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Tipos de Cancer / Cánceres Gastrointestinal / Cáncer de la Vesícula / Recursos de NCI
National Cancer Institute®
Ultima Vez Modificado: 21 de noviembre del 2001
1
UI - 21436792
AU - Dixit VK; Singh S; Shukla VK
TI -
Aetiopathogenesis of carcinoma gallbladder.
SO - Trop Gastroenterol 2001 Apr-Jun;22(2):103-6
AD - Department of Surgery, Institute of Medical Sciences, Banaras Hindu
University, Varanasi-221 005, India.
2
UI - 99444171
AU - Paolucci V; Schaeff B; Schneider M; Gutt C
TI -
Tumor seeding following laparoscopy: international survey.
SO - World J Surg 1999 Oct;23(10):989-95; discussion 996-7
AD - Klinikum der Johann Wolfgang Goethe Universitat, Zentrum der Chirurgie,
Klinik fur Allgemeinchirurgie, Theodor-Stern-Kai 7, D-60590 Frankfurt am
Main, Germany.
The aim of the study was to determine if tumor seeding during
laparoscopic surgery for cancer is a rare event or a typical
complication of this procedure. Laparoscopic staging and treatment of
intraabdominal tumors is increasing in gastroenterology, gynecology, and
general surgery. A total of 1052 questionnaires were mailed to surgical
department chairmen, members of the German Society of Surgery, Swiss
Association for Laparoscopic and Thoracoscopic Surgery, and Austrian
Society of Minimal Invasive Surgery asking them to list their
department's experience with tumor seeding after laparoscopy for
nonapparent or known malignancy. There were 607 (57.7%) surgeons who
reported a total of 117,840 laparoscopic cholecystectomies, 409
incidental gallbladder carcinomas, and 412 laparoscopies on patients
with colorectal carcinoma. Altogether 109 patients who developed tumor
recurrence in connection with laparoscopic surgery have been reported.
Port-site recurrence was identified in 70 of 409 patients (17.1%) with a
median of 180 days following laparoscopic cholecystectomy for
nonapparent gallbladder carcinoma. In 8 cases (11.5%) a protective
plastic bag had been used for gallbladder retrieval. Six patients
without port-site metastases were found to have a diffuse peritoneal
carcinomatosis a median of 120 days after cholecystectomy. Of 412
laparoscopies for colorectal cancer, 19 cases (4.6%) of tumor seeding
have been reported, 16 of which (3.9%) had documented port-site and scar
recurrences a median of 196 days after laparoscopy. The tumor specimen
was intact, and a plastic bag was used for extraction in seven cases. In
14 patients trocar-site metastases have been reported a median of 70
days after laparoscopy for different nonapparent or known malignancies.
The probability of developing abdominal wall metastasis is higher after
laparoscopy for cancer than after open surgery. An intact surgical
specimen and the use of a plastic retrieval bag do not exclude the risk
of port-site recurrences. These facts and the early appearance of
peritoneal carcinosis in a few cases of intraabdominal malignancies seem
to confirm a specific laparoscopic risk for intraperitoneal tumor cell
seeding and implantation.
3
UI - 21241218
AU - Sarli L; Costi R
TI -
Re: Paolucci, V et al: Tumor seeding following laparoscopy:
international survey. World J. Surg. 23:989,1999.
SO - World J Surg 2001 Mar;25(3):387
4
UI - 21271462
AU - Elnemr A; Ohta T; Kayahara M; Kitagawa H; Yoshimoto K; Tani T; Shimizu
TI -
K; Nishimura G; Terada T; Miwa K
Anomalous pancreaticobiliary ductal junction without bile duct
dilatation in gallbladder cancer.
SO - Hepatogastroenterology 2001 Mar-Apr;48(38):382-6
AD - Department of Surgery II, School of Medicine Kanazawa University,
Takara-machi 13-1, Kanazawa 920-0934, Japan.
BACKGROUND/AIMS: Anomalous pancreaticobiliary junction is a rare anomaly
but is a risk factor for primary carcinoma of the gallbladder. To define
the relationship between anomalous pancreaticobiliary junction,
especially if it is not associated with common bile duct dilatation, and
gallbladder carcinoma, we retrospectively reviewed data of 126 patients
with gallbladder carcinoma. METHODOLOGY: All these patients had
undergone direct cholangiography either by endoscopic retrograde
cholangiopancreaticography or percutaneous transhepatic cholangiography.
