Relevant bibliographies by topics / Pancreatic cancer / Journal articles

Journal articles on the topic 'Pancreatic cancer'

To see the other types of publications on this topic, follow the link: Pancreatic cancer.
Author: Grafiati
Published: 4 June 2021
Last updated: 7 July 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Pancreatic cancer.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Li, Yumin, and Xiaohui Wang. "PET Imaging in Pancreatic Cancer." SDRP Journal of Food Science & Technology 4, no. 3 (2019): 659–69. http://dx.doi.org/10.25177/jfst.4.3.ra.493.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kashyap, Monika. "Pancreatic Cancer: A Silent Killer." International Journal of Science and Research (IJSR) 13, no. 5 (May 5, 2024): 136–38. http://dx.doi.org/10.21275/mr24430192939.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Shi, Chanjuan, Ralph H. Hruban, and Alison P. Klein. "Familial Pancreatic Cancer." Archives of Pathology & Laboratory Medicine 133, no. 3 (March 1, 2009): 365–74. http://dx.doi.org/10.5858/133.3.365.

Full text
Abstract:
Abstract Context.—Approximately 5% to 10% of individuals with pancreatic cancer report a history of pancreatic cancer in a close family member. In addition, several known genetic syndromes, such as familial breast cancer (BRCA2), the Peutz-Jeghers syndrome, and the familial atypical multiple mole melanoma syndrome, have been shown to be associated with an increased risk of pancreatic cancer. The known genes associated with these conditions can explain only a portion of the clustering of pancreatic cancer in families, and research to identify additional susceptibility genes is ongoing. Objective.—To provide an understanding of familial pancreatic cancer and the pathology of familial exocrine pancreatic cancers. Data Sources.—Published literature on familial aggregation of pancreatic cancer and familial exocrine pancreatic tumors. Conclusions.—Even in the absence of predictive genetic testing, the collection of a careful, detailed family history is an important step in the management of all patients with pancreatic cancer. While most pancreatic cancers that arise in patients with a family history are ductal adenocarcinomas, certain subtypes of pancreatic cancer have been associated with familial syndromes. Therefore, the histologic appearance of the pancreatic cancer itself, and/or the presence and appearance of precancerous changes in the pancreas, may increase the clinical index of suspicion for a genetic syndrome.
APA, Harvard, Vancouver, ISO, and other styles
4

Gubergrits, N. B., N. V. Byelyayeva, A. A. Suprun, and I. A. Kozinskaya. "Pancreatic syphilis mimicking cancer." Herald of Pancreatic Club 59, no. 2 (May 15, 2023): 35–38. http://dx.doi.org/10.33149/vkp.2023.02.06.

Full text
Abstract:
Since the incidence of syphilis is increasing, the number of pancreatic lesions is expected to increase too. Pancreatic syphilis can be congenital or acquired. The pancreas is affected in 10–80% of patients with congenital syphilis. Infection of the pancreas occurs most often during the second half of pregnancy. Morphologically, there are five types of congenital pancreatic syphilis: gummy; diffuse interstitial pancreatitis, which can be combined with multiple miliary gummas and atrophy of the pancreatic parenchyma; indurative fibrous type; with atrophy of the lobules (atrophic type); and with a predominant lesion of the pancreatic ducts —sialangitis pancreatica. In congenital syphilis, the pancreatic head is mostly affected. Early and severe damage to the islets of Langerhans is typical. Acquired pancreatic syphilis is less common than congenital syphilis. Morphologically, it has three types: the edematous-infiltrative type, in secondary syphilis; the gummy type (pancreatitis gummosa), in tertiary syphilis; and sclerotic pancreatitis, or pancreatitis sclerotica, or “syphilitic cirrhosis of the pancreas”. The latter type is usually the outcome of the first two morphological types. Clinically acquired pancreatic syphilis proceeds according to the type of recurrent chronic pancreatitis, i.e., with periodic exacerbations (pancreatic attacks), but the pain is rarely intense, and the phenomenon of “deviation” of enzymes into the blood is rarely observed. This clinical type more often corresponds to the edematous-infiltrative morphological type of syphilitic organ damage, and less often to the gummy type. It should be noted that acquired pancreatic syphilis occurs against the background of specific damage to the liver, heart, aorta, kidneys, skin, stomach, central nervous system, etc. The differential diagnosis of gummy pancreatic lesions and pancreatic cancer is especially complicated. Antisyphilitic treatment should be administered. Due to a toxic-allergic reaction, the symptoms of pancreatitis may exacerbate at the start of a specific therapy.
APA, Harvard, Vancouver, ISO, and other styles
5

VG, Zaitsev. "Risks of Pancreatic Cancer and Dietary Glucosinolates." Gastroenterology & Hepatology International Journal 6, no. 2 (July 1, 2021): 1–3. http://dx.doi.org/10.23880/ghij-16000186.

Full text
Abstract:
Pancreatic cancer has poor prognosis and is detected in the late stages usually. There is no way for specific prevention of pancreatic cancer. Brassicaceae vegetable-produced glucosinolates and isothiocyanates are known as anticancer substances. Aim of this mini-review was to estimate opportunities of pancreatic cancer prevention by glucosinolates and their derivatives. Results of ten clinical and epidemiologic studies were discussed. It was shown no clear and solid evidence for positive effects of glucosinolates, isothiocyanates or plants containing these substances in pancreatic cancer prevention or treatment have been observed
APA, Harvard, Vancouver, ISO, and other styles
6

Krishnamoorthy, Mithunah, John G. Lenehan, Jeremy P. Burton, and Saman Maleki Vareki. "Immunomodulation in Pancreatic Cancer." Cancers 12, no. 11 (November 12, 2020): 3340. http://dx.doi.org/10.3390/cancers12113340.

