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1. Khoury JD, Jones D, Yared MA, Manning JT Jr, Abruzzo LV, Hagemeister FB, Medeiros LJ: Bone marrow involvement in patients with nodular lymphocyte predominant Hodgkin lymphoma. Am J Surg Pathol; 2004 Apr;28(4):489-95
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  • Of 275 patients diagnosed as lymphocyte predominant Hodgkin lymphoma at our institution (1983-2003), we identified 7 patients with purely nodular disease in the diagnostic lymph node biopsy specimen who also had bone marrow involvement.
  • The latter was detected at the time of initial diagnosis in four patients, after one cycle of chemotherapy in one patient, and at relapse in two patients.
  • All patients had laboratory, radiologic, and/or morphologic evidence of aggressive disease at the time of detection of bone marrow involvement.
  • At last follow-up, four patients had died of their disease and three were alive following therapy.
  • Bone marrow involvement is associated with laboratory, radiologic, or morphologic evidence of aggressive disease and poor prognosis.
  • Although the best terminology for these bone marrow lymphomas is uncertain, the aggressive clinical behavior of these neoplasms supports the need for intensive therapy.
  • [MeSH-major] Bone Marrow Neoplasms / pathology. Hodgkin Disease / pathology. Lymphocytes

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  • (PMID = 15087668.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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2. Alvarez Kindelán J, López Beltrán A, Anglada Curado F, Moreno Arcas P, Carazo Carazo JL, Regueiro López JC, Leva Vallejo M, Prieto Castro R, Requena Tapia MJ: [Clinico-pathologic differences between bladder neoplasm with low malignant potential and low-grade carcinoma]. Actas Urol Esp; 2001 Oct;25(9):645-50
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  • [Title] [Clinico-pathologic differences between bladder neoplasm with low malignant potential and low-grade carcinoma].
  • [Transliterated title] Diferencias clínico-patológicas entre neoplasia vesical de bajo potencial maligno y carcinoma de bajo grado.
  • OBJECTIVE: To determine if the morphologic subgrouping of grade I bladder tumors between papillary neoplasm of low malignant potential and low grade papillary carcinoma is of clinical and survival value.
  • MATERIAL AND METHODS: All 257 consecutive patients diagnosed of superficial bladder cancer between 1990 and 1995 in HU Reina Sofia of Cordoba were reviewed and further reclassified according to WHO/ISUP consensus classification of urothelial neoplasms of the bladder.
  • Of the tumors 12 were urothelial papilloma, 51 were papillary neoplasm of low malignant potential, 43 were low grade papillary carcinoma Ta, 65 were low grade papillary carcinoma T1 and 37 were high grade papillary carcinoma.
  • The differences in the multiplicity are not significant and only the mean size is higher in papillary low grade carcinoma.
  • About the risk factors for recurrence and progression of the disease, only is significative the tumor size.
  • Rarely, the use of chemotherapy seems to play a role in the recurrence.
  • There are no differences in recurrence and progression between the groups, although the percentages are always higher in the papillary low grade carcinoma group.
  • We think that the use of chemotherapy must be avoided in this low grade bladder tumors.
  • [MeSH-major] Carcinoma / pathology. Urinary Bladder Neoplasms / pathology

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  • (PMID = 11765548.001).
  • [ISSN] 0210-4806
  • [Journal-full-title] Actas urologicas espanolas
  • [ISO-abbreviation] Actas Urol Esp
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
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3. Jeibmann A, Hasselblatt M, Pfister S, Sträter R, Brentrup A, Holling M, Niederstadt T, Paulus W, Frühwald MC: From glioblastoma to gangliocytoma: an unforeseen but welcome shift in biological behavior. J Neurosurg Pediatr; 2009 Nov;4(5):475-8
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  • [Title] From glioblastoma to gangliocytoma: an unforeseen but welcome shift in biological behavior.
  • Few GBMs in children, however, seem to respond quite well to adjuvant chemotherapy.
  • The biological basis for such chemotherapy sensitivity remains uncertain.
  • In this paper the authors report the case of a 2-month-old girl with a histologically confirmed GBM (WHO Grade IV) in whom chemotherapy was accompanied by differentiation of the malignant primary tumor into a typical gangliocytoma (WHO Grade I) showing ganglioid differentiation and expression of neuronal markers synaptophysin, neurofilament, and NeuN as well as a low Ki 67/MIB-1 proliferation index.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / therapy. Ganglioneuroma / pathology. Ganglioneuroma / therapy. Glioblastoma / pathology. Glioblastoma / therapy
  • [MeSH-minor] Antigens, Nuclear / metabolism. Antineoplastic Agents / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor. Carboplatin / administration & dosage. Cell Differentiation. Cell Proliferation. Etoposide / administration & dosage. Female. Humans. Hydrocephalus / pathology. Infant. Nerve Tissue Proteins / metabolism. Neurofilament Proteins / metabolism. Neurosurgical Procedures. Reverse Transcriptase Polymerase Chain Reaction. Synaptophysin / metabolism

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  • (PMID = 19877783.001).
  • [ISSN] 1933-0715
  • [Journal-full-title] Journal of neurosurgery. Pediatrics
  • [ISO-abbreviation] J Neurosurg Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Biomarkers, Tumor; 0 / Nerve Tissue Proteins; 0 / Neurofilament Proteins; 0 / Synaptophysin; 0 / neuronal nuclear antigen NeuN, human; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin
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4. Azad NS, Annunziata CM, Steinberg SM, Minasian L, Premkumar A, Chow C, Kotz HL, Kohn EC: Lack of reliability of CA125 response criteria with anti-VEGF molecularly targeted therapy. Cancer; 2008 Apr 15;112(8):1726-32
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  • [Title] Lack of reliability of CA125 response criteria with anti-VEGF molecularly targeted therapy.
  • BACKGROUND: CA125 is an accepted indicator of epithelial ovarian cancer (EOC) response and is used to monitor patients treated with cytotoxic chemotherapy.
  • It is uncertain how CA125 is affected by molecularly targeted drugs.
  • In this pilot study, the authors analyzed the utility of CA125 to predict disease behavior in patients who were receiving sorafenib, a Raf-kinase/VEGFR2 inhibitor, and bevacizumab, an anti-VEGF monoclonal antibody.
  • Computed tomography (CT) scans were performed every 2 cycles for restaging, and CA125 was measured monthly.
  • CA125 concentrations were retrospectively analyzed as a function of clinical behavior.
  • Three patients with objective partial response by imaging lasting >20, >22, and >24 cycles would have terminated treatment prematurely if CA125 had been used.
  • [MeSH-major] CA-125 Antigen / analysis. Neoplasms, Glandular and Epithelial / drug therapy. Ovarian Neoplasms / drug therapy. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Vascular Endothelial Growth Factor A / antagonists & inhibitors
  • [MeSH-minor] Adult. Angiogenesis Inhibitors / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzenesulfonates / administration & dosage. Bevacizumab. Cohort Studies. Female. Humans. Middle Aged. Neoplasm Staging. Niacinamide / analogs & derivatives. Phenylurea Compounds. Pilot Projects. Pyridines / administration & dosage. Remission Induction. Reproducibility of Results. Retrospective Studies. Tomography, X-Ray Computed. Treatment Outcome. raf Kinases / antagonists & inhibitors

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  • [CommentIn] Cancer. 2008 Nov 15;113(10):2832-3; author reply 2833-4 [18846540.001]
  • (PMID = 18300236.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Clinical Trial, Phase I; Comparative Study; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / CA-125 Antigen; 0 / Phenylurea Compounds; 0 / Pyridines; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 25X51I8RD4 / Niacinamide; 2S9ZZM9Q9V / Bevacizumab; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.11.1 / raf Kinases
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5. Theodoropoulos G, Wise WE, Padmanabhan A, Kerner BA, Taylor CW, Aguilar PS, Khanduja KS: T-level downstaging and complete pathologic response after preoperative chemoradiation for advanced rectal cancer result in decreased recurrence and improved disease-free survival. Dis Colon Rectum; 2002 Jul;45(7):895-903
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  • [Title] T-level downstaging and complete pathologic response after preoperative chemoradiation for advanced rectal cancer result in decreased recurrence and improved disease-free survival.
  • PURPOSE: Preoperative chemoradiation therapy is used widely in the treatment of rectal cancer.
  • The predictive value of response to neoadjuvant remains uncertain.
  • We retrospectively evaluated the impact of response to preoperative and, specifically, of T-level downstaging, nodal downstaging, and complete pathologic response after chemoradiation therapy on oncologic outcome of patients with locally advanced rectal cancer.
  • METHODS: There were 88 patients with ultrasound Stage T3/T4 midrectal (n = 37) and low rectal (n = 51) cancers (63 males; mean age 62.6 years).
  • All patients were treated by preoperative 5-fluorouracil-based chemotherapy and pelvic radiation followed by surgical resection in six weeks or longer (56 sphincter-preserving resections).
  • RESULTS: T-level downstaging after neoadjuvant treatment was demonstrated in 36 (41 percent) of 88 patients, and complete pathologic response was observed in 16 (18 percent) of the 88.
  • Patients with T-level downstaging and complete pathologic response were characterized by significantly better disease-free survival (P = 0.03, P = 0.04) and better overall survival (P = 0.07, P = 0.08), according to Wilcoxon's test comparing Kaplan-Meier survival curves.
  • None of the patients with complete pathologic response developed recurrence or died during the follow-up period.
  • CONCLUSION: T-level downstaging and complete pathologic response after preoperative chemoradiation therapy followed by definitive surgical resection for advanced rectal cancer resulted in decreased recurrence and improved disease-free survival.
  • Advanced rectal cancers that undergo T-level downstaging and complete pathologic response after chemoradiation therapy may represent subgroups that are characterized by better biologic behavior.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Neoplasm Recurrence, Local / prevention & control. Rectal Neoplasms / drug therapy. Rectal Neoplasms / radiotherapy
  • [MeSH-minor] Disease-Free Survival. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoadjuvant Therapy. Neoplasm Staging. Preoperative Care. Remission Induction. Retrospective Studies. Treatment Outcome

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  • (PMID = 12130878.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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6. Bergmann F, Breinig M, Höpfner M, Rieker RJ, Fischer L, Köhler C, Esposito I, Kleeff J, Herpel E, Ehemann V, Friess H, Schirmacher P, Kern MA: Expression pattern and functional relevance of epidermal growth factor receptor and cyclooxygenase-2: novel chemotherapeutic targets in pancreatic endocrine tumors? Am J Gastroenterol; 2009 Jan;104(1):171-81
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  • OBJECTIVES: Pancreatic endocrine tumors represent morphologically and biologically heterogeneous neoplasms.
  • Well-differentiated endocrine tumors (benign or of uncertain behavior) can be distinguished from well-differentiated and poorly differentiated endocrine carcinomas.
  • Although many well-differentiated endocrine carcinomas show rather low rates of tumor growth, more than two-thirds of pancreatic endocrine carcinomas display distant metastases at the time of diagnosis.
  • As the currently applied therapies beyond surgery only achieve partial or complete response rates of approximately 15%, additional chemotherapeutic targets are needed, especially in the therapy of inoperable and progressive pancreatic endocrine carcinomas.
  • RESULTS: The expression of EGFR correlated significantly with the grade of malignancy, increasing from low rates of expression in benign tumors and tumors of uncertain behavior to high rates of expression in well- and poorly differentiated endocrine carcinomas.
  • The expression of COX-2 was independent of the malignant potential, but was more frequently expressed in primary tumors than in metastases.
  • The treatment of the human pancreas carcinoid cell line BON and the mouse insulinoma cell line beta-TC-3 with EGFR and COX-2 inhibitors (monotherapy and combined therapy) resulted in a significant, dose-dependent reduction of cell viability coupled with increased apoptosis.
  • [MeSH-major] Cyclooxygenase 2 / metabolism. Pancreatic Neoplasms / metabolism. Pyrazoles / therapeutic use. Receptor, Epidermal Growth Factor / metabolism. Sulfonamides / therapeutic use. Tyrphostins / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Animals. Apoptosis / drug effects. Blotting, Western. Carcinoid Tumor / metabolism. Celecoxib. Cell Line, Tumor. Cell Survival / drug effects. Cyclooxygenase 2 Inhibitors / therapeutic use. Dose-Response Relationship, Drug. Female. Humans. Insulinoma / metabolism. Male. Mice. Mice, Transgenic. Middle Aged. Quinazolines. Tumor Cells, Cultured. Young Adult

