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Tipos de Cancer / Cánceres Gastrointestinal / Cáncer de la Vesícula / Recursos de NCI
National Cancer Institute®
Ultima Vez Modificado: 1 de febrero del 2002
1
UI - 11808954
AU - Sarli L; Costi R; Roncoroni L
TI -
Laparoscopy and gallbladder cancer.
SO - Am J Gastroenterol 2002 Jan;97(1):206
2
UI - 11677943
AU - Ajiki T; Kamigaki T; Hasegawa Y; Fujino Y; Suzuki Y; Takeyama Y; Ku Y;
TI -
Kuroda Y
Proliferating cell nuclear antigen, p53, and c-erbB-2 expression in
relation to clinicopathological variables and prognosis in cancer of the
ampulla of Vater.
SO - Hepatogastroenterology 2001 Sep-Oct;48(41):1266-70
AD - First Department of Surgery, Kobe University School of Medicine, 7-5-1
Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan. ajiki@med.kobe-u.ac.jp
BACKGROUND/AIMS: Various clinicopathological factors have been thought
to influence the prognosis of ampullary cancers. Recent advances in
molecular biology should provide much useful information on the
prognostic factors of ampullary carcinomas. METHODOLOGY: PCNA
(proliferating cell nuclear antigen), p53, and c-erbB-2 were
immunohistochemically evaluated in 30 resectable ampullary carcinomas.
PCNA, p53, and c-erbB-2 expression, 6 clinicopathological variables, and
prognosis were studied and correlations among these factors were
investigated. RESULTS: The mean PCNA-positive rate was 39.1%. The
percentages of cases positive for p53 and c-erbB-2 were 53% and 23%,
respectively. No correlation was seen between PCNA, p53, or c-erbB-2
expression and clinicopathological variables. The optimum cut-off of
PCNA indices influencing recurrence was decided as 40% by receiver
operator characteristic curves. The cumulative disease-free survival
rate of patients from the > or = 40% PCNA positive rate group was
significantly poorer than that of the < 40% PCNA positive rate group (P
< 0.01). p53 accumulation and c-erbB-2 expression were not correlated
with prognosis. Multivariate analysis revealed that the PCNA positive
rate and lymph node metastasis independently contributed to survival (P
< 0.05). CONCLUSIONS: PCNA expression is a useful prognostic marker;
however, p53 and c-erbB-2 overexpression are not useful as biomarkers
for ampullary cancers.
3
UI - 11677947
AU - Saetta A; Lazaris AC; Michalopoulos NV; Davaris PS
TI -
Genetic alterations involved in the development of gallbladder
carcinomas from Greek patients.
SO - Hepatogastroenterology 2001 Sep-Oct;48(41):1284-8
AD - Department of Pathology, Medical School, National and Kapodistrian
University of Athens, Athens, Greece. asaetta@cc.uoa.gr
BACKGROUND/AIMS: The genetic pathways of gallbladder cancer are not yet
well defined since the contribution of genetic abnormalities clarified
in other organs remains questionable. METHODOLOGY: We investigated a
group of 22 gallbladder carcinomas from Greek patients with regard to
p53 mutations, bax and TGF-beta RII alterations--as indicators of
microsatellite instability. The findings were correlated to the presence
of ras mutations, patients' clinicopathologic features and survival.
PCR-SSCP analysis was performed for the detection of p53 mutations in
conserved domains IV and V. RESULTS: In five tumors p53 mutations were
detected; none of them was ras mutated. Although these tumors were
characterized by flat morphology, low histologic grade and rather
advanced stage, no statistical correlation could be determined. No
indications of microsatellite instability were found. CONCLUSIONS: Ras
and p53 genes do not appear to cooperate during gallbladder cancer, at
least as far as the flat type of cancer is concerned. p53 alterations
are likely to take part in the de novo pathway of gallbladder
carcinogenesis.
4
UI - 11677948
AU - Bathe OF; Pacheco JT; Ossi PB; Hamilton KL; Franceschi D; Sleeman D;
TI -
Levi JU; Livingstone AS
Management of hilar bile duct carcinoma.