Full text
Abstract:
Pancreatic cancer has a high mortality rate, and its incidence is increasing worldwide. The almost universal poor prognosis of pancreatic cancer is partly due to symptoms presenting only at late stages and limited effective treatments. Recently, immune checkpoint blockade inhibitors have drastically improved patient survival in metastatic and advanced settings in certain cancers. Unfortunately, these therapies are ineffective in pancreatic cancer. However, tumor biopsies from long-term survivors of pancreatic cancer are more likely to be infiltrated by cytotoxic T-cells and certain species of bacteria that activate T-cells. These observations suggest that T-cell activation is essential for anti-tumor immunity in pancreatic cancers. This review discusses the immunological mechanisms responsible for effective anti-tumor immunity and how immune-based strategies can be exploited to develop new pancreatic cancer treatments.
APA, Harvard, Vancouver, ISO, and other styles
7

Jeekel, J. "Pancreatic Cancer: Surgery of pancreatic cancer." Annals of Oncology 5 (1994): S73—S74. http://dx.doi.org/10.1093/annonc/5.suppl_3.s73.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Shaeir, Sayed Shaker, Mohamed Atef ElKordy, Mohamed Emam Sobeih, Rasha Mahmoud Allam, and Ayman Hanafy. "Pancreatico-jejunostomy versus pancreatico-gasrostomy after pancreatico-duodenectomy in decreasing postoperative pancreatic fistula." Egyptian Journal of Surgery 42, no. 2 (April 2023): 473–81. http://dx.doi.org/10.4103/ejs.ejs_91_23.

Full text
Abstract:
Background Pancreatico-duodenectomy is still the cornerstone in curating pancreatic and periampullary cancers. Many techniques for pancreatic anastomosis were described. Pancreatico-gastrostomy (PG) may be a suitable technique, especially in small pancreatic ducts where the stitching of duct to mucosa may be difficult. Still, the results of pancreatico-gastrostomy compared to pancreatico-jejunostomy (PJ) in terms of morbidity are not well studied; hence, this study was designed to investigate. Objective To compare pancreatico-gastrostomy versus pancreatico-jejunostomy post pancreatico-duodenectomy from points of operative techniques and characteristics, and postoperative morbidity and mortality. Patients and methods The Cohort study included all cases diagnosed with either pancreatic head or periampullary cancers and underwent pancreatico-duodenectomy at National Cancer Institute (NCI), Cairo University, between January 2021 and February 2023. Cases were enrolled into one of the two groups, group 1: underwent pancreatico-gastrostomy, while group 2 underwent pancreatico-jejunostomy. The two groups were compared by: Demographic characteristics, preoperative investigations results, operative, postoperative data and histopathological results of the specimens resected. Results Incidence of the pancreatic leak was not significantly different in both groups (17.6% versus 15.8% for PG and PJ respectively, P=0.833), operative time was shorter in a pancreatico-gastrostomy group (310, 355 min, P=0.001), Delayed gastric emptying (DGE) was less occurred in cases of pancreatico-gastrostomy (5.9%, 31.6%, P=0.006). Postoperative mortality was not different in both groups (8.8%, 2.6% for PG and PJ respectively, P=0.338). Conclusion Regarding the incidence of postoperative pancreatic fistula, both reconstruction methods produce comparable postoperative results. Pancreatico-gastrostomy is a good alternative technique to the standard pancreatico-jejunostomy.
APA, Harvard, Vancouver, ISO, and other styles
9

Kasuga, Akiyoshi, Takeshi Okamoto, Shohei Udagawa, Chinatsu Mori, Takafumi Mie, Takaaki Furukawa, Yuto Yamada, et al. "Molecular Features and Clinical Management of Hereditary Pancreatic Cancer Syndromes and Familial Pancreatic Cancer." International Journal of Molecular Sciences 23, no. 3 (January 21, 2022): 1205. http://dx.doi.org/10.3390/ijms23031205.

Full text
Abstract:
Hereditary pancreatic cancers are caused by several inherited genes. Familial pancreatic cancer is defined as pancreatic cancer arising in a patient with at least two first-degree relatives with pancreatic cancer in the absence of an identified genetic cause. Hereditary pancreatic cancer syndromes and familial pancreatic cancers account for about 10% of pancreatic cancer cases. Germline mutations in BRCA1, BRCA2, ATM, PALB2, CDKN2A, STK11, and TP53 and mismatch repair genes (MLH1, MSH2, MSH6, PMS2, and EPCAM) are among the well-known inherited susceptibility genes. Currently available targeted medications include poly (ADP-ribose) polymerase inhibitors (PARP) for cases with mutant BRCA and immune checkpoint inhibitors for cases with mismatch repair deficiency. Loss of heterozygosity of hereditary pancreatic cancer susceptibility genes such as BRCA1/2 plays a key role in carcinogenesis and sensitivity to PARP inhibitors. Signature 3 identified by whole genome sequencing is also associated with homologous recombination deficiency and sensitivity to targeted therapies. In this review, we summarize molecular features and treatments of hereditary pancreatic cancer syndromes and surveillance procedures for unaffected high-risk cases. We also review transgenic murine models to gain a better understanding of carcinogenesis in hereditary pancreatic cancer.
APA, Harvard, Vancouver, ISO, and other styles
10

Ahn, Daniel H., and Tanios Bekaii-Saab. "Ampullary Cancer: An Overview." American Society of Clinical Oncology Educational Book, no. 34 (May 2014): 112–15. http://dx.doi.org/10.14694/edbook_am.2014.34.112.