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  • (PMID = 19098866.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazoles; 0 / Quinazolines; 0 / Sulfonamides; 0 / Tyrphostins; 170449-18-0 / tyrphostin AG 1478; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; JCX84Q7J1L / Celecoxib
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7. Malpica A, Deavers MT, Lu K, Bodurka DC, Atkinson EN, Gershenson DM, Silva EG: Grading ovarian serous carcinoma using a two-tier system. Am J Surg Pathol; 2004 Apr;28(4):496-504
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  • The study included 50 cases of low-grade ovarian serous carcinoma and 50 cases of high-grade ovarian serous carcinoma retrieved from the files of the Department of Pathology at the University of Texas M. D.
  • Cases assigned to the low-grade category were characterized by the presence of mild to moderate nuclear atypia.
  • Patients in the low-grade ovarian serous carcinoma group ranged in age from 19 to 75 years (mean 41.7 years) while patients in the high-grade ovarian serous carcinoma group ranged in age from 27 to 76 years (mean 55 years).
  • Using the Shimizu/Silverberg system, the low-grade ovarian serous carcinoma cases were distributed as follows: grade 1, 47 cases; grade 2, 3 cases.
  • Most of the patients in both groups were treated with total abdominal hysterectomy and bilateral salpingo-oophorectomy and also received cisplatinum-based chemotherapy.
  • On follow-up, 37 patients in the low-grade ovarian serous carcinoma group had died of disease at a median 4.2 years after diagnosis compared with 46 patients in the high-grade ovarian serous carcinoma group who died of disease at a median of 1.7 years.
  • Eight patients in the low-grade ovarian serous carcinoma group and 4 patients in the high-grade ovarian serous carcinoma group were alive with disease at median follow-ups of 4.3 and 3.85 years, respectively.
  • Four patients with low-grade serous carcinoma were alive without evidence of disease after a follow-up that ranged from 4.4 to 22.6 years (median 6.85 years), and one died of other causes 14 years after the diagnosis of her ovarian tumor.
  • Of interest, 60% of the low-grade ovarian serous carcinomas in this study were associated with a serous neoplasm of low malignant potential, whereas this association was present in only 2% of the high-grade ovarian serous carcinomas.
  • [MeSH-major] Cystadenocarcinoma, Serous / pathology. Ovarian Neoplasms / pathology

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  • (PMID = 15087669.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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8. Jedlicka P: Ewing Sarcoma, an enigmatic malignancy of likely progenitor cell origin, driven by transcription factor oncogenic fusions. Int J Clin Exp Pathol; 2010;3(4):338-47
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  • [Title] Ewing Sarcoma, an enigmatic malignancy of likely progenitor cell origin, driven by transcription factor oncogenic fusions.
  • Since its first description by James Ewing in 1921, Ewing Sarcoma has been a cryptic malignancy.
  • A poorly differentiated tumor of uncertain histogenesis and aggressive biologic behavior, it is the second most common malignancy of bone and soft tissue affecting adolescents and young adults.
  • Some two decades ago, the understanding of Ewing Sarcoma biology took a leap forward with the identification of recurrent EWS/Ets fusions, which drive onco-genesis in this disease.
  • A further leap forward occurred over the last half decade with the application of gene silencing, global expression profiling and primary cell culture technologies to the study of this disease.
  • Improved understanding of EWS/Ets biology and relevant oncogenic pathways has in turn led to the development of targeted therapies, including, recently, small molecules targeting key complexes involving the oncogenic fusion itself.
  • In many respects still remaining an enigma, Ewing Sarcoma is an important model for cancers originating in progenitor-type cells or manifesting progenitor-type cell features, and cancers containing recurrent oncogenic fusions, the latter a surprisingly expanding number.
  • [MeSH-minor] Animals. Bone Neoplasms / drug therapy. Bone Neoplasms / genetics. Bone Neoplasms / pathology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Gene Expression. Humans. Soft Tissue Neoplasms / drug therapy. Soft Tissue Neoplasms / genetics. Soft Tissue Neoplasms / pathology

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  • [Cites] Cancer Res. 2009 May 15;69(10):4363-71 [19417137.001]
  • [Cites] Br J Cancer. 2009 Jul 7;101(1):80-90 [19491900.001]
  • [Cites] Nat Med. 2009 Jul;15(7):750-6 [19584866.001]
  • [Cites] Cancer Res. 2009 Dec 1;69(23):9047-55 [19920188.001]
  • [Cites] Adv Anat Pathol. 2010 Jan;17(1):1-11 [20032633.001]
  • [Cites] Carcinogenesis. 2010 Mar;31(3):394-401 [20019092.001]
  • [Cites] Cancer Lett. 2007 Aug 28;254(1):1-10 [17250957.001]
  • [Cites] Cancer Res. 1999 Nov 15;59(22):5745-50 [10582694.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(1):204-13 [10623711.001]
  • [Cites] Cancer Res. 2000 Mar 15;60(6):1536-40 [10749119.001]
  • [Cites] J Biol Chem. 2000 Aug 11;275(32):24865-71 [10827180.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Jul 15;120(2):91-8 [10942797.001]
  • [Cites] Oncogene. 2000 Sep 14;19(39):4523-30 [11002425.001]
  • [Cites] J Biol Chem. 2000 Dec 1;275(48):37612-8 [10982800.001]
  • [Cites] Oncogene. 2001 Feb 1;20(5):626-33 [11313995.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3586-90 [11325824.001]
  • [Cites] Lab Invest. 2001 Jun;81(6):803-14 [11406642.001]
  • [Cites] J Biol Chem. 2001 Jun 22;276(25):22317-22 [11301318.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5747-54 [11607824.001]
  • [Cites] J Biol Chem. 2001 Nov 9;276(45):41977-84 [11553628.001]
  • [Cites] Int J Cancer. 2002 Mar 10;98(2):193-8 [11857407.001]
  • [Cites] Oncogene. 2002 May 30;21(24):3847-54 [12032822.001]
  • [Cites] Cancer Res. 2002 Aug 15;62(16):4583-7 [12183411.001]
  • [Cites] Cancer Biol Ther. 2002 Jul-Aug;1(4):330-6 [12432241.001]
  • [Cites] Br J Cancer. 2003 Jan 13;88(1):137-45 [12556973.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3464-8 [12839926.001]
  • [Cites] Oncogene. 2003 Oct 9;22(44):6819-29 [14534527.001]
  • [Cites] Int J Cancer. 2004 Jan 20;108(3):358-66 [14648701.001]
  • [Cites] Oncogene. 2003 Dec 18;22(58):9282-7 [14681687.001]
  • [Cites] Oncogene. 2004 May 6;23(21):3830-40 [15021903.001]
  • [Cites] Mol Cell Biol. 2004 Aug;24(16):7275-83 [15282325.001]
  • [Cites] Oncogene. 2004 Sep 16;23(42):7087-94 [15273724.001]
  • [Cites] Mol Genet Metab. 2004 Sep-Oct;83(1-2):60-73 [15464421.001]
  • [Cites] J Clin Invest. 1990 Dec;86(6):1806-14 [2174908.001]
  • [Cites] Mol Cell Biol. 1993 Dec;13(12):7393-8 [8246959.001]
  • [Cites] Cancer Res. 1996 Oct 15;56(20):4570-4 [8840962.001]
  • [Cites] Oncogene. 1997 Jan 16;14(2):213-21 [9010223.001]
  • [Cites] Oncogene. 1998 Aug 6;17(5):603-10 [9704926.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1428-32 [10197607.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):222-7 [10508522.001]
  • [Cites] Oncogene. 1999 Sep 30;18(40):5592-7 [10523836.001]
  • [Cites] Semin Cancer Biol. 2005 Jun;15(3):189-96 [15826833.001]
  • [Cites] Cancer Res. 2005 May 1;65(9):3868-76 [15867386.001]
  • [Cites] Cancer Res. 2005 Oct 1;65(19):8698-705 [16204038.001]
  • [Cites] Cancer Res. 2005 Oct 1;65(19):8984-92 [16204072.001]
  • [Cites] Gene. 2005 Dec 19;363:1-14 [16202544.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11459-68 [16357154.001]
  • [Cites] Mol Cell Biol. 2006 Apr;26(7):2467-78 [16537893.001]
  • [Cites] Future Oncol. 2005 Aug;1(4):521-8 [16556028.001]
  • [Cites] Cancer Cell. 2006 May;9(5):405-16 [16697960.001]
  • [Cites] Cancer Res. 2006 Jun 1;66(11):5574-81 [16740692.001]
  • [Cites] Clin Cancer Res. 2006 Jun 1;12(11 Pt 1):3532-40 [16740780.001]
  • [Cites] Brief Funct Genomic Proteomic. 2006 Mar;5(1):8-14 [16769671.001]
  • [Cites] Mol Cancer Res. 2006 Nov;4(11):851-9 [17114343.001]
  • [Cites] Clin Cancer Res. 2006 Nov 15;12(22):6781-90 [17121899.001]
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1322-30 [17317844.001]
  • [Cites] Cancer Cell. 2007 May;11(5):421-9 [17482132.001]
  • [Cites] Cancer Res. 2008 Sep 1;68(17):7100-9 [18757425.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8968-75 [18974141.001]
  • [Cites] Lab Invest. 2008 Dec;88(12):1291-302 [18838963.001]
  • [Cites] Oncologist. 2009 Jan;14(1):83-91 [19126579.001]
  • [Cites] PLoS One. 2009;4(2):e4634 [19247449.001]
  • [Cites] Cancer Res. 2009 Mar 1;69(5):1776-81 [19208848.001]
  • [Cites] PLoS One. 2009;4(3):e4932 [19305498.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 31;106(13):5324-9 [19289832.001]
  • [Cites] Ann Clin Lab Sci. 2009 Spring;39(2):160-6 [19429803.001]
  • [Cites] Mol Cell Biol. 2007 Nov;27(22):7918-34 [17875932.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2176-85 [18381423.001]
  • [Cites] PLoS One. 2008;3(4):e1965 [18414662.001]
  • [Cites] Oncogene. 2008 May 22;27(23):3282-91 [18084326.001]
  • [Cites] Curr Opin Oncol. 2008 Jul;20(4):412-8 [18525337.001]
  • [Cites] PLoS One. 2008;3(7):e2634 [18648544.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Jul 22;105(29):10149-54 [18626011.001]
  • (PMID = 20490326.001).
  • [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; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / RNA-Binding Protein EWS
  • [Number-of-references] 73
  • [Other-IDs] NLM/ PMC2872742
  • [Keywords] NOTNLM ; Ewing Sarcoma / fusion oncogene / progenitor cell / transcription factor
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9. Celikel C, Yumuk PF, Basaran G, Yildizeli B, Kodalli N, Ahiskali R: Epithelioid hemangioendothelioma with multiple organ involvement. APMIS; 2007 Jul;115(7):881-8
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  • Epithelioid hemangioendothelioma is a rare vascular neoplasm of uncertain malignant potential.
  • The concurrent involvement of multiple sites at presentation may cause diagnostic problems because epithelioid hemangioendothelioma can mimic other neoplastic processes.
  • Although it is a chemo-resistant disease, chemotherapy is usually advised for patients with metastatic or concurrent involvement.
  • Here we document the presentation, treatment, and outcome of two cases with concurrent involvement of the lung and liver.
  • [MeSH-major] Hemangioendothelioma, Epithelioid / radiography. Liver Neoplasms / radiography. Lung Neoplasms / radiography
  • [MeSH-minor] Female. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 17614859.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Denmark
  • [Number-of-references] 30
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10. Cheng L, Foster SR, MacLennan GT, Lopez-Beltran A, Zhang S, Montironi R: Inflammatory myofibroblastic tumors of the genitourinary tract--single entity or continuum? J Urol; 2008 Oct;180(4):1235-40
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  • PURPOSE: Inflammatory myofibroblastic tumor of the genitourinary tract is a spindled soft tissue lesion that is often mistaken for sarcoma.
  • We investigated whether inflammatory myofibroblastic tumors in adults and children are the same entity, and whether inflammatory myofibroblastic tumor is part of a biological spectrum that includes benign and malignant entities at opposite ends.
  • RESULTS: The literature suggests that with evidence of anaplastic lymphoma kinase rearrangement and expression, the lesion is neoplastic rather than reactive, differentiating it from previously described lesions.
  • CONCLUSIONS: Inflammatory myofibroblastic tumor of the genitourinary tract should be considered a neoplasm of uncertain malignant potential, and routine surveillance and close clinical followup are recommended.
  • Aggressive therapy (radical cystectomy, radiation or chemotherapy) is unwarranted given the indolent and often benign clinical course for the majority of cases.
  • To understand the diagnostic and prognostic implications future emphasis should be placed on the link between genetic abnormalities, and clinical course, therapeutic response and ultimate outcome.
  • [MeSH-major] Carcinoma / pathology. Granuloma, Plasma Cell / pathology. Sarcoma / pathology. Urogenital Neoplasms / pathology
  • [MeSH-minor] Biopsy, Needle. Diagnosis, Differential. Humans. Immunohistochemistry. Incidence. Neoplasm Staging. Prognosis. Risk Assessment. Ureteral Neoplasms / diagnosis. Ureteral Neoplasms / pathology. Urethral Neoplasms / diagnosis. Urethral Neoplasms / pathology. Urinary Bladder Neoplasms / diagnosis. Urinary Bladder Neoplasms / pathology

