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Tipos de Cancer / Cánceres Gastrointestinal / Cáncer de la Vesícula / Recursos de NCI
National Cancer Institute®
Ultima Vez Modificado: 1 de agosto del 2002
1
UI - 12090103
AU - Roa I; de Aretxabala X; Araya JC; Villaseca M; Roa J; Gilda IT; Burgos
TI -
L; Munoz S
[Morphological prognostic elements in gallbladder cancer]
SO - Rev Med Chil 2002 Apr;130(4):387-95
AD - Departamento de Anatomia Patologica y Cirugia Facultad de Medicina,
Unidad de Epidemiologia Clinica, Universidad de la Frontera, Chile.
iroa@ufro.cl
BACKGROUND: The exact survival rates and prognostic factors of
gallbladder cancer are still incompletely known. AIM: To report the
actuarial survival of patients with gallbladder cancer. MATERIAL AND
METHODS: Six hundred thirty seven women, aged 59 years old as a mean and
108 men, aged 64 years old as a mean, with gallbladder cancer are
reported. Patients were followed for up to 150 months. RESULTS: Two
hundred twenty four patients had an early and 521 had an advanced
carcinoma. Overall survival was 38% at ten years. Sex or ethnic origin
did not influence survival. Early tumors had a 92% survival at 10 years
whereas the survival of advanced tumors was 16% at 5 years. Subserous
tumors had a 5 years survival of 32% whereas serous tumors had a 5 years
survival of 11%. Well-differentiated advanced tumors had a significantly
better survival than moderately or poorly differentiated tumors.
Vascular or lymphatic infiltration was also associated to a lower
survival. All patients with advanced tumors and vascular infiltration
died before 5 years. CONCLUSIONS: Tumor infiltration and differentiation
degree were the most important prognostic independent factors in
gallbladder cancer.
2
UI - 11992815
AU - Serra I; Diehl AK
TI -
Number and size of stones in patients with asymptomatic and symptomatic
gallstones and gallbladder carcinoma.
SO - J Gastrointest Surg 2002 Mar-Apr;6(2):272-3; discussion 273
3
UI - 12131166
AU - Wolfson WL
TI -
Colloid carcinomas of the pancreas and periamullary region.
SO - Am J Surg Pathol 2002 Jul;26(7):952; discussion 952-3
4
UI - 12130444
AU - Yoshimitsu K; Honda H; Shinozaki K; Aibe H; Kuroiwa T; Irie H; Chijiiwa
TI -
K; Asayama Y; Masuda K
Helical CT of the local spread of carcinoma of the gallbladder:
evaluation according to the TNM system in patients who underwent
surgical resection.
SO - AJR Am J Roentgenol 2002 Aug;179(2):423-8
AD - Department of Clinical Radiology, Kyushu University Graduate School of
Medical Sciences, 3-1-1, Maidashi, Higashi-ku Fukuoka 812-8582, Japan.
OBJECTIVE: Our aim was to evaluate the performance of helical CT as an
aid in the preoperative diagnosis of the spread of carcinomas of the
gallbladder. MATERIALS AND METHODS: Two radiologists retrospectively
reviewed both hard-copy and soft-copy (on a monitor with multiplanar
reconstruction capability) versions of helical CT scans (3-mm
collimation and 3-mm reconstruction) of 21 patients who had undergone
surgical resection for carcinomas of the gallbladder. The local spread
of the disease was evaluated according to the TNM system, and the
results were correlated to the pathologic findings. Inter- and
intraobserver differences were checked with kappa statistics. Results of
the consensus interpretations were used to calculate sensitivity,
specificity, and accuracy of helical CT. RESULTS: No significant inter-
or intraobserver differences were found in any T category evaluation.
The sensitivities of the hard-copy consensus interpretations in the
diagnosis of T1, T2, T3, and T4 lesions were 33%, 64%, 80%, and 100%,
respectively; specificities of hard-copy interpretations were 94%, 80%,
81%, and 95%, respectively. For soft-copy (monitor) consensus
interpretations, the sensitivities for the diagnosis of T1, T2, T3, and
T4 lesions were 33%, 73%, 80%, and 100%, respectively; the specificities
of soft-copy interpretations were 94%, 80%, 88%, and 95%, respectively.
