stereotactic body radiation therapy in locally advanced pancreatic cancer. Front Oncol. 2022;12:1050070.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
31.  Wilson RR. Radiological use of fast protons. Radiology. 1946;47:487-491.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 825]  [Cited by in F6Publishing: 845]  [Article Influence: 65.0]  [Reference Citation Analysis (0)]
32.  Missaglia A, Bourkadi-Idrissi A, Casamichiela F, Mazzucconi D, Carminati M, Agosteo S, Fiorini C. Prompt-gamma fall-off estimation with C-ion irradiation at clinical energies, using a knife-edge slit camera: A Monte Carlo study. Phys Med. 2023;107:102554.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
33.  Broerse JJ, Barendsen GW, van Kersen GR. Survival of cultured human cells after irradiation with fast neutrons of different energies in hypoxic and oxygenated conditions. Int J Radiat Biol Relat Stud Phys Chem Med. 1968;13:559-572.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 71]  [Cited by in F6Publishing: 71]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
34.  Charalampopoulou A, Barcellini A, Frittitta GE, Fulgini G, Ivaldi GB, Magro G, Liotta M, Orlandi E, Pullia MG, Tabarelli de Fatis P, Facoetti A. In Vitro Effects of Photon Beam and Carbon Ion Radiotherapy on the Perineural Invasion of Two Cell Lines of Neurotropic Tumours. Life (Basel). 2023;13.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
35.  Wozny AS, Rodriguez-Lafrasse C. The 'stealth-bomber' paradigm for deciphering the tumour response to carbon-ion irradiation. Br J Cancer. 2023;128:1429-1438.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
36.  Kanai T, Endo M, Minohara S, Miyahara N, Koyama-ito H, Tomura H, Matsufuji N, Futami Y, Fukumura A, Hiraoka T, Furusawa Y, Ando K, Suzuki M, Soga F, Kawachi K. Biophysical characteristics of HIMAC clinical irradiation system for heavy-ion radiation therapy. Int J Radiat Oncol Biol Phys. 1999;44:201-210.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 654]  [Cited by in F6Publishing: 660]  [Article Influence: 27.5]  [Reference Citation Analysis (0)]
37.  Reese AS, Lu W, Regine WF. Utilization of intensity-modulated radiation therapy and image-guided radiation therapy in pancreatic cancer: is it beneficial? Semin Radiat Oncol. 2014;24:132-139.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 37]  [Article Influence: 4.1]  [Reference Citation Analysis (0)]
38.  Bittner MI, Grosu AL, Brunner TB. Comparison of toxicity after IMRT and 3D-conformal radiotherapy for patients with pancreatic cancer - a systematic review. Radiother Oncol. 2015;114:117-121.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 57]  [Cited by in F6Publishing: 61]  [Article Influence: 7.6]  [Reference Citation Analysis (0)]
39.  Naumann M, Czempiel T, Lößner AJ, Pape K, Beyreuther E, Löck S, Drukewitz S, Hennig A, von Neubeck C, Klink B, Krause M, William D, Stange DE, Bütof R, Dietrich A. Combined Systemic Drug Treatment with Proton Therapy: Investigations on Patient-Derived Organoids. Cancers (Basel). 2022;14.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
40.  Brahmer JR, Tykodi SS, Chow LQ, Hwu WJ, Topalian SL, Hwu P, Drake CG, Camacho LH, Kauh J, Odunsi K, Pitot HC, Hamid O, Bhatia S, Martins R, Eaton K, Chen S, Salay TM, Alaparthy S, Grosso JF, Korman AJ, Parker SM, Agrawal S, Goldberg SM, Pardoll DM, Gupta A, Wigginton JM. Safety and activity of anti-PD-L1 antibody in patients with advanced cancer. N Engl J Med. 2012;366:2455-2465.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5599]  [Cited by in F6Publishing: 5770]  [Article Influence: 524.5]  [Reference Citation Analysis (0)]
41.  Jiang Y, Li Y, Zhu B. T-cell exhaustion in the tumor microenvironment. Cell Death Dis. 2015;6:e1792.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 503]  [Cited by in F6Publishing: 531]  [Article Influence: 66.4]  [Reference Citation Analysis (0)]
42.  Nevala-Plagemann C, Hidalgo M, Garrido-Laguna I. From state-of-the-art treatments to novel therapies for advanced-stage pancreatic cancer. Nat Rev Clin Oncol. 2020;17:108-123.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 143]  [Cited by in F6Publishing: 150]  [Article Influence: 37.5]  [Reference Citation Analysis (0)]
43.  Le DT, Durham JN, Smith KN, Wang H, Bartlett BR, Aulakh LK, Lu S, Kemberling H, Wilt C, Luber BS, Wong F, Azad NS, Rucki AA, Laheru D, Donehower R, Zaheer A, Fisher GA, Crocenzi TS, Lee JJ, Greten TF, Duffy AG, Ciombor KK, Eyring AD, Lam BH, Joe A, Kang SP, Holdhoff M, Danilova L, Cope L, Meyer C, Zhou S, Goldberg RM, Armstrong DK, Bever KM, Fader AN, Taube J, Housseau F, Spetzler D, Xiao N, Pardoll DM, Papadopoulos N, Kinzler KW, Eshleman JR, Vogelstein B, Anders RA, Diaz LA Jr. Mismatch repair deficiency predicts response of solid tumors to PD-1 blockade. Science. 2017;357:409-413.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3799]  [Cited by in F6Publishing: 3974]  [Article Influence: 662.3]  [Reference Citation Analysis (0)]
44.  Morphotek  A Single-Dose Pilot Study of Radiolabeled Amatuximab (MORAb-009) in Mesothelin Over Expressing Cancers. [accessed 2023 Apr 25]. In: [Internet]. Bethesda (MD): U.S. National Library of Medicine. Available from: Identifier: NCT01521325.  [PubMed]  [DOI]  [Cited in This Article: ]
45.  Patel SP, Bristol A, Saric O, Wang XP, Dubeykovskiy A, Arlen PM, Morse MA. Anti-tumor activity of a novel monoclonal antibody, NPC-1C, optimized for recognition of tumor antigen MUC5AC variant in preclinical models. Cancer Immunol Immunother. 2013;62:1011-1019.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 15]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
46.  Georgetown University  Durvalumab Plus CV301 With Maintenance Chemotherapy in Metastatic Colorectal or Pancreatic Adenocarcinoma. [accessed 2023 Apr 25]. In: [Internet]. Bethesda (MD): U.S. National Library of Medicine. Available from: Identifier: NCT03376659.  [PubMed]  [DOI]  [Cited in This Article: ]
47.   M.D. Anderson Cancer Center. Bevacizumab, Erlotinib and Capecitabine for Advanced Pancreatic Cancer. [accessed 2023 Apr 25]. In: [Internet]. Bethesda (MD): U.S. National Library of Medicine. Available from: Identifier: NCT00614653.  [PubMed]  [DOI]  [Cited in This Article: ]
48.  O'Sullivan D, Dowling P, Joyce H, McAuley E, McCann A, Henry M, McGovern B, Barham P, Kelleher FC, Murphy J, Kennedy S, Swan N, Moriarty M, Clynes M, Larkin A. A novel inhibitory anti-invasive MAb isolated using phenotypic screening highlights AnxA6 as a functionally relevant target protein in pancreatic cancer. Br J Cancer. 2017;117:1326-1335.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 13]  [Cited by in F6Publishing: 13]  [Article Influence: 2.2]  [Reference Citation Analysis (0)]
49.  Smith DC, Eisenberg PD, Manikhas G, Chugh R, Gubens MA, Stagg RJ, Kapoun AM, Xu L, Dupont J, Sikic B. A phase I dose escalation and expansion study of the anticancer stem cell agent demcizumab (anti-DLL4) in patients with previously treated solid tumors. Clin Cancer Res. 2014;20:6295-6303.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 104]  [Cited by in F6Publishing: 113]  [Article Influence: 12.6]  [Reference Citation Analysis (0)]
50.  OncoMed Pharmaceuticals, Inc.   A Phase 1b Study of Demcizumab Plus Pembrolizumab in Locally Advanced or Metastatic Solid Tumors. [accessed 2023 Apr 25]. In: [Internet]. Bethesda (MD): U.S. National Library of Medicine. Available from: Identifier: NCT02722954.  [PubMed]  [DOI]  [Cited in This Article: ]
51.  51 Argani P, Iacobuzio-Donahue C, Ryu B, Rosty C, Goggins M, Wilentz RE, Murugesan SR, Leach SD, Jaffee E, Yeo CJ, Cameron JL, Kern SE, Hruban RH. Mesothelin is overexpressed in the vast majority of ductal adenocarcinomas of the pancreas: identification of a new pancreatic cancer marker by serial analysis of gene expression (SAGE). Clin Cancer Res. 2001;7:3862-3868.  [PubMed]  [DOI]  [Cited in This Article: ]
52.  Lan T, Luo M, Wei X. Mesenchymal stem/stromal cells in cancer therapy. J Hematol Oncol. 2021;14:195.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 39]  [Cited by in F6Publishing: 31]  [Article Influence: 15.5]  [Reference Citation Analysis (0)]
53.  Weng Z, Zhang B, Wu C, Yu F, Han B, Li B, Li L. Therapeutic roles of mesenchymal stem cell-derived extracellular vesicles in cancer. J Hematol Oncol. 2021;14:136.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 62]  [Cited by in F6Publishing: 50]  [Article Influence: 25.0]  [Reference Citation Analysis (0)]
54.  Timaner M, Tsai KK, Shaked Y. The multifaceted role of mesenchymal stem cells in cancer. Semin Cancer Biol. 2020;60:225-237.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 53]  [Cited by in F6Publishing: 57]  [Article Influence: 14.3]  [Reference Citation Analysis (0)]
55.  Hassan R, Cohen SJ, Phillips M, Pastan I, Sharon E, Kelly RJ, Schweizer C, Weil S, Laheru D. Phase I clinical trial of the chimeric anti-mesothelin monoclonal antibody MORAb-009 in patients with mesothelin-expressing cancers. Clin Cancer Res. 2010;16:6132-6138.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 139]  [Cited by in F6Publishing: 157]  [Article Influence: 12.1]  [Reference Citation Analysis (0)]
56.  Fujisaka Y, Kurata T, Tanaka K, Kudo T, Okamoto K, Tsurutani J, Kaneda H, Okamoto I, Namiki M, Kitamura C, Nakagawa K. Phase I study of amatuximab, a novel monoclonal antibody to mesothelin, in Japanese patients with advanced solid tumors. Invest New Drugs. 2015;33:380-388.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 26]  [Article Influence: 2.9]  [Reference Citation Analysis (0)]
57.  Qu CF, Li Y, Song YJ, Rizvi SM, Raja C, Zhang D, Samra J, Smith R, Perkins AC, Apostolidis C, Allen BJ. MUC1 expression in primary and metastatic pancreatic cancer cells for in vitro treatment by (213)Bi-C595 radioimmunoconjugate. Br J Cancer. 2004;91:2086-2093.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 77]  [Cited by in F6Publishing: 83]  [Article Influence: 4.6]  [Reference Citation Analysis (0)]
58.  Besmer DM, Curry JM, Roy LD, Tinder TL, Sahraei M, Schettini J, Hwang SI, Lee YY, Gendler SJ, Mukherjee P. Pancreatic ductal adenocarcinoma mice lacking mucin 1 have a profound defect in tumor growth and metastasis. Cancer Res. 2011;71:4432-4442.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 86]  [Cited by in F6Publishing: 93]  [Article Influence: 7.8]  [Reference Citation Analysis (0)]
59.  Striefler JK, Riess H, Lohneis P, Bischoff S, Kurreck A, Modest DP, Bahra M, Oettle H, Sinn M, Bläker H, Denkert C, Stintzing S, Sinn BV, Pelzer U. Mucin-1 Protein Is a Prognostic Marker for Pancreatic Ductal Adenocarcinoma: Results From the CONKO-001 Study. Front Oncol. 2021;11:670396.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 3]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
60.  Nagai K, Adachi T, Harada H, Eguchi S, Sugiyama H, Miyazaki Y. Dendritic Cell-based Immunotherapy Pulsed With Wilms Tumor 1 Peptide and Mucin 1 as an Adjuvant Therapy for Pancreatic Ductal Adenocarcinoma After Curative Resection: A Phase I/IIa Clinical Trial. Anticancer Res. 2020;40:5765-5776.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 12]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]
61.  Hisatsune A, Nakayama H, Kawasaki M, Horie I, Miyata T, Isohama Y, Kim KC, Katsuki H. Anti-MUC1 antibody inhibits EGF receptor signaling in cancer cells. Biochem Biophys Res Commun. 2011;405:377-381.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 28]  [Cited by in F6Publishing: 32]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
62.  Wu G, Maharjan S, Kim D, Kim JN, Park BK, Koh H, Moon K, Lee Y, Kwon HJ. A Novel Monoclonal Antibody Targets Mucin1 and Attenuates Growth in Pancreatic Cancer Model. Int J Mol Sci. 2018;19.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 19]  [Article Influence: 3.8]  [Reference Citation Analysis (0)]
63.  Kelly PN. The Cancer Immunotherapy Revolution. Science. 2018;359:1344-1345.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 79]  [Cited by in F6Publishing: 86]  [Article Influence: 17.2]  [Reference Citation Analysis (0)]
64.  Ferrara N, Adamis AP. Ten years of anti-vascular endothelial growth factor therapy. Nat Rev Drug Discov. 2016;15:385-403.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 527]  [Cited by in F6Publishing: 562]  [Article Influence: 80.3]  [Reference Citation Analysis (0)]
65.  Apte RS, Chen DS, Ferrara N. VEGF in Signaling and Disease: Beyond Discovery and Development. Cell. 2019;176:1248-1264.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 742]  [Cited by in F6Publishing: 817]  [Article Influence: 272.3]  [Reference Citation Analysis (0)]
66.  Enrich C, Rentero C, de Muga SV, Reverter M, Mulay V, Wood P, Koese M, Grewal T. Annexin A6-Linking Ca(2+) signaling with cholesterol transport. Biochim Biophys Acta. 2011;1813:935-947.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 55]  [Cited by in F6Publishing: 60]  [Article Influence: 4.6]  [Reference Citation Analysis (0)]
67.  Rentero C, Blanco-Muñoz P, Meneses-Salas E, Grewal T, Enrich C. Annexins-Coordinators of Cholesterol Homeostasis in Endocytic Pathways. Int J Mol Sci. 2018;19.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 33]  [Cited by in F6Publishing: 33]  [Article Influence: 6.6]  [Reference Citation Analysis (0)]
68.  Keklikoglou I, Cianciaruso C, Güç E, Squadrito ML, Spring LM, Tazzyman S, Lambein L, Poissonnier A, Ferraro GB, Baer C, Cassará A, Guichard A, Iruela-Arispe ML, Lewis CE, Coussens LM, Bardia A, Jain RK, Pollard JW, De Palma M. Chemotherapy elicits pro-metastatic extracellular vesicles in breast cancer models. Nat Cell Biol. 2019;21:190-202.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 267]  [Cited by in F6Publishing: 278]  [Article Influence: 55.6]  [Reference Citation Analysis (0)]
69.  Leca J, Martinez S, Lac S, Nigri J, Secq V, Rubis M, Bressy C, Sergé A, Lavaut MN, Dusetti N, Loncle C, Roques J, Pietrasz D, Bousquet C, Garcia S, Granjeaud S, Ouaissi M, Bachet JB, Brun C, Iovanna JL, Zimmermann P, Vasseur S, Tomasini R. Cancer-associated fibroblast-derived annexin A6+ extracellular vesicles support pancreatic cancer aggressiveness. J Clin Invest. 2016;126:4140-4156.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 131]  [Cited by in F6Publishing: 139]  [Article Influence: 19.9]  [Reference Citation Analysis (0)]
70.  Fasoulakis Z, Koutras A, Ntounis T, Pergialiotis V, Chionis A, Katrachouras A, Palios VC, Symeonidis P, Valsamaki A, Syllaios A, Diakosavvas M, Angelou K, Samara AA, Pagkalos A, Theodora M, Schizas D, Kontomanolis EN. The Prognostic Role and Significance of Dll4 and Toll-like Receptors in Cancer Development. Cancers (Basel). 2022;14.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 1]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
71.  Cubillo Gracian A, Dean A, Muñoz A, Hidalgo M, Pazo-Cid R, Martin M, Macarulla Mercade T, Lipton L, Harris M, Manzano-Mozo JL, Maurel J, Guillen-Ponce C, Tebbutt N, Cooray P, Sohal D, Zalupski M, Kolevska T, Stagg R, Goldstein D. YOSEMITE: A 3 arm double-blind randomized phase 2 study of gemcitabine, paclitaxel protein-bound particles for injectable suspension, and placebo (GAP) vs gemcitabine, paclitaxel protein-bound particles for injectable suspension and either 1 or 2 truncated courses of demcizumab (GAD). Ann Oncol. 2017;28:v211.  [PubMed]  [DOI]  [Cited in This Article: ]
72.  Sahlin M, Bauden MP, Andersson R, Ansari D. Radioimmunotherapy--a potential novel tool for pancreatic cancer therapy? Tumour Biol. 2015;36:4053-4062.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 10]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
73.  Sugyo A, Tsuji AB, Sudo H, Koizumi M, Ukai Y, Kurosawa G, Kurosawa Y, Saga T, Higashi T. Efficacy Evaluation of Combination Treatment Using Gemcitabine and Radioimmunotherapy with (90)Y-Labeled Fully Human Anti-CD147 Monoclonal Antibody 059-053 in a BxPC-3 Xenograft Mouse Model of Refractory Pancreatic Cancer. Int J Mol Sci. 2018;19.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 13]  [Article Influence: 2.6]  [Reference Citation Analysis (0)]
74.  Kasten BB, Gangrade A, Kim H, Fan J, Ferrone S, Ferrone CR, Zinn KR, Buchsbaum DJ. (212)Pb-labeled B7-H3-targeting antibody for pancreatic cancer therapy in mouse models. Nucl Med Biol. 2018;58:67-73.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 28]  [Cited by in F6Publishing: 31]  [Article Influence: 5.2]  [Reference Citation Analysis (0)]
75.  Li E, Huang X, Zhang G, Liang T. Combinational blockade of MET and PD-L1 improves pancreatic cancer immunotherapeutic efficacy. J Exp Clin Cancer Res. 2021;40:279.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 12]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
76.  Zhang X, Huang X, Xu J, Li E, Lao M, Tang T, Zhang G, Guo C, Zhang X, Chen W, Yadav DK, Bai X, Liang T. NEK2 inhibition triggers anti-pancreatic cancer immunity by targeting PD-L1. Nat Commun. 2021;12:4536.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 13]  [Article Influence: 6.5]  [Reference Citation Analysis (0)]
77.  Huang X, Zhang G, Tang TY, Gao X, Liang TB. Personalized pancreatic cancer therapy: from the perspective of mRNA vaccine. Mil Med Res. 2022;9:53.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
78.  Miao L, Zhang Y, Huang L. mRNA vaccine for cancer immunotherapy. Mol Cancer. 2021;20:41.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 134]  [Cited by in F6Publishing: 153]  [Article Influence: 76.5]  [Reference Citation Analysis (0)]
79.  Kang X, Lin Z, Xu M, Pan J, Wang ZW. Deciphering role of FGFR signalling pathway in pancreatic cancer. Cell Prolif. 2019;52:e12605.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 23]  [Article Influence: 5.8]  [Reference Citation Analysis (0)]
80.  Lai E, Puzzoni M, Ziranu P, Pretta A, Impera V, Mariani S, Liscia N, Soro P, Musio F, Persano M, Donisi C, Tolu S, Balconi F, Pireddu A, Demurtas L, Pusceddu V, Camera S, Sclafani F, Scartozzi M. New therapeutic targets in pancreatic cancer. Cancer Treat Rev. 2019;81:101926.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 47]  [Cited by in F6Publishing: 53]  [Article Influence: 13.3]  [Reference Citation Analysis (0)]
81.  Ebrahimi S, Hosseini M, Shahidsales S, Maftouh M, Ferns GA, Ghayour-Mobarhan M, Hassanian SM, Avan A. Targeting the Akt/PI3K Signaling Pathway as a Potential Therapeutic Strategy for the Treatment of Pancreatic Cancer. Curr Med Chem. 2017;24:1321-1331.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 100]  [Cited by in F6Publishing: 109]  [Article Influence: 18.2]  [Reference Citation Analysis (0)]
82.  Polireddy K, Chen Q. Cancer of the Pancreas: Molecular Pathways and Current Advancement in Treatment. J Cancer. 2016;7:1497-1514.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 47]  [Cited by in F6Publishing: 53]  [Article Influence: 7.6]  [Reference Citation Analysis (0)]
83.  Drilon A, Laetsch TW, Kummar S, DuBois SG, Lassen UN, Demetri GD, Nathenson M, Doebele RC, Farago AF, Pappo AS, Turpin B, Dowlati A, Brose MS, Mascarenhas L, Federman N, Berlin J, El-Deiry WS, Baik C, Deeken J, Boni V, Nagasubramanian R, Taylor M, Rudzinski ER, Meric-Bernstam F, Sohal DPS, Ma PC, Raez LE, Hechtman JF, Benayed R, Ladanyi M, Tuch BB, Ebata K, Cruickshank S, Ku NC, Cox MC, Hawkins DS, Hong DS, Hyman DM. Efficacy of Larotrectinib in TRK Fusion-Positive Cancers in Adults and Children. N Engl J Med. 2018;378:731-739.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1577]  [Cited by in F6Publishing: 1520]  [Article Influence: 304.0]  [Reference Citation Analysis (0)]
84.  Miknyoczki SJ, Lang D, Huang L, Klein-Szanto AJ, Dionne CA, Ruggeri BA. Neurotrophins and Trk receptors in human pancreatic ductal adenocarcinoma: expression patterns and effects on in vitro invasive behavior. Int J Cancer. 1999;81:417-427.  [PubMed]  [DOI]  [Cited in This Article: ]
85.  Lal G, Liu G, Schmocker B, Kaurah P, Ozcelik H, Narod SA, Redston M, Gallinger S. Inherited predisposition to pancreatic adenocarcinoma: role of family history and germ-line p16, BRCA1, and BRCA2 mutations. Cancer Res. 2000;60:409-416.  [PubMed]  [DOI]  [Cited in This Article: ]
86.  Iqbal J, Ragone A, Lubinski J, Lynch HT, Moller P, Ghadirian P, Foulkes WD, Armel S, Eisen A, Neuhausen SL, Senter L, Singer CF, Ainsworth P, Kim-Sing C, Tung N, Friedman E, Llacuachaqui M, Ping S, Narod SA; Hereditary Breast Cancer Study Group. The incidence of pancreatic cancer in BRCA1 and BRCA2 mutation carriers. Br J Cancer. 2012;107:2005-2009.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 180]  [Cited by in F6Publishing: 189]  [Article Influence: 17.2]  [Reference Citation Analysis (0)]
87.  Macherla S, Laks S, Naqash AR, Bulumulle A, Zervos E, Muzaffar M. Emerging Role of Immune Checkpoint Blockade in Pancreatic Cancer. Int J Mol Sci. 2018;19.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 51]  [Cited by in F6Publishing: 53]  [Article Influence: 10.6]  [Reference Citation Analysis (0)]
88.  O'Reilly EM, Lee JW, Zalupski M, Capanu M, Park J, Golan T, Tahover E, Lowery MA, Chou JF, Sahai V, Brenner R, Kindler HL, Yu KH, Zervoudakis A, Vemuri S, Stadler ZK, Do RKG, Dhani N, Chen AP, Kelsen DP. Randomized, Multicenter, Phase II Trial of Gemcitabine and Cisplatin With or Without Veliparib in Patients With Pancreas Adenocarcinoma and a Germline BRCA/PALB2 Mutation. J Clin Oncol. 2020;38:1378-1388.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 165]  [Cited by in F6Publishing: 174]  [Article Influence: 58.0]  [Reference Citation Analysis (0)]
89.  Park W, Chen J, Chou JF, Varghese AM, Yu KH, Wong W, Capanu M, Balachandran V, McIntyre CA, El Dika I, Khalil DN, Harding JJ, Ghalehsari N, McKinnell Z, Chalasani SB, Makarov V, Selenica P, Pei X, Lecomte N, Kelsen DP, Abou-Alfa GK, Robson ME, Zhang L, Berger MF, Schultz N, Chan TA, Powell SN, Reis-Filho JS, Iacobuzio-Donahue CA, Riaz N, O'Reilly EM. Genomic Methods Identify Homologous Recombination Deficiency in Pancreas Adenocarcinoma and Optimize Treatment Selection. Clin Cancer Res. 2020;26:3239-3247.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 72]  [Cited by in F6Publishing: 79]  [Article Influence: 26.3]  [Reference Citation Analysis (0)]
90.  Pastushenko I, Blanpain C. EMT Transition States during Tumor Progression and Metastasis. Trends Cell Biol. 2019;29:212-226.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 920]  [Cited by in F6Publishing: 1040]  [Article Influence: 208.0]  [Reference Citation Analysis (0)]
91.  Dongre A, Weinberg RA. New insights into the mechanisms of epithelial-mesenchymal transition and implications for cancer. Nat Rev Mol Cell Biol. 2019;20:69-84.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1356]  [Cited by in F6Publishing: 1457]  [Article Influence: 364.3]  [Reference Citation Analysis (0)]
92.  van Mackelenbergh MG, Stroes CI, Spijker R, van Eijck CHJ, Wilmink JW, Bijlsma MF, van Laarhoven HWM. Clinical Trials Targeting the Stroma in Pancreatic Cancer: A Systematic Review and Meta-Analysis. Cancers (Basel). 2019;11.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 34]  [Article Influence: 8.5]  [Reference Citation Analysis (0)]
93.  Hou YC, Chao YJ, Hsieh MH, Tung HL, Wang HC, Shan YS. Low CD8⁺ T Cell Infiltration and High PD-L1 Expression Are Associated with Level of CD44⁺/CD133⁺ Cancer Stem Cells and Predict an Unfavorable Prognosis in Pancreatic Cancer. Cancers (Basel). 2019;11.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 56]  [Cited by in F6Publishing: 59]  [Article Influence: 14.8]  [Reference Citation Analysis (0)]
94.  Laura A, Anna C, Cinquepalmi M, Giovanni M, Sole MM, Nava AK, Niccolò P, Giuseppe N, Stefano V, Paolo A, Francesco D, Giovanni R. Is Complete Pathologic Response in Pancreatic Cancer Overestimated? A Systematic Review of Prospective Studies. J Gastrointest Surg. 2020;24:2336-2348.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 4]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
95.  Gugenheim J, Crovetto A, Petrucciani N. Neoadjuvant therapy for pancreatic cancer. Updates Surg. 2022;74:35-42.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 1]  [Article Influence: 0.5]  [Reference Citation Analysis (0)]
96.  Zhang Y, Huang ZX, Song B. Role of imaging in evaluating the response after neoadjuvant treatment for pancreatic ductal adenocarcinoma. World J Gastroenterol. 2021;27:3037-3049.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 8]  [Cited by in F6Publishing: 8]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]
97.  Borhani AA, Dewan R, Furlan A, Seiser N, Zureikat AH, Singhi AD, Boone B, Bahary N, Hogg ME, Lotze M, Zeh HJ III, Tublin ME. Assessment of Response to Neoadjuvant Therapy Using CT Texture Analysis in Patients With Resectable and Borderline Resectable Pancreatic Ductal Adenocarcinoma. AJR Am J Roentgenol. 2020;214:362-369.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 19]  [Article Influence: 4.8]  [Reference Citation Analysis (0)]
98.  ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium. Pan-cancer analysis of whole genomes. Nature. 2020;578:82-93.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1416]  [Cited by in F6Publishing: 1348]  [Article Influence: 449.3]  [Reference Citation Analysis (0)]
99.  Peng L, Bian XW, Li DK, Xu C, Wang GM, Xia QY, Xiong Q. Large-scale RNA-Seq Transcriptome Analysis of 4043 Cancers and 548 Normal Tissue Controls across 12 TCGA Cancer Types. Sci Rep. 2015;5:13413.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 83]  [Cited by in F6Publishing: 82]  [Article Influence: 10.3]  [Reference Citation Analysis (0)]
100.  Traub B, Link KH, Kornmann M. Curing pancreatic cancer. Semin Cancer Biol. 2021;76:232-246.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 6]  [Cited by in F6Publishing: 8]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]