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  • (PMID = 18707729.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 40
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11. Zaino R, Whitney C, Brady MF, DeGeest K, Burger RA, Buller RE: Simultaneously detected endometrial and ovarian carcinomas--a prospective clinicopathologic study of 74 cases: a gynecologic oncology group study. Gynecol Oncol; 2001 Nov;83(2):355-62
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  • It is often unclear whether this represents synchronous primary tumors or metastasis from endometrium to ovary, or from ovary to endometrium; consequently, staging, therapy, and expected outcome are uncertain.
  • The Gynecologic Oncology Group sought to study patients with simultaneously detected adenocarcinomas in the endometrium and ovary with disease grossly confined to the pelvis to explore the possible correlation among discrete tumor subsets, natural history, and survival.
  • All were initially treated with total abdominal hysterectomy, bilateral salpingo-oophorectomy, and staging laparotomy, with radiation and chemotherapy left to the discretion of the treating physician and patient.
  • Fifteen pathologic variables were examined to identify differences in tumor behavior.
  • The histologic grades of ovarian and uterine tumors also distinguished groups of patients with different probabilities of recurrence at 5 years: 8.0% (95% CI: 2.8-21.3%) for those patients with no more than grade 1 disease at either site and 22.4% (95% CI: 11.8-38.4%) for those with a higher grade in either the ovary or the endometrium (hazard ratio = 3.1, P = 0.047).
  • CONCLUSION: The prognosis for women with simultaneously detected carcinomas in the uterus and ovary with gross disease confined to the pelvis is surprisingly good, particularly for those with disease microscopically limited to the uterus and ovary or of low histologic grade.
  • [MeSH-major] Adenocarcinoma / pathology. Endometrial Neoplasms / pathology. Neoplasms, Multiple Primary / pathology. Ovarian Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Female. Humans. Middle Aged. Neoplasm Recurrence, Local / pathology. Prognosis. Prospective Studies

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  • [Copyright] Copyright 2001 Academic Press.
  • (PMID = 11606097.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 12482; United States / NCI NIH HHS / CA / CA 12534; United States / NCI NIH HHS / CA / CA 13630; United States / NCI NIH HHS / CA / CA 15975; United States / NCI NIH HHS / CA / CA 16386; United States / NCI NIH HHS / CA / CA 16938; United States / NCI NIH HHS / CA / CA 19502; United States / NCI NIH HHS / CA / CA 21720; United States / NCI NIH HHS / CA / CA 21946; United States / NCI NIH HHS / CA / CA 23501; United States / NCI NIH HHS / CA / CA 23765; United States / NCI NIH HHS / CA / CA 37535; United States / NCI NIH HHS / CA / CA 37569; United States / NCI NIH HHS / CA / CA 40296
  • [Publication-type] Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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12. Malpica A, Deavers MT, Gershenson D, Tortolero-Luna G, Silva EG: Serous tumors involving extra-abdominal/extra-pelvic sites after the diagnosis of an ovarian serous neoplasm of low malignant potential. Am J Surg Pathol; 2001 Aug;25(8):988-96
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  • [Title] Serous tumors involving extra-abdominal/extra-pelvic sites after the diagnosis of an ovarian serous neoplasm of low malignant potential.
  • The involvement of extra-abdominal/extra-pelvic sites by serous tumors after the diagnosis of an ovarian serous neoplasm of low malignant potential is extremely rare.
  • Ten patients also received adjuvant therapy (radiotherapy, 2; chemotherapy and radiotherapy, 4; chemotherapy, 3; intraperitoneal 32P, 1).
  • The interval between the diagnosis of the ovarian neoplasm and the subsequent tumor involving an extra-abdominal/extra-pelvic site ranged from 4 to 240 months (mean 124 months).
  • Eight patients were treated with chemotherapy, 1 with radiotherapy, 2 with chemotherapy and radiotherapy, and 1 with surgery alone.
  • Six patients died of disease and 5 patients were alive with no evidence of disease.
  • In this small series of cases, no definitive clinical or pathologic feature related to the occurrence of extra-abdominal/extra-pelvic serous tumors was found.
  • Based on the LN involvement and the endosalpingiosis seen in some cases, these tumors might develop from circulating neoplastic serous cells or from areas of endosalpingiosis involving extra-abdominal/extra-pelvic sites.
  • [MeSH-major] Cystadenocarcinoma / pathology. Neoplasms, Second Primary / pathology. Ovarian Neoplasms / pathology

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  • (PMID = 11474282.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Chan AT, Giovannucci EL: Primary prevention of colorectal cancer. Gastroenterology; 2010 Jun;138(6):2029-2043.e10
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  • In the past several decades, much has been learned about the dietary, lifestyle, and medication risk factors for this malignancy.
  • Although a role for supplements, including vitamin D, folate, and vitamin B6, remains uncertain, calcium supplementation is likely to be at least modestly beneficial.
  • Medications such as aspirin and nonsteroidal anti-inflammatory drugs and postmenopausal hormones for women are associated with substantial reductions in colorectal cancer risk, though their utility is affected by associated risks.