Full text
Abstract:
Ampullary cancers are rare, accounting for only 0.2% of gastrointestinal cancers and approximately 7% of all periampullary cancers.1They arise from the ampullary complex, distal to the confluence of the common bile and pancreatic duct ( Fig. 1 ). In contrast to other periampullary malignancies, true ampullary cancers present earlier in their disease course with symptoms that result from biliary obstruction. It is often difficult to distinguish primary ampullary cancers from other periampullary cancers preoperatively. In early stages, ampullary cancers are surgically treated, similar to pancreatic cancers, and typically with a pancreatico-duodenoectomy (or Whipple procedure). Because of their earlier presentation, resection rates for all patients are much higher than other periampullary carcinomas. Moreover, their prognosis tends to be better than those with other periampullary- and pancreatic-originating cancers. In patients with true ampullary cancer, there is very limited data to guide physicians on the choice of therapy, largely because of the rarity of the disease and the paucity of related research. Herein, we provide an overview of the biology, histology, current therapeutic strategies, and potential future therapies for carcinomas arising from the ampulla of Vater.
APA, Harvard, Vancouver, ISO, and other styles
11

NK, Sunčana. "Occurrence of Pancreatic Cancer Associated Insulin Dependent Diabetes." Cancer Research and Cellular Therapeutics 1, no. 3 (September 8, 2017): 01–03. http://dx.doi.org/10.31579/2640-1053/016.

Full text
Abstract:
Patients with pancreatic cancer often present with non-specific symptoms and are often diagnosed at an advanced stage. The relationship between diabetes and the development of pancreatic cancer has been an area of intense research. In the present study we specifically aim to look at the hypothesis that the incidence of insulin dependent diabetes increases after the onset of pancreatic cancer. Materials and Methods: We retrospectively reviewed the chart of all pancreatic cancer patients in tumor registry admitted to University of Florida Tumor Registry in Jacksonville, Florida. Data was collective from January 2000 and December 2006. Each patient’s record was reviewed for histologic biopsy, demographic information, presence of risk factors, co-morbidities, presence and duration of diabetes. Assessment of diabetes was based on the guidelines provided by American Diabetes Association. Results: 82 patients were identified from the University of Florida Cancer Registry from the year 2000-2006. Complete data was available on 76 patients. Mean age at diagnosis was 66.4 years. 53 (69.7%) were African American, 23 (30.26%) were white. There was an equal male/female distribution of 1:1.07 (43 males; 40 females). 35 (46.0%) patients were smokers. Most common presentation was with obstructive jaundice (33/76 or 43.4%) followed by typical symptoms of weight loss, fatigue, abdominal and back pain (31/76 or 40.78%). In 11 (14.47%) patients, pancreatic cancer was noted as an incidental finding. Staging at the time of diagnosis was available in 76 patients. 48 (63.1%) patients were in Stage 4, 13 (17.1%) patients were in Stage 3, 10 (13.15%) patients were at stage 2 and 5 (6.5%) patients were in Stage 1. 15(19.7%) patients had diabetes at the time of diagnosis of pancreatic cancer. 5 (6.5%) developed one or more deep vein thrombosis (DVTs) after the diagnosis of PC. Diabetes was present in 15 (19.7%) for an average duration of 19 months. Only 4(26.6%) out of 15 patients were on insulin therapy before the diagnosis of pancreatic cancer. Six additional patients (an increase of 7.93%) developed diabetes after the diagnosis of pancreatic cancer. 13 (61.9%) of the 21 patients required insulin therapy after the diagnosis of pancreatic cancer. As many as 27 (35%) patients opted for hospice care after the diagnosis of pancreatic cancer. Whipple’s procedure or exploratory debulking surgery of the tumor was performed in 33 (43%) patients. 29 (38.1%) patients received Gemcitabine/carboplatin/5 FU based chemotherapy. Conclusion: We found that the Incidence of Insulin-dependent diabetes increased in patients diagnosed with pancreatic cancer.
APA, Harvard, Vancouver, ISO, and other styles
12

Lee, Cheong J., Joseph Dosch, and Diane M. Simeone. "Pancreatic Cancer Stem Cells." Journal of Clinical Oncology 26, no. 17 (June 10, 2008): 2806–12. http://dx.doi.org/10.1200/jco.2008.16.6702.

Full text
Abstract:
Cellular heterogeneity in cancer was observed decades ago by studies in mice which showed that distinct subpopulations of cells within a tumor mass are capable of driving tumorigenesis. Conceptualized from this finding was the stem-cell hypothesis for cancer, which suggests that only a specific subset of cancer cells within each tumor is responsible for tumor initiation and propagation, termed tumor initiating cells or cancer stem cells (CSCs). Recent data has been provided to support the existence of CSCs in human blood cell–derived cancers and solid organ tumors of the breast, brain, prostate, colon, and skin. Study of human pancreatic cancers has also revealed a specific subpopulation of cancer cells that possess the characteristics of CSCs. These pancreatic cancer stem cells express the cell surface markers CD44, CD24, and epithelial-specific antigen, and represent 0.5% to 1.0% of all pancreatic cancer cells. Along with the properties of self-renewal and multilineage differentiation, pancreatic CSCs display upregulation of important developmental genes that maintain self-renewal in normal stem cells, including Sonic hedgehog (SHH) and BMI-1. Signaling cascades that are integral in tumor metastasis are also upregulated in the pancreatic CSC. Understanding the biologic behavior and the molecular pathways that regulate growth, survival, and metastasis of pancreatic CSCs will help to identify novel therapeutic approaches to treat this dismal disease.
APA, Harvard, Vancouver, ISO, and other styles
13

Ghabache, B., J. Cole, and S. Vasireddy. "Pancreatic cancer in breast cancer patients: Incidence and relation with hormone receptor status." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 17079. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.17079.

