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1. Silva RG, Dahmoush L, Gerke H: Pancreatic metastasis of an ovarian malignant mixed Mullerian tumor identified by EUS-guided fine needle aspiration and Trucut needle biopsy. JOP; 2006;7(1):66-9
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  • [Title] Pancreatic metastasis of an ovarian malignant mixed Mullerian tumor identified by EUS-guided fine needle aspiration and Trucut needle biopsy.
  • CONTEXT: Malignant mixed Mullerian tumors are rare ovarian neoplasms that account for less than 2% of ovarian malignancies.
  • To our knowledge, this is the first report of a malignant mixed Mullerian tumor with metastasis to the pancreas.
  • The metastatic tumor was identified by endoscopic ultrasound guided fine needle aspiration (EUS-FNA) and Trucut needle biopsy of the pancreas.
  • CASE REPORT: We describe a 69-year-old female with concomitant Duke's C adenocarcinoma of the colon and stage III-C malignant mixed Mullerian tumor that presented with malignant ascites, increasing abdominal girth and a pancreatic head mass.
  • EUS revealed an 11 cm cystic mass in the head of the pancreas that was characterized as a carcinosarcoma/malignant mesodermal mixed tumor by EUS-FNA and Trucut needle biopsy.
  • The tumor was morphologically identical to the surgical specimen of her ovarian mass.
  • The patient was treated with palliative chemotherapy and a three-month follow up CT scan did not reveal any new metastatic lesions.
  • CONCLUSION: The pancreas is a rare site of metastasis and more commonly seen in renal cell carcinoma, melanoma or lung tumors; amongst others.
  • Although ovarian adenocarcinoma has been reported as a primary site of pancreatic metastasis, it has not been previously described originating from a mixed Mullerian tumor of the ovary presenting as a cystic pancreatic head mass.
  • [MeSH-major] Mixed Tumor, Mullerian / secondary. Ovarian Neoplasms / pathology. Pancreatic Neoplasms / secondary
  • [MeSH-minor] Aged. Biopsy, Fine-Needle / methods. Endosonography. Female. Humans. Neoplasm Staging. Pancreas / pathology. Pancreas / radiography. Prognosis. Tomography, X-Ray Computed


2. Plotnikov A, Tichler T, Korenstein R, Keisari Y: Involvement of the immune response in the cure of metastatic murine CT-26 colon carcinoma by low electric field-enhanced chemotherapy. Int J Cancer; 2005 Dec 10;117(5):816-24
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  • [Title] Involvement of the immune response in the cure of metastatic murine CT-26 colon carcinoma by low electric field-enhanced chemotherapy.
  • Low electric field cancer treatment-enhanced chemotherapy (LEFCT-EC) is a new treatment modality that combines chemotherapeutic agents and low electric field stimulation.
  • LEFCT-EC was found to destroy malignant mouse tumors and cause massive death of tumor cells.
  • This may enable the immune system cells to efficiently recognize and eliminate tumor cells at the primary tumor site and at metastatic foci.
  • Mice with 15 mm diameter intracutaneous colon carcinomas (CT-26) were injected with BCNU (35 mg/kg), and 2 min later the tumors were exposed to low electric fields (intensity 40 V/cm, pulse duration 180 micros, frequency 500 Hz) for 12 min (LEFCT-EC).
  • We found that treatment with LEFCT-EC achieved complete cure of 93% of the animals.
  • In comparison, electric fields alone (13% cure), chemotherapy alone (0%), surgery (15%) or a combination of surgery and bis-chloroethyl-nitrosurea, carmustine (BCNU; 84%) treatments resulted in lower cure rates.
  • After treatment and cure with LEFCT-EC, 50% of the cured mice developed resistance to a tumor challenge (surgery + BCNU only 15%).
  • Furthermore, splenocytes from cured animals protected naive animals from a tumorigenic dose of tumor cells.
  • FACS analysis revealed restoration of normal splenocyte subpopulation proportions impaired by cytotoxic chemotherapy.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Carmustine / therapeutic use. Colonic Neoplasms / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. Flow Cytometry. Mice. Mice, Inbred BALB C. Neoplasm Metastasis

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 15981217.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; U68WG3173Y / Carmustine
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3. Ulusan S, Koç Z, Kayaselçuk F: Imaging characteristics of liver metastasis from gastrointestinal stromal tumor before and after imatinib mesylate treatment. Turk J Gastroenterol; 2008 Jun;19(2):129-32
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  • [Title] Imaging characteristics of liver metastasis from gastrointestinal stromal tumor before and after imatinib mesylate treatment.
  • Our objective was to show the unusual imaging characteristics of cystic liver metastases from a malignant gastrointestinal stromal tumor before and after treatment with imatinib mesylate.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Gastrointestinal Stromal Tumors / pathology. Gastrointestinal Stromal Tumors / ultrasonography. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Aged. Benzamides. Colon / pathology. Fatal Outcome. Humans. Imatinib Mesylate. Intestinal Neoplasms / drug therapy. Intestinal Neoplasms / ultrasonography. Intestine, Small / pathology. Liver / drug effects. Liver / pathology. Liver / ultrasonography. Male. Neoplasm Invasiveness. Stomach / pathology. Stomach Neoplasms / drug therapy. Stomach Neoplasms / ultrasonography