RESULTS: Among 126 patients with gallbladder cancer, 23 patients (18.3%)
exhibited anomalous pancreaticobiliary junction. Patients with anomalous
pancreaticobiliary junction were younger (mean age: 54 +/- 9.1 years)
than patients without anomalous pancreaticobiliary junction (mean age:
65 +/- 9.7 years). The incidence of gallstones in patients with
anomalous pancreaticobiliary junction (17%) was significantly lower than
in those without this anomaly (64%) (P < 0.01). Among the 23 patients
with anomalous pancreaticobiliary junction, 12 patients (52%) had no
bile duct dilatation and, 11 patients (48%) had bile duct dilatation in
the form of fusiform or cylindrical dilatation. However, no cases with
severe cystic dilatation were found. Patients of anomalous
pancreaticobiliary junction without common bile duct dilatation had more
advanced disease and poor prognosis than those with common bile duct
dilatation. CONCLUSIONS: The present study revealed that gallbladder
cancer in the patients of anomalous pancreaticobiliary junction without
common bile duct dilatation was diagnosed at advanced stage and the
prognosis was very poor. Therefore, if a minor abnormality is detected
in the wall of acalculous gallbladder on ultrasonography, direct
cholangiography should be done to exclude this anomaly.
5
UI - 21274204
AU - Esposito I; Friess H; Buchler MW
TI -
Carcinogenesis of cancer of the papilla and ampulla: pathophysiological
facts and molecular biological mechanisms.
SO - Langenbecks Arch Surg 2001 Apr;386(3):163-71
AD - Department of Visceral and Transplantation Surgery, University of Bern,
Inselspital, Switzerland.
BACKGROUND: Ampullary cancer has one of the highest resectability rates
and best prognoses among neoplasms arising in the periampullary region.
DISCUSSION: Early diagnosis due to early symptoms can partially explain
the better prognosis as compared to other cancers of the periampullary
region, but biologic factors should also be taken in account. In the
past few years, the molecular mechanisms underlying this disease have
been investigated and alterations of genes that regulate different cell
functions have been described. Mutations of K-ras and of the tumor
suppressor genes APC, p16 and p53 indicate a major disturbance in cell
cycle regulation. CONCLUSIONS: If the molecular profile of ampullary
cancer is examined in terms of rate and type of molecular changes, it
seems to be more similar to intestinal than to pancreatic cancer.
Furthermore, the fact that many ampullary carcinomas arise from adenomas
and the frequent finding of ampullary tumors in patients affected by
polyposis syndromes also suggest that ampullary and colon cancers share
common molecular mechanisms of carcinogenesis.
6
UI - 21274205
AU - Wittekind C; Tannapfel A
TI -
Adenoma of the papilla and ampulla--premalignant lesions?
SO - Langenbecks Arch Surg 2001 Apr;386(3):172-5
AD - Institute of Pathology, University of Leipzig, Germany.
tana@medizin.uni-leipzig.de
Ampullary adenomas arising in the papilla or the ampulla Vateri, are
rare, benign, neoplastic lesions. No specific aetiological factors, such
as diet, chemical or environmental causes, have been identified yet. An
established risk factor which is accompanied by the development of
adenoma is the presence of genetically inherited polyposis syndromes,
e.g. familial adenomatosis coli (FAP). Adenomas assume tubular,
tubulovillous, or villous architecture and are not different from
adenomas arising elsewhere in the gastrointestinal tract. The full
neoplastic spectrum, ranging from mild to high grade dysplasia, up to
invasive carcinoma, resembles the adenoma-carcinoma sequence of the
large bowels.
7
UI - 21274206
AU - Vogt M; Jakobs R; Riemann JF
TI -
Rationale for endoscopic management of adenoma of the papilla of Vater:
options and limitations.
SO - Langenbecks Arch Surg 2001 Apr;386(3):176-82
AD - Klinikum der Stadt Ludwigshafen GmbH, Ludwigshafen am Rhein, Germany.