Full text
Abstract:
17079 Background: There has been a long-standing interest in the role of estrogens in pancreatic tumors and several reports regarding the expression of hormone receptors in pancreatic tumors and the relation between estrogen stimulation and the development of pancreatic cancer have been inconsistent . This raised questions about the increased risk of pancreatic cancer among breast cancer survivors and the possible role of antihormonal therapy in the prevention and treatment of these malignancies. Methods: The Tumor registry at the Ochsner Clinic Foundation in New Orleans was queried to identify new cases of pancreatic cancer among patients previously diagnosed with breast cancer. This was done by matching data on pancreatic and breast cancer diagnosed between January 1996 and January 2006. For each case of pancreatic cancer, data was collected from the initial breast cancer pathology report, this included : Cancer type, Grade, Estrogen Receptor status, Progesterone Receptor, HER- 2 Receptor status , BRCA gene mutation and cancer stage on diagnosis. Clinic notes and radiology reports were also reviewed to determine the presence of risk factors for pancreatic cancer, the interval of time between the two diagnosis and the stage of breast cancer at the time of diagnosis of pancreatic cancer. Results: A total of 2,669 breast cancer cases were reviewed and 5 cases of pancreatic cancers were found among patients with a previous diagnosis of breast cancer. In all these cases the breast cancer tumor was positive for Estrogen and Progesteron receptor and negative for Her2 overexpression. The incidence of pancreatic cancer in this subgroup of patients (Breast cancer, ER+,PR+, HER2-) was 1% much higher than the incidence in the general female population. Conclusions: In our experience patients with breast cancer might have a higher risk of developping pancreatic cancer. This is especially true for patients whose tumors over-express the estrogen and progesterone receptors and which do not over-express the Her2 receptor. Further studies are needed to evaluate the overall incidence of pancreatic cancer in this population and to determine the role of anti-hotmonal therapy in the prevention of these cancers. No significant financial relationships to disclose.
APA, Harvard, Vancouver, ISO, and other styles
14

Kanamori, Akane, Daisuke Matsubara, Yurika Saitoh, Yuya Fukui, Noriko Gotoh, Shuichi Kaneko, Motoharu Seiki, Yoshinori Murakami, Jun-ichiro Inoue, and Takeharu Sakamoto. "Mint3 depletion restricts tumor malignancy of pancreatic cancer cells by decreasing SKP2 expression via HIF-1." Oncogene 39, no. 39 (August 21, 2020): 6218–30. http://dx.doi.org/10.1038/s41388-020-01423-8.

Full text
Abstract:
Abstract Pancreatic cancer is one of the most fatal cancers without druggable molecular targets. Hypoxia inducible factor-1 (HIF-1) is a heterodimeric transcriptional factor that promotes malignancy in various cancers including pancreatic cancer. Herein, we found that HIF-1 is accumulated in normoxic or moderate hypoxic areas of pancreatic cancer xenografts in vivo and is active even during normoxia in pancreatic cancer cells in vitro. This prompted us to analyze whether the HIF-1 activator Mint3 contributes to malignant features of pancreatic cancer. Mint3 depletion by shRNAs attenuated HIF-1 activity during normoxia and cell proliferation concomitantly with accumulated p21 and p27 protein in pancreatic cancer cells. Further analyses revealed that Mint3 increased transcription of the oncogenic ubiquitin ligase SKP2 in pancreatic cancer cells via HIF-1. This Mint3-HIF-1-SKP2 axis also promoted partial epithelial-mesenchymal transition, stemness features, and chemoresistance in pancreatic cancer cells. Even in vivo, Mint3 depletion attenuated tumor growth of orthotopically inoculated human pancreatic cancer AsPC-1 cells. Database and tissue microarray analyses showed that Mint3 expression is correlated with SKP2 expression in human pancreatic cancer specimens and high Mint3 expression is correlated with poor prognosis of pancreatic cancer patients. Thus, targeting Mint3 may be useful for attenuating the malignant features of pancreatic cancer.
APA, Harvard, Vancouver, ISO, and other styles
15

Zhao, Jiangang, Jiahui Li, Hans A. Schlößer, Felix Popp, Marie Christine Popp, Hakan Alakus, Karl-Walter Jauch, Christiane J. Bruns, and Yue Zhao. "Targeting Cancer Stem Cells and Their Niche: Current Therapeutic Implications and Challenges in Pancreatic Cancer." Stem Cells International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/6012810.

Full text
Abstract:
Cancer stem cells (CSCs) have been identified as a subpopulation of stem-like cancer cells with the ability of self-renewal and differentiation in hematological malignancies and solid tumors. Pancreatic cancer is one of the most lethal cancers worldwide. CSCs are thought to be responsible for cancer initiation, progression, metastasis, chemoresistance, and recurrence in pancreatic cancer. In this review, we summarize the characteristics of pancreatic CSCs and discuss the mechanisms involved in resistance to chemotherapy, the interactions with the niche, and the potential role in cancer immunoediting. We propose that immunotherapy targeting pancreatic CSCs, in combination with targeting the niche components, may provide a novel treatment strategy to eradicate pancreatic CSCs and hence improve outcomes in pancreatic cancer.
APA, Harvard, Vancouver, ISO, and other styles
16

Hu, Chunling, Holly LaDuca, Hermela Shimelis, Eric C. Polley, Jenna Lilyquist, Steven N. Hart, Jie Na, et al. "Multigene Hereditary Cancer Panels Reveal High-Risk Pancreatic Cancer Susceptibility Genes." JCO Precision Oncology, no. 2 (November 2018): 1–28. http://dx.doi.org/10.1200/po.17.00291.

Full text
Abstract:
Purpose The relevance of inherited pathogenic mutations in cancer predisposition genes in pancreatic cancer is not well understood. We aimed to assess the characteristics of patients with pancreatic cancer referred for hereditary cancer genetic testing and to estimate the risk of pancreatic cancer associated with mutations in panel-based cancer predisposition genes in this high-risk population. Methods Patients with pancreatic cancer (N = 1,652) were identified from a 140,000-patient cohort undergoing multigene panel testing of predisposition genes between March 2012 and June 2016. Gene-level mutation frequencies relative to Exome Aggregation Consortium and Genome Aggregation Database reference controls were assessed. Results The frequency of germline cancer predisposition gene mutations among patients with pancreatic cancer was 20.73%. Mutations in ATM, BRCA2, CDKN2A, MSH2, MSH6, PALB2, and TP53 were associated with high pancreatic cancer risk (odds ratio, > 5), and mutations in BRCA1 were associated with moderate risk (odds ratio, > 2). In a logistic regression model adjusted for age at diagnosis and family history of cancer, ATM and BRCA2 mutations were associated with personal history of breast or pancreatic cancer, whereas PALB2 mutations were associated with family history of breast or pancreatic cancer. Conclusion These findings provide insight into the spectrum of mutations expected in patients with pancreatic cancer referred for cancer predisposition testing. Mutations in eight genes confer high or moderate risk of pancreatic cancer and may prove useful for risk assessment for pancreatic and other cancers. Family and personal histories of breast cancer are strong predictors of germline mutations.
APA, Harvard, Vancouver, ISO, and other styles
17

Domagała-Haduch, Małgorzata, Anita Gorzelak-Magiera, Łukasz Michalecki, and Iwona Gisterek-Grocholska. "Radiochemotherapy in Pancreatic Cancer." Current Oncology 31, no. 6 (June 6, 2024): 3291–300. http://dx.doi.org/10.3390/curroncol31060250.

