K-ras Oncogene Mutations Indicate Malignancy in Cystic Tumors of the Pancreas

Bartsch, Detlef K.; Daniel, Bastian; Barth, Peter; Schudy, Andreas; Nies, C.; Kisker, Oliver; Wagner, Hans‐Joachim; Rothmund, M.

doi:10.1097/00000658-199807000-00012

Cited by 81 publications

(48 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Neither ras gene family mutations nor alterations in p53 have been found in SPT (Lee et al, 1997;Bartsch et al, 1998). Our 5 cases confirmed this data.…”

Section: Solid Pseudopapillary Tumourssupporting

confidence: 88%

Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis

et al. 2001

View full text Add to dashboard Cite

Summary Alterations of K-ras, p53, p16 and DPC4/Smad4 characterize pancreatic ductal cancer (PDC). Reports of inactivation of these latter two genes in pancreatic endocrine tumours (PET) suggest that common molecular pathways are involved in the tumorigenesis of pancreatic exocrine and endocrine epithelia. We characterized 112 primary pancreatic tumours for alterations in p16 and DPC4 and immunohistochemical expression of DPC4. The cases included 34 PDC, 10 intraductal papillary-mucinous tumours (IPMT), 6 acinar carcinomas (PAC), 5 solid-pseudopapillary tumours (SPT), 16 ampulla of Vater cancers (AVC) and 41 PET. All tumours were also presently or previously analysed for K-ras and p53 mutations and allelic loss at 9p, 17p and 18q. Alterations in K-ras, p53, p16 and DPC4 were found in 82%, 53%, 38% and 9% of PDC, respectively and in 47%, 60%, 25% and 6% of AVC. Alterations in these genes were virtually absent in PET, PAC or SPT, while in IPMT only K-ras mutations were present (30%). Positive immunostaining confirmed the absence of DPC4 alterations in all IPMT, SPT, PAC and PET, while 47% of PDC and 38% of AVC were immunonegative. These data suggest that pancreatic exocrine and endocrine tumourigenesis involves different genetic targets and that among exocrine pancreatic neoplasms, only ductal and ampullary cancers share common molecular events.

show abstract

“…Neither ras gene family mutations nor alterations in p53 have been found in SPT (Lee et al, 1997;Bartsch et al, 1998). Our 5 cases confirmed this data.…”

Section: Solid Pseudopapillary Tumourssupporting

confidence: 88%

Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis

et al. 2001

View full text Add to dashboard Cite

show abstract

“…82 Solid-pseudopapillary neoplasms lack the genetic alterations of infiltrating ductal adenocarcinomas (KRAS, p16, DPC4, and p53 genes). 53,83,186,190,[196][197][198] Almost all, however, have somatic point mutations in exon 3 of the b-catenin gene, 83,189 implicating the same genetic pathway that is abnormal in acinar neoplasms (acinar cell carcinoma and pancreatoblastoma). As expected in the presence of b-catenin activation, solid-pseudopapillary neoplasms typically have cyclin D1 overexpression.…”

Section: Solid-pseudopapillary Neoplasmmentioning

confidence: 99%

Nonductal neoplasms of the pancreas

2007

View full text Add to dashboard Cite

Although the majority of pancreatic neoplasms are infiltrating ductal adenocarcinomas or other neoplasms with ductal differentiation, neoplasms with acinar, endocrine, mixed, or uncertain differentiation constitute a diverse and distinctive group. The most common and best-characterized nonductal neoplasms are pancreatic endocrine neoplasm, acinar cell carcinoma, pancreatoblastoma, and solid pseudopapillary neoplasm. This review details the clinical and pathologic features of these nonductal neoplasms, highlighting diagnostic criteria including the use of specific immunohistochemical stains to define the cellular differentiation of the neoplasms. Modern Pathology (2007) 20, S94-S112.

show abstract

“…The first attempt to vaccinate patients with pancreatic cancer involved the vaccination with large amounts of autologous antigen presenting cells pulsed with K-Ras [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21] . Five patients with pancreatic carcinoma and identified ras mutations participated in this study, 76 none of whom showed any T cell responsiveness against any of the Ras mutant peptides before vaccination.…”

Section: Activated Ras As a Tumor Antigenmentioning

confidence: 99%

Modulation of the immune response and tumor growth by activated Ras

Weijzen

Kast

1999

Leukemia

View full text Add to dashboard Cite

As a result of its transforming abilities, activated Ras is expressed in a great number of cancers. The ras mutation frequency varies between 95% in pancreatic cancer and 5% in breast cancer. In leukemia, the highest frequency (30%) is found in acute myeloid leukemia. The presence of ras mutations has been correlated with a poor prognosis and negative clinical outcome. This suggests that mutated Ras activates mechanisms, which favor tumor growth, enhance the metastatic capacity of tumors or modulate tumor-specific immune responses. Several new functions of Ras, such as downregulation of major histocompatibility complex molecules, upregulation of certain cytokines, growth factors and degradative enzymes have been uncovered in the last decade. Additionally, mutated Ras can also serve as a primary target for the development of immunotherapy or drug therapy. This review will discuss the mechanisms by which Ras expressing tumors are able to evade destruction by the immune system and enhance their growth and metastatic potential. It will further elaborate on the attempts to develop successful immunotherapy and drug therapy targeting Ras expressing tumors.

show abstract

K-ras Oncogene Mutations Indicate Malignancy in Cystic Tumors of the Pancreas

Cited by 81 publications

References 32 publications

Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis

Pancreatic tumours: molecular pathways implicated in ductal cancer are involved in ampullary but not in exocrine nonductal or endocrine tumorigenesis

Nonductal neoplasms of the pancreas

Modulation of the immune response and tumor growth by activated Ras

Contact Info

Product

Resources

About