Overall accuracy of the hard-copy interpretation was 83%; the overall
accuracy of the soft-copy interpretation was not significantly
different-86%. CONCLUSION: Helical CT provided 83-86% accuracy in the
diagnosis of the local extent of carcinomas of the gallbladder, showing
acceptable sensitivity and specificity for the T2 and more advanced
lesions but poor sensitivity for the T1 lesions. Use of a monitor with
multiplanar reconstructions of the CT data did not significantly improve
the diagnostic accuracy.
5
UI - 11948128
AU - Asano T; Shoda J; Ueda T; Kawamoto T; Todoroki T; Shimonishi M; Tanabe
TI -
T; Sugimoto Y; Ichikawa A; Mutoh M; Tanaka N; Miwa M
Expressions of cyclooxygenase-2 and prostaglandin E-receptors in
carcinoma of the gallbladder: crucial role of arachidonate metabolism in
tumor growth and progression.
SO - Clin Cancer Res 2002 Apr;8(4):1157-67
AD - Department of Gastroenterology, Institute of Clinical Medicine,
University of Tsukuba, Tsukuba-shi, Ibaraki, Japan.
An association of gallbladder carcinoma with cholelithiasis suggests
that chronic inflammation may modulate tumorigenesis and/or progression
of the carcinoma. An enhanced expression of cyclooxygenase-2 (COX-2) is
observed frequently in advanced carcinomas of gastrointestinal tracts,
which in turn suggests that potentiated arachidonate metabolism may play
a crucial role in tumor biology. In the present study, the expression
levels of COX-2 and prostaglandin E receptor subtypes were determined in
16 cases of gallbladder carcinomas of different depths of invasion
(pT(1) 3, pT(2) 2, pT(3) 4, and pT(4) 7) to determine the role of
arachidonate metabolism in tumor growth and progression. The mRNA levels
of COX-2 were increased significantly in pT(3) and pT(4) carcinomas
compared with the levels in pT(1) and pT(2) carcinomas.
Immunohistochemistry and in situ hybridization revealed the existence of
COX-2 mRNA and protein in both the cancerous epithelia and adjacent
stroma of pT(1)-pT(4) carcinomas. Only in pT(3) and pT(4) carcinomas was
intense expression of COX-2 observed in the adjacent stroma. The tissue
concentration of PGE(2) was significantly increased in pT(3) and pT(4)
carcinomas. The mRNAs of PGE receptor subtypes EP(2), EP(3), and EP(4)
were amplified in pT(1)-pT(4) gallbladder carcinomas, in which their
mRNAs and EP(4) protein were expressed mostly in the cancerous
epithelia. Treatment with a specific EP(4) agonist, as well as PGE(2)
but not EP(2) and EP(3) agonists, up-regulated the expression of c-fos,
an induced growth response gene, and increased colony formation. In
advanced gallbladder carcinoma, enhanced expression of COX-2 is observed
in the adjacent stroma rather than in the cancerous epithelia, and the
stroma is a potent source of PG synthesis. In epithelial-stromal
interactions, the increased PGE(2) synthesis in the adjacent stroma and
its biological effect via EP(4) on the carcinoma cells may contribute to
tumor growth and progression of gallbladder carcinoma.
6
UI - 12113034
AU - Hejna M; Zielinski CC
TI -
Nonsurgical management of gallbladder cancer: cytotoxic treatment and
radiotherapy.
SO - Expert Rev Anticancer Ther 2001 Aug;1(2):291-300
AD - Department of Medicine 1, Division of Oncology, University Hospital,
18-20 Waebringer Guertel, A-1090 Vienna, Austria.
Carcinoma of the gallbladder is a rare tumor entity. Apart from surgical
intervention, there is no therapeutic measure with curative potential.
Therefore, patients with advanced--i.e., unresectable or
metastatic-disease present a difficult problem to clinicians, whether to
choose a strictly symptomatic treatment or expose the patient to the
side effects of potentially ineffective treatment. Despite anecdotal
reports about symptomatic palliation and survival advantages, only
unrandomized Phase II studies too small to draw meaningful conclusions
have been published thus far. Since there is no standard therapy for
advanced gallbladder cancer, patients should be offered the opportunity
to participate in controlled clinical trials.
7
UI - 11808954
AU - Sarli L; Costi R; Roncoroni L
TI -
Laparoscopy and gallbladder cancer.