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  • (PMID = 19110671.001).
  • [ISSN] 2148-5607
  • [Journal-full-title] The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology
  • [ISO-abbreviation] Turk J Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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4. Ebisui C, Ohkubo K, Akitake H, Ohtsuka M, Maekawa T, Yoshioka S, Hama N, Kashiwazaki M, Taniguchi M, Tsujie M, Konishi M, Fujimoto T: [A case of ovarian metastasis from colon cancer successfully treated with multidisciplinary therapy]. Gan To Kagaku Ryoho; 2010 Nov;37(12):2542-4
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  • [Title] [A case of ovarian metastasis from colon cancer successfully treated with multidisciplinary therapy].
  • An 80-year-old female patient was undergone sigmoidectomy with D2 lymph node dissection for type 2 sigmoid colon cancer in February 2007.
  • CT scan and MRI revealed a mass of 10 cm in diameter with multiple cysts in the pelvic cavity, which was diagnosed a malignant ovarian tumor.
  • In May 2008, total hysterectomy, bilateral oophorectomy, and partial omentectomy were performed and its pathological finding was metastatic ovarian tumor originating from colon cancer.
  • Adjuvant chemotherapy was administered, as cancer cells were detected in the ascites.
  • [MeSH-major] Adenocarcinoma / pathology. Krukenberg Tumor / secondary. Krukenberg Tumor / therapy. Ovarian Neoplasms / secondary. Ovarian Neoplasms / therapy. Sigmoid Neoplasms / pathology
  • [MeSH-minor] Aged, 80 and over. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Drug Combinations. Female. Humans. Hysterectomy. Ovariectomy. Oxonic Acid / administration & dosage. Tegafur / administration & dosage. Uracil / administration & dosage

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  • (PMID = 21224633.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 56HH86ZVCT / Uracil; 5VT6420TIG / Oxonic Acid; 1-UFT protocol
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5. Curtis BR, Kaliszewski J, Marques MB, Saif MW, Nabelle L, Blank J, McFarland JG, Aster RH: Immune-mediated thrombocytopenia resulting from sensitivity to oxaliplatin. Am J Hematol; 2006 Mar;81(3):193-8
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  • Thrombocytopenia developing in the course of chemotherapy for malignant disease is usually attributed to drug-induced marrow suppression and/or marrow replacement by tumor.
  • We describe two patients who developed severe thrombocytopenia and hemorrhagic symptoms while being treated with oxaliplatin, 5-fluorouracil, and leukovorin for metastatic colon cancer in whom platelet destruction appears to have been caused by oxaliplatin-dependent antibodies specific for the platelet glycoprotein IIb/IIIa complex (alpha(IIb)/beta(3) integrin).
  • Drug-induced immune thrombocytopenia (DITP) should be considered in patients who experience a sudden, isolated drop in platelet levels while being treated with chemotherapeutic agents, especially when adequate numbers of megakaryocytes are present in the bone marrow.

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  • (PMID = 16493620.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL013629; United States / NHLBI NIH HHS / HL / HL-13629
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Autoantibodies; 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; 12001-76-2 / Vitamin B Complex; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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6. Valdespino-Castillo VE, Ruiz-Jaime A: [Renal cell carcinoma with colon metastases: an infrequent site for metastases]. Cir Cir; 2008 Jul-Aug;76(4):339-42
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  • [Title] [Renal cell carcinoma with colon metastases: an infrequent site for metastases].
  • [Transliterated title] Cáncer de riñón con metástasis a colon. Un sitio poco frecuente de metástasis.
  • BACKGROUND: Renal cell carcinoma (RCC) represents approximately 3% of malignant tumors in adults and occurs in a M:F ratio of 1.5:1.0.
  • Clear cell carcinoma is the most frequent histological type, and 30% of renal carcinomas have metastasized at the time of diagnosis.
  • The objective of the present study is to report colon metastasis of clear cell carcinoma that required surgery and chemotherapy.
  • His treatment consisted of cytoreductive radical nephrectomy and interferon because of pulmonary disease.
  • Nevertheless, he presented with hematochezia and underwent colonoscopy where a splenic flexure tumor was demonstrated.
  • Biopsy reported a clear cell tumor.
  • Pathology report was clear cell carcinoma with involvement of the colon from the mucosa to serosa.
  • Currently, there is no evidence of tumor activity and the patient is being followed-up.
  • CONCLUSIONS: RCC metastases are most frequent in lung, liver, and bone and less frequent in brain, skin, and soft tissue.
  • Survival of patients who present metastasis <1 year after nephrectomy is 33 months vs. patients who present metastasis after 1 year from nephrectomy (55 months).
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Colectomy / methods. Combined Modality Therapy. Follow-Up Studies. Gastrointestinal Hemorrhage / etiology. Humans. Immunotherapy. Interferon-alpha / therapeutic use. Lung Neoplasms / secondary. Male. Middle Aged. Nephrectomy / methods. Remission Induction

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  • (PMID = 18778546.001).
  • [ISSN] 0009-7411
  • [Journal-full-title] Cirugía y cirujanos
  • [ISO-abbreviation] Cir Cir
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha
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7. Ren JZ, Huo JR: [Effect of 5-Aza-CdR on expression and methylation of E-cadherin gene in human colon carcinoma cells]. Chin J Cancer; 2010 Jan;29(1):38-42
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  • [Title] [Effect of 5-Aza-CdR on expression and methylation of E-cadherin gene in human colon carcinoma cells].
  • BACKGROUND AND OBJECTIVE: Colon cancer is one of the most common malignant tumors, and its pathogenesis is not fully understood.
  • E-cadherin can suppress tumor cell invasion and metastasis, and is considered as an invasion/metastasis suppressor gene.
  • Inactivation of E-cadherin gene often occurs in colon carcinoma.
  • This study was to investigate the correlation between E-cadherin gene expression and the methylation status of E-cadherin 5' CpG islands in human colon carcinoma cell line HT-29, and to explore the mechanism of carcinogenesis of colon cancer.
  • METHODS: Immunocytochemical dicho-step method and reverse transcription-polymerase chain reaction (RT-PCR) were used to detect the expression of E-cadherin protein and mRNA in HT-29 cells after 5-Aza-CdR treatment; methylation specific PCR was used to analyze the methylation status at promoter of E-cadherin gene.
  • RESULTS: The expression of E-cadherin gene could be restored by 5-Aza-CdR treatment, immunocytochemical staining showed the positive expression ratio of E-cadherin increased from (21+/-7)% (1 micromol/L) to (39+/-13)% (5 micromol/L); E-cadherin genes were methylated and not expressed in HT-29 cells in the colon carcinoma.
  • CONCLUSIONS: E-cadherin methylation plays an important role in the carcinogenesis of colon carcinoma cells and can re-express after the treatment with 5-Aza-CdR.
  • [MeSH-major] Azacitidine / analogs & derivatives. Cadherins / metabolism. Cell Proliferation / drug effects. DNA Methylation
  • [MeSH-minor] Antimetabolites, Antineoplastic / pharmacology. Colonic Neoplasms / drug therapy. Gene Expression Regulation, Neoplastic. HT29 Cells / metabolism. HT29 Cells / pathology. Humans. RNA, Messenger / metabolism