BACKGROUND: Several studies and our own results prove that endoscopic
therapy in selected cases of benign adenomas is safe and technically
feasible. In patients refusing surgery or patients with high comorbidity
and poor physical health status, endoscopic resection is an excellent
alternative. DISCUSSION: The decision for endoscopic or surgical
excision of adenomas is determined by general health status, histology,
size, location, and depth of the lesion. In carcinoma of the papilla of
Vater it is important to assess the tumoral ductal infiltration
correctly to determine whether endoscopic resection is a viable option.
Intraductal ultrasound is essential before initiating treatment and it
therefore contributes to conservative therapy in patients with tumors of
the papilla of Vater. Temporary placement of a short pancreatic duct
stent may protect against pancreatitis and might allow more excessive
ablation of adenomatous tissue, especially around the pancreatic duct
orifice. After endoscopic sphincterotomy, biliary and pancreatic
endoprostheses can be inserted easily in cases of obstructed pathways or
cholangitis and pancreatitis due to tumor obstruction. Argon plasma
coagulation can be used to treat oozing tumor hemorrhages or to vaporize
tumoral residues after endoscopic snare resection. Endoscopic
surveillance is essential after surgical or endoscopic resection of
adenomas of the papilla of Vater.
8
UI - 21274214
AU - Tazuma S; Kajiyama G
TI -
Carcinogenesis of malignant lesions of the gall bladder. The impact of
chronic inflammation and gallstones.
SO - Langenbecks Arch Surg 2001 Apr;386(3):224-9
AD - First Department of Internal Medicine, Hiroshima University School of
Medicine, Japan. stazuma@mcai.med.hiroshima-u.ac.jp
Gallbladder carcinoma is an uncommon but highly malignant tumor with a
poor 5-year survival rate. The presence of gallstones is a
well-established risk factor for gallbladder carcinoma, and the risk
seems to correlate with stone size. Metaplastic changes of the
gallbladder epithelium present in chronic cholecystitis may be a
premalignant lesion. Solitary polyps with a size of greater than 1 cm
are recognized as a predisposing factor for gallbladder carcinoma when
their characteristics are echopenic, sessile, and high cell density.
Endoscopic ultrasound is the most useful technique to detect the early
changes of malignancy in polyps. Anomalous junction of
pancreaticobiliary ducts (AJPBD) without a choledochal cyst and
porcelain gallbladder is an additional risk factor for gallbladder
malignancy. At the molecular level, it has been proposed that chronic
inflammation of the gallbladder may lead to the loss of p53 gene
heterozygosity and excessive expression of p53 protein. Furthermore, a
proposed mechanism underlying the high risk of gallbladder carcinoma in
patients with AJPBD is that chronic reflux of pancreatic juice causes
intestinal metaplasia, hyperplasia, and dysplasia with the mutation of
p53 and K-ras. In contrast, the causal relationship between porcelain
gallbladder and malignancy is yet to be established. In this article,
recognition of risk factors for gallbladder carcinoma was summarized
with special attention to gallstones and chronic inflammation.
9
UI - 21419011
AU - Aoki T; Inoue K; Tsuchida A; Kasuya K; Koyanagi Y
TI -
Dye-staining stereomicroscopic examinations for fine mucosal structures
of the gallbladder.
SO - Dig Surg 2001;18(4):298-304
AD - Department of Surgery, Tokyo Medical University, Tokyo, Japan.
BACKGROUND: In order to diagnose an unsuspected gallbladder carcinoma
and to examine whether a differential diagnosis could be made between
cancer and noncancerous lesions during surgery, we evaluated the
findings of fine structures of various types of gallbladder mucosa.
METHODS: We used stereomicroscopy with a dye-contrast technique under
water and measured the maximum blood vessel diameters of the gallbladder
mucosa: normal gallbladder, chronic cholecystitis, and carcinoma.
RESULTS: All normal gallbladders showed fine-reticular-type findings. In
chronic cholecystitis, 5.8% of the specimens (n = 69) had fine reticular
type, 87.0% had rough reticular type, and 7.2% had atrophic type. All
the cases of adenomyomatosis (n = 16) showed rough reticular type. In
eight specimens of pancreaticobiliary maljunction, 75% of them showed
high reticular type, and the other 25% showed papillary type. The two
adenoma specimens showed fine granular type. In five gallbladder
carcinomas, the lattice-like pattern completely disappeared and showed
rough granular type. The average of maximum vessel diameters in the
gallbladder mucosa were 41.0 microm in normal gallbladders, 99.1 microm
in patients with chronic cholecystitis, and 614.8 microm in patients
with a carcinoma. There were significant differences among them (p <
0.05). CONCLUSION: This study showed that differential diagnosis between
cancer and noncancerous lesion is possible by dye-staining mucosal
pattern and measurement of maximum vessel diameters by stereoscopic
examination. Copyright 2001 S. Karger AG, Basel
10
UI - 21463167
AU - Muguruma N; Okamura S; Ichikawa S; Tsujigami K; Suzuki M; Tadatsu M;
TI -
Kusaka Y; Okita Y; Yano M; Ito S
Endoscopic sonography in the diagnosis of gallbladder wall lesions in
patients with gallstones.