SO - Am J Gastroenterol 2002 Jan;97(1):206
8
UI - 12082295
AU - Gustafsson U; Einarsson C; Eriksson LC; Gadaleanu V; Sahlin S; Tribukait
TI -
B
DNA ploidy and S-phase fraction in carcinoma of the gallbladder related
to histopathology, number of gallstones and survival.
SO - Anal Cell Pathol 2001;23(3-4):143-52
AD - Department of Surgery, Danderyd Hospital, Sweden.
Ulf.Gustafsson@kir.ds.sll.se
Gallstones are a risk factor for the development of gallbladder cancer.
We studied DNA ploidy and cell cycle composition by flow cytometry in
archival specimens from 52 gall bladder carcinomas in relation to
histopathological grade, tumour stage, gallstone number and survival.
69% of the gallbladder carcinomas showed aneuploidy. All tumours with
single stones (N=11) were aneuploid while only 61% of tumours with
multiple stones (N=41) were aneuploid (p=0.002). DNA aneuploidy was
related to increase in T-category (p=0.01), grade (p=0.02), and nuclear
pleomorphism (p=0.0005). The distribution of DNA ploidy shifted from
tetraploid in low stage towards triploid positions in high stage tumours
(p=0.02) combined with higher S-phase values in triploid tumours
(p=0.05). S-phase fraction increased during development from normal
tissue to dysplasia, cancer in situ and cancer in diploid cases
(p=0.0002), and further at the change from diploid to aneuploid
(p=0.004). At a median cancer specific survival time of four months
patients with diploid tumours had a better survival than those with
aneuploid tumours (p=0.02). In multivariate analysis of the tumour
characteristic, only T-category and tumour grade were independent
prognostic factors.The shift from diploid to aneuploid and the further
shift of ploidy within aneuploid tumours are in agreement with the
concept of a clonal development of gallbladder cancer. These changes are
combined with a stepwise increase in the fraction of S-phase cells. Low
frequency of symptoms in single stone patients may be the reason for
detection of malignancy at a late stage of tumour development.
9
UI - 12101481
AU - Dobritz M; Fellner FA; Baum U; Nomayr A; Lell M; Klein P; Papadopoulos
TI -
T; Bautz W
[MR imaging of pancreatic lesions with Mn-DPDP. A histopathologic
correlation]
SO - Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 2002 Jul;174(7):893-7
AD - Institut fur Diagnostische Radiologie, Friedrich-Alexander Universitat
Erlangen, Nurnberg, Germany.
PURPOSE: To examine the diagnostic accuracy of pancreatic lesions using
mangafodipir-trisodium (Mn-DPDP) enhanced MR imaging. The imaging
results were correlated with the histopathological results. MATERIAL AND
METHODS: 40 patients with suspicion of pancreatic carcinoma were
examined with MRI before and after i. v. administration of Mn-DPDP
(Philips Gyroscan ACS NT 1.5 T, phased array body-coil: TSE T 2 with and
without SPIR, TR 2000 ms, TE 120ms; FFE T 1 breathhold, TR 115 ms, TE
4.6 ms; MRCP, TR 6000 ms, TE 1200 ms; Teslascan i. v. 5 micromol Mn/kg;
FFE T 1 breathhold SPIR, TR 140 ms, TE 4,6 ms). Two observers evaluated
in consensus the number and characteristics of focal pancreatic lesions.
The MR findings were correlated with histopathological findings
retrospectively. RESULTS: The following lesions were found:
adenocarcinoma (19), pancreatitis (8), adenocarcinoma within
pancreatitis (3), insulinoma (2), hematoma (1), papillitis stenosans
(1), signet ring cell carcinoma (1), metastasis of rectal carcinoma (1),
papillary mesothelioma (1). In three patients there was no pathological
finding. Mn-DPDP enhanced MRI showed a sensitivity of 100 % and a
specificity of 56 %. CONCLUSION: Mn-DPDP enhanced MRI in conjunction
with MRCP showed a high sensitivity for the detection of pancreatic
lesions. However, the specificity is low, thus recommending Mn-DPDP
enhanced MRI only as a complementary imaging method.