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  • (PMID = 20038309.001).
  • [ISSN] 1000-467X
  • [Journal-full-title] Chinese journal of cancer
  • [ISO-abbreviation] Chin J Cancer
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Cadherins; 0 / RNA, Messenger; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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8. Matusiak D, Benya RV: CYP27A1 and CYP24 expression as a function of malignant transformation in the colon. J Histochem Cytochem; 2007 Dec;55(12):1257-64
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  • [Title] CYP27A1 and CYP24 expression as a function of malignant transformation in the colon.
  • Because of the propensity of bioactive 1,25-dihydroxyvitamin D3 to cause toxic hypercalcemia, considerable effort has been directed to identifying safer drugs while retaining the efficacy of the parent compound.
  • However, vitamin D precursors do not present toxicity concerns and may be sufficient for CRC chemoprevention or chemotherapy, providing the appropriate enzymes are present in colonic epithelia.
  • We previously showed that CYP27B1 is present at equally high levels in the colon and CRC irrespective of differentiation but was not present in metastases.
  • Whereas total cellular CYP27A1 remains high in CRC and lymph node metastases, the amount of enzyme present in the nuclei decreases with tumor cell dedifferentiation while rising in the cytoplasm.
  • Although the amount of total CYP24 decreases slightly in CRC as a function of tumor cell dedifferentiation and metastasis, location of this enzyme shifts almost entirely from the nuclear compartment to the cytoplasmic compartment.
  • These data indicate that non-toxic vitamin D precursors should be sufficient for CRC chemoprevention, but that neither vitamin D nor its precursors may be sufficient for CRC chemotherapy.
  • [MeSH-minor] Adenomatous Polyps / enzymology. Adenomatous Polyps / ultrastructure. Colon / enzymology. Colon / pathology. Colon / ultrastructure. Humans. Immunohistochemistry. Intestinal Mucosa / enzymology. Intestinal Mucosa / ultrastructure. Lymphatic Metastasis. Vitamin D3 24-Hydroxylase

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  • (PMID = 17875655.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-094346
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.126 / Vitamin D3 24-Hydroxylase; EC 1.14.13.15 / CYP27A1 protein, human; EC 1.14.13.15 / Cholestanetriol 26-Monooxygenase
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9. Ripoll GV, Garona J, Hermo GA, Gomez DE, Alonso DF: Effects of the synthetic vasopressin analog desmopressin in a mouse model of colon cancer. Anticancer Res; 2010 Dec;30(12):5049-54

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  • [Title] Effects of the synthetic vasopressin analog desmopressin in a mouse model of colon cancer.
  • The compound seems to act by inducing an agonist effect on specific V2 vasopressin membrane receptors present in both tumor cells and endothelial cells.
  • Here we explored the antitumor effects of DDAVP in cultured colon carcinoma cells and in a syngeneic Balb/c mouse model.
  • Both human Colo-205 and mouse CT-26 colon carcinoma cell lines expressed the V2 receptor, as revealed by immunofluorescence.
  • In vivo, DDAVP (2 intravenous doses of 2 μg/kg) reduced accumulation of ascites and formation of intestinal tumor nodules in mice intraperitoneally inoculated with CT-26 cells.
  • Perioperative administration of DDAVP significantly inhibited tumor progression in animals surgically implanted in the spleen with CT-26 cells, and caused some reduction in liver metastasis.
  • Although DDAVP and 5-fluorouracil demonstrated additive cytostatic effects in vitro, no antitumor effects were observed in this study in mice receiving a single cycle of chemotherapy (25 mg/kg) in combination with the peptide.
  • Our data suggest that DDAVP may be potentially used to minimize spread or survival of residual malignant cells during surgical procedures for colon and other gastrointestinal tumors.
  • [MeSH-major] Colonic Neoplasms / drug therapy. Deamino Arginine Vasopressin / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Fluorescent Antibody Technique. Humans. Male. Mice. Mice, Inbred BALB C. Receptors, Vasopressin / biosynthesis

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  • (PMID = 21187489.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Vasopressin; ENR1LLB0FP / Deamino Arginine Vasopressin
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10. Azab AK, Kleinstern J, Srebnik M, Rubinstein A: The metastatic stage-dependent mucosal expression of sialic acid is a potential marker for targeting colon cancer with cationic polymers. Pharm Res; 2008 Feb;25(2):379-86
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  • [Title] The metastatic stage-dependent mucosal expression of sialic acid is a potential marker for targeting colon cancer with cationic polymers.
  • PURPOSE: Locoregional recurrence is the most common complication after adenocarcinoma resection in the colon, despite adjuvant chemotherapy.
  • Therapy efficacy could be improved if designed to target malignant cells by incorporating specific recognition factors in the drugs or the drug vehicles.
  • The aim of this study was to elucidate whether the overexpression of sialic acid (SA) on colonic malignant tissues could be utilized for drug targeting by cationic polymers.
  • MATERIALS AND METHODS: Cell lines (IEC-6, SW-480 and SW-620) and colon polyps and normal adjacent tissues harvested from dimethylhydrazine (DMH) induced rats were used as in vitro and in vivo models of different metastatic stages of colon cancer.
  • The binding of FITC labeled cationic polymers of various degrees of cationization to normal and malignant colonic cells and tissue was measured.
  • RESULTS: SA was overexpressed on malignant colonic cells and tissues, and its expression correlated to the metastatic stage in vitro.
  • The binding of the cationic copolymers to the cell lines and tissues correlated with the charge density of the polymer and with the metastatic stage of the cell line.
  • The interaction between the malignant colonic cells and tissues with the polymers was SA dependent and increased after mucus removal.
  • CONCLUSION: Cationic polymers could be used as a targeting tool to colonic malignant epithelium, to be implemented in drug delivery and diagnosis.
  • [MeSH-major] Acrylamides / pharmacology. Colonic Neoplasms / drug therapy. N-Acetylneuraminic Acid / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Intestinal Mucosa / metabolism. Neoplasm Metastasis. Neoplasm Staging. Rats. Wheat Germ Agglutinins / metabolism

