Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an attempt to improve the guidelines for concurrent management of concomitant abdominal aortic aneurysm (AAA) and symptomatic malignancy, a retrospective study was undertaken. A total of 186 AAA repairs were performed electively, and 25 patients (13.4%) had concurrent symptomatic malignancy from April 1986 to March 1997. Fourteen patients underwent a one-stage operation, including five abdominoperineal rectal resections, four subtotal gastrectomies, three total gastrectomies, and two right hemicolectomies. Eleven others underwent a two-stage operation, including four with total gastrectomy and left hemicolectomy followed by AAA repair, as well as two with right hemicolectomy and one with left hemicolectomy prior to AAA repair. There were no operative deaths or severe postoperative complications. Of the 25 patients, 22 (88.0%) are still alive during follow-up ranging from 8 months to 11 years. Our surgical approach to both lesions is as follows: (1) Using the transperitoneal approach alone, subtotal gastrectomy and abdominoperineal rectal resection can be safely done simultaneously. (2) Although total gastrectomy can also be performed concurrently, the approach used for each lesion is separate. (3) Colorectal resection is generally done separately. However, a one-stage operation can be performed using the thromboexclusion procedure for AAA repair in patients with right-sided colonic cancer or a temporary transverse colostomy for left-sided colorectal cancer.
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PMID:Surgical strategy for abdominal aortic aneurysm with concurrent symptomatic malignancy. 993 94

The therapeutic approach to a patient who has an abdominal aortic aneurysm (AAA) and an intraabdominal nonvascular surgical disorder simultaneously remains controversial. To establish guidelines for the management of those patients, a retrospective review of patients who had concomitant AAA and intraabdominal nonvascular surgical disorders was undertaken. During the period January 1988 to December 1997 a series of 162 patients underwent surgical repairs of AAA in our hospital. Among them 16 patients (9.9%) had several kinds of intraabdominal nonvascular surgical disorders, and 13 underwent one-stage operation for both diseases. That is, cholelithiasis coexisted in five patients, inguinal hernia in four, gastric cancer in two, and retroperitoneal tumor and renal tumor in one each. All AAAs were the infrarenal type, and there were no inflammatory or ruptured aneurysms. In cases of cholelithiasis coexistent with AAA, aneurysmectomy was performed first. After tight closure of the retroperitoneum, cholecystectomy was done. In cases of cholelithiasis coexistent with AAA, aneurysmectomy was performed first. After tight closure of the retroperitoneum, cholecystectomy was done. In cases of inguinal hernia coexistent with AAA, the AAA was first replaced with a prosthetic vascular graft and a residual piece of the graft was used as a patch for hernioplasty. This procedure was similar to laparoscopic hernioplasty. In two cases of gastric cancer concomitant with AAA, the AAA was first replaced. Subtotal gastrectomy with D2 lymphatic dissection was done after tight closure of the retroperitoneum. A drain was inserted into the epiploic foramen to detect anastomotic leakage. A retroperitoneal tumor coexisting with AAA was dissected and resected en bloc with the aneurysmal wall because the tumor firmly adhered to the aneurysm. The abdominal aorta was then replaced with a prosthetic graft. In a case of renal tumor concomitant with AAA, nephrectomy was done first to perform a complete lymphatic dissection around the renal artery. Then AAA repair was performed with a conventional procedure. There were no fatal complications, such as pneumonitis, hemorrhage, anastomotic leakage, or graft infection. All 13 patients were discharged from our hospital and are currently free from recurrence of malignancy or hernia. In summary, properly selected one-stage operations for intraabdominal nonvascular surgical disorders and AAA may be safe and bring physical and economic benefit to the patient.
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PMID:Intraabdominal nonvascular operations combined with abdominal aortic aneurysm repair. 1008 95

ErbB-2 is overexpressed in several human cancers and conveys a transforming activity that is dependent on tyrosine kinase activity. Antibodies and T cells to ErbB-2 have been isolated from cancer patients, indicating ErbB-2 as a potential target of active vaccination. In this study, 3 mutant ErbB-2 DNA constructs encoding full-length, ErbB-2 proteins were tested as tumor vaccines. To eliminate tyrosine kinase activity, the ATP binding lysine residue 753 was substituted with alanine by replacing codon AAA with GCA in mutant ErbB-2A. To direct recombinant ErbB-2 to the cytoplasm where major histocompatibility complex (MHC) I peptide processing takes place, the endoplasmic reticulum (ER) signal sequence was deleted in cyt ErbB-2. The third construct cyt ErbB-2A contained cytoplasmic ErbB-2 with the K to A mutation. Expression of recombinant proteins was measured by flow cytometry in transfected murine mammary tumor cell line D2F2. Transmembrane ErbB-2 and ErbB-2A were readily detected. Cytoplasmic ErbB-2 and ErbB-2A were detected only after the transfected cells were incubated overnight with a proteasome inhibitor, indicating prompt degradation upon synthesis. ErbB-2 autophosphorylation was eliminated by the K to A mutation as demonstrated by Western blot analysis. Growth of ErbB-2-positive tumor in BALB/c mice was inhibited after vaccination with ErbB-2 or ErbB-2A, but not with cyt ErbB-2 or cyt ErbB-2A. ErbB-2A that is free of tyrosine kinase activity is a potential candidate for anticancer vaccination. The 3 mutant constructs should be useful tools to delineate the role of individual immune effector cell in ErbB-2-specific antitumor immunity and to develop strategies for enhancing such immunity.
Int J Cancer 1999 May 31
PMID:Protection against mammary tumor growth by vaccination with full-length, modified human ErbB-2 DNA. 1032 28