SO - J Clin Ultrasound 2001 Sep;29(7):395-400
AD - Second Department of Internal Medicine, School of Medicine, The
University of Tokushima, 3-18-15, Kuramoto-cho, Tokushima 770-8503,
Japan.
PURPOSE: The purpose of this study was to evaluate the diagnostic
accuracy of endoscopic sonography (EUS) in the detection of gallbladder
wall lesions in patients with and without gallstones. METHODS: We
retrospectively reviewed the medical records, sonograms, and sonographic
reports of 62 patients who underwent cholecystectomy for gallbladder
wall lesions evaluated by EUS. We assessed the accuracy of EUS in
diagnosing gallbladder wall lesions in the presence or absence of
gallstones and on the basis of the size and number of stones and the
size of the gallbladder wall lesions. We also evaluated the effect of
acoustic shadowing. The EUS results were compared with the
histopathologic results. RESULTS: EUS correctly diagnosed the
gallbladder wall lesions in 17 (71%) of 24 patients with gallstones and
in 34 (89%) of 38 patients without gallstones. The diagnostic accuracy
of EUS was 86% in patients with gallbladder wall lesions smaller than 20
mm and 79% in patients with gallbladder wall lesions 20 mm or larger.
The diagnostic accuracy was 75% in patients with gallstones smaller than
5 mm and 67% in patients with stones 5 mm or larger. The accuracy was
67% in patients with 1-5 stones and 83% in patients with 6 or more
stones. None of these differences was statistically significant.
Acoustic shadowing did not affect the diagnostic accuracy of EUS.
CONCLUSIONS: The diagnostic accuracy of EUS for gallbladder wall lesions
is not affected by the presence of gallstones. However, better
diagnostic criteria must be established based on larger studies, and
technical refinements of the equipment are needed to increase the
accuracy of EUS in the diagnosis of gallbladder wall lesions. Copyright
2001 John Wiley & Sons, Inc.
11
UI - 21436738
AU - Roa I; Villaseca M; Araya J; Roa J; de Aretxabala X; Ibacache G; Garcia
TI -
M
[CD44 (HCAM) expression in subserous gallbladder carcinoma]
SO - Rev Med Chil 2001 Jul;129(7):727-34
AD - Unidad de Anatomia Patologica y Citopatologia Hospital Temuco,
Departamento de Cirugia, Facultad de Medicina, Universidad de la
Frontera, Temuco, Chile.
BACKGROUND: HCAM or CD44 is a multifunctional cell adhesion molecule,
related to cell-cell, cell-extracellular matrix interactions and
involved in tumor invasion. AIM: To study the importance of CD44
expression in subserous gallbladder carcinoma. MATERIAL AND METHODS: One
hundred five samples (93 female) of subserous gallbladder carcinoma and
33 non tumoral gallbladder were studied. CD44 was stained using the
streptavidine-biotin technique, using human anti CD44 antibodies. Eighty
subjects with carcinoma were followed for a period up to 105 months.
RESULTS: Mean age of patients was 62.6 years old, all tumors were
adenocarcinoma, all were silent and 13% were well differentiated. CD44
was expressed in all controls and in 91%, the expression was normal. In
57% of cancer samples, CD44 expression was abnormal, in 50% it was less
expressed and in 24%, it was not expressed. No differences in CD44
expression was observed between mucosa from control samples and mucosa
adjacent to the tumor or superficial or deep tumoral areas. Global five
years survival was 40%. No significant differences in survival were
observed in those tumors with a lower of absent CD44 expression. Six
patients with a higher expression died before 18 months of follow up.
CONCLUSIONS: Nearly 50% of subserous gallbladder carcinomas show an
abnormal CD44 expression.
12
UI - 21457660
AU - Inui K
TI -
Three-dimensional intraductal ultrasonography.
SO - J Gastroenterol 2000 Dec;35(12):951-2
13
UI - 21410261
AU - Schrem H; Schutze S; Klempnauer J
TI -
[What's new in hepatobiliary surgery?]
SO - Zentralbl Chir 2001 Aug;126(8):569-70
14
UI - 21439475
AU - Kaushik SP
TI -
Current perspectives in gallbladder carcinoma.
SO - J Gastroenterol Hepatol 2001 Aug;16(8):848-54
AD - Department of General Surgery, Government Medical College and Hospital,
Chandigarh, India. spkaushik@hotmail.com
Carcinoma gallbladder (CaGB) is not a common malignancy in a large
number of countries in the world, except Chile, Japan, some parts of
India, and a few other regions. Lacunae exist even today in terms of
understanding of its epidemiology, aetiopathogenesis, and in the early
pick up of malignanacy, as well as in choosing the most appropriate
treatment option for a given case. While Japanese surgeons have
advocated radical resections for CaGB and have shown good outcome
resulting in long- term survival, others have not felt convinced about
the desirability of undertaking such morbid surgical procedures in all
patients. Also, radical resections have not always resulted in a
tumor-free state and a cure in a large percentage of cases. Under the
circumstances, the clinician's mind is often confused as to the most
beneficial option for that patient once curative resection is not
possible. Palliation of the jaundice and/or gastric outlet obstruction
relieves the symptoms but does not prolong survival. The role of
adjuvant chemotherapy with or without cytoreductive surgery has not been
fully explored in CaGB. The present review quotes experience that seems
to support the above contention. However, a number of well-designed
multicentric trials are required to confirm the above philosophy of
treatment for the benefit of patients suffering from CaGB.
15
UI - 21439496
AU - Watanabe O; Haga S; Okabe T; Kumazawa K; Shiozawa S; Tsuchiya A;
TI -
Kajiwara T; Hirotani T; Aiba M
Amputation neuroma of common bile duct with obstructive jaundice.
SO - J Gastroenterol Hepatol 2001 Aug;16(8):945-6
16
UI - 21468691
AU - Quan ZW; Wu K; Wang J; Shi W; Zhang Z; Merrell RC
TI -
Association of p53, p16, and vascular endothelial growth factor protein
expressions with the prognosis and metastasis of gallbladder cancer.
SO - J Am Coll Surg 2001 Oct;193(4):380-3
AD - Department of Surgery, Xinhua Hospital, Shanghai Second Medical
University, China.
BACKGROUND: Tumor suppressor genes were studied in gallbladder disease
including cancer for correlation. VEGF (vascular endothelial growth
factor) expression was assessed against Nevin staging and metastasis of
gallbladder carcinoma. The importance of p53, p16, and VEGF in
gallbladder cancer was estimated. STUDY DESIGN: Twenty-four gallbladder
carcinomas, 20 gallbladder adenomas, and 18 chronic cholecystitis
specimens were immunohistochemically and histopathologically
investigated for the relation of p53, p16, and VEGF to Nevin staging and
pathologic grading. RESULTS: The expression rate of abnormal p53 in
gallbladder carcinomas was significantly higher than that in gallbladder
adenoma and chronic cholecystitis (p = 0.003, p = 0.014). The expression
rate of abnormal p53 in Nevin staging S1, S2, S3 gallbladder carcinoma
was significantly higher than that in S4, S5 (p = 0.01). Abnormal p16
was highest in carcinoma, next in adenoma, and lowest in chronic
cholecystitis (p = 0.031, p = 0.017). Gallbladder carcinoma expressed
VEGF far more often than adenoma or cholecystitis (p = 0.001);
VEGF-positive rates were lower in S1, S2, S3 than S4, S5 by Nevin
staging of gallbladder cancer (p = 0.044). CONCLUSION: Mutation of p53
and p16 genes might correlate with progression of of gallbladder
carcinoma. Analysis of p53 and p16 can estimate the prognosis of
gallbladder cancer. VEGF expression correlates with Nevin staging in
gallbladder cancer.
17
UI - 21268433
AU - Schauer RJ; Meyer G; Baretton G; Schildberg FW; Rau HG
TI -
Prognostic factors and long-term results after surgery for gallbladder
carcinoma: a retrospective study of 127 patients.