10
UI - 12111196
AU - Beghelli S; Orlandini S; Moore PS; Talamini G; Capelli P; Zamboni G;
TI -
Falconi M; Scarpa A
Ampulla of vater cancers: T-stage and histological subtype but not Dpc4
expression predict prognosis.
SO - Virchows Arch 2002 Jul;441(1):19-24
AD - Department of Pathology, University of Verona, Strada Le Grazie, 37134
Verona, Italy.
Loss of immunohistochemical expression of Dpc4 occurs in about 50% of
pancreatic ductal cancers and its loss correlates with DPC4/Smad4 gene
inactivation. Dpc4 expression was also lost in 6 of 16 (37%) ampulla of
Vater cancers (AVCs) previously analyzed. Furthermore, chromosomal
losses involving 18q, where DPC4 is located, have been observed in 34%
of AVCs and are associated with decreased survival. To evaluate the
possibility that expression of Dpc4 may be correlated with survival, we
analyzed 89 AVCs for inactivation of DPC4 by immunohistochemical
staining. Thirty-seven cases showed no expression of Dpc4 (41%).
Multivariate survival analysis was performed including age, sex, tumor
size, histological subtype (intestinal or pancreatobiliary), grade of
differentiation, T-stage, lymph-node metastases and Dpc4 status. T-stage
and histological subtype were selected as independent prognostic
factors, while Dpc4 immunostaining was not significantly associated with
any clinicopathological variable, including histological subtype.
Although Dpc4 expression is of no clinical relevance, its involvement in
AVC gives additional weight to the hypothesis that, among all pancreatic
exocrine and endocrine tumors, only AVC and common ductal
adenocarcinomas have similar molecular fingerprints. Moreover,
comparison of the frequencies of allelic loss on chromosomal arm 18q and
the loss of Dpc4 expression (34% and 41%, respectively) is highly
suggestive that DPC4 is the major target of these losses.
11
UI - 11726870
AU - Shah SK; Costamagna G
TI -
Can unilateral stent placement be adequate in patients with Klatskin
tumors of Bismuth-type III and IV?
SO - Gastrointest Endosc 2001 Dec;54(6):804-5
12
UI - 11972211
AU - Martin RC 2nd; Vitale GC; Reed DN; Larson GM; Edwards MJ; McMasters KM
TI -
Cost comparison of endoscopic stenting vs surgical treatment for
unresectable cholangiocarcinoma.
SO - Surg Endosc 2002 Apr;16(4):667-70
AD - Department of Surgery, University of Louisville School of Medicine,
Louisville, KY 40292, USA.
BACKGROUND: Total lifetime costs of endoscopic vs surgical treatment for
obstructive jaundice due to cholangiocarcinoma are difficult to assess.
The purpose of this study was to compare total costs in these two
groups, including all treatment and retreatments. METHODS: This
retrospective study identified patients with biopsy-proven
cholangiocarcinoma treated this decade with either endoscopic biliary
stenting or surgical biliary-enteric bypass with or without resection.
Outcomes and hospital charges were recorded. Ten matched control
patients were compared from each group. Costs included those for cost of
repeat endoscopy in the endoscopic group and for the management of
recurrent obstructive jaundice in the surgical group. RESULTS: The
groups were similar in age and gender ratio. The surgical approach was
frequently for cure; therefore, surgical patients were by and large at
an earlier stage of their disease than those in the endoscopic group.
Mean survival for the endoscopic group was 19 months vs 16.5 months for
the surgical group. The median total lifetime cost for surgical therapy
was $60,986 vs $24,251 for endoscopic therapy. CONCLUSION: Endoscopic
therapy is an effective palliative therapy for unresectable
cholangiocarcinoma. Endoscopic therapy for this entity costs
significantly less than surgical treatment. The cost benefit of
endoscopic stenting over standard surgical bypass in the management of
patients with unresectable cholangiocarcinoma, when considered along
with its minimally invasive approach, makes this the procedure of choice
for palliative therapy.
13
UI - 12053224
AU - Heidecke CD; Rosenberg R; Bauer M; Werner M; Weigert N; Ulm K; Roder JD;
TI -
Siewert JR
Impact of grade of dysplasia in villous adenomas of Vater's papilla.
SO - World J Surg 2002 Jun;26(6):709-14
AD - Chirurgische Klinik und Poliklinik, Klinikum rechts der Isar der
Technischen Universitat Munchen, Ismaningerstrasse 22, 81675 Munich,
Germany.