SO - Hepatogastroenterology 2001 Sep-Oct;48(41):1289-94
AD - Department of Surgery, University of Miami, Miami, Florida, USA.
bathe@ucalgary.ca
BACKGROUND/AIMS: Hilar cholangiocarcinoma is a rare tumor with a dismal
prognosis. Because proximal bile duct cancers are uncommon, outcomes
related to various therapeutic interventions are not well defined.
METHODOLOGY: Between 1985 and 1997, 55 patients with bile duct cancers
involving the proximal third of the extrahepatic bile ducts were seen.
The management of patients with resectable and unresectable disease was
retrospectively reviewed. All but four patients were followed until the
time of death. RESULTS: Forty patients underwent laparotomy following
preoperative assessment of extent of disease and 19 patients (35%)
ultimately underwent resection with curative intent. Survival was
significantly longer in patients who underwent resection (2-year
survival 47% vs. 18%; P = 0.027). Of those patients whose disease was
resected, 11 patients received adjuvant radiotherapy. Survival for this
group was not significantly different from that seen in patients who did
not receive adjuvant radiotherapy. Similarly, in patients with
unresectable disease, administration of radiotherapy was not associated
with an improved outcome. CONCLUSIONS: Locoregional extent of disease is
the greatest problem in cases of proximal bile duct cancers. Resection
provides the best hope for long-term survival, but new adjuvant
strategies are needed.
5
UI - 11677950
AU - Kim MW; Kim WH; Wang HJ; Chung JB; Chun M
TI -
The experiences of hilar skeletonization for the treatment of locally
advanced proximal bile duct cancer.
SO - Hepatogastroenterology 2001 Sep-Oct;48(41):1298-301
AD - Department of Surgery, Ajou University School of Medicine San 5,
Wonchon-dong, Paldal-gu, Suwon 442-749, Korea. ajgs@madang.ajou.ac.kr
BACKGROUND/AIMS: Because proximal bile duct cancer easily involves the
surrounding tissue, tumor cells often remain after apparent
macroscopically complete radical resection. We evaluated the effect of
resective modality of these tumors on prognosis and the effect of
postoperative radiotherapy on survival of patients with microscopic
residual tumor following local resection in locally advanced proximal
bile duct cancer. METHODOLOGY: From November, 1990 to October, 1993, 45
proximal bile duct cancer patients who received local excision were
entered onto this prospective, nonrandomized study. The patients were
divided into three groups after operation, 16 patients with curative
resection; 15 noncurative resection; and 14 nonresection. Patients who
had positive lymph nodes or microscopic cancer cells in resection margin
or adjacent major vessels, were treated with postoperative external
radiotherapy, 5040 cGy for 40 days. RESULTS: The overall 1-, 2-, and
5-year survival of the patients was 62.2%, 24.4%, and 15.6%,
respectively. The overall mean and median survival of patients was 24.1
+/- 3.98 (mean +/- SE) months and 13 +/- 0.74 months, respectively.
Survival rates between resection and nonresection showed a statistically
significant difference (P < 0.05). However, survival rates between
curative resection and noncurative resection with postoperative
radiotherapy were not statistically significant (P > 0.05). CONCLUSIONS:
The resection is the treatment of choice for locally advanced proximal
bile duct cancer, if resectable and the noncurative resection followed
by postoperative external radiotherapy may be beneficial to the patients
with locally advanced proximal bile duct cancer.
6
UI - 11677994
AU - Schwarz RE; Keny H
TI -
Preoperative platelet count predicts survival after resection of
periampullary adenocarcinoma.