SO - Langenbecks Arch Surg 2001 Mar;386(2):110-7
AD - Department of Surgery, Klinikum Grosshadern, Ludwig-Maximilian
University, 81377 Munich, Germany.
BACKGROUND: The surgical management of gallbladder cancer is
controversial, especially as to the indications for reoperation,
extended resection, and aggressive treatment in advanced tumor stages.
METHODS: Records and follow-ups of 127 patients with gallbladder
carcinoma who underwent surgery between 1980 and 1997 were examined
according to the pTNM and Nevin staging systems. Factors predictive for
survival were obtained from histopathologic staging and surgical
procedures. RESULTS: Surgery for gallbladder cancer was associated with
an overall 5-year survival rate of 6.6%. Curative resection was possible
in 35.5% of cases, which resulted in 5-year survival rates of 20%.
Noncurative surgery revealed poor prognosis, with median survival time
limited to 3.2 months, independently of macroscopic or microscopic tumor
residues. None of the latter patients survived longer than 24 months.
Surgery of stage I/II cancer showed a 5-year survival rate of 64.5%. In
stage III/IV tumors, resectability was only 20.4%. However, curative
surgery in advanced stages significantly increased median survival from
3.2 to 19.4 months. CONCLUSIONS: Only complete tumor resection can
provide long-term survival, even in advanced stages. Because negative
surgical margins and UICC stage are the strongest predictors for
survival, reoperation is required with all incidental findings above the
T1b stage.
18
UI - 21291615
AU - Sanz-Altamira PM; O'Reilly E; Stuart KE; Raeburn L; Steger C; Kemeny NE;
TI -
Saltz LB
A phase II trial of irinotecan (CPT-11) for unresectable biliary tree
carcinoma.
SO - Ann Oncol 2001 Apr;12(4):501-4
AD - Division of Hematology/Oncology, Boston Center for Liver Cancer, Beth
Israel Deaconess Medical Center, Harvard Medical School, Boston,
Massachusetts 02215, USA.
BACKGROUND: Unresectable adenocarcinomas of the biliary tree have a very
poor prognosis. No good chemotherapeutic regimen is available.
Irinotecan has not yet been fully tested in this disease. We evaluated
its activity in unresectable bile duct cancers. PATIENTS AND METHODS:
Twenty-five consecutive eligible patients at our two institutions were
treated with irinotecan at a starting dose of 125 mg/m2. A cycle
consisted of once-a-week treatments for four consecutive weeks, followed
by two weeks of rest. All patients were required to have histologically
confirmed diagnosis, clinically documented metastatic or unresectable
carcinoma and measurable disease. Patients were evaluated for response,
toxicity, and survival. RESULTS: A total of 83 cycles of therapy were
delivered. Two patients had a partial response (8%; 95% confidence
interval (CI): 0%-18%) and ten additional patients had stable disease
for at least two months (40%; 95% CI: 20.8%-59.2%). The therapy was well
tolerated, with moderate myelosuppression and diarrhea as the main
toxicities. The overall median survival was 10 months. CONCLUSIONS:
Irinotecan has minimal activity in biliary tree carcinomas, but is well
tolerated with appropriate supportive care, and produces occasional
objective responses.
19
UI - 21457977
AU - Afzal S; Kristiansen VB; Rosenberg J
TI -
[Gallbladder polyps]
SO - Ugeskr Laeger 2001 Sep 10;163(37):5003-6
AD - Kirurgisk afdeling D, Amtssygehuset i Glostrup.
Polyps in the gall bladder are detected in 4-5% of the population and
most of them are benign. However, they can be premalignant and the
prognosis for gall bladder carcinoma is still poor. As with other
cancers, treatment at an early stage is therefore, considered essential
to improve the prognosis. Because of the very low morbidity after
laparoscopic cholecystectomy we recommend laparoscopic cholecystectomy
when a polyp in the gall bladder is detected by ultrasonography. A wait
and see attitude with repeated ultrasonography twice a year may be
chosen, if there are contra-indications to laparoscopic cholecystectomy.
If the lesion increases in size, cholecystectomy should be performed.
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.
As an oncologist, Dr. Giantonio provides care for many patients at the end of life, which he describes as a privilege and rewarding. Read more.
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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®)