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  • (PMID = 17960470.001).
  • [ISSN] 0724-8741
  • [Journal-full-title] Pharmaceutical research
  • [ISO-abbreviation] Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acrylamides; 0 / Wheat Germ Agglutinins; GZP2782OP0 / N-Acetylneuraminic Acid
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11. Sakakibara T, Kurasawa T, Narumi K, Kamano T, Tsurumaru M: T-cell malignant lymphoma of the ileum causing ileac fistulas: report of a case. Surg Today; 2002;32(6):536-40
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  • [Title] T-cell malignant lymphoma of the ileum causing ileac fistulas: report of a case.
  • Upper and lower gastrointestinal examinations did not reveal any abnormal findings, but an abdominal aortic aneurysm was diagnosed by computed tomography, and thus was determined to be the source of the pain.
  • The patient was referred to our hospital to undergo a grafting operation; however, a laparotomy performed in July 1997 revealed an unexpected small intestinal tumor, and therefore a partial ileectomy between 15 and 70cm in an oral direction from the terminal ileum was carried out instead.
  • Histopathological and genetic examinations demonstrated diffuse small malignant lymphocytic T-cell lymphomas of the ileum invading all layers.
  • Metastasis of the facial skin and local recurrence were recognized 5 months later, and chemotherapy with THP-COP and ESHAP only resulted in progressive disease.
  • An autopsy revealed three fistulas caused by metastatic tumors, one of which communicated with the duodenum from the ileum, one with the skin from the ileum, and one to the transverse colon from the ileum.
  • [MeSH-minor] Aged. Fatal Outcome. Humans. Male. Neoplasm Recurrence, Local

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  • (PMID = 12107782.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 10
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12. Barthomeuf C, Lim S, Iranshahi M, Chollet P: Umbelliprenin from Ferula szowitsiana inhibits the growth of human M4Beu metastatic pigmented malignant melanoma cells through cell-cycle arrest in G1 and induction of caspase-dependent apoptosis. Phytomedicine; 2008 Jan;15(1-2):103-11
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  • [Title] Umbelliprenin from Ferula szowitsiana inhibits the growth of human M4Beu metastatic pigmented malignant melanoma cells through cell-cycle arrest in G1 and induction of caspase-dependent apoptosis.
  • Metastatic malignant melanoma have a bad prognosis (median survival: 6-8 months) mainly due to the development of lung, hepatic and brain metastases.
  • We have observed that the cell susceptibility to umbelliprenin decreases in the order M4Beu (metastatic pigmented malignant melanoma)>A549 (nonsmall cell lung carcinoma) approximately PC3 (androgen-resistant prostate carcinoma)>PA1 (ovary teratocarcinoma)>human primary fibroblasts approximately MCF7 (breast adenocarcinoma)>DLD1 (colon adenocarcinoma).
  • The finding that the cytotoxic effect of umbelliprenin is markedly more pronounced in M4Beu cells than in primary fibroblasts, suggests a therapeutic margin.
  • As M4Beu cell proliferation is more potently inhibited by umbelliprenin (IC50 12.3 microM) than by the citrus coumarin auraptene (7-geranyloxycoumarin, IC50 17.1 microM) previously reported capable of inhibiting the prevalence of lung metastasis in mice bearing B16BL6 murine melanoma, our data suggest that umbelliprenin orally administered and foods and folk medicines containing this coumarin, may afford protection against the development and early recurrence of malignant melanoma.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma / drug therapy. Cell Proliferation / drug effects. Ferula / chemistry. G1 Phase / drug effects. Melanoma / drug therapy. Umbelliferones / pharmacology
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. Caspases / metabolism. Cell Line, Tumor. Cells, Cultured. Cisplatin / pharmacology. Coumarins / pharmacology. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Fibroblasts / drug effects. Humans. Inhibitory Concentration 50. Plant Roots / chemistry

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  • (PMID = 17689942.001).
  • [ISSN] 0944-7113
  • [Journal-full-title] Phytomedicine : international journal of phytotherapy and phytopharmacology
  • [ISO-abbreviation] Phytomedicine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Coumarins; 0 / Umbelliferones; 495-02-3 / aurapten; EC 3.4.22.- / Caspases; MSD8N8A1LQ / umbelliprenin; Q20Q21Q62J / Cisplatin
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13. Karnak I, Senocak ME, Ciftci AO, Cağlar M, Bingöl-Koloğlu M, Tanyel FC, Büyükpamukçu N: Inflammatory myofibroblastic tumor in children: diagnosis and treatment. J Pediatr Surg; 2001 Jun;36(6):908-12
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  • [Title] Inflammatory myofibroblastic tumor in children: diagnosis and treatment.
  • BACKGROUND/PURPOSE: Inflammatory myofibroblastic tumor (IMT) is a rare benign neoplasm.
  • Furthermore, malignant degeneration or transformation to lymphoma in the recurrent or residual IMT have directed attention to this interesting entity.
  • Herein, the authors present their experience with IMT with special emphasis on diagnosis and treatment.
  • METHODS: All records of children treated with diagnosis of IMT between 1977 and 1999 inclusive were evaluated retrospectively.
  • Except the case with intrathoracic IMT, all the tumors were located in the abdomen at various sites such as cardioesophageal junction (n = 1), left hepatic lobe (n = 1), mesentery of the small bowel (n = 2), and antimesenteric wall of the descending colon (n = 1), gastrosplenic region and porta hepatis (n = 1).
  • Tumor sizes ranged from 3 x 2 x 2 cm to 15 x 15 x 13 cm.
  • Total surgical excision of IMT was considered adequate for treatment in 6 cases.
  • One patient with aggressive IMT required further treatments such as immunomodulation and chemotherapy and died of neutropenic sepsis.
  • CONCLUSIONS: IMT is a benign neoplasm rarely presented with malignant features such as local invasiveness, recurrence, distant metastasis, or malignant transformation.
  • IMT can be suspected preoperatively through some hematologic abnormalities and radiologic findings, but precise diagnosis should be made on the basis of histologic findings.
  • Complete surgical resection and close follow-up are all necessary for appropriate treatment to avoid recurrences as well as unnecessary and potentially harmful therapy.
  • [MeSH-minor] Child. Female. Humans. Male. Recurrence. Retrospective Studies. Tomography, X-Ray Computed