Full text
Abstract:
Despite the advancements made in oncology in recent years, the treatment of pancreatic cancer remains a challenge. Five-year survival rates for this cancer do not exceed 10%. Among the reasons contributing to poor treatment outcomes are the oligosymptomatic course of the tumor, diagnostic difficulties due to the anatomical location of the organ, and the unique biological features of pancreatic cancer. The mainstay of treatment for resectable cancer is surgery and adjuvant chemotherapy. For unresectable and metastatic cancers, chemotherapy remains the primary method of treatment. At the same time, for about thirty years, there have been attempts to improve treatment outcomes by using radiotherapy combined with systemic treatment. Unlike chemotherapy, radiotherapy has no established place in the treatment of pancreatic cancer. This paper addresses the topic of radiotherapy in pancreatic cancer as a valuable method that can improve treatment outcomes alongside chemotherapy.
APA, Harvard, Vancouver, ISO, and other styles
18

Lan, Bin, Siyuan Zeng, Robert Grützmann, and Christian Pilarsky. "The Role of Exosomes in Pancreatic Cancer." International Journal of Molecular Sciences 20, no. 18 (September 4, 2019): 4332. http://dx.doi.org/10.3390/ijms20184332.

Full text
Abstract:
Pancreatic cancer remains one of the deadliest cancers in the world, as a consequence of late diagnosis, early metastasis and limited response to chemotherapy, under which conditions the potential mechanism of pancreatic cancer progression requires further study. Exosomes are membrane vesicles which are important in the progression, metastasis and chemoresistance in pancreatic cancer. Additionally, they have been verified to be potential as biomarkers, targets and drug carriers for pancreatic cancer treatment. Thus, studying the role of exosomes in pancreatic cancer is significant. This paper focuses on the role of exosomes in the proliferation, metastasis and chemoresistance, as well as their potential applications for pancreatic cancer.
APA, Harvard, Vancouver, ISO, and other styles
19

Bruno, M. J., E. B. Haverkort, G. P. Tijssen, G. N. J. Tytgat, and D. J. van Leeuwen. "Placebo controlled trial of enteric coated pancreatin microsphere treatment in patients with unresectable cancer of the pancreatic head region." Gut 42, no. 1 (January 1, 1998): 92–96. http://dx.doi.org/10.1136/gut.42.1.92.

Full text
Abstract:
Background—Impeded flow of pancreatic juice due to mechanical obstruction of the pancreatic duct in patients with cancer of the pancreatic head region causes exocrine pancreatic insufficiency with steatorrhoea and creatorrhoea. This may contribute to the profound weight loss that often occurs in these patients.Aims—To investigate whether pancreatic enzyme replacement therapy prevents this weight loss.Patients—Twenty one patients with unresectable cancer of the pancreatic head region with suspected pancreatic duct obstruction, a biliary endoprosthesis in situ, and a Karnofsky performance status greater than 60.Methods—Randomised double blind trial of eight weeks with either placebo or high dose enteric coated pancreatin enzyme supplementation. All patients received dietary counselling.Results—The mean difference in the percentage change of body weight was 4.9% (p=0.02, 95% confidence interval for the difference: 0.9 to 8.9). Patients on pancreatic enzymes gained 1.2% (0.7 kg) body weight whereas patients on placebo lost 3.7% (2.2 kg). The fat absorption coefficient in patients on pancreatic enzymes improved by 12% whereas in placebo patients it dropped by 8% (p=0.13, 95% confidence interval for the difference: –6 to 45). The daily total energy intake was 8.42 MJ in patients on pancreatic enzymes and 6.66 MJ in placebo patients (p=0.04, 95% confidence interval for the difference: 0.08 to 3.44).Conclusions—Weight loss in patients with unresectable cancer of the pancreatic head region and occlusion of the pancreatic duct can be prevented, at least for the period immediately after insertion of a biliary endoprosthesis, by high dose enteric coated pancreatin enzyme supplementation in combination with dietary counselling.
APA, Harvard, Vancouver, ISO, and other styles
20

Yamaue, Hiroki, Seiko Hirono, Manabu Kawai, Ken-Ichi Okada, Motoki Miyazawa, Atsushi Shimizu, Yuji Kitahata, et al. "The characteristics of pancreatic neck cancer." Journal of Clinical Oncology 34, no. 4_suppl (February 1, 2016): 337. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.337.