Therapeutic strategies for villous adenoma of the papilla of Vater
remain controversial. This study evaluates the accuracy of preoperative
histopathologic diagnosis and the impact of the grade of dysplasia on
recurrence as well as on potential alteration of the surgical approach.
A series of 32 patients with an adenoma of Vater's papilla who underwent
local resection or pylorus-preserving pancreaticoduodenectomy between
endoscopic biopsies had been performed preoperatively. The
histopathology of the preoperatively obtained biopsy specimens and
subsequent surgical specimens were evaluated for grade of dysplasia by
two pathologists and correlated with the clinical course after operative
treatment. Altogether, 3 of 11 patients (27%) with a low-grade (LG)
dysplasia adenoma and 6 of 21 patients (29%) with a high-grade (HG)
dysplasia adenoma in the initial endoscopic biopsy specimens exhibited
invasive carcinoma at the postoperative histologic examination (NS).
Recurrence was not observed in the 6 patients from the LG dysplasia
adenoma group following local resection and benign postoperative
histology. In contrast, recurrence of villous adenoma was discovered in
2 of 12 patients (17%) and development of invasive carcinoma in 5 of 12
patients (42%) from the preoperative HG dysplasia group (p <0.05). The
overall risk of carcinoma after primary diagnosis of an HG dysplasia
adenoma was 44% (14/32). Adenoma of the papilla of Vater including HG
dysplasia appears to be associated with a high risk of exhibiting
invasive carcinoma postoperatively and a high rate of recurrence.
Therefore pylorus-preserving pancreaticoduodenectomy should be offered
to patients with an HG dysplasia adenoma.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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Calcium Leucovorin, Citrovorum Factor, Folinic Acid
Cladribine (2-CDA, Leustatin®)
Cyclophosphamide (Cytoxan®, Neosar®, Endoxan®)
Cyclosporine (Neoral®, Sandimmune®, Restasis®, Gengraf®)
Cytarabine (Cytosar-U®, Ara-C)
Irinotecan (Camptosar®, CPT-11)
Leucovorin (Calcium Leucovorin, Citrovorum Factor, Folinic Acid)
Calcium Leucovorin, Citrovorum Factor, Folinic Acid
Leucovorin (Calcium Leucovorin, Citrovorum Factor, Folinic Acid)
Leuprolide Acetate (Lupron®, Lupron Depot®, Eligard®, Prostap®, Viadur®) - For Men
Leuprolide Acetate (Lupron®, Lupron Depot®, Eligard®, Prostap®, Viadur®) - For Women
Lupron®, Lupron Depot®, Eligard®, Prostap®, Viadur®
Lupron®, Lupron Depot®, Eligard®, Prostap®, Viadur®
Busulfan (Myleran®, Busulfex®)
Intravesicular Mitomycin (Mutamycin®, Mitomycin-C, given into the bladder)
Mechlorethamine (Mustargen®, Nitrogen Mustard)
mechlorethamine, mustine, Mustargen®
Megestrol (Megace®, Megace-ES®)
Mercaptopurine (Purinethol®, 6-MP)
Methotrexate (Mexate®, Folex®, Rheumatrex®, Amethopterin, MTX)
Mexate®, Folex®, Rheumatrex®, Amethopterin, MTX
Mitomycin (Mutamycin®, Mitomycin-C)
Morphine Sulfate (Given by IV)
Morphine Sulfate (MS Contin®, Avinza®, Kadian®, Oramorph SR®)
MS Contin®, Avinza®, Kadian®, Oramorph SR®
Mutamycin®, Mitomycin-C, given into the bladder
Nitrogen mustard (mechlorethamine, mustine, Mustargen®)
Bendamustine Hydrochloride (Treanda®)
Bexarotene (Targretin®), Oral Formulation
Bexarotene Gel (Targretin® Gel Formulation)
Etoposide (Toposar®, VePesid®, Etopophos®,VP-16)
Thioguanine (6-TG, Thioguanine Tabloid®)
Toposar®, VePesid®, Etopophos®,VP-16
Trelstar LA® and Trelstar Depot®
Tretinoin (Vesanoid®, All-Trans-Retinoic Acid, ATRA)
Triptorelin (Trelstar LA® and Trelstar Depot®)