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  • [Copyright] Copyright 2001 by W.B. Saunders Company.
  • (PMID = 11381424.001).
  • [ISSN] 0022-3468
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 21
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14. Mauritz R, Giovannetti E, Beumer IJ, Smid K, Van Groeningen CJ, Pinedo HM, Peters GJ: Polymorphisms in the enhancer region of the thymidylate synthase gene are associated with thymidylate synthase levels in normal tissues but not in malignant tissues of patients with colorectal cancer. Clin Colorectal Cancer; 2009 Jul;8(3):146-54
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  • [Title] Polymorphisms in the enhancer region of the thymidylate synthase gene are associated with thymidylate synthase levels in normal tissues but not in malignant tissues of patients with colorectal cancer.
  • The analysis of the relationship between TSER genotype and TS mRNA and activity in normal and malignant tissues might explain the previous controversial data and help in the selection of useful markers to predict drug response and/or toxicity.
  • MATERIALS AND METHODS: To address this issue, we studied TSER genotype, TS expression, and activity with specific polymerase chain reaction and activity assays (TS catalytic activity and FdUMP binding) in normal (liver, mucosa) and malignant (primary tumor and liver metastasis) tissues from 83 patients with CRC.
  • RESULTS: No correlation between TSER genotype and TS mRNA and protein levels was observed in malignant tissues.
  • In contrast, normal tissues harboring one or two 3RG alleles were characterized by higher TS protein levels (2.4-fold; P = .008) and catalytic activity (P < .05) compared with the other TSER genotypes.
  • CONCLUSION: These results suggest that TSER polymorphisms do not predict tumoral TS levels possibly depending on altered TS regulation in cancer tissues, and might explain the lack of clear correlation with clinical outcome after chemotherapy with fluoropyrimidines.
  • However, the relationship between TS phenotype and TSER genotype in normal tissues warrants further investigations in large-scale prospective studies evaluating TS genotype and fluoropyrimidine tolerability.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Colon / enzymology. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / enzymology. Neoplasm Recurrence, Local / genetics. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Rectum / enzymology. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

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  • (PMID = 19632929.001).
  • [ISSN] 1938-0674
  • [Journal-full-title] Clinical colorectal cancer
  • [ISO-abbreviation] Clin Colorectal Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.1.1.45 / Thymidylate Synthase
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15. Izawa N, Matsumoto S, Manabe J, Tanizawa T, Hoshi M, Shigemitsu T, Machinami R, Kanda H, Takeuchi K, Miki Y, Arai M, Shirahama S, Kawaguchi N: A Japanese patient with Li-Fraumeni syndrome who had nine primary malignancies associated with a germline mutation of the p53 tumor-suppressor gene. Int J Clin Oncol; 2008 Feb;13(1):78-82
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  • [Title] A Japanese patient with Li-Fraumeni syndrome who had nine primary malignancies associated with a germline mutation of the p53 tumor-suppressor gene.
  • We describe a patient who had nine primary malignant tumors and a germline mutation in the p53 tumor-suppressor gene, characteristically found in the Li-Fraumeni syndrome (LFS).
  • The patient received chemotherapy followed by surgery and had a remission.
  • After the age of 28 years, nine primary malignant tumors developed successively, including right breast cancer, colon cancer, malignant fibrous histiocytoma (MFH) of the abdominal wall, right lung double cancers, bilateral breast cancers, and MFH of the left thigh.
  • This is the second highest number of types of primary malignant tumors to be reported in LFS.
  • The patient died of lung metastasis from MFH at the age of 37 years.
  • Our findings suggest that a multidisciplinary approach to treatment, including surgery, is beneficial in patients with LFS.
  • [MeSH-minor] Adolescent. Female. Humans. Neoplasms / genetics. Neoplasms / pathology. Neoplasms / therapy. Pedigree