Full text
Abstract:
337 Background: Pancreatic neck cancer occurs in the small region surrounded by the common hepatic artery (CHA), gastroduodenal artery (GDA), and portal vein (PV). The specific clinicopathological characteristics of pancreatic neck cancer remain unclear. This study aimed to identify specific biological behaviors of pancreatic neck cancer for the improvement of treatment outcomes. Methods: This study was a retrospective cohort study and comparative outcomes design. In 63 (19.4%) of 325 consecutive pancreatic cancer patients who underwent surgery, the tumor was located in the pancreatic neck. Clinicopathological characteristics and prognostic factors specific to pancreatic neck cancer were analyzed by comparison to those of pancreatic head or body/tail cancers. Results: The rates of radiographic and pathological PV and/or superior mesenteric vein (PV/SMV) invasion were higher in patients with pancreatic neck cancer (radiographic: 84.1%, pathological: 36.5%) than those with pancreatic head and body/tail cancers (radiographic, head: 67.3%, body/tail: 25.0%, pathological, head: 26.0%, body/tail: 6.3%). The most frequent lymph node metastasis was found in the region along the CHA in pancreatic neck cancer, and the spots most likely to show a positive surgical margin were the dissected surface of the PV and the root of the GDA and/or CHA. For pancreatic neck cancer patients, five independent poor prognostic factors were found: pathological PV/SMV invasion (P= 0.005), moderately or poorly differentiation (P= 0.001), positive lymph node ratio ≥ 0.1 (P< 0.001), surgical margin length ≤ 1 mm (P= 0.018), and no completion of planned postoperative adjuvant therapy (P< 0.001). Conclusions: Pancreatic neck cancer showed specific clinicopathological characteristics and prognostic factors after resection. Patients with these risk factors might need multimodality treatment strategies, including neoadjuvant therapy, in order to prolong the survival, although further studies will be necessary to confirm our findings.
APA, Harvard, Vancouver, ISO, and other styles
21

Mukherji, Reetu, Dipanjan Debnath, Marion L. Hartley, and Marcus S. Noel. "The Role of Immunotherapy in Pancreatic Cancer." Current Oncology 29, no. 10 (September 23, 2022): 6864–92. http://dx.doi.org/10.3390/curroncol29100541.

Full text
Abstract:
Pancreatic adenocarcinoma remains one of the most lethal cancers globally, with a significant need for improved therapeutic options. While the recent breakthroughs of immunotherapy through checkpoint inhibitors have dramatically changed treatment paradigms in other malignancies based on considerable survival benefits, this is not so for pancreatic cancer. Chemotherapies with modest benefits are still the cornerstone of advanced pancreatic cancer treatment. Pancreatic cancers are inherently immune-cold tumors and have been largely refractory to immunotherapies in clinical trials. Understanding and overcoming the current failures of immunotherapy through elucidating resistance mechanisms and developing novel therapeutic approaches are essential to harnessing the potential durable benefits of immune-modulating therapy in pancreatic cancer patients.
APA, Harvard, Vancouver, ISO, and other styles
22

Goggins, Michael. "Molecular Markers of Early Pancreatic Cancer." Journal of Clinical Oncology 23, no. 20 (July 10, 2005): 4524–31. http://dx.doi.org/10.1200/jco.2005.19.711.

Full text
Abstract:
Pancreatic cancer is a deadly disease and the fourth most common cause of cancer death in the United States. Since chemotherapy and radiotherapy have thus far largely failed to significantly improve the survival of patients with pancreatic ductal adenocarcinoma, there is considerable interest in identifying better diagnostic markers of pancreatic neoplasia. Not only could better markers improve the early diagnosis of pancreatic cancer and allow more patients to undergo curative surgical resection, but also could potentially be used for patients at high risk of developing pancreatic cancer to identify precancerous lesions while they are amenable to cure. A wealth of information has recently become available about gene expression, DNA methylation, and proteomics alterations that occur in pancreatic cancers creating hope that better diagnostic markers of pancreatic cancer will be soon forthcoming.
APA, Harvard, Vancouver, ISO, and other styles
23

Yoshida, Takeichi, Yasunobu Yamashita, and Masayuki Kitano. "Endoscopic Ultrasound for Early Diagnosis of Pancreatic Cancer." Diagnostics 9, no. 3 (July 24, 2019): 81. http://dx.doi.org/10.3390/diagnostics9030081.

Full text
Abstract:
Detection of small pancreatic cancers, which have a better prognosis than large cancers, is needed to reduce high mortality rates. Endoscopic ultrasound (EUS) is the most sensitive imaging modality for detecting pancreatic lesions. The high resolution of EUS makes it particularly useful for detecting small pancreatic lesions that may be missed by other imaging modalities. Therefore, EUS should be performed in patients with obstructive jaundice in whom computed tomography (CT) or magnetic resonance imaging (MRI) does not identify a definite pancreatic lesion. Interest in the use of EUS for screening individuals at high risk of pancreatic cancer, including those with intraductal papillary mucinous neoplasms (IPMNs) and familial pancreatic cancer is growing. Contrast-enhanced EUS can facilitate differential diagnosis of small solid pancreatic lesions as well as malignant cystic lesions. In addition, EUS-guided fine needle aspiration can provide samples of small pancreatic lesions. Thus, EUS and EUS-related techniques are essential for early diagnosis of pancreatic cancer.
APA, Harvard, Vancouver, ISO, and other styles
24

Vargas, Alejandra, Priyata Dutta, Eileen S. Carpenter, and Jorge D. Machicado. "Endoscopic Ultrasound-Guided Ablation of Premalignant Pancreatic Cysts and Pancreatic Cancer." Diagnostics 14, no. 5 (March 6, 2024): 564. http://dx.doi.org/10.3390/diagnostics14050564.

Full text
Abstract:
Pancreatic cancer is on the rise and expected to become the second leading cause of cancer-related death by 2030. Up to a one-fifth of pancreatic cancers may arise from mucinous pancreatic cysts, which are frequently present in the general population. Currently, surgical resection is the only curative approach for pancreatic cancer and its cystic precursors. However, only a dismal proportion of patients are eligible for surgery. Therefore, novel treatment approaches to treat pancreatic cancer and precancerous pancreatic cysts are needed. Endoscopic ultrasound (EUS)-guided ablation is an emerging minimally invasive method to treat pancreatic cancer and premalignant pancreatic cysts. Different ablative modalities have been used including alcohol, chemotherapy agents, and radiofrequency ablation. Cumulative data over the past two decades have shown that endoscopic ablation of mucinous pancreatic cysts can lead to cyst resolution in a significant proportion of the treated cysts. Furthermore, novel data are emerging about the ability to endoscopically ablate early and locally advanced pancreatic cancer. In this review, we aim to summarize the available data on the efficacy and safety of the different EUS-ablation modalities for the management of premalignant pancreatic cysts and pancreatic cancer.
APA, Harvard, Vancouver, ISO, and other styles
25

Szajda, Sławomir Dariusz, Napoleon Waszkiewicz, Sylwia Chojnowska, and Krzysztof Zwierz. "Carbohydrate markers of pancreatic cancer." Biochemical Society Transactions 39, no. 1 (January 19, 2011): 340–43. http://dx.doi.org/10.1042/bst0390340.

Full text
Abstract:
Pancreatic cancer is the fourth most common cause of death from cancer in the world and the sixth in Europe. Pancreatic cancer is more frequent in males than females. Worldwide, following diagnosis of pancreatic cancer, <2% of patients survive for 5 years, 8% survive for 2 years and <50% survive for only approx. 3 months. The biggest risk factor in pancreatic cancer is age, with a peak of morbidity at 65 years. Difficulty in the diagnosis of pancreatic cancer causes a delay in its detection. It is one of the most difficult cancers to diagnose and therefore to treat successfully. Additional detection of carbohydrate markers may offer a better diagnosis of pancreatic cancer. Carbohydrate markers of cancer may be produced by the cancer itself or by the body in response to cancer, whose presence in body fluids suggests the presence and growth of the cancer. The most widely used, and best-recognized, carbohydrate marker of pancreatic cancer is CA 19–9 [CA (carbohydrate antigen) 19–9]. However, the relatively non-specific nature of CA 19–9 limits its routine use in the early diagnosis of pancreatic cancer, but it may be useful in monitoring treatment of pancreatic cancer (e.g. the effectiveness of chemotherapy), as a complement to other diagnostic methods. Some other carbohydrate markers of pancreatic cancer may be considered, such as CEA (carcinoembryonic antigen), CA 50 and CA 242, and the mucins MUC1, MUC2 and MUC5AC, but enzymes involved in the processing of glycoconjugates could also be involved. Our preliminary research shows that the activity of lysosomal exoglycosidases, including HEX (N-acetyl-β-D-hexosaminidase), GAL (β-D-galactosidase), FUC (α-L-fucosidase) and MAN (α-D-mannosidase), in serum and urine may be used in the diagnosis of pancreatic cancer.
APA, Harvard, Vancouver, ISO, and other styles
26

Kumar, Lokender, Sanjay Kumar, Kumar Sandeep, and Sanjay Kumar Singh Patel. "Therapeutic Approaches in Pancreatic Cancer: Recent Updates." Biomedicines 11, no. 6 (June 1, 2023): 1611. http://dx.doi.org/10.3390/biomedicines11061611.

Full text
Abstract:
Cancer is a significant challenge for effective treatment due to its complex mechanism, different progressing stages, and lack of adequate procedures for screening and identification. Pancreatic cancer is typically identified in its advanced progression phase with a low survival of ~5 years. Among cancers, pancreatic cancer is also considered a high mortality-causing casualty over other accidental or disease-based mortality, and it is ranked seventh among all mortality-associated cancers globally. Henceforth, developing diagnostic procedures for its early detection, understanding pancreatic cancer-linked mechanisms, and various therapeutic strategies are crucial. This review describes the recent development in pancreatic cancer progression, mechanisms, and therapeutic approaches, including molecular techniques and biomedicines for effectively treating cancer.
APA, Harvard, Vancouver, ISO, and other styles
27

Yousaf, Muhammad Nadeem, Fizah S. Chaudhary, Amrat Ehsan, Alejandro L. Suarez, Thiruvengadam Muniraj, Priya Jamidar, Harry R. Aslanian, and James J. Farrell. "Endoscopic ultrasound (EUS) and the management of pancreatic cancer." BMJ Open Gastroenterology 7, no. 1 (May 2020): e000408. http://dx.doi.org/10.1136/bmjgast-2020-000408.

Full text
Abstract:
Pancreatic cancer is one of the leading causes of cancer-related mortality in western countries. Early diagnosis of pancreatic cancers plays a key role in the management by identification of patients who are surgical candidates. The advancement in the radiological imaging and interventional endoscopy (including endoscopic ultrasound (EUS), endoscopic retrograde cholangiopancreatography and endoscopic enteral stenting techniques) has a significant impact in the diagnostic evaluation, staging and treatment of pancreatic cancer. The multidisciplinary involvement of radiology, gastroenterology, medical oncology and surgical oncology is central to the management of patients with pancreatic cancers. This review aims to highlight the diagnostic and therapeutic role of EUS in the management of patients with pancreatic malignancy, especially pancreatic ductal adenocarcinoma.
APA, Harvard, Vancouver, ISO, and other styles
28

Cheng, Xianliang, Gang Zhao, and Yunqi Zhao. "Combination Immunotherapy Approaches for Pancreatic Cancer Treatment." Canadian Journal of Gastroenterology and Hepatology 2018 (2018): 1–7. http://dx.doi.org/10.1155/2018/6240467.

Full text
Abstract:
Pancreatic ductal adenocarcinoma is a lethal malignant disease with a very low medium survival. Currently, metastatic pancreatic cancer poorly responds to conventional treatments and exhibits an acute resistance to most chemotherapy. Few approaches have been shown to be effective for metastatic pancreatic cancer treatment. Novel therapeutic approaches to treat patients with pancreatic adenocarcinoma are in great demand. Last decades, immunotherapies have been evaluated in clinical trials and received great success in many types of cancers. However, it has very limited success in treating pancreatic cancer. As pancreatic cancer poorly responds to many single immunotherapeutic agents, combination immunotherapy was introduced to improve efficacy. The combination therapies hold great promise for enhancing immune responses to achieve better therapeutic effects. This review summarizes the existing and potential combination immunotherapies for the treatment of pancreatic cancer.
APA, Harvard, Vancouver, ISO, and other styles
29

Hruban, Ralph H., and Giuseppe Zamboni. "Pancreatic Cancer." Archives of Pathology & Laboratory Medicine 133, no. 3 (March 1, 2009): 347–49. http://dx.doi.org/10.5858/133.3.347.