Mxi1 is thought to negatively regulate Myc function and may therefore be a potential tumor suppressor gene. Little effort has yet been made to find alterations involving this gene in human solid tumors. We screened 31 human gastric cancers, 7 esophageal cancers, 85 bone and soft tissue tumors of various types, including 4 neurofibrosarcomas. We also examined 29 human tumor cell lines consisting of 12 esophageal cancers, 7 glioma/glioblastomas and 10 others for Mxi1 mutations in exons 1, 2, 4 (HLH domain), 5 and 6. Polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and subsequent sequencing revealed three distinct polymorphisms in the intron-exon boundary upstream from exon 6. We discovered a missense mutation, GCA to GTA (Ala 54 Val), in exon 2 in a neurofibrosarcoma patient (case 1), two missense mutations, AAA to CAA (Lys 118 Gln) and GAA to GGA (Glu 154 Gly) in exon 5 of another neurofibrosarcoma patient (case 2), and 3 amino acid substitutions, GTG to GCG (Val 179 Ala), GTT to GCT (Val 181 Ala) and TTC to CTC (Phe 186 Leu), in a third neurofibrosarcoma patient (case 3). In case 3, loss of heterozygosity was also demonstrated by informative (TTC)3/(TTC)2 polymorphism. Our data demonstrate that mutations occur in the Mxi1 gene in neurofibrosarcoma. Missense mutations in the functional domain of Mxi1 in these cases may be involved in the pathogenesis of neurofibrosarcoma.
Jpn J Cancer Res 1999 Jul
PMID:Mxi1 mutations in human neurofibrosarcomas. 1047 Feb 86

Li-Fraumeni syndrome is an autosomal dominant disorder that is characterized by various types of cancer in childhood and adult cases. Although hereditary TP53 mutation is very rare in different human cancers, it has been frequently reported in Li-Fraumeni syndrome. On the other hand, hereditary mutations of TP57KIP2, P15INK4B, and P16INK4A, which affect the cell cycle similar to TP53, were observed in some types of cancer. In a Turkish family with the diagnosis of Li-Fraumeni syndrome, we analyzed the mutation pattern of TP53, P57KIP2, P15INK4B, and P16INK4A in the peripheral blood, and loss of heterozygosity (homo/hemizygous deletion) pattern of TP53 and P15INK4B/P16INK4A in two tumor tissues. The propositus had a seminoma, his daughter a medulloblastoma, and one of his healthy cousins, a TP53 codon 292 missense point mutation (AAA-->ATA; Lys-->Ile) in the peripheral blood cells. Tumor tissue obtained from the propositus with the seminoma revealed loss of heterozygosity in the TP53 gene. In the analyses of tumor tissues from the propositus and his daughter, a P16INK4A codon 94 missense point mutation (GCG-->GAG; Ala-->Glu) was observed with the hereditary TP53 mutation. P16INK4A codon 94 mutation observed in our family is a novel mutation in Li-Fraumeni syndrome. No other gene alteration in TP53, P57KIP2, P15INK4B, and P16INK4A was observed. Existence of the P16INK4A mutation and the hereditary TP53 mutation with or without loss of heterozygosity in the TP53 gene (seminoma/medulloblastoma) may be evidence for a common mechanism involved in tumorogenesis. The gene alterations in TP53 and P16INK4A genes may be used as tumor markers in our family.
Cancer Genet Cytogenet 1999 Sep
PMID:Hereditary TP53 codon 292 and somatic P16INK4A codon 94 mutations in a Li-Fraumeni syndrome family. 1572 47

Juvenile polyposis is an uncommon condition characterized by the development of multiple (usually more than 5) juvenile polyps in the gastrointestinal tract, especially in the colon. This disease usually occurs during childhood, and is inherited in an autosomal dominant fashion. It has been suggested that the dpc4 (deleted in pancreatic carcinoma, locus 4) gene, which is located on chromosome 18q21.1, might cause juvenile polyposis. The dpc4 (smad4) gene is a candidate tumor-suppressor gene and may play a role in the TGF-beta-signaling pathway. To confirm the idea that alterations of the dpc4 gene may result in juvenile polyposis, we screened 5 Korean juvenile-polyposis patients by PCR-SSCP (single-strand conformation polymorphism) analysis and bi-directional sequencing. There were germline mutations of the dpc4 gene in 3 out of the 5 patients: 2 had a genetic alteration in exon 9 and the third had a mutation in exon 8. These germline mutations occurred in the C-terminus of the dpc4 gene, similar to most published mutations. One patient exhibited a non-sense mutation (codon 388), which changed a glutamine codon (CAG) to a stop codon (TAG). The second patient harbored a mis-sense mutation (codon 390), causing a non-conservative amino-acid change <glutamate (GAA) to lysine (AAA)>. The third patient had a mis-sense mutation in exon 8 (codon 361), which altered an arginine codon (CGC) into a histidine codon (CAC).
Int J Cancer 2000 May 15
PMID:Germline mutations of the dpc4 gene in Korean juvenile polyposis patients. 1079 67

The management of simultaneously occurring abdominal aortic aneurysm and malignancy is controversial. It is unclear whether to treat the aneurysm first or the malignancy, or both simultaneously. If the malignancy is resected first there is a risk of postoperative rupture of the aneurysm. If simultaneous surgery is performed there is a risk of prosthetic graft infection. This condition leads to many therapeutic problems which, by the light of 18 personal cases occurred in almost ten years and the recent literature, are discussed in this paper.
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PMID:[The surgery of abdominal aortic aneurysms synchronous with neoplastic lesions (apropos of 18 personal observations)]. 1080 74

A deficiency in DNA repair is associated with increased cancer risk. Inter-individual variations in DNA repair capacity observed in humans may result from genetic polymorphisms in DNA repair genes. In order to provide a basis for future functional and molecular epidemiology studies on cancer susceptibility, we screened 35 individuals for polymorphisms in coding regions of XPA and XPB genes involved in nucleotide excision repair (NER). Relevant cDNA sequences were amplified by PCR, sequenced with fluorescently labeled terminators and analyzed with automated sequencer. Two polymorphisms in XPB were found: AAA-->AGA (445A>G; GenBank M31899) causing K117R substitution and GGC-->TGC (1299G>T; GenBank M31899) causing G402C exchange. Also, two polymorphisms in XPB were detected: CGA-->CAA (709G>A; GenBank D14533) causing R228Q exchange, and A-->G (23A>G; GenBank D14533) substitution in the 5' non-coding region of the gene. The three aforementioned amino acid substitutions were uncommon in this population (1.4%). In contrast, the substitution located 4 nucleotides upstream of the ATG start codon of XPB was frequent (57%). To our best knowledge this is the first report of these sequence variants. The location of these polymorphisms in evolutionary conserved regions suggest that they may be of functional significance.
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PMID:Identification of four single nucleotide polymorphisms in DNA repair genes: XPA and XPB (ERCC3) in Polish population. 1086 89

We report a case of ruptured abdominal aortic aneurysm (AAA) in a patient receiving chemotherapy for pancreatic cancer. We reviewed the literature on the effects of corticosteroids and chemotherapy on aaa formation and discuss possible mechanisms for drug action to promote aneurysm expansion and rupture. If cancer and AAA coincide and curative chemotherapy is possible, a potential impact of chemotherapy on AAA expansion should be considered.
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PMID:Acute enlargement and subsequent rupture of an abdominal aortic aneurysm in a patient receiving chemotherapy for pancreatic carcinoma. 1124 Nov 50

Abdominal aortic aneurysm and cholelithiasis are two common diseases in the elderly population. The prevalence of abdominal aortic aneurysms ranges between 1.8 and 6.6% in autoptic series and it's estimated that 2.5% of the over sixty year old population is affected. Carcinoma of the gallbladder is the most common malignant tumor of the biliary tract and in the United States is the fifth most frequent digestive tract malignancy; it's incidence ranges between 2 to 10 cases of 100,000 persons/year. No adequate guidelines are now available to assist the surgeon, in the case of concomitant gallbladder disease and abdominal aortic aneurysm. In this paper the management of abdominal aortic aneurysm in a patient with gallbladder disease is discussed in order to assist the surgeon deciding whether to perform concomitant aneurysm resection and cholecystectomy. In 162 aneurysmectomies (1987-1997) 18 (11.11%) patients underwent combined aneurysmectomy and cholecystectomy operation. The patients ranged in age from 49 to 88 years (average 69 years). In two cases the anatomo-histological specimen examinations (twelve sections) demonstrated a gallbladder carcinoma. The overall mortality rate was 5.56% either for aneurysmectomy alone or for combined therapy. In case of abdominal aortic aneurysm and concomitant gallbladder disease, in choosing simple endoaneurysmectomy, the surgeon has to consider the risk of early and late complications of leaving a diseased gallbladder in place. In case of concomitant performance of both operations, the risks of a possible septic graft contamination must be considered. We believe that the patient may be best served by performing the vascular and nonvascular procedures in the same operation. In this paper a new proof, till now never considered in the international literature, is presented to support our opinion: the possibility of concomitant unknown cancer or precancerous lesions in a lithiasic gallbladder. Diagnosis of these lesions is, indeed, not easy to perform in the preoperative phase and is often a postoperative anatomo-histological detection.
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PMID:Two incidental cases of abdominal aortic aneurysm and gallbladder cancer. Further data influencing the management of patients affected by aneurysm and gallbladder disease. 1095 49


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