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16. Rad FH, Le Buanec H, Paturance S, Larcier P, Genne P, Ryffel B, Bensussan A, Bizzini B, Gallo RC, Zagury D, Uzan G: VEGF kinoid vaccine, a therapeutic approach against tumor angiogenesis and metastases. Proc Natl Acad Sci U S A; 2007 Feb 20;104(8):2837-42
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  • [Title] VEGF kinoid vaccine, a therapeutic approach against tumor angiogenesis and metastases.
  • Tumor growth depends on blood supply, requiring the development of new vessels, and vascular endothelial growth factor (VEGF) plays a central role in neoangiogenic processes.
  • For this reason, VEGF represents a target for the development of new therapeutic antiangiogenic molecules.
  • Clinical trials using anti-VEGF mAbs such as bevacizumab have validated the efficacy of this therapeutic approach but have also revealed adverse effects.
  • In mVEGF kinoid-immunized BALB/c mice challenged with syngeneic CT26 colorectal tumor cells, the number and size of lung metastases were significantly decreased.
  • In human (h)VEGF kinoid-immunized BALB/c mice, high levels of serum Abs to hVEGF were present, and purified IgG from these mice decreased by > or =50% the tumor growth of human A673 rhabdomyosarcoma cells and HT29 colon carcinoma xenografted in Swiss nude and NOD/SCID mice, respectively.
  • Tumor cell growth inhibition was similar to that observed in mice receiving therapeutic doses of bevacizumab.
  • These experiments suggest that a therapeutic vaccine containing VEGF kinoid may represent a strategy for safely combating VEGF-dependent neovascularization and metastases occurring in malignant tumors.
  • [MeSH-major] Cancer Vaccines / immunology. Cancer Vaccines / therapeutic use. Neoplasms / blood supply. Neoplasms / drug therapy. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / prevention & control. Vascular Endothelial Growth Factor A / immunology
  • [MeSH-minor] Animals. Antibodies / isolation & purification. Antibody Formation / immunology. Cell Line, Tumor. Colorectal Neoplasms / pathology. Female. HT29 Cells. Humans. Immune Sera. Immunization. Lung Neoplasms / secondary. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Metastasis. Paclitaxel / therapeutic use. Rhabdomyosarcoma / pathology. Xenograft Model Antitumor Assays

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  • (PMID = 17301234.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Cancer Vaccines; 0 / Immune Sera; 0 / Vascular Endothelial Growth Factor A; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC1797624
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17. Manuelli M, De Luca L, Iaria G, Tatangelo P, Sforza D, Perrone L, Bellini MI, Angelico R, Anselmo A, Tisone G: Conversion to rapamycin immunosuppression for malignancy after kidney transplantation. Transplant Proc; 2010 May;42(4):1314-6
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  • INTRODUCTION: Malignancies are a well-known complication of immunosuppressive therapy among renal transplant recipients, representing an important cause of long-term morbidity and mortality.
  • Rapamycin has been shown to limit the proliferation of a number of malignant cell lines in vivo and in vitro.
  • METHODS: Fifteen patients developed the following malignancies at a mean of 90.3 months (range = 10-252) after kidney transplantation: metastatic gastric cancer (n = 1), metastatic colon cancer (n = 1), bilateral nephrourothelioma (n = 1), skin cancer (n = 2), Kaposi's sarcoma (n = 2), posttransplant lymphoproliferative disorder (PTLD; n = 4), renal cell carcinoma T1 (n = 1), MALT lymphoma (n = 1), intramucous colon carcinoma (n = 1), liposarcoma of the spermatic cord (n = 1).
  • After the diagnosis of malignancy, the patients were switched from calcineurin inhibitor-based immunosuppression to rapamycin (monotherapy, n = 3), or associated with steroids (n = 6) or with mycophenolate mofetil (n = 6).
  • RESULTS: Both patients with metastatic cancer underwent chemotherapy but succumbed after 6 and 13 months.
  • Two patients with PTLD who underwent chemotherapy died after 12 and 36 months.
  • Renal graft function remained stable in all other patients from diagnosis throughout follow-up.
  • Nevertheless, it is difficult to assess whether tumor regression was due to rapamycin treatment or to the reduced immunosuppression.
  • [MeSH-major] Kidney Transplantation / immunology. Neoplasms / immunology. Sirolimus / therapeutic use
  • [MeSH-minor] Cell Division / drug effects. Cell Line, Tumor. Colonic Neoplasms / immunology. Colonic Neoplasms / pathology. Genital Neoplasms, Male / immunology. Genital Neoplasms, Male / pathology. Humans. Immunosuppression / methods. Immunosuppressive Agents / therapeutic use. Liposarcoma / immunology. Liposarcoma / pathology. Male. Neoplasm Metastasis. Skin Neoplasms / immunology. Skin Neoplasms / pathology. Stomach Neoplasms / immunology. Stomach Neoplasms / pathology

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  • [Copyright] Copyright (c) 2010. Published by Elsevier Inc.
  • (PMID = 20534289.001).
  • [ISSN] 1873-2623
  • [Journal-full-title] Transplantation proceedings
  • [ISO-abbreviation] Transplant. Proc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; W36ZG6FT64 / Sirolimus
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18. Shen R, Tao L, Xu Y, Chang S, Van Brocklyn J, Gao JX: Reversibility of aberrant global DNA and estrogen receptor-alpha gene methylation distinguishes colorectal precancer from cancer. Int J Clin Exp Pathol; 2009;2(1):21-33
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  • However, the significance of epigenetic changes for diagnosis and/or prognosis of colorectal cancer have not been established, although it has been extensively investigated.
  • Recently we have identified a new type of cancer cell called precancerous stem cells (pCSCs) and proposed that cancer may arise from a lengthy development process of tumor initiating cells (TICs) --> pCSCs --> cancer stem cells (CSCs) --> cancer, which is in parallel to histological changes of hyperplasia (TICs) --> precancer (pCSCs) --> carcinoma (CSCs/cancer cells), accompanied by clonal evolutionary epigenetic and genetic alterations.
  • In this study, we investigated whether aberrant DNA methylation can be used as a biomarker for the differentiation between premalignant and malignant lesions in the colorectum.
  • The aberrant methylation can be completely reversed in APs, but not in AdCa by a nonsteroidal anti-inflammatory drug (NSAID) celecoxib, which is a selective inhibitor of cyclooxygenase-2 (Cox-2), suggesting that the epigenetic alterations between colorectal precancer (AP) and cancer (AdCa) are fundamentally different in response to anti-cancer therapy.