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  • [Cites] Environ Mol Mutagen. 2004;44(1):10-25 [15199543.001]
  • [Cites] J Natl Cancer Inst. 2004 Jun 16;96(12):921-5 [15199111.001]
  • [Cites] Am J Clin Nutr. 2004 Jul;80(1):108-13 [15213036.001]
  • [Cites] J Nutr. 2004 Jul;134(7):1806-11 [15226473.001]
  • [Cites] J Natl Cancer Inst. 2004 Jul 7;96(13):1015-22 [15240785.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1192-8 [15247130.001]
  • [Cites] J AOAC Int. 2004 May-Jun;87(3):775-86 [15287679.001]
  • [Cites] J Nutr. 2004 Sep;134(9):2475S-2481S [15333745.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Sep;13(9):1502-8 [15342452.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Sep;13(9):1509-14 [15342453.001]
  • [Cites] Am J Clin Nutr. 2004 Oct;80(4):1003-11 [15447912.001]
  • [Cites] Lancet. 2004 Oct 2-8;364(9441):1219-28 [15464182.001]
  • [Cites] Natl Cancer Inst Monogr. 1966 Jan;19:1-125 [5905668.001]
  • [Cites] Lancet. 1969 Dec 6;2(7632):1229-31 [4187817.001]
  • [Cites] Br Med J. 1976 Dec 25;2(6051):1525-36 [1009386.001]
  • [Cites] J Natl Cancer Inst. 1977 Mar;58(3):525-47 [557114.001]
  • [Cites] Proc Natl Acad Sci U S A. 1977 Aug;74(8):3555-9 [333441.001]
  • [Cites] Am J Obstet Gynecol. 1979 Mar 1;133(5):537-47 [220875.001]
  • [Cites] Obstet Gynecol. 1979 Jul;54(1):74-9 [221871.001]
  • [Cites] Public Health Rep. 1980 May-Jun;95(3):213-22 [7384406.001]
  • [Cites] Int J Epidemiol. 1980 Sep;9(3):227-31 [7440046.001]
  • [Cites] J Natl Cancer Inst. 1981 Jul;67(1):57-60 [6942196.001]
  • [Cites] Int J Cancer. 1982 Jul 15;30(1):9-11 [7118300.001]
  • [Cites] Int J Cancer. 1983 Aug 15;32(2):155-61 [6307893.001]
  • [Cites] J Surg Oncol. 1983 Sep;24(1):83-7 [6887943.001]
  • [Cites] J Natl Cancer Inst. 1983 Oct;71(4):703-9 [6578365.001]
  • [Cites] Cancer Res. 1984 Jan;44(1):363-9 [6690049.001]
  • [Cites] N Engl J Med. 1984 Mar 8;310(10):617-21 [6694673.001]
  • [Cites] Am J Public Health. 1995 Aug;85(8 Pt 1):1128-32 [7625511.001]
  • [Cites] Am J Epidemiol. 1995 Sep 15;142(6):608-11 [7653469.001]
  • [Cites] Cancer Res. 1995 Nov 1;55(21):4906-9 [7585528.001]
  • [Cites] J Natl Cancer Inst. 1995 Dec 6;87(23):1760-6 [7473832.001]
  • [Cites] Eur J Cancer Prev. 1995 Oct;4(5):345-52 [7496322.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1995 Oct-Nov;4(7):703-7 [8672985.001]
  • [Cites] Cancer Causes Control. 1995 Nov;6(6):513-8 [8580299.001]
  • [Cites] Lancet. 1996 May 18;347(9012):1372-4 [8637343.001]
  • [Cites] Am J Epidemiol. 1996 Jul 1;144(1):34-41 [8659483.001]
  • [Cites] Dig Dis Sci. 1996 Jul;41(7):1319-26 [8689906.001]
  • [Cites] Int J Cancer. 1996 Jul 29;67(3):327-32 [8707404.001]
  • [Cites] Cancer Causes Control. 1996 Mar;7(2):253-63 [8740738.001]
  • [Cites] J Natl Cancer Inst. 1996 Oct 2;88(19):1375-82 [8827015.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1996 Jul;5(7):503-7 [8827353.001]
  • [Cites] Ann Epidemiol. 1996 Jul;6(4):276-82 [8876837.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1997 Dec;6(12):1029-32 [9419398.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Feb;7(2):163-8 [9488592.001]
  • [Cites] Gastroenterology. 1998 Mar;114(3):441-7 [9496933.001]
  • [Cites] Ann Intern Med. 1998 May 1;128(9):705-12 [9556463.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Apr;7(4):329-33 [9568789.001]
  • [Cites] J Gen Intern Med. 1998 May;13(5):303-10 [9613885.001]
  • [Cites] J Natl Cancer Inst. 1984 Jun;72(6):1323-5 [6587152.001]
  • [Cites] Cancer Res. 1984 Oct;44(10):4633-7 [6467218.001]
  • [Cites] Mutat Res. 1985 Jun-Jul;150(1-2):33-41 [3889618.001]
  • [Cites] J Natl Cancer Inst. 1985 Aug;75(2):185-91 [3894750.001]
  • [Cites] Biochem J. 1985 Jul 1;229(1):265-8 [4038261.001]
  • [Cites] N Engl J Med. 1985 Nov 28;313(22):1381-4 [4058532.001]
  • [Cites] J Natl Cancer Inst. 1986 Apr;76(4):557-69 [3007842.001]
  • [Cites] Nutr Cancer. 1987;9(1):43-56 [3808969.001]
  • [Cites] Int J Epidemiol. 1986 Dec;15(4):494-501 [3818156.001]
  • [Cites] Br J Cancer. 1987 Jun;55(6):687-94 [3620314.001]
  • [Cites] Cancer Res. 1988 Aug 1;48(15):4399-404 [3390835.001]
  • [Cites] Int J Cancer. 1988 Aug 15;42(2):167-75 [3403062.001]
  • [Cites] Am J Epidemiol. 1988 Nov;128(5):1007-15 [3189277.001]
  • [Cites] Am J Surg. 1989 Jan;157(1):175-9 [2535920.001]
  • [Cites] Int J Cancer. 1989 Jun 15;43(6):1007-16 [2731998.001]
  • [Cites] Int J Cancer. 1989 Jul 15;44(1):1-6 [2545631.001]
  • [Cites] Cancer Res. 1989 Sep 1;49(17):4936-40 [2758422.001]
  • [Cites] Cancer Res. 1989 Oct 1;49(19):5459-68 [2766308.001]
  • [Cites] Lancet. 1989 Sep 23;2(8665):725-7 [2570969.001]
  • [Cites] Int J Epidemiol. 1989 Sep;18(3):556-62 [2807657.001]
  • [Cites] Lancet. 1989 Nov 18;2(8673):1176-8 [2572900.001]
  • [Cites] Gastroenterology. 1990 Feb;98(2):406-13 [2295396.001]
  • [Cites] Int J Cancer. 1990 Jan 15;45(1):69-76 [2298506.001]
  • [Cites] Nutr Cancer. 1990;13(1-2):101-9 [2300490.001]
  • [Cites] Am J Epidemiol. 1990 Apr;131(4):612-24 [2156419.001]
  • [Cites] J Natl Cancer Inst. 1990 Apr 18;82(8):650-61 [2157027.001]
  • [Cites] Br J Cancer. 1990 May;61(5):741-8 [2337511.001]
  • [Cites] Dig Dis Sci. 1990 Nov;35(11):1414-20 [2226103.001]
  • [Cites] N Engl J Med. 1990 Dec 13;323(24):1664-72 [2172820.001]
  • [Cites] Epidemiology. 1990 Mar;1(2):141-5 [2073501.001]
  • [Cites] Diabetes Care. 1991 Apr;14(4):271-82 [2060430.001]
  • [Cites] Gastroenterology. 1991 Sep;101(3):635-9 [1650315.001]
  • [Cites] Cancer Causes Control. 1990 Jul;1(1):5-14 [2102276.001]
  • [Cites] Int J Cancer. 1991 Sep 9;49(2):161-7 [1652565.001]
  • [Cites] Int J Cancer. 1993 Sep 9;55(2):213-9 [8370618.001]
  • [Cites] BMJ. 1993 Jul 31;307(6899):285-9 [8374373.001]
  • [Cites] Cancer Causes Control. 1993 Sep;4(5):405-11 [8218871.001]
  • [Cites] J Natl Cancer Inst. 1994 Feb 2;86(3):183-91 [8283490.001]
  • [Cites] J Natl Cancer Inst. 1994 Feb 2;86(3):192-9 [8283491.001]
  • [Cites] Cancer Res. 1994 Feb 1;54(3):718-23 [8306333.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3694-700 [15150130.001]
  • [Cites] Am J Clin Nutr. 2004 Jun;79(6):935-45 [15159222.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jun;13(6):915-9 [15184246.001]
  • [Cites] Carcinogenesis. 2005 Mar;26(3):637-42 [15579480.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] J Natl Cancer Inst. 2005 Mar 16;97(6):457-60 [15770010.001]
  • [Cites] N Engl J Med. 2005 Mar 17;352(11):1092-102 [15713943.001]
  • [Cites] N Engl J Med. 2005 Mar 17;352(11):1071-80 [15713944.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Apr;14(4):835-41 [15824153.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Apr;14(4):850-5 [15824155.001]
  • [Cites] Int J Cancer. 2005 Jul 1;115(4):648-52 [15700302.001]
  • [Cites] Eur J Clin Invest. 2005 May;35(5):290-304 [15860041.001]
  • [Cites] Cancer Causes Control. 2005 Mar;16(2):83-95 [15868450.001]
  • [Cites] J Natl Cancer Inst. 2005 May 4;97(9):684-92 [15870439.001]
  • [Cites] Clin Cancer Res. 2005 May 15;11(10):3642-6 [15897559.001]
  • [Cites] Gastroenterology. 2005 Jun;128(7):1830-7 [15940618.001]
  • [Cites] J Natl Cancer Inst. 2005 Jun 15;97(12):906-16 [15956652.001]
  • [Cites] J Natl Cancer Inst. 2005 Jun 15;97(12):917-26 [15956653.001]
  • [Cites] J Natl Cancer Inst. 1991 Sep 18;83(18):1324-9 [1886158.001]
  • [Cites] Int J Cancer. 1991 Sep 30;49(3):381-6 [1917136.001]
  • [Cites] Int J Cancer. 1991 Oct 21;49(4):520-5 [1917152.001]
  • [Cites] Am J Ther. 2004 May-Jun;11(3):156-63 [15133529.001]
  • [Cites] Int J Epidemiol. 1991 Jun;20(2):362-7 [1917235.001]
  • [Cites] Anticancer Drugs. 1990 Oct;1(1):15-21 [2131030.001]
  • [Cites] J Clin Epidemiol. 1991;44(11):1255-61 [1941019.001]
  • [Cites] Ann Intern Med. 1991 Dec 15;115(12):952-4 [1659272.001]
  • [Cites] Int J Cancer. 1992 Jan 21;50(2):223-9 [1730516.001]
  • [Cites] J Natl Cancer Inst. 1992 Jan 15;84(2):91-8 [1310511.001]
  • [Cites] Diabetes Care. 1991 Nov;14(11):1066-74 [1797488.001]
  • [Cites] Cancer Causes Control. 1992 Sep;3(5):457-73 [1525327.001]
  • [Cites] J Natl Cancer Inst. 1992 Oct 7;84(19):1491-500 [1433333.001]
  • [Cites] Nutr Cancer. 1992;18(2):97-111 [1437657.001]
  • [Cites] J Natl Cancer Inst. 1992 Dec 16;84(24):1887-96 [1334153.001]
  • [Cites] Ann Intern Med. 1993 Jan 15;118(2):91-5 [8416323.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1993 Jan-Feb;2(1):41-6 [8420611.001]
  • [Cites] J Natl Cancer Inst. 1993 Feb 3;85(3):224-9 [8423627.001]
  • [Cites] Int J Cancer. 1993 Mar 12;53(5):720-7 [8449595.001]
  • [Cites] N Engl J Med. 1993 May 6;328(18):1313-6 [8385741.001]
  • [Cites] Gut. 1993 Apr;34(4):531-6 [8387940.001]
  • [Cites] J Natl Cancer Inst. 1993 Jun 2;85(11):875-84 [8492316.001]
  • [Cites] J Natl Cancer Inst. 1993 Aug 4;85(15):1220-4 [8331682.001]
  • [Cites] Am J Epidemiol. 1993 Aug 15;138(4):225-36 [8395140.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 May;15(5):892-6 [16702366.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1120-5 [16775169.001]
  • [Cites] J Natl Cancer Inst. 2006 Jul 5;98(13):920-31 [16818856.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4320-4 [10485479.001]
  • [Cites] Br J Cancer. 1999 Sep;81(1):62-8 [10487613.001]
  • [Cites] Dis Colon Rectum. 1999 Oct;42(10):1300-5 [10528768.001]
  • [Cites] J Natl Cancer Inst. 1994 Mar 16;86(6):455-60 [8120921.001]
  • [Cites] Cancer Causes Control. 1994 Jan;5(1):38-52 [8123778.001]
  • [Cites] N Engl J Med. 1994 Apr 14;330(15):1029-35 [8127329.001]
  • [Cites] Gynecol Endocrinol. 1993 Dec;7(4):251-8 [8147234.001]
  • [Cites] N Engl J Med. 1994 Jul 21;331(3):141-7 [8008027.001]
  • [Cites] Science. 1994 Aug 12;265(5174):956-9 [8052854.001]
  • [Cites] Cancer Causes Control. 1994 Jul;5(4):359-66 [8080948.001]
  • [Cites] Cancer. 1994 Oct 1;74(7):1847-54 [8082089.001]
  • [Cites] Gastroenterology. 1994 Oct;107(4):1183-8 [7926468.001]
  • [Cites] Nat Genet. 1994 Aug;7(4):536-40 [7951326.001]
  • [Cites] Int J Cancer. 1994 Dec 15;59(6):728-38 [7989109.001]
  • [Cites] Ann Intern Med. 1995 Mar 1;122(5):327-34 [7847643.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1994 Dec;3(8):675-82 [7881341.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1995 Jan-Feb;4(1):21-8 [7894320.001]
  • [Cites] Ann Med. 1994 Dec;26(6):443-52 [7695871.001]
  • [Cites] J Natl Cancer Inst. 1995 Feb 15;87(4):265-73 [7707417.001]
  • [Cites] J Natl Cancer Inst. 1995 Apr 5;87(7):517-23 [7707438.001]
  • [Cites] Cancer Res. 1995 May 15;55(10):2017-20 [7743494.001]
  • [Cites] Cancer Causes Control. 1995 Mar;6(2):164-79 [7749056.001]
  • [Cites] Int J Cancer. 2008 Apr 15;122(8):1690-4 [18092326.001]
  • [Cites] Circulation. 2008 Apr 22;117(16):2104-13 [18378608.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1136-43 [18483335.001]
  • [Cites] Am J Clin Nutr. 2008 Jun;87(6):1793-801 [18541570.001]
  • [Cites] Gastroenterology. 2008 Sep;135(3):770-80 [18619459.001]
  • [Cites] Am J Clin Nutr. 2008 Oct;88(4):1074-82 [18842796.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Oct;17(10):2609-18 [18829444.001]
  • [Cites] Cancer Causes Control. 2008 Dec;19(10):1291-8 [18618276.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Nov;17(11):3108-15 [18990751.001]
  • [Cites] Lancet. 2008 Nov 15;372(9651):1756-64 [18922570.001]
  • [Cites] J Nutr. 2008 Dec;138(12):2372-8 [19022960.001]
  • [Cites] Am J Epidemiol. 2008 Dec 1;168(11):1292-300 [18945689.001]
  • [Cites] N Engl J Med. 2008 Dec 11;359(24):2567-78 [19073976.001]
  • [Cites] JAMA. 2008 Dec 17;300(23):2765-78 [19088354.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):196-203 [19124498.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1996 Oct;5(10):779-84 [8896888.001]
  • [Cites] Am J Epidemiol. 1996 Dec 1;144(11):1005-14 [8942430.001]
  • [Cites] Cell. 1996 Nov 29;87(5):803-9 [8945508.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1996 Dec;5(12):955-60 [8959316.001]
  • [Cites] JAMA. 1996 Dec 25;276(24):1957-63 [8971064.001]
  • [Cites] Int J Cancer. 1996 Dec 11;68(6):744-8 [8980177.001]
  • [Cites] Cancer Res. 1997 Jan 1;57(1):75-80 [8988044.001]
  • [Cites] J Biol Chem. 1997 Feb 7;272(6):3406-10 [9013583.001]
  • [Cites] Eur J Cancer Prev. 1996 Dec;5(6):445-54 [9061275.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):2869-73 [9096313.001]
  • [Cites] Cancer Causes Control. 1997 Mar;8(2):130-8 [9134236.001]
  • [Cites] Cancer Causes Control. 1997 Mar;8(2):146-58 [9134238.001]
  • [Cites] Cancer Causes Control. 1997 Mar;8(2):175-83 [9134241.001]
  • [Cites] Nutr Cancer. 1997;28(1):52-62 [9200151.001]
  • [Cites] Mutat Res. 1997 May 12;376(1-2):211-9 [9202758.001]
  • [Cites] J Natl Cancer Inst. 1997 Jul 2;89(13):948-55 [9214674.001]
  • [Cites] Cancer Causes Control. 1997 Jul;8(4):615-25 [9242478.001]
  • [Cites] Cancer Causes Control. 1997 Jul;8(4):649-67 [9242482.001]
  • [Cites] Nutr Cancer. 1997;28(2):125-9 [9290116.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1997 Sep;6(9):671-5 [9298573.001]
  • [Cites] Br J Cancer. 1997;76(5):675-7 [9303370.001]
  • [Cites] Nutr Cancer. 1997;28(3):276-81 [9343837.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4787-94 [9354440.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1997 Dec;6(12):1007-10 [9419395.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Aug;18(8):2195-201 [19661077.001]
  • [Cites] JAMA. 2009 Aug 12;302(6):649-58 [19671906.001]
  • [Cites] Am J Epidemiol. 2009 Oct 1;170(7):863-72 [19723749.001]
  • [Cites] J Clin Oncol. 2009 Sep 20;27(27):4542-7 [19704062.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Oct;18(10):2726-33 [19755647.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Oct;18(10):2745-50 [19755657.001]
  • [Cites] Am J Epidemiol. 1998 Jul 1;148(1):4-16 [9663397.001]
  • [Cites] Cancer Res. 1998 Aug 1;58(15):3307-11 [9699660.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Aug;7(8):653-9 [9718216.001]
  • [Cites] J Natl Cancer Inst. 1998 Aug 19;90(16):1212-8 [9719082.001]
  • [Cites] N Engl J Med. 1999 Jan 14;340(2):101-7 [9887161.001]
  • [Cites] N Engl J Med. 1999 Jan 21;340(3):169-76 [9895396.001]
  • [Cites] Arch Intern Med. 1999 Jan 25;159(2):161-6 [9927099.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1999 Jan;8(1):15-24 [9950235.001]
  • [Cites] J Nutr. 1999 Feb;129(2S Suppl):560S-564S [10064332.001]
  • [Cites] J Natl Cancer Inst. 1999 Mar 17;91(6):542-7 [10088625.001]
  • [Cites] Am J Med. 1999 May;106(5):574-82 [10335731.001]
  • [Cites] Jpn J Cancer Res. 1999 Jul;90(7):711-9 [10470282.001]
  • [Cites] Int J Cancer. 2005 Feb 20;113(5):825-8 [15499620.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 14;101(50):17468-73 [15574495.001]
  • [Cites] Eur J Immunol. 2005 Jan;35(1):217-24 [15593122.001]
  • [Cites] JAMA. 2005 Jan 12;293(2):172-82 [15644544.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Jan;14(1):133-7 [15668486.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Jan;14(1):138-47 [15668487.001]
  • [Cites] Genet Test. 2004 Winter;8(4):417-20 [15684874.001]
  • [Cites] Am J Epidemiol. 2007 Feb 1;165(3):256-61 [17118965.001]
  • [Cites] Carcinogenesis. 2007 Feb;28(2):240-5 [17166881.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Feb;16(2):314-21 [17301265.001]
  • [Cites] Ann Intern Med. 2007 Mar 6;146(5):361-4 [17339621.001]
  • [Cites] Ann Intern Med. 2007 Mar 6;146(5):365-75 [17339622.001]
  • [Cites] Ann Intern Med. 2007 Mar 6;146(5):376-89 [17339623.001]
  • [Cites] Int J Cancer. 2007 May 1;120(9):2007-12 [17266031.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):676-83 [17416757.001]
  • [Cites] J Natl Cancer Inst. 2007 Apr 18;99(8):608-15 [17440162.001]
  • [Cites] Int J Cancer. 2007 Jul 1;121(1):136-42 [17354224.001]
  • [Cites] Gastroenterology. 2007 May;132(6):2169-80 [17498510.001]
  • [Cites] Lancet. 2007 May 12;369(9573):1603-13 [17499602.001]
  • [Cites] Hum Reprod. 2007 Jun;22(6):1769-77 [17347166.001]
  • [Cites] Int J Cancer. 2007 Jul 15;121(2):368-76 [17372899.001]
  • [Cites] N Engl J Med. 2007 May 24;356(21):2131-42 [17522398.001]
  • [Cites] Diabetes Care. 2005 Jul;28(7):1805-7 [15983343.001]
  • [Cites] JAMA. 2005 Jul 6;294(1):47-55 [15998890.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Aug;14(8):2030-4 [16103456.001]
  • [Cites] JAMA. 2005 Aug 24;294(8):914-23 [16118381.001]
  • [Cites] Am J Epidemiol. 2005 Sep 15;162(6):548-58 [16093288.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):8034-41 [16140978.001]
  • [Cites] Am J Clin Nutr. 2005 Sep;82(3):575-80 [16155270.001]
  • [Cites] J Natl Cancer Inst. 2005 Sep 21;97(18):1317-9 [16174847.001]
  • [Cites] Nat Clin Pract Gastroenterol Hepatol. 2005 Jul;2(7):308-15 [16265284.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 Oct;97(1-2):179-94 [16236494.001]
  • [Cites] J Natl Cancer Inst. 2005 Nov 16;97(22):1688-94 [16288122.001]
  • [Cites] JAMA. 2005 Dec 14;294(22):2849-57 [16352792.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Dec;14(12):3010-2 [16365028.001]
  • [Cites] Am J Gastroenterol. 2005 Dec;100(12):2789-95 [16393237.001]
  • [Cites] Am J Epidemiol. 2006 Jan 15;163(2):108-15 [16339055.001]
  • [Cites] Int J Cancer. 2006 Apr 1;118(7):1777-81 [16217756.001]
  • [Cites] Immunology. 2006 Mar;117(3):310-8 [16476050.001]
  • [Cites] N Engl J Med. 2006 Feb 16;354(7):684-96 [16481636.001]
  • [Cites] Cancer Causes Control. 2006 Apr;17(3):257-66 [16489533.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):315-20 [16492922.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):486-93 [16537706.001]
  • [Cites] Circulation. 2006 Mar 28;113(12):1578-87 [16534006.001]
  • [Cites] Aliment Pharmacol Ther. 2006 Apr 1;23(7):1007-16 [16573803.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Apr;15(4):750-5 [16614119.001]
  • [Cites] J Clin Invest. 2000 Jun;105(11):1589-94 [10841517.001]
  • [Cites] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):625-30 [10868699.001]
  • [Cites] Epidemiology. 2000 Jul;11(4):376-81 [10874542.001]
  • [Cites] Gut. 2000 Aug;47(2):211-4 [10896912.001]
  • [Cites] Cancer Causes Control. 2000 Aug;11(7):579-88 [10977102.001]
  • [Cites] Cancer Causes Control. 1999 Oct;10(5):379-86 [10530607.001]
  • [Cites] Cancer Causes Control. 1999 Oct;10(5):387-96 [10530608.001]
  • [Cites] J Natl Cancer Inst. 2004 Nov 17;96(22):1669-75 [15547179.001]
  • [Cites] Int J Cancer. 2005 Feb 20;113(5):829-34 [15499619.001]
  • [Cites] Am J Epidemiol. 2007 Nov 15;166(10):1116-25 [17823383.001]
  • [Cites] Int J Cancer. 2008 Feb 1;122(3):620-9 [17935129.001]
  • [Cites] PLoS Med. 2007 Dec;4(12):e325 [18076279.001]
  • [Cites] Ann Oncol. 2008 Jan;19(1):150-5 [17785762.001]
  • [Cites] Gastroenterology. 2008 Jan;134(1):21-8 [18005960.001]
  • [Cites] Gastroenterology. 2008 Jan;134(1):29-38 [18022173.001]
  • [Cites] Cancer Res. 2008 Jan 1;68(1):323-8 [18172326.001]
  • [Cites] Mutat Res. 2008 Feb 1;638(1-2):162-74 [18022202.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Jan;17(1):171-82 [18199722.001]
  • [Cites] Cancer Res. 2008 Jan 15;68(2):553-60 [18199552.001]
  • [Cites] Gastroenterology. 2008 Feb;134(2):388-95 [18242207.001]
  • [Cites] Gastroenterology. 2008 Feb;134(2):617-9 [18242224.001]
  • [Cites] Cancer Biol Ther. 2007 Oct;6(10):1621-6 [17932462.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Feb;17(2):320-9 [18268115.001]
  • [Cites] Int J Obes (Lond). 2008 Feb;32(2):304-14 [17878894.001]
  • [Cites] J Natl Cancer Inst. 2002 Mar 20;94(6):437-46 [11904316.001]
  • [Cites] JAMA. 2002 Jul 17;288(3):321-33 [12117397.001]
  • [Cites] J Nutr. 2002 Aug;132(8 Suppl):2350S-2355S [12163691.001]
  • [Cites] Mutat Res. 2002 Sep 30;506-507:175-85 [12351157.001]
  • [Cites] Mutat Res. 2002 Sep 30;506-507:205-14 [12351160.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Oct;11(10 Pt 1):1012-8 [12376501.001]
  • [Cites] Eur J Cancer Prev. 2002 Oct;11(5):465-72 [12394244.001]
  • [Cites] Gastroenterology. 2002 Dec;123(6):1770-7 [12454832.001]
  • [Cites] QJM. 2002 Dec;95(12):787-96 [12454321.001]
  • [Cites] J Natl Cancer Inst. 2003 Jan 15;95(2):154-9 [12529348.001]
  • [Cites] Arch Intern Med. 2003 Feb 10;163(3):309-14 [12578511.001]
  • [Cites] Br J Cancer. 2003 Mar 10;88(5):684-8 [12618874.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):883-90 [12621132.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Mar;12(3):201-8 [12646508.001]
  • [Cites] JAMA. 2009 Jan 7;301(1):39-51 [19066370.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Dec;1(7):514-21 [19139001.001]
  • [Cites] Am J Clin Nutr. 2009 Feb;89(2):568-76 [19088152.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Feb;18(2):516-25 [19190143.001]
  • [Cites] Gut. 2009 Mar;58(3):413-20 [18978177.001]
  • [Cites] Br J Cancer. 2009 Feb 24;100(4):611-6 [19209175.001]
  • [Cites] J Natl Cancer Inst. 2009 Feb 18;101(4):267-76 [19211442.001]
  • [Cites] J Natl Cancer Inst. 2009 Feb 18;101(4):256-66 [19211452.001]
  • [Cites] Carcinogenesis. 2009 Mar;30(3):472-9 [19029193.001]
  • [Cites] Cancer Prev Res (Phila). 2009 Mar;2(3):209-12 [19258540.001]
  • [Cites] Cancer Prev Res (Phila). 2009 Mar;2(3):213-23 [19258546.001]
  • [Cites] Int J Cancer. 2009 May 15;124(10):2406-15 [19142968.001]
  • [Cites] Cancer Prev Res (Phila). 2009 Apr;2(4):310-21 [19336730.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Apr;18(4):1197-202 [19336555.001]
  • [Cites] Am J Clin Nutr. 2009 May;89(5):1441-52 [19339391.001]
  • [Cites] Lancet Oncol. 2009 May;10(5):501-7 [19410194.001]
  • [Cites] Am J Gastroenterol. 2009 May;104(5):1231-40 [19367270.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 May;18(5):1531-7 [19423530.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 May;18(5):1552-61 [19423533.001]
  • [Cites] World J Gastroenterol. 2009 May 21;15(19):2336-9 [19452574.001]
  • [Cites] Cancer Causes Control. 2009 Jul;20(5):731-40 [19122977.001]
  • [Cites] Eur J Cancer Prev. 2009 Jun;18(3):179-90 [19238085.001]
  • [Cites] Clin Gastroenterol Hepatol. 2009 Jun;7(6):682-688.e1-5 [19245853.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jun 9;106(23):9409-13 [19470469.001]
  • [Cites] J Natl Cancer Inst. 2004 Mar 3;96(5):403-7 [14996862.001]
  • [Cites] Clin Gastroenterol Hepatol. 2003 May;1(3):202-10 [15017492.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Apr;13(4):538-45 [15066917.001]
  • [Cites] J Natl Cancer Inst. 2004 Apr 7;96(7):546-53 [15069117.001]
  • [Cites] Ann Intern Med. 2004 Apr 20;140(8):603-13 [15096331.001]
  • [Cites] Am J Epidemiol. 2004 May 15;159(10):983-92 [15128611.001]
  • [Cites] Am J Epidemiol. 2009 Nov 15;170(10):1207-21 [19846566.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Nov;18(11):2835-41 [19843681.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Nov;18(11):2933-41 [19861511.001]
  • [Cites] Am J Clin Nutr. 2009 Dec;90(6):1623-31 [19864409.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Dec;18(12):3362-7 [19959683.001]
  • [Cites] Cancer. 2009 Dec 15;115(24):5662-71 [19827153.001]
  • [Cites] Cancer Causes Control. 2009 Oct;20(8):1397-408 [19466571.001]
  • [Cites] Obes Rev. 2010 Jan;11(1):19-30 [19538439.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 8;103(32):12098-102 [16880406.001]
  • [Cites] Am J Gastroenterol. 2006 Aug;101(8):1872-9 [16790032.001]
  • [Cites] N Engl J Med. 2006 Aug 31;355(9):873-84 [16943400.001]
  • [Cites] N Engl J Med. 2006 Aug 31;355(9):885-95 [16943401.001]
  • [Cites] Circulation. 2006 Sep 5;114(10):1028-35 [16943394.001]
  • [Cites] J Clin Oncol. 2006 Nov 1;24(31):5010-6 [17075120.001]
  • [Cites] Am J Clin Nutr. 2006 Nov;84(5):1184-92 [17093173.001]
  • [Cites] Cancer Causes Control. 2006 Dec;17(10):1299-304 [17111262.001]
  • [Cites] Nature. 2006 Dec 14;444(7121):860-7 [17167474.001]
  • [Cites] Gastroenterology. 2006 Dec;131(6):1674-82 [17087947.001]
  • [Cites] J Natl Cancer Inst. 2007 Jan 17;99(2):129-36 [17227996.001]
  • [Cites] Lancet. 2003 May 3;361(9368):1496-501 [12737858.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):412-8 [12750235.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):464-7 [12750244.001]
  • [Cites] Br J Cancer. 2003 Jun 2;88(11):1687-92 [12771981.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7859-64 [12810952.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Jul;12(7):631-7 [12869402.001]
  • [Cites] Gastroenterology. 2003 Aug;125(2):328-36 [12891533.001]
  • [Cites] Cancer Causes Control. 2003 Jun;14(5):403-11 [12946034.001]
  • [Cites] Dig Dis Sci. 2003 Oct;48(10):1998-2002 [14627347.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 Nov;12(11 Pt 1):1253-6 [14652290.001]
  • [Cites] J Natl Cancer Inst. 2003 Dec 3;95(23):1765-71 [14652238.001]
  • [Cites] Mol Endocrinol. 2003 Dec;17(12):2386-92 [14500760.001]
  • [Cites] JAMA. 2003 Dec 10;290(22):2959-67 [14665657.001]
  • [Cites] Ann Intern Med. 2004 Feb 3;140(3):157-66 [14757613.001]
  • [Cites] J Natl Cancer Inst. 2004 Feb 4;96(3):229-33 [14759990.001]
  • [Cites] J Natl Cancer Inst. 2007 Jun 6;99(11):881-9 [17551148.001]
  • [Cites] JAMA. 2007 Jun 6;297(21):2351-9 [17551129.001]
  • [Cites] J Nutr. 2007 Jul;137(7):1808-14 [17585035.001]
  • [Cites] Carcinogenesis. 2007 Jul;28(7):1426-9 [17277232.001]
  • [Cites] Cancer Causes Control. 2007 Oct;18(8):853-63 [17605083.001]
  • [Cites] Br J Cancer. 2007 Aug 6;97(3):446-51 [17622244.001]
  • [Cites] Cancer Res. 2007 Aug 1;67(15):7534-9 [17671225.001]
  • [Cites] Am J Clin Nutr. 2007 Sep;86(3):556-65 [17823417.001]
  • [Cites] Int J Cancer. 2007 Nov 1;121(9):2065-72 [17640039.001]
  • [Cites] J Surg Res. 2007 Oct;142(2):239-45 [17574271.001]
  • [Cites] JAMA. 2007 Sep 26;298(12):1412-9 [17895457.001]
  • [Cites] Carcinogenesis. 2007 Sep;28(9):1991-5 [17634405.001]
  • [Cites] Carcinogenesis. 2007 Sep;28(9):2019-27 [17690112.001]
  • [Cites] J Natl Cancer Inst. 2007 Oct 3;99(19):1471-83 [17895473.001]
  • [Cites] Nutr J. 2007;6:20 [17767717.001]
  • [Cites] J Nutr. 1999 Nov;129(11):1945-50 [10539767.001]
  • [Cites] Cell. 1999 Oct 29;99(3):335-45 [10555149.001]
  • [Cites] Digestion. 2000;61(2):129-34 [10705177.001]
  • [Cites] N Engl J Med. 2000 Apr 20;342(16):1149-55 [10770979.001]
  • [Cites] N Engl J Med. 2000 Apr 20;342(16):1156-62 [10770980.001]
  • [Cites] J Biol Chem. 2000 Apr 14;275(15):11397-403 [10753955.001]
  • [Cites] Cancer Causes Control. 2000 Mar;11(3):249-55 [10782659.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Apr;9(4):443-7 [10794491.001]
  • [Cites] Aliment Pharmacol Ther. 2000 Apr;14 Suppl 1:64-7 [10807405.001]
  • [Cites] J Natl Cancer Inst. 2000 Oct 4;92(19):1592-600 [11018095.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Oct;9(10):1059-65 [11045788.001]
  • [Cites] J Nutr. 2000 Nov;130(11):2648-52 [11053501.001]
  • [Cites] J Natl Cancer Inst. 2000 Nov 1;92(21):1740-52 [11058617.001]
  • [Cites] Lancet. 2000 Oct 14;356(9238):1300-6 [11073017.001]
  • [Cites] J Natl Cancer Inst. 2000 Dec 6;92(23):1888-96 [11106680.001]
  • [Cites] Epidemiology. 2001 Jan;12(1):88-93 [11138826.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):126-30 [11196149.001]
  • [Cites] Ann Oncol. 2001 Feb;12(2):173-8 [11300319.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Mar;10(3):265-8 [11303597.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3566-9 [11325819.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 May;10(5):439-46 [11352852.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 May;10(5):559-62 [11352869.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Jul;10(7):725-31 [11440957.001]
  • [Cites] Nutr Cancer. 2001;39(1):35-41 [11588900.001]
  • [Cites] Eur J Cancer. 2001 Nov;37(16):2091-6 [11597389.001]
  • [Cites] J Natl Cancer Inst. 2001 Dec 5;93(23):1799-805 [11734596.001]
  • [Cites] Br J Cancer. 2001 Nov 30;85(11):1700-5 [11742491.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Dec;10(12):1259-66 [11751443.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2001 Dec;10(12):1267-74 [11751444.001]
  • [Cites] J Am Med Assoc. 1958 March 15;166(11):1294-308 [12308037.001]
  • [Cites] Int J Cancer. 2002 Mar 10;98(2):241-56 [11857415.001]
  • [Cites] Gastroenterology. 2002 Mar;122(3):641-5 [11874996.001]
  • [Cites] Nat Med. 2002 Mar;8(3):289-93 [11875501.001]
  • [Cites] Pharmacogenetics. 2002 Mar;12(2):145-50 [11875368.001]
  • (PMID = 20420944.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA107412; United States / NCI NIH HHS / CA / CA133891; United States / NCI NIH HHS / CA / P01 CA055075-120001; United States / NCI NIH HHS / CA / CA137178; United States / NCI NIH HHS / CA / P01 CA087969; United States / NCI NIH HHS / CA / P01 CA055075; United States / NCI NIH HHS / CA / CA 055075; United States / NCI NIH HHS / CA / CA087969-100006; United States / NCI NIH HHS / CA / K07 CA107412; United States / NCI NIH HHS / CA / CA137178-02; United States / NCI NIH HHS / CA / R01 CA137178-02; United States / NCI NIH HHS / CA / R01 CA137178; United States / NCI NIH HHS / CA / CA055075-120001; United States / NCI NIH HHS / CA / K07 CA107412-05S1; United States / NCI NIH HHS / CA / CA107412-05S1; United States / NCI NIH HHS / CA / K07 CA107412-05; United States / NCI NIH HHS / CA / R01 CA133891; United States / NCI NIH HHS / CA / CA087969; United States / NCI NIH HHS / CA / P50 CA127003-01; United States / NCI NIH HHS / CA / P01 CA087969-100006; United States / NCI NIH HHS / CA / P50 CA127003; United States / NCI NIH HHS / CA / CA107412-05
  • [Publication-type] Journal Article; Portraits; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Anticarcinogenic Agents
  • [Number-of-references] 419
  • [Other-IDs] NLM/ NIHMS233908; NLM/ PMC2947820
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14. Kerrigan SA, Turnnir RT, Clement PB, Young RH, Churg A: Diffuse malignant epithelial mesotheliomas of the peritoneum in women: a clinicopathologic study of 25 patients. Cancer; 2002 Jan 15;94(2):378-85
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  • [Title] Diffuse malignant epithelial mesotheliomas of the peritoneum in women: a clinicopathologic study of 25 patients.
  • BACKGROUND: The behavior of diffuse peritoneal mesotheliomas in women and the possible relation between tumor morphology and outcome are uncertain.
  • The authors examined the behavior of diffuse epithelial peritoneal mesotheliomas in women and the possible relation between pathologic features and outcome.
  • METHODS: Twenty-five female patients with diffuse peritoneal epithelial malignant mesotheliomas were divided into two groups: those who survived for < 4 years (60%) and those who survived for > 4 years (40%).
  • Both groups were compared in terms of age, presentation, treatment, survival, tumor architecture, mitotic rate, necrosis, nuclear grade, and immunohistochemical profile.
  • RESULTS: Patients in the two groups were similar in terms of age at diagnosis (median ages, 50.7 years and 49.9 years), presentation, initial tumor burden, and treatment.
  • Slightly less than 50% of patients in both groups received some form of chemotherapy or radiation therapy after undergoing tumor-reductive surgery or biopsy.
  • One patient was alive with disease 15 years after diagnosis.
  • However, because there do not appear to be morphologic features that reliably identify favorable tumors versus unfavorable tumors, aggressive therapy for all women with diffuse peritoneal mesotheliomas may be warranted.
  • [MeSH-major] Mesothelioma / pathology. Peritoneal Neoplasms / pathology

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  • (PMID = 11905410.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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15. Yang F, Jin C, Long J, Yu XJ, Xu J, Di Y, Li J, Fu de L, Ni QX: Solid pseudopapillary tumor of the pancreas: a case series of 26 consecutive patients. Am J Surg; 2009 Aug;198(2):210-5
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  • The aim of this study is to describe the clinicopathologic features and surgical management of this disease in our institution.
  • Clinicopathologic factors were compared between benign and malignant cases to determine what features of the tumor could suggest malignant potential.
  • The neoplasm was localized in the pancreatic head/neck in 14 patients and in the body/tail in 12 patients.
  • All of the tumors-including 8 pancreaticoduodenectomies, 10 distal pancreatectomies, 6 local resections, 1 total pancreatectomy, and 1 central pancreatectomy-were resected successfully.
  • No patient received chemotherapy or radiotherapy after surgery.
  • One of the 2 patients with malignant SPT, in whom Ki-67 immunoreactivity was >25%, developed local recurrence with liver metastasis 4 months and died 6 months after surgery.
  • There were no significant associations between clinicopathologic factors and malignancy.
  • CONCLUSIONS: SPT is a rare neoplasm with low malignant potential.
  • Characteristic computed axial tomography and magnetic resonance imaging scans combined with age and sex profile should be sufficient for the decision to operate.
  • Patients with malignant SPT should have careful follow-up.
  • The high proliferative index assessed by immunohistochemical staining for Ki-67 may predict poor outcome of malignant SPT.
  • [MeSH-major] Carcinoma, Papillary / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 19268906.001).
  • [ISSN] 1879-1883
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Leydon GM: 'Yours is potentially serious but most of these are cured': optimistic communication in UK outpatient oncology consultations. Psychooncology; 2008 Nov;17(11):1081-8
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  • OBJECTIVE: To describe how experienced doctors discuss radiotherapy and chemotherapy with cancer patients about to undergo such treatment.
  • Participants included three experienced consultant oncologists and 27 patients diagnosed with cancer attending outpatient oncology consultations to discuss radiotherapy or chemotherapy.
  • RESULTS: Doctors repeatedly invoked optimism when discussing bad and uncertain information about radiotherapy and chemotherapy.
  • This was achieved by following relatively bad or uncertain information with some good information.
  • CONCLUSIONS: Doctors talked optimistically while sharing information about chemotherapy and radiotherapy with patients about to undergo such treatment.
  • Research indicates that patients want their doctors to openly share bad and uncertain information, but to do so sensitively.
  • Following uncertain or bad tidings with relatively better news was one way in which doctors delivered information honestly without diminishing opportunities for hope in the consultation room or optimism about the future.
  • [MeSH-major] Neoplasms / drug therapy. Neoplasms / radiotherapy. Patient Education as Topic. Physician-Patient Relations. Truth Disclosure. Uncertainty
  • [MeSH-minor] Adaptation, Psychological. Adult. Aged. Aged, 80 and over. Comprehension. Emotions. Female. Humans. Male. Middle Aged. Prognosis. Referral and Consultation. Semantics. Verbal Behavior


17. Zavadil M, Feyereisl J, Safár P, Pán M: [Undifferentiated choriocarcinoma--epithelioid trophoblastic tumors treated at the Center for Trophoblastic Diseases in the Czech Republic 1955-2003]. Ceska Gynekol; 2003 Nov;68(6):420-6
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  • OBJECTIVE: The clinical-pathological picture, pathogenesis, biological behavior and therapy of epithelioid trophoblastic tumor (ETT) alias undifferentiated choriocarcinoma (CH-Ned).
  • SETTING: Trophoblastic Disease Center in the Czech Republic (TDC-CZ), Department of Gynecology and Obstetrics, 3rd Medical Faculty, Charles University, Institute for the Care of Mother and Child, Prague.
  • METHODS: The identification of all tumors complying with histopathological criteria of ETT-CHNed among 372 malignant tumors of trophoblast (MTT), treated at TDC-CZ in the years 1955-2003.
  • Their morphological analysis was done from the standpoint of formal pathogenesis, correlation with clinical picture, laboratory and therapeutic results.
  • RESULTS: Among 372 malignant tumors of trophoblast (MTT) we detected 25 ETT-CHNed.
  • In 18 cases (72%) the tumor displayed gynecological symptomatology, in 7 cases (28%) a non-gynecological one (pulmonary 3 times, thyroid once, CNS once, GIT once, mamma once).
  • In the case history there was delivery in 10 cases, abortion in eight, mola hydatiosa completa twice, anamnesis was uncertain once and extra-uterine pregnancy was suspected also once.
  • The interval between pregnancy and established diagnosis was in the range of one to 64 months.
  • The ETT-CHNed diagnosis was established 18 times from curettage of endometrium, six times from biopsies of organs considered as primary localization of the tumor and once during post mortem examination.
  • In the first period (1955-1963) before introduction of chemotherapy all five patients died (100%) in the range of 4 months to 3 years.
  • In the third period (1981-2003), hysterectomy with subsequent polychemotherapy resulted in complete remission from two to 18 years in 9 out of 11 women (82%), while in two cases with absent ETT-CHNed in uterus the intervention was limited to tumor extirpation in the lung or mamma with subsequent treatment with chemotherapy.
  • Their clinical-pathological analysis revealed that ETT-CHNed is a malignant tumor, which is not less aggressive than choriocarcinoma (CH-NST).
  • It represents a less differentiated form of MTT, becoming manifest in a low production of hCG.
  • There are differentiated transitions between ETT-CHNed and CH-NST, which are analogous to grading of other malignant epithelial tumors.
  • Hysterectomy with subsequent intensive chemotherapy decreased the original 100% mortality in the years 1955-1963 to 18.1% in the years 1980-2003.

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  • (PMID = 15042852.001).
  • [ISSN] 1210-7832
  • [Journal-full-title] Ceska gynekologie
  • [ISO-abbreviation] Ceska Gynekol
  • [Language] CZE
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
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18. Carretta A, Ceresoli GL, Arrigoni G, Canneto B, Reni M, Cigala C, Zannini P: Diagnostic and therapeutic management of neuroendocrine lung tumors: a clinical study of 44 cases. Lung Cancer; 2000 Sep;29(3):217-25
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  • [Title] Diagnostic and therapeutic management of neuroendocrine lung tumors: a clinical study of 44 cases.
  • Neuroendocrine tumors of the lung (NTL) are a distinct subset of tumors with a wide range of histological patterns and clinical behavior.
  • Controversy still exists as to the ideal diagnostic and therapeutic approach to these neoplasms.
  • A series of 44 consecutive NTL patients operated on at our Institution was retrospectively reviewed in order to critically analyze the diagnostic and therapeutic management.
  • A preoperative diagnosis was obtained in 11 patients (25%).
  • Pathological diagnosis was typical carcinoid (TC) tumor in 36 cases, atypical carcinoid (AC) in three and large-cell neuroendocrine carcinoma (LCNEC) in five.
  • One patient had preoperative chemotherapy.
  • Median follow-up time was 40 months for TC and 51.5 months for AC/LCNEC.
  • Recurrence of disease was observed in three patients with TC and in two with AC/LCNEC.
  • In conclusion, our study confirms findings in the literature showing that TC and AC/LCNEC are clinically different, and that a differential preoperative diagnosis and treatment is necessary.
  • Surgery, with anatomical resection and lymphoadenectomy, remains the treatment of choice in all these tumors.
  • Laser treatment should be considered only as a palliative procedure or as a complementary technique to surgery.
  • The role of adjuvant treatments in AC and LCNEC is uncertain and should be evaluated in larger trials.
  • The prognostic role of biological factors such as cytometry and genetic markers requires further investigation before any definitive conclusions can be drawn.
  • [MeSH-major] Lung Neoplasms / surgery. Neuroendocrine Tumors / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / analysis. Chemotherapy, Adjuvant. Diagnosis, Differential. Female. Humans. Lymph Node Excision. Lymphatic Metastasis. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis

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  • (PMID = 10996424.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] IRELAND
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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19. Ferrari A, Casanova M, Bisogno G, Cecchetto G, Meazza C, Gandola L, Garaventa A, Mattke A, Treuner J, Carli M: Malignant vascular tumors in children and adolescents: a report from the Italian and German Soft Tissue Sarcoma Cooperative Group. Med Pediatr Oncol; 2002 Aug;39(2):109-14
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  • [Title] Malignant vascular tumors in children and adolescents: a report from the Italian and German Soft Tissue Sarcoma Cooperative Group.
  • BACKGROUND: Malignant vascular tumors are extremely rare in childhood and few data on their clinical management are available.
  • We report on a series of 18 children who had malignant vascular tumors, treated from 1980 to 2000 by the Italian and German Soft Tissue Sarcoma Cooperative Group.
  • PROCEDURE: Twelve patients had angiosarcoma, four had malignant hemangioendothelioma, and two had Kaposi's sarcoma.
  • Surgical resection was completed in six cases; radiotherapy was administered to 6 children, and chemotherapy to 14.
  • Response to chemotherapy was evaluable in nine cases and was: six no response, two partial remission, one complete remission.
  • CONCLUSIONS: Angiosarcoma and related malignant vascular tumors are aggressive neoplasms with a poor prognosis; their behavior in children seems no different from their adult counterparts.
  • Complete surgical resection remains the mainstay of treatment, but is probably sufficient in only a minority of cases.
  • The role of chemotherapy is uncertain, but the high rate of metastatic spread prompts investigation into new chemotherapeutic approaches.
  • [MeSH-major] Neoplasms, Vascular Tissue / pathology. Sarcoma / pathology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Clinical Trials as Topic. Germany. Hemangioendothelioma / pathology. Hemangiosarcoma / pathology. Humans. Infant. Italy. Prognosis. Sarcoma, Kaposi / pathology. Treatment Outcome

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12116058.001).
  • [ISSN] 0098-1532
  • [Journal-full-title] Medical and pediatric oncology
  • [ISO-abbreviation] Med. Pediatr. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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20. Ruoppolo M, Pezzica E, Milesi R, Corti D, Mercurio P, Fragapane G: [Neuroendocrine small-cell bladder cancer: our experience]. Urologia; 2010 Oct-Dec;77 Suppl 17:64-71
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  • Small-cell carcinoma is an epithelial tumor associated with a more aggressive behavior and poorer prognosis than transitional cell bladder carcinoma.
  • At the time of presentation 59% of patients have clinical stage >T2 and 56% show metastatic disease.
  • Local advanced disease was present in all the cases with stage >T2, metastatic disease in 1 case, lymph node involvement and ureteral bilateral obstruction in 2.
  • Platinum-based adjuvant chemotherapy was proposed but only two patients received the treatment.
  • All of the three patients died of metastatic disease at 5, 7, and 13 months.
  • The most common site of relapse and spread of disease was the peritoneum and intestinal tract, and the reason of death was uncontrolled acute hemorrhage from gastro-intestinal district.
  • CONCLUSIONS: In the absence of a prospective study, and because of the rarity of the disease, the best treatment for small-cell bladder cancer remains uncertain.
  • Neoadjuvant chemotherapy with platinum regimen plus aggressive surgical approach will be the treatment of choice.
  • The association of chemotherapy and radiotherapy should also be considered.
  • [MeSH-major] Carcinoma, Neuroendocrine / pathology. Carcinoma, Small Cell / pathology. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Combined Modality Therapy. Cystectomy. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Disease Progression. Fatal Outcome. Gastrointestinal Hemorrhage / etiology. Hematuria / etiology. Humans. Intestinal Neoplasms / complications. Intestinal Neoplasms / secondary. Leukemia, Lymphocytic, Chronic, B-Cell. Liver Neoplasms / secondary. Lymph Node Excision. Male. Middle Aged. Neoplasms, Second Primary. Peritoneal Neoplasms / secondary. Prostatic Neoplasms. Stomach Neoplasms. Survival Rate

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  • (PMID = 21308678.001).
  • [ISSN] 1724-6075
  • [Journal-full-title] Urologia
  • [ISO-abbreviation] Urologia
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin
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21. Uhm JE, Park YH, Yi SY, Cho EY, Choi YL, Lee SJ, Park MJ, Lee SH, Jun HJ, Ahn JS, Kang WK, Park K, Im YH: Treatment outcomes and clinicopathologic characteristics of triple-negative breast cancer patients who received platinum-containing chemotherapy. Int J Cancer; 2009 Mar 15;124(6):1457-62
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  • [Title] Treatment outcomes and clinicopathologic characteristics of triple-negative breast cancer patients who received platinum-containing chemotherapy.
  • The aim of this study was to evaluate the role of platinum-containing chemotherapy for metastatic triple-negative breast cancer (TNBC) patients in terms of the response rate (RR) and progression-free survival.
  • A second aim was to characterize the clinical behavior at the time of relapse of TNBC.
  • We retrospectively analyzed the clinical outcomes of patients with metastatic breast cancer who received taxane-platinum chemotherapy as the first- or second-line treatment, focusing on the TN phenotype.
  • In total, 257 patients with metastatic breast cancer received platinum-containing chemotherapy at Samsung Medical Center from 1999 to 2006.
  • Of these patients, 106 patients with available data on estrogen (ER), progesterone (PgR) and human epidermal growth factor receptor-2 (HER2) receptor status received taxane-platinum regimen as the first- or second-line treatment.
  • The time to death after chemotherapy (19 vs. 50 months, p = 0.037) and overall survival (OS) (21 vs. 56 months, p = 0.030) differed significantly between patients with TNBC and non-TNBC.
  • TNBC showed a unique locoregional infiltration pattern at relapse, which might reflect its aggressive clinical behavior.
  • Despite the similar response to platinum-containing chemotherapy, patients with TNBC had a shorter OS than patients with non-TNBC.
  • The implication of TN phenotype as poor prognostic factor is uncertain, because it needs to be defined whether poor outcome is related to the rapid growing characteristics of tumor itself or the resistance to drug therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Platinum Compounds / therapeutic use
  • [MeSH-minor] Adult. Aged. Bridged Compounds / therapeutic use. Disease-Free Survival. Female. Humans. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Phenotype. Receptor, ErbB-2 / drug effects. Receptor, ErbB-2 / genetics. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis. Recurrence. Retrospective Studies. Taxoids / therapeutic use. Treatment Outcome. Young Adult


22. Akbulut M, Kelten C, Bir F, Soysal ME, Duzcan SE: Primary peritoneal serous psammocarcinoma with recurrent disease and metastasis: a case report and review of the literature. Gynecol Oncol; 2007 Apr;105(1):248-51
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  • [Title] Primary peritoneal serous psammocarcinoma with recurrent disease and metastasis: a case report and review of the literature.
  • Although behavior of tumor is uncertain, it has been suggested to be similar to serous carcinomas of low malignant potential.
  • Computed tomography showed a heavily calcified rectovaginal mass that was histologically characterized by numerous psammoma bodies and low-grade cytological features.
  • Following the primary surgery, the patient received 9 cycles of chemotherapy.
  • CONCLUSION: Although psammocarcinoma is known to behave in a more indolent course, clinicians should be aware that patients with this disease may have a clinically aggressive, recurrent, and metastatic tumor that necessitated systemic therapy.
  • [MeSH-major] Cystadenocarcinoma, Serous / pathology. Neoplasm Recurrence, Local / pathology. Peritoneal Neoplasms / pathology
  • [MeSH-minor] Aged. Female. Humans. Neoplasm Metastasis

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  • (PMID = 17222893.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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23. Torres Lobatón A, Cruz Ortiz H, Rojo Herrera G, Avila Medrano L: [Sarcomas of the vulva. Report of 2 cases]. Ginecol Obstet Mex; 2000 Oct;68:429-34
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  • [Transliterated title] Sarcomas de la vulva. Informe de dos casos.
  • The first case was a teenager of 14 years-old with a low grade leiomyosarcoma surgically treated.
  • Along a 22 years follow-up the disease has had four local recurrences of more than 5 cm each one: two after surgery and two after surgery plus chemotherapy and surgery plus radiotherapy respectively.
  • She is alive disease evidence after two years from the last combined treatment.
  • The second one, was a 26 years-old patient with a malignant schwannoma of 12 cm in diameter treated with combined radical surgery, radiotherapy, and chemotherapy.
  • She is alive and without disease evidence 52 months after surgery.
  • Treatment of vulvar sarcomas is radical local excision followed mainly by radiotherapy with infiltrating margins.
  • The value of postoperative adjuvant chemotherapy is uncertain.
  • According to the natural history and behavior of vulvar sarcomas, we conclude that the elective treatment of these tumors should be carry out in institutions of high level.
  • [MeSH-major] Leiomyosarcoma. Neurilemmoma. Vulvar Neoplasms
  • [MeSH-minor] Abdominal Neoplasms / drug therapy. Abdominal Neoplasms / radiotherapy. Abdominal Neoplasms / secondary. Adolescent. Adult. Antineoplastic Agents, Alkylating / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bartholin's Glands. Chemotherapy, Adjuvant. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cystectomy. Cysts / diagnosis. Dacarbazine / administration & dosage. Dacarbazine / therapeutic use. Diagnosis, Differential. Disease-Free Survival. Doxorubicin / administration & dosage. Female. Follow-Up Studies. Humans. Neoplasm Recurrence, Local. Pelvic Neoplasms / drug therapy. Pelvic Neoplasms / radiotherapy. Pelvic Neoplasms / secondary. Radioisotope Teletherapy. Retrospective Studies. Treatment Outcome. Urinary Bladder Neoplasms / secondary. Urinary Bladder Neoplasms / surgery

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  • (PMID = 11138405.001).
  • [ISSN] 0300-9041
  • [Journal-full-title] Ginecología y obstetricia de México
  • [ISO-abbreviation] Ginecol Obstet Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7GR28W0FJI / Dacarbazine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide
  • [Number-of-references] 12
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24. De Munnynck K, Van Gool S, Van Calenbergh F, Demaerel P, Uyttebroeck A, Buyse G, Sciot R: Desmoplastic infantile ganglioglioma: a potentially malignant tumor? Am J Surg Pathol; 2002 Nov;26(11):1515-22
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  • [Title] Desmoplastic infantile ganglioglioma: a potentially malignant tumor?
  • Desmoplastic infantile ganglioglioma is a rare intracranial tumor of early childhood with a usually excellent prognosis despite malignant features both radiologically and histologically.
  • A combination of vincristine and carboplatinum was used according to the Low Grade Glioma Protocol of the International Society of Pediatric Oncology, with a temporary good response.
  • When histologically characterized by highly anaplastic features, it seems the biologic behavior of this tumor remains uncertain.
  • The aggressive behavior and the responsiveness to chemotherapy in this case may challenge the belief in the benign nature of these rare tumors.
  • [MeSH-major] Brain Neoplasms / pathology. Ganglioglioma / secondary
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Brain / pathology. Carboplatin / administration & dosage. Child, Preschool. Desmin. Fatal Outcome. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Neoplasm Proteins / analysis. Vincristine / administration & dosage


25. Casper ES: Gastrointestinal stromal tumors. Curr Treat Options Oncol; 2000 Aug;1(3):267-73
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  • The nonepithelial, nonlymphoid tumors of the gastrointestinal tract are heterogeneous in terms of clinical presentation, behavior, pathology, and genetic features.
  • Many of these tumors have no muscle differentiation, and designations such as leiomyoma or leiomyosarcoma are inappropriate for many of these neoplasms.
  • Both benign and malignant types are recognized.
  • Complete en bloc surgical resection, when possible, is the cornerstone of therapy.
  • Incomplete surgical resection and metastatic disease indicate a dismal prognosis in the majority of patients.
  • Recurrent or metastatic disease is often resected, but this has an uncertain impact on outcome.
  • For patients with unresectable disease, the results with systemic chemotherapy have been dismal.
  • Treatment with doxorubicin/ifosfamide combinations is of dubious value.
  • Hepatic arterial embolization, with and without intra-arterial chemotherapy, results in regression of liver metastases in selected patients.
  • The impact of such treatment on outcome, however, is poorly studied.
  • Aggressive surgical resection of peritoneal metastases with intraperitoneal chemotherapy has been advocated, but requires formal study in large trials.
  • [MeSH-major] Gastrointestinal Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Humans. Radiotherapy. Stromal Cells / pathology. Survival Rate

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  • [Cites] Histopathology. 1991 Jul;19(1):1-11 [1916682.001]
  • [Cites] J Natl Cancer Inst. 1991 Jul 3;83(13):926-32 [2067035.001]
  • [Cites] Ultrastruct Pathol. 1996 Jul-Aug;20(4):373-93 [8837346.001]
  • [Cites] Cancer. 1995 Apr 15;75(8):2083-8 [7697597.001]
  • [Cites] Radiographics. 1998 Mar-Apr;18(2):379-92 [9536485.001]
  • [Cites] Eur J Cancer. 1999 Mar;35(3):413-9 [10448292.001]
  • [Cites] J Clin Oncol. 1999 Jan;17(1):150-7 [10458228.001]
  • [Cites] Am J Surg Pathol. 1993 Sep;17(9):887-97 [8394653.001]
  • [Cites] Am J Surg Pathol. 1986;10 Suppl 1:83-99 [3296804.001]
  • [Cites] Cancer. 1992 Mar 15;69(6):1334-41 [1540870.001]
  • [Cites] Lab Invest. 1998 Dec;78(12):1633-6 [9881963.001]
  • [Cites] Ann Chir Gynaecol. 1998;87(4):287-90 [9891767.001]
  • [Cites] N Engl J Med. 1993 Apr 15;328(15):1107-14 [8455669.001]
  • [Cites] Ann Surg Oncol. 1995 Jan;2(1):26-31 [7834450.001]
  • [Cites] J Clin Oncol. 1989 Jan;7(1):126-31 [2491883.001]
  • [Cites] Gastrointest Endosc. 1997 Jun;45(6):468-73 [9199902.001]
  • [Cites] Ann Surg. 1987 Dec;206(6):706-10 [3689007.001]
  • [Cites] Am J Surg Pathol. 1999 Jan;23(1):82-7 [9888707.001]
  • [Cites] Mayo Clin Proc. 1999 Jun;74(6):543-52 [10377927.001]
  • [Cites] Ann Surg. 1995 Apr;221(4):392-7 [7726675.001]
  • [Cites] J Allergy Clin Immunol. 1997 Oct;100(4):435-40 [9338533.001]
  • [Cites] Ann Chir Gynaecol. 1998;87(4):278-81 [9891765.001]
  • [Cites] Am J Pathol. 1999 Jan;154(1):53-60 [9916918.001]
  • [Cites] Nat Genet. 1998 Aug;19(4):323-4 [9697690.001]
  • [Cites] Am J Surg Pathol. 1999 Sep;23(9):1109-18 [10478672.001]
  • [Cites] Hum Pathol. 1999 Oct;30(10):1213-20 [10534170.001]
  • [Cites] J Clin Oncol. 1993 Jul;11(7):1269-75 [8315424.001]
  • [Cites] Am J Surg Pathol. 1999 Apr;23(4):377-89 [10199467.001]
  • (PMID = 12057170.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 30
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26. Coelho Neto M, Ramina R, de Meneses MS, Arruda WO, Milano JB: Peritoneal dissemination from central neurocytoma: case report. Arq Neuropsiquiatr; 2003 Dec;61(4):1030-4
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  • OBJECTIVE: Central neurocytoma is a low grade tumor of neuroglial origin and a relatively new histological entity.
  • Only a few cases have been reported and its biological behavior is still uncertain.
  • Some cases have shown an aggressive behavior (local recurrence, malignant dedifferentiation or CSF dissemination) and challenged the initial view of its relative benignity.
  • Chemotherapy was initiated immediately after diagnosis of peritoneal dissemination (etoposide, carboplatin, doxorubicin and cyclophosphamide).
  • The patient developed metabolic imbalance and respiratory failure due to rapid formation of ascitic fluid and died 3 days after the diagnosis of peritoneal dissemination was established.
  • CONCLUSION: Central neurocytoma is a low grade tumor with low values of the proliferative index in the majority of cases.
  • In spite of that, some tumors may present a very aggressive behavior and extraneural dissemination.
  • Evaluation of proliferative index may be a guideline parameter for planning adjuvant therapies after surgical treatment in selected cases.
  • [MeSH-major] Cerebral Ventricle Neoