Cancer statistics: Current diagnosis and treatment of pancreatic cancer in Shanghai, China

Jiang, Long; Luo, Guopei; Xiao, Zhi; Liu, Zu qiang; Guo, Meng; Liu, Liang; Liu, Chen; Xu, Jin; Gao, Yu Tang; Zheng, Ying; Wu, Chunxiao; Ni, Quan Xing; Li, Min; Lei, Yu

doi:10.1016/j.canlet.2014.01.004

Cited by 105 publications

(77 citation statements)

References 33 publications

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“…Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant cancers of the digestive system, with incidence invisible and rapid disease progression [1]. Therefore, most PDAC patients are at an advanced stage, owning a bad prognosis [2] with limited opportunity for surgery.…”

Section: Introductionmentioning

confidence: 99%

Circulating Tumor DNA as a Sensitive Marker in Patients Undergoing Irreversible Electroporation for Pancreatic Cancer

Lin

Alnaggar

Liang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Pancreatic ductal adenocarcinoma (PDAC) is often diagnosed at an advanced stage, resulting in extremely poor 5-year survival. Late diagnosis of PDAC is mainly due to lack of a reliable method of early detection. Carbohydrate antigen (CA) 19-9 is often used as a tumor biomarker in PDAC; however, the test lacks sensitivity and specificity. Therefore, new sensitive and minimally invasive diagnostic tools are required to detect pancreatic cancer. Methods: Here, we investigated circulating tumor DNA (ctDNA) which contained KRAS-mutated as a potential diagnostic tool for PDAC patients who underwent irreversible electroporation (IRE). We used droplet digital polymerase chain reaction (ddPCR) to detect the expression of KRAS-mutated genes in plasma samples of 65 PDAC patients who underwent IRE. Results: In these 65 cases, ctDNA was detected in 20 (29.2%) samples. The median overall survival (OS) was 11.4 months with ctDNA+ patients and 14.3 months for ctDNA- patients. ctDNA+ patients had a obviously poorer prognosis associated to overall survival (P < 0.001). Conclusion: Our results suggested that the existence of ctDNA was a predictor of survival for PDAC patients. Therefore, ctDNA may be a new sensitive biomarker for monitoring treatment outcome in PDAC.

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Section: Introductionmentioning

confidence: 99%

Circulating Tumor DNA as a Sensitive Marker in Patients Undergoing Irreversible Electroporation for Pancreatic Cancer

Lin

Alnaggar

Liang

et al. 2018

Cell Physiol Biochem

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“…Despite many advances in molecular and targeted anticancer therapeutics over the past 30 years, pancreatic cancer has remained one of the most aggressive types of malignancies with less than a 5% survival rate within 5 years of diagnosis (1)(2)(3)(4). Gemcitabine is considered the "gold" standard chemotherapeutic agent for treatment of pancreatic cancer; however, the response rate to gemcitabine alone or in combination with other chemotherapeutics is only marginal (1,2,4,5).…”

Section: Introductionmentioning

confidence: 99%

“…Gemcitabine is considered the "gold" standard chemotherapeutic agent for treatment of pancreatic cancer; however, the response rate to gemcitabine alone or in combination with other chemotherapeutics is only marginal (1,2,4,5). Among many reasons that have been investigated to explain this chemotherapeutic inefficiency (6)(7)(8)(9)(10)(11), reduced cellular uptake of gemcitabine as a result of down regulation of influx proteins and/or upregulation of the efflux proteins has been highlighted in several studies (12)(13)(14)(15) .…”

Section: Introductionmentioning

confidence: 99%

Calcitriol Reverses Induced Expression of Efflux Proteins and Potentiates Cytotoxic Activity of Gemcitabine in Capan-2 Pancreatic Cancer Cells

Kohan¹,

Sani²,

Boroujerdi³

2017

J Pharm Pharm Sci

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ABSTRACT-Purpose. Efflux and influx proteins play a major role in chemo-resistance by affecting the net cellular uptake of anti-cancer drugs. Hence, alteration of the efflux and influx protein expression may result in variations of chemotherapeutics uptake and consequently cell death rate. The present study investigated the effects of pre-treatment of capan-2 pancreatic cancer cells with calcitriol, butylated hydroxytoluene (BHT), butylated hydroxyanisole (BHA) or silibinin on the induction of three major efflux proteins and the main gemcitabine influx protein. The influence of the pre-treatments on the net cellular uptake of gemcitabine, total ATPase activity, and cell death rate were also evaluated. Methods. Capan-2 pancreatic cancer cells were pre-treated for 24 h with calcitriol, BHT, BHA, or silibinin, followed by gemcitabine treatment. The concentration of gemcitabine was quantified using ultra-performance liquid chromatography (UPLC). Real-time polymerase chain reaction (RT-PCR) was utilized in order to investigate the expression of the mRNAs. The expression of the proteins was assessed using western blotting. Measurement of the ATPase activity was conducted utilizing a colorimetric method and viability of the cells was determined using a luminescent cell viability assay. Results. Protein expression studies showed that BHT, silibinin, and BHA increased expression of the efflux proteins and decreased the overall uptake of gemcitabine, whereas calcitriol significantly inhibited expression of the efflux proteins and increased gemcitabine uptake. Expression of specific mRNAs correlated reasonably well with the levels of corresponding proteins. Additionally, the expression of efflux proteins and ATPase activity were well correlated, signifying that the induced efflux proteins are functionally active. Moreover, pre-treatment with calcitriol resulted in a significant increase in cell death with gemcitabine treatment, whereas, BHA significantly reduced the cell death rate. On the other hand, pre-treatment with BHT and silibinin had no significant effect on the cell death rate. Conclusions. Pre-treatment of the pancreatic cancer cells with calcitriol significantly increased gemcitabine cellular uptake and consequently decreased cell viability after treatment with gemcitabine, whereas BHA significantly reduced gemcitabine uptake and decreased cell death rate, which were at least partially attributed to the alteration of expression of efflux and influx proteins.

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“…Similarly, extended lymphadenectomy does not improve survival over standard lymphadenectomy. However, extended lymphadenectomy is associated with increased early morbidity [87].A surgical mortality of <5% has been achieved in most specialized centers but resection for pancreatic cancer continues to have a morbidity rate of >30% [83,88]. Complications following pancreatectomy include pancreatic fistulae, delayed gastric emptying, hemorrhage, wound infection, intraabdominal sepsis, acute pancreatitis, portal vein thrombosis, chylous ascites and bile leaks.…”

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confidence: 99%

The Pathogenesis, Diagnosis, and Management of Pancreatic Cancer

Malhotra¹,

Ahn²,

Bloomston

2015

J Gastrointest Dig Syst

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Pancreatic cancer is an aggressive and devastating disease accounting for 44,000 new cases per year in US. It is characterized by invasiveness, rapid progression and profound resistance to treatment. The majority of cases are diagnosed above age 65 with about 60% of cases at an advanced stage and 5 year survival less than 10%. Advances in molecular biology have greatly improved our understanding of pathogenesis of pancreatic cancer. Many patients have mutations of K-ras oncogene and various tumor suppressor genes are also investigated. Radical surgery remains the only curative treatment option for pancreatic cancer in early stages. For locally advanced, unresectable and metastatic disease, treatment is palliative, in form of adjuvant or neoadjuvant chemotherapy with or without radiotherapy. Gemcitabine based combinations have essentially failed to provide a substantial prolongation of survival and constitute treatment option only in patients with a good performance status. This article provides an overview of epidemiology; risks factors, molecular genetics, biomarkers, diagnostic modality and evidence based therapeutic options for resectable and palliative options for unresectable disease. Keywords: Pancreatic cancer; Diagnosis EpidemiologyPancreatic cancer is one of the most lethal human cancers and is the fourth leading cause of cancer-related deaths in the United States [1,2]. It is estimated that 38,460 of 45,220 people diagnosed with pancreatic cancer in the United States in 2013 will die of their disease, representing approximately 6% of total U.S. cancer deaths [1]. Typically a cancer of the elderly, only 13% of cases occur in patients younger than 55 years, whereas 69% of cases occur in those older than 65. There is a slight predilection for men over women in most countries. Furthermore the incidence of pancreatic cancer in the United States increased from 1999 to 2008, possibly because of the increasing prevalence of obesity and other unknown factors [1,[3][4][5]. Mortality rates have remained largely unchanged [6].The etiology of pancreatic cancer remains unclear, thus making specific risk factors allusive. Still, accepted associated risk factors include smoking, family history of chronic pancreatitis, advancing age, male gender, diabetes mellitus, obesity, non-O blood group, occupational exposures (to chlorinated hydrocarbon solvents and nickel), African American ethnic origin, a high-fat diet, diets high in meat and low in vegetables and folate, and possibly Helicobacter pylori infection and periodontal disease [7]. Findings of preliminary studies suggest that metformin could protect against development of pancreatic cancer [8,9]. A retrospective analysis of 302 patients with pancreatic cancer and diabetes found that metformin use was associated with increased survival at 2 years (30.1% vs. 15.4%; P=0.004) and increased overall survival (OS) (15.2 months vs. 11.1; P=0.009). The OS difference was significant only in patients without distant metastases and remained significant when insulin user...

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Cancer statistics: Current diagnosis and treatment of pancreatic cancer in Shanghai, China

Cited by 105 publications

References 33 publications

Circulating Tumor DNA as a Sensitive Marker in Patients Undergoing Irreversible Electroporation for Pancreatic Cancer

Circulating Tumor DNA as a Sensitive Marker in Patients Undergoing Irreversible Electroporation for Pancreatic Cancer

Calcitriol Reverses Induced Expression of Efflux Proteins and Potentiates Cytotoxic Activity of Gemcitabine in Capan-2 Pancreatic Cancer Cells

The Pathogenesis, Diagnosis, and Management of Pancreatic Cancer

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