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  • (PMID = 18830381.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; DNA methylation / Precancer / cancer progression / colorectal cancer / epigenetic / estrogen receptor-α / nonsteroidal anti-inflammatory drugs / tumor initiation
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19. Pahlavan PS, Kanthan R: Goblet cell carcinoid of the appendix. World J Surg Oncol; 2005 Jun 20;3:36

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Goblet cell carcinoid (GCC) of the appendix is a rare neoplasm that share histological features of both adenocarcinoma and carcinoid tumor.
  • While its malignant potential remains unclear, GCC's are more aggressive than conventional carcinoid.
  • The clinical presentations of this neoplasm are also varied.
  • The focus is on its diagnosis, histopathological aspects, clinical manifestations, and management.
  • Accurate diagnosis of this neoplasm requires astute observations within an acutely inflamed appendix as this neoplasm has a prominent pattern of submucosal growth and usually lacks the formation of a well-defined tumor mass.
  • The most common surgical treatment of choice was appendectomy with right hemicolectomy in 34.70% followed by simple appendectomy in 24.57%.
  • Concomitant distant metastasis at diagnosis was present in 11.16% of patients with the ovaries being the most common site in 3.60% followed by disseminated abdominal carcinomatosis in 1.03%.
  • Local lymph node involvement was seen in 8.76% of patients at the time of diagnosis.
  • GCC's of the appendix remains a neoplasm of unpredictable biological behavior and thus warrants lifelong surveillance for recurrence of the disease upon diagnosis and successful surgical extirpation.
  • CONCLUSION: GCC of the appendix is a rare neoplasm.
  • Due to its wide range of presentation, this tumor should be considered as a possible diagnosis in many varied situations leading to abdominal surgery.
  • In cases with obvious spread of the disease chemotherapy, mostly with 5-FU and leucovorin is advised.
  • Cytoreductive surgery with adjuvant intraperitoneal chemotherapy can offer improved survival in cases with advanced peritoneal dissemination.

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  • (PMID = 15967038.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1182398
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20. Hao LS, Zhu X, Zhao LH, Qian K, Zhou Y, Bu J, Wu XT: Clear cell adenocarcinoma of colorectum: a case report and review of the literature. Acta Gastroenterol Belg; 2007 Apr-Jun;70(2):235-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary clear cell adenocarcinoma of the colorectum is a rare neoplasm, which differs from ordinary carcinomas of the colorectum in morphological features, but shares some traits of clear cell carcinoma of other organs.
  • The tumor is usually composed of polygonal or oval cells with abundant granular and clear cytoplasm.
  • The tumor was located in descending colon of a 37-year-old man, and was rich in glycogen but poor in mucin.
  • By immunoperoxidase and histochemical staining, we clarified the clinicopathological characteristics, diagnosis and differential diagnoses, and pursued its potential pathogenesis.
  • In our case, necrosis, high mitotic activity and lymph node metastasis may suggest a highly malignant tumor and an advanced pathological stage.
  • Nevertheless, the patient has survived for one year with the help of operation and postoperative adjuvant chemotherapy.
  • Regardless of the stage and differentiation, surgical therapy and proper adjuvant chemotherapy are effective means to treat the clear cell adenocarcinoma of the colorectum.
  • [MeSH-minor] Adult. Biopsy. Colonoscopy. Diagnosis, Differential. Follow-Up Studies. Humans. Male

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  • (PMID = 17715642.001).
  • [ISSN] 1784-3227
  • [Journal-full-title] Acta gastro-enterologica Belgica
  • [ISO-abbreviation] Acta Gastroenterol. Belg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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21. Zou GM: Cancer initiating cells or cancer stem cells in the gastrointestinal tract and liver. J Cell Physiol; 2008 Dec;217(3):598-604
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It has been suggested that cancer stem cells population within the solid tumor with indefinite proliferation potential drives the growth and metastasis of cancer.
  • In literature, these malignant stem cells also named Cancer initiating cells.
  • Cancer stem cells exhibit low rate of division and proliferation in their niche that help them to avoid chemotherapy and radiation.
  • Epithelial cancers are believed to originate from transformation of tissue stem cells.
  • Bone marrow-derived cells, which are frequently recruited to sites of tissue injury and inflammation, might also represent a potential source of malignancy in the gastrointestinal tract.
  • More recently, other cancer stem cells in gastrointestinal tract, such as colon cancer stem cells, liver cancer stem cells, have been also characterized in their phenotype.
  • These advances clearly will bring the new strategy in cancer treatment and control in the gastrointestinal tract.
  • [MeSH-minor] Animals. Antigens, CD / metabolism. Biomarkers, Tumor / metabolism. Cell Proliferation. Glycoproteins / metabolism. Humans. Peptides / metabolism

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  • (PMID = 18651561.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / Peptides
  • [Number-of-references] 55
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22. Katunuma N, Tsuge H, Nukatsuka M, Asao T, Fukushima M: Structure-based design of specific cathepsin inhibitors and their application to protection of bone metastases of cancer cells. Arch Biochem Biophys; 2002 Jan 15;397(2):305-11
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The decalcification during bone absorption is followed by the degradation of type-1 collagen by osteoclastic cathepsins.
  • Tumor-bearing osteoclasts or TNF-alpha-activated osteoclasts secrete large amounts of cysteine proteases, especially procathepsin L, which powerfully degrade type-1 collagen leading to tumor-associated bone absorption and release of bone calcium.
  • The bone pit formations in vitro, which are caused by osteoclasts derived from human bone marrow cells activated by RANKL and M-CSF and also by mice osteoclasts activated by TNF-alpha, are significantly prevented by CLIK-148 treatment.
  • We evaluated the in vivo inhibitory effect of malignant hypercalcemia induced by LJC-1 human mandibular cancer inoculation by CLIK-148 treatment, and the CLIK-148 treatment significantly protected against the tumor-induced hypercalcemia.
  • On the protection of bone metastasis of colon 26 PMF-15 implanted to mouse calvaria, CLIK-148 treatment significantly inhibited calvaria bone absorption (direct metastasis).
  • The CLIK-148 treatment also reduced distant bone metastasis to the femur and tibia of melanoma A375 tumors implanted into the left ventricle of the heart.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Cathepsins / antagonists & inhibitors. Cysteine Proteinase Inhibitors / therapeutic use. Epoxy Compounds / therapeutic use. Hypercalcemia / drug therapy. Pyridines / therapeutic use
  • [MeSH-minor] Animals. Bone Resorption / drug therapy. Collagen / metabolism. Colonic Neoplasms / drug therapy. Drug Design. Femur / pathology. Humans. Melanoma / drug therapy. Mice. Neoplasm Metastasis

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  • [Copyright] (c)2002 Elsevier Science.
  • (PMID = 11795887.001).
  • [ISSN] 0003-9861
  • [Journal-full-title] Archives of biochemistry and biophysics
  • [ISO-abbreviation] Arch. Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CLIK 148; 0 / Cysteine Proteinase Inhibitors; 0 / Epoxy Compounds; 0 / Pyridines; 9007-34-5 / Collagen; EC 3.4.- / Cathepsins
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23. Voelkel-Johnson C, Hannun YA, El-Zawahry A: Resistance to TRAIL is associated with defects in ceramide signaling that can be overcome by exogenous C6-ceramide without requiring down-regulation of cellular FLICE inhibitory protein. Mol Cancer Ther; 2005 Sep;4(9):1320-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor superfamily that selectively induces apoptosis in malignant cells.
  • Colon cancer cells isolated from the primary tumor (SW480) and a subsequent metastasis (SW620) of the same patient have different sensitivities to TRAIL.
  • Upon TRAIL treatment, ceramide (primarily C(16)-ceramide) increased in SW480 but not SW620 cells.
  • Our results suggest that ceramide plays a role in promoting TRAIL-mediated apoptosis and that TRAIL-resistant cancers may benefit from combination therapy with ceramide or agents that enhance ceramide accumulation.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / pharmacology. Ceramides / pharmacology. Colonic Neoplasms / metabolism. Intracellular Signaling Peptides and Proteins / metabolism. Membrane Glycoproteins / pharmacology. Signal Transduction. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. CASP8 and FADD-Like Apoptosis Regulating Protein. Caspases / metabolism. Down-Regulation. Drug Combinations. Enzyme Activation / drug effects. Flow Cytometry. Glucose / metabolism. Humans. Kinetics. Paclitaxel / pharmacology. TNF-Related Apoptosis-Inducing Ligand. Tumor Cells, Cultured

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  • (PMID = 16170023.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 1P20-RR17698-01; United States / NCI NIH HHS / CA / P01 CA97132
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Apoptosis Regulatory Proteins; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Ceramides; 0 / Drug Combinations; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 038753E78J / N-caproylsphingosine; EC 3.4.22.- / Caspases; IY9XDZ35W2 / Glucose; P88XT4IS4D / Paclitaxel
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24. Marshall JC, Fernandes BF, Di Cesare S, Maloney SC, Logan PT, Antecka E, Burnier MN Jr: The use of a cyclooxygenase-2 inhibitor (Nepafenac) in an ocular and metastatic animal model of uveal melanoma. Carcinogenesis; 2007 Sep;28(9):2053-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The expression of cyclooxygenase-2 (COX-2) has been reported as an indicator of poor prognosis in a wide variety of human tumors, including colon, breast and uveal melanoma (UM).
  • COX-2 inhibitors have shown promise in controlling the malignancy of several types of tumors.
  • Intraocular tumor growth was evaluated weekly by fundoscopic examination and each animal was weighed prior to examination.
  • Blood samples were taken weekly from all rabbits to detect circulating malignant cells (CMCs) throughout the experiment.
  • The control group developed more intraocular tumors and presented with metastases and higher detectable levels of CMCs before the treated group.
  • [MeSH-major] Benzeneacetamides / therapeutic use. Cyclooxygenase 2 Inhibitors / therapeutic use. Melanoma / drug therapy. Phenylacetates / therapeutic use. Uveal Neoplasms / drug therapy
  • [MeSH-minor] Animals. Models, Animal. Neoplasm Metastasis. Rabbits

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  • (PMID = 17434930.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzeneacetamides; 0 / Cyclooxygenase 2 Inhibitors; 0 / Phenylacetates; 0J9L7J6V8C / nepafenac
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25. Tsuruta D, Kobayashi H, Imanishi H, Sugawara K, Ishii M, Jones JC: Laminin-332-integrin interaction: a target for cancer therapy? Curr Med Chem; 2008;15(20):1968-75
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  • [Title] Laminin-332-integrin interaction: a target for cancer therapy?
  • For many years, extracellular matrix (ECM) was considered to function as a tissue support and filler.
  • We focus in this review on a laminin isoform, laminin-332 (formerly termed laminin-5), a major component of the basement membrane (BM) of skin and other epithelial tissues.
  • Mutations in either laminin-332 or integrin alpha6beta4 result in junctional epidermolysis bullosa, a blistering skin disease, while targeting of laminin-332 by autoantibodies in cicatricial pemphigoid leads to dysadhesion of epithelial cells from their underlying connective tissue.
  • Abnormal expression of laminin-332 and its integrin receptors is also a hallmark of certain tumor types and is believed to promote invasion of colon, breast and skin cancer cells.
  • Moreover, there is emerging evidence that laminin-332 and its protease degradation products are not only found at the leading front of several tumors but also likely induce and/or promote tumor cell migration.
  • Finally, we discuss strategies for the development of laminin-332-based antagonists for the treatment of malignant tumors.

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  • (PMID = 18691052.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / AR054184-18; United States / NIAMS NIH HHS / AR / R01 AR054184; United States / NIAMS NIH HHS / AR / R01 AR054184-20; United States / NIAMS NIH HHS / AR / R01 AR054184-18
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Integrins; 0 / kalinin; EC 2.7.- / Protein Kinases; EC 3.4.- / Metalloproteases
  • [Number-of-references] 133
  • [Other-IDs] NLM/ NIHMS251751; NLM/ PMC2992754
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