SO - Hepatogastroenterology 2001 Sep-Oct;48(41):1493-8
AD - City of Hope National Medical Center, Department of General Oncologic
Surgery, Duarte, CA, USA. Roderich.Schwarz@umdnj.edu
BACKGROUND/AIMS: Thrombocytosis or thrombocytopenia have been shown to
act as negative predictors of outcome for various solid tumors. No such
effect is known for periampullary cancer. The preoperative peripheral
blood platelet count impacts on outcome after resection of pancreatic
and other periampullary adenocarcinomas. METHODOLOGY: Clinicopathologic
information, treatment aspects, and outcome parameters of patients
undergoing pancreatectomy at City of Hope Cancer Center were
retrospectively collected and tabulated. The impact of the preoperative
platelet count on postoperative recovery, disease-free survival, and
overall survival was analyzed. RESULTS: Between 1988 and 1998, 65
patients underwent partial or total pancreatectomy at City of Hope
Cancer Center, 49 of whom had a diagnosis of pancreatic or periampullary
adenocarcinoma. There were 26 females and 23 males, with a median age of
64 years (range: 24-86). Median preoperative platelet count was 308
(x10(9)/L; range: 104 to 547). Diagnoses were pancreatic (n = 28),
duodenal (n = 12), and bile duct/ampullary cancer (n = 9). Procedures
included pancreatoduodenectomy (n = 42), distal pancreatectomy (n = 4),
and total pancreatectomy (n = 3). Six patients underwent a splenectomy.
A lower preoperative platelet count was correlated to a shortened
prothrombin time (P = 0.02), and a positive resection margin (P = 0.01),
but not operative blood loss or transfusion requirements. Postoperative
complications and hospital stay were not affected by the platelet count.
Preoperative platelets of < 300 were associated with a decreased median
overall survival (13 vs. 33 months, P = 0.02) and disease-free survival
(11 vs. 29 months, P = 0.02), at a median follow-up of 14 months (18 for
survivors). On multivariate analysis, the platelet count remained a
significant predictor of survival in addition to grade, perineural
invasion, the primary tumor size, and the surgeon. CONCLUSIONS: Based on
these retrospective data, a lower preoperative platelet count correlates
with inferior, a higher count with superior survival outcome after
resection of periampullary cancer. The mechanism is unclear, but may
relate to general factors (bone-marrow suppression or hypersplenism for
low platelets, systemic antitumor mediators for high platelets) or
platelet-specific effects (platelet influence on tumor angiogenesis or
metastatic efficiency). The preoperative thrombocyte count should be
considered a parameter with potential clinical significance in
prospective clinical studies of periampullary neoplasms.
7
UI - 11802210
AU - Caca K; Feisthammel J; Klee K; Tannapfel A; Witzigmann H; Wittekind C;
TI -
Mossner J; Berr F
Inactivation of the INK4a/ARF locus and p53 in sporadic extrahepatic
bile duct cancers and bile tract cancer cell lines.
SO - Int J Cancer 2002 Feb 1;97(4):481-8
AD - Department of Medicine II, University of Leipzig, Leipzig, Germany.
caca@medizin.uni-leipzig.de
The tumor-suppressor genes p14(ARF), p16(INK4a) and Tp53 are commonly
inactivated in many tumors. We investigated their role in the
pathogenesis of 9 bile tract cancer cell lines and 21 primary sporadic
extrahepatic bile duct carcinomas. p53 and p16 protein expression was
examined by Western blot analysis and immunohistochemistry. Mutation
screening of p53 was done by SSCP and direct sequencing. Inactivating
mechanisms of p14 and p16 were addressed by screening for mutations,
homozygous deletions, chromosomal loss of 9p21 (loss of heterozygosity
[LOH] analysis) and promoter hypermethylation of the p14/p16 genes. p53
overexpression could be detected in 7 of 9 cell lines and 7 of 21
primary tumors, but mutations were found in 3 cell lines only. p16
expression was absent in all cell lines, due to homozygous deletion of
the gene in 8 of 9 cell lines and hypermethylation of the p16 promoter
in one cell line (CC-LP-1). p14 exon 1beta was homozygously deleted in 6
of 9 cell lines, while retained in CC-LP-1 and 2 additional lines. No
p14 promoter hypermethylation could be detected. p16 expression was lost
in 11 of 21 primary tumors. p16 promoter hypermethylation was present in
9 of 21 primary tumors, all with lost p16 expression. Allelic loss at
9p21 was detected in 13 of 21 primary tumors, 10 of 11 with lost p16
expression and 8 of 9 with methylated p16 promoter. No p14 promoter
hypermethylation or p14/p16 mutations could be detected. Neither Tp53
nor p16 alterations showed obvious association with histopathologic or
clinical characteristics. In conclusion, inactivation of the p16 gene is
a frequent event in primary sporadic extrahepatic bile duct cancers,
9p21 LOH and promoter hypermethylation being the principal inactivating
mechanisms. Therefore, p16, but not p14, seems to be the primary target
of inactivation at the INK4a locus in bile duct cancers. Other
mechanisms than Tp53 mutations seems to be predominantly responsible for
stabilization of nuclear p53 protein in bile duct cancers. Copyright
2002 Wiley-Liss, Inc.
8
UI - 11780432
AU - Wang C; Lu X; Liu G; Dai L; Xu T; Chen Y; Gao C; Wen X; Qian J
TI -
Detailed deletion mapping on chromosome region 9p21 in human
periampullary neoplasms.
SO - Chin Med J (Engl) 2001 Jun;114(6):588-91
AD - Department of Gastroenterology, Peking Union Medical College Hospital,
Chinese Academy of Medical Sciences, Peking Union Medical College,
Beijing 100730, China. wangchunwei@btamail.net.cn
OBJECTIVE: To further define the extent of chromosome 9p21 deletion in
periampullary neoplasms. METHODS: The loss of heterozygosity at 5
microsatellite polymorphic markers on chromosome 9p21 was detected by
polymerase chain reaction (PCR), polyacrylamide gel electrophoresis
(PAGE) and silver staining in 35 specimens of periampullary neoplasms
and their matching blood samples. RESULTS: Fifty percent (4/8) of
pancreatic cancer cases showed the loss of heterozygosity at one or more
microsatellite loci, with the more frequent sites of D9S974 (37.5%) and
D9S942 (28.6%), and some showing consecutive allelic loss. Sixty-two
point five percent (5/8) of ampullary carcinoma cases showed loss of
heterozygosity at one or more of the loci, frequent site of loss being
D9S942 (42.9%) and the next most frequent being IFNA (37.5%) and D9S171
(37.5%). Loss of one locus was observed in 14.2% (1/7) of insulinoma.
CONCLUSION: The minimal common region of chromosome deletion in
periampullary neoplasms is defined between the D9S974 and D9S942 loci
within a 15 kb interval in 9p21, suggesting the involvement of a novel
tumor suppressor gene in their carcinogenesis.
9
UI - 11569922
AU - Chen Y; Satoh T; Sasatomi E; Miyazaki K; Tokunaga O
TI -
Critical role of type IV collagens in the growth of bile duct carcinoma.
In vivo and in vitro studies.
SO - Pathol Res Pract 2001;197(9):585-96
AD - Department of Pathology, Saga Medical School, Japan.
g9804@post.saga-med.ac.jp
Most extrahepatic bile duct carcinomas (EBDC) are characterized by a
striking stromal response (desmoplasia). Our previous studies showed
deposition of type IV collagen in the desmoplastic stroma beyond the
basement membrane. Although type IV collagen is expressed in EBDC,
little is known about the pattern of deposition in tumor stroma and how
this matrix component influences the behavior of tumor cells. With the
progression of desmoplasia in EBDC, different changes occurred in the
quantity and localization of type IV collagen from that of type I
collagen. Type I collagen was diffusely distributed in the stroma and
appeared to be concentrated in the center of the tumors. In contrast,
type IV collagen was deposited in the interstitium alongside carcinoma
cells at the tumors' periphery. Weak or no type IV collagen deposition
was detected in the more central portion of the tumors containing
sclerotic collagens. To investigate the role of stromal type IV collagen
in tumor cell proliferation, EBDC cell lines were cultured in a
three-dimensional matrix containing varying compositions of type I
collagen and type IV collagen. They were also assayed for cell adhesion
and migration using in vitro models. Type IV collagen more extensively
stimulated tumor cell proliferation, adhesion and migration in a
dose-dependent manner than did type I collagen. All of these results
suggest that modified tumor stroma with the presence of type IV collagen
in EBDC provides a better environment for tumor growth and invasion.
10
UI - 9424866
AU - Knast W; Markocka-Maczka K; Wierzbicki J; Wozniak S; Nienartowicz M;
TI -
Pelczar P
[Tumor in Vater's ampulla--local excision or Whipple's resection]
SO - Wiad Lek 1997;50 Suppl 1 Pt 2():158-61
AD - Katedry i Kliniki Chirurgii Przewodu Pokarmowego Akademii Medycznej we
Wroclawiu.
Results of the operative treatment of Vater's papilla carcinoma in
fifteen cases were analysed. Eleven patients had pancreatoduodenectomy
according to Whipple, four had only local excision of Vater's papilla
along with the tumour. All four had early recurrence and were
re-operated by Whipple method. In our experience only radical
pancreatoduodenectomy with regional lymphadenectomy, preferably Whipple
type, gives chance of achieving the radical cure.
11
UI - 11796009
AU - Matsuo K; Kuroki T; Kitaoka F; Tajima Y; Kanematsu T
TI -
Loss of heterozygosity of chromosome 16q in gallbladder carcinoma.
SO - J Surg Res 2002 Feb;102(2):133-6
AD - Department of Surgery II, Nagasaki University School of Medicine,
Nagasaki 852-8501, Japan. matsk@mebe.sphere.ne.jp
BACKGROUND: The present study was planned to investigate cumulative
genetic changes during development and progression of gallbladder
carcinoma (GBC) in clinical patients. MATERIALS AND METHODS: We examined
GBC DNA from resected tissue isolated from 56 cases of GBC for loss of
heterozygosity (LOH) at six loci on five chromosomal arms (1p36, 9p21,
13q14, 16q24, 17p13), using highly polymorphic microsatellite markers.
RESULTS: High incidences of LOH at 1p36 (19/36: 53%), 9p21 (12/32: 38%),
13q14 (20/36: 56%), 16q24 (31/54: 61%), and 17p13 (15/36: 42%) were
detected. When comparing genetic features with clinicopathological
stages of these tumors, it appeared that only LOH at 16q24 had a high
incidence (5/6: 83%) at an early stage (T1a: tumor invades lamina
propria) of the disease, although large numbers of LOH were found on all
chromosomal arms in tumors of more advanced stages (T1b, T2, T3, and
T4). CONCLUSION: These results suggested that the putative tumor
suppressor gene on 16q24 may be strongly related to an early step of
carcinogenesis in GBC and that GBC acquires a high malignant potential
when the tumor invades the muscle layer. (c)2001 Elsevier Science.
12
UI - 11747335
AU - Oshikiri T; Hida Y; Miyamoto M; Hashida H; Katoh K; Suzuoki M; Nakakubo
TI -
Y; Hiraoka K; Shinohara T; Itoh T; Kondo S; Katoh H
RCAS1 as a tumour progression marker: an independent negative prognostic
factor in gallbladder cancer.
SO - Br J Cancer 2001 Dec 14;85(12):1922-7
AD - Department of Surgical Oncology, Division of Cancer Medicine, Hokkaido
University Graduate School of Medicine, North 15, West 7, Kita-ku,
Sapporo, 060-8638, Japan.
Receptor-binding cancer antigen expressed on SiSo cells (RCAS1) induces
apoptosis in immune cells bearing the RCAS1 receptor. We sought to
determine RCAS1 involvement in the origin and progression of gallbladder
cancer, and also implications of RCAS1 for patient survival. RCAS1
expression was examined immunohistochemically in 110 surgically resected
gallbladder specimens. The gallbladders represented 20 cases of
cholecystitis with no associated pancreaticobiliary maljunction; 23
cases of cholecystitis with pancreaticobiliary maljunction; 14 cases of
adenomyomatosis; 7 adenomas; and 46 cancers. High expression of RCAS1
(immunoreactivity in over 25% of cells) was observed in 32 of the 46
cancers (70%), but not in other diseases, including pre-cancerous
conditions. RCAS1 immunoreactivity was associated with depth of tumour
invasion (P = 0.0180), lymph node metastasis (P = 0.0033), lymphatic
involvement (P = 0.0104), venous involvement (P = 0.0224), perineural
involvement (P = 0.0351) and stage by the tumour, nodes and metastases
(TNM) classification (P = 0.0026). Thus, RCAS1 expression may be a
relatively late event in gallbladder carcinogenesis, possibly promoting
tumour progression. Cox regression multivariate analysis demonstrated
RCAS1 positivity to be an independent negative predictor for survival (P
= 0.0337; risk ratio, 12.690; 95% confidence interval, 1.216-132.423).
High expression of RCAS1 significantly correlated with tumour
progression and predicted poor outcome in gallbladder cancer.
13
UI - 11830924
AU - Eriguchi N; Aoyagi S; Tamae T; Nishimura K; Hamada S; Kawabata M; Kodama
TI -
T; Jimi A
Carcinoma of the ampulla of Vater associated with other organ
malignancies.
SO - Kurume Med J 2001;48(4):255-9
AD - Department of Surgery, Sasebo Kyosai Hospital, 10-17 Shimanji-cho,
Sasebo 857-8575, Japan.
Because of its location with respect to the biliary system, carcinoma of
the ampulla of Vater is considered to manifest earlier in its course of
development than carcinoma of the pancreas. The most common physical
finding is jaundice, which occurs in 93-100% of cases [1,2]. This
retrospective study describes the results of the treatment and prognosis
for double primary cancers in which cancer of the ampulla of Vater was
associated with malignancies in other organs in 5 patients who were
diagnosed and treated at Kurume University Hospital. The patients
included 5 men with an average age of 72.8 years. There were 3
synchronous double and 2 metachronous double cancer patients. Regarding
prognoses of these patients, 1 patient with associated lung cancer died
because of postoperative complications after pneumonectomy, 1 patient
died due to carcinomatosa peritonei developing from the ampulla Vater
carcinoma, and 1 patient died because of metastatic liver tumors from
the ampullary carcinoma. In multiple cancers including ampulla Vater
carcinoma, gastrointestinal cancers such as gastric or colon cancer
occur frequently. Therefore, a careful gastrointestinal examination
should be done preoperatively. We report our experience with 5 cases of
ampullary carcinoma associated with malignancies in other organs and
review the literature.
14
UI - 11830926
AU - Kinoshita H; Hashino K; Hashimoto M; Kodama T; Nishimura K; Kawabata M;
TI -
Furukawa S; Tamae T; Nagashima J; Hara M; Imayama H; Aoyagi S
Clinicopathological evaluation of surgical treatment for early
gallbladder cancer.
SO - Kurume Med J 2001;48(4):267-71
AD - Department of Surgery, Kurume University School of Medicine, Kurume
830-0011, Japan.
We evaluated the therapeutic principles for early gallbladder cancer
based on clinicopathological characteristics and outcomes in 27 patients
encountered at the Kurume University Hospital between January, 1975 and
December, 1999. Concerning the depth of wall penetration, 15 patients
had mucosal cancers (m-cancers), and 12 patients muscularis propria
cancers(mp-cancers). The gross patterns were lp (pedunculated) in 16
patients, ls (sessile) in 3 patients, IIa (flat elevated) in 4 patients,
and IIb (flat) in 4 patients. The operative procedure used was
cholecystectomy (C) in 12 patients, 4 of whom underwent lymph node
dissection. Full-thickness cholecystectomy (FTC) was carried out in 3
patients, one of whom had lymph node dissection. Combination of C and
gallbladder bed resection (GbBR) was performed in 7 patients, 6 of whom
had lymph node dissection. Combination of C and bile duct resection
(BDR), and lymph node dissection was performed in 1 patient. Combination
of C and GbBR and BDR, and lymph node dissection was performed in 6
patients. All the patients who underwent lymph node dissection were
negative for metastasis. Of the 27 patients, 2 underwent laparoscopic
operation: one with m-cancer was 79 years old, and the other with
mp-cancer 86 years old. In the m-cancers, no lymphatic, venous or
perineural infiltration was observed. In contrast, in the mp-cancers,
lymphatic and venous infiltration each were observed in 4 patients
(33.3%), although no perineural infiltration was observed. A diagnosis
of gallbladder cancer was made postoperatively in 6 patients, of whom 4
had the IIb pattern and all were complicated by gallstone, indicating
the difficulty of diagnosing the IIb pattern. The 5-year survival rates
for the m- and mp-cancers were as high as 90.9% and 80.8%, respectively.
As a curative surgical technique for m- and mp-cancers, lymph node
dissection should be performed in addition to FTC, GbBR, and BDR, in
combination. When a postoperative histopathologic diagnosis of
gallbladder cancer has been made, no second-look operation should be
performed for m-cancers, but lymph node dissection of up to the second
group should be performed for mp-cancers in a second-look operation.
15
UI - 11848630
AU - Wagholikar GD; Behari A; Krishnani N; Kumar A; Sikora SS; Saxena R;
TI -
Kapoor VK
Early gallbladder cancer.
SO - J Am Coll Surg 2002 Feb;194(2):137-41
AD - Department of Surgical Gastroenterology, Sanjay Gandhi Post Graduate
Institute of Medical Sciences, Lucknow, India.
BACKGROUND: The majority of patients with gallbladder cancer (GBC) have
advanced disease at the time of diagnosis and are unresectable. Longterm
survival is usually seen in a subset of patients with early GBC
(EGBC)-cancer confined to the mucosa (pT1a) and muscularis (pT1b).
Management guidelines of EGBC are not yet defined and are controversial.
The purpose of this article is to evaluate the diagnostic aspects and
effects of resectional procedures on survival outcome in patients with
EGBC. STUDY DESIGN: EGBC was defined as cancer confined to the mucosa
(pT1a) or muscularis (pT1b) according to the TNM classification.
Clinicopathological details and survival data of 14 patients who had
EGBC were analyzed. There were 9 women and 5 men, with a mean age of 60
years. RESULTS: A definite preoperative diagnosis was possible in only
three patients and three patients were diagnosed at surgery; the
majority of patients were diagnosed incidentally after cholecystectomy
for associated gallstones. Two patients underwent extended
cholecystectomy and 12 patients underwent simple cholecystectomy. Two
patients had pT1a and 12 had pT1b lesions. Mean (SD) survival was 71.5
(12.2) months and median survival was 42 months. There were five
treatment failures with locoregional recurrence and death. All patients
with pT1b tumors were treated by simple cholecystectomy. Cumulative 1-,
3-, and 5-year survival was 92%, 68%, and 68% respectively. CONCLUSIONS:
Simple cholecystectomy is an adequate treatment only for mucosal GBC.
Patients with pT1b tumors require extended cholecystectomy. Incidental
GBC extending up to the muscularis merits early reoperation for
completion of extended cholecystectomy, which offers the only chance of
cure.
16
UI - 11579805
AU - Fong Y; Malhotra S
TI -
Gallbladder cancer: recent advances and current guidelines for surgical
therapy.
SO - Adv Surg 2001;35():1-20
AD - Cornell University Medical College, Memorial Sloan-Kettering Cancer
Center, New York, USA.
17
UI - 11804747
AU - Hui AM; Shi YZ; Li X; Sun L; Guido T; Takayama T; Makuuchi M
TI -
Proliferative marker Ki-67 in gallbladder carcinomas: high expression
level predicts early recurrence after surgical resection.
SO - Cancer Lett 2002 Feb 25;176(2):191-8
AD - Hepato-Biliary-Pancreatic Surgery Division, Department of Surgery,
Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo,
Bunkyo-ku, Tokyo 113-0033, Japan. huia@mail,nih.gov
To evaluate the prognostic value of proliferative maker Ki-67, its
expression was determined immunohistochemically in 37 gallbladder
carcinomas (GBCs). A high Ki-67 index was significantly correlated with
tumor lymphatic invasion (P=0.007) and vascular invasion (P=0.04). High
Ki-67 index group and low Ki-67 index group showed different clinical
courses. Five patients who experienced recurrences in high Ki-67 index
group developed their recurrent diseases within one year after surgery
and died soon after recurrence, while the recurrences (five cases) in
low Ki-67 index group were distributed all stages after surgery. In
conclusion, high Ki-67 index predicts early recurrence after surgery for
GBCs.
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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®)