Full text
APA, Harvard, Vancouver, ISO, and other styles
30

O'Neal, Cheryl, and Joyce Emerson Cleary. "Pancreatic Cancer." American Journal of Nursing 100, no. 4 (April 2000): 23. http://dx.doi.org/10.2307/3521931.

Full text
APA, Harvard, Vancouver, ISO, and other styles
31

Friess, Helmut, and Florian Scheufele. "Pancreatic cancer." Translational Gastroenterology and Hepatology 5 (July 2020): 32. http://dx.doi.org/10.21037/tgh.2019.12.15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
32

Murr, M. M., M. G. Sarr, A. J. Oishi, and J. A. van Heerden. "Pancreatic cancer." CA: A Cancer Journal for Clinicians 44, no. 5 (September 1, 1994): 304–18. http://dx.doi.org/10.3322/canjclin.44.5.304.

Full text
APA, Harvard, Vancouver, ISO, and other styles
33

Rosenberg, Lawrence. "Pancreatic Cancer." Drugs 59, no. 5 (May 2000): 1071–89. http://dx.doi.org/10.2165/00003495-200059050-00004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
34

Park, Wungki, Akhil Chawla, and Eileen M. O’Reilly. "Pancreatic Cancer." JAMA 326, no. 9 (September 7, 2021): 851. http://dx.doi.org/10.1001/jama.2021.13027.

Full text
APA, Harvard, Vancouver, ISO, and other styles
35

Pawlik, Timothy M. "Pancreatic Cancer." Surgical Oncology Clinics of North America 30, no. 4 (October 2021): xiii—xv. http://dx.doi.org/10.1016/j.soc.2021.07.002.

Full text
APA, Harvard, Vancouver, ISO, and other styles
36

Okamura, Yukiyasu. "Pancreatic Cancer." Journal of Nihon University Medical Association 80, no. 6 (December 1, 2021): 275–80. http://dx.doi.org/10.4264/numa.80.6_275.

Full text
APA, Harvard, Vancouver, ISO, and other styles
37

Rajkomar, Kheman, and Nigel B. Jamieson. "Pancreatic cancer." Surgery (Oxford) 40, no. 4 (April 2022): 237–48. http://dx.doi.org/10.1016/j.mpsur.2022.02.001.

Full text
APA, Harvard, Vancouver, ISO, and other styles
38

RUBINSON, DOUGLAS A., and MATTHEW B. YURGELUN. "Pancreatic Cancer." Hematology/Oncology Clinics of North America 36, no. 5 (October 2022): i. http://dx.doi.org/10.1016/s0889-8588(22)00108-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
39

Song, Si Young. "Pancreatic Cancer." Journal of the Korean Medical Association 46, no. 8 (2003): 729. http://dx.doi.org/10.5124/jkma.2003.46.8.729.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

Abate-Daga, Daniel, Steven A. Rosenberg, and Richard A. Morgan. "Pancreatic cancer." OncoImmunology 3, no. 6 (June 2014): e29194. http://dx.doi.org/10.4161/onci.29194.

Full text
APA, Harvard, Vancouver, ISO, and other styles
41

Tuma, Rabiya S. "Pancreatic Cancer." Oncology Times 35, no. 4 (February 2013): 6–8. http://dx.doi.org/10.1097/01.cot.0000427826.53087.1a.

Full text
APA, Harvard, Vancouver, ISO, and other styles
42

Tuma, Rabiya S. "Pancreatic Cancer." Oncology Times 35, no. 4 (February 2013): 8. http://dx.doi.org/10.1097/01.cot.0000427827.53087.53.

Full text
APA, Harvard, Vancouver, ISO, and other styles
43

Carlson, Robert H. "Pancreatic Cancer." Oncology Times 36, no. 18 (September 2014): 56–58. http://dx.doi.org/10.1097/01.cot.0000454899.51058.3c.

Full text
APA, Harvard, Vancouver, ISO, and other styles
44

Carlson, Robert H. "Pancreatic Cancer." Oncology Times 36, no. 18 (September 2014): 27. http://dx.doi.org/10.1097/01.cot.0000454903.81552.bd.

Full text
APA, Harvard, Vancouver, ISO, and other styles
45

Susman, Ed. "Pancreatic Cancer." Oncology Times 37, no. 4 (February 2015): 28–30. http://dx.doi.org/10.1097/01.cot.0000461864.07623.89.

Full text
APA, Harvard, Vancouver, ISO, and other styles
46

Stockwell, Serena. "Pancreatic Cancer." Oncology Times 37, no. 18 (September 2015): 31. http://dx.doi.org/10.1097/01.cot.0000471991.33987.c8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
47

Carlson, Robert H. "Pancreatic Cancer." Oncology Times 37, no. 23 (December 2015): 40–41. http://dx.doi.org/10.1097/01.cot.0000475711.27331.70.

Full text
APA, Harvard, Vancouver, ISO, and other styles
48

Watson, John, Katrina Hydon, and Robert Adair. "Pancreatic cancer." InnovAiT: Education and inspiration for general practice 9, no. 8 (July 28, 2016): 490–95. http://dx.doi.org/10.1177/1755738016655559.

Full text
APA, Harvard, Vancouver, ISO, and other styles
49

Carlson, Robert H. "Pancreatic Cancer." Oncology Times 29, no. 2 (January 2007): 43–44. http://dx.doi.org/10.1097/01.cot.0000265649.02207.a8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
50

Tuma, Rabiya S. "Pancreatic Cancer." Oncology Times 29, no. 3 (February 2007): 44–45. http://dx.doi.org/10.1097/01.cot.0000266379.83708.0b.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Pancreatic cancer' for other source types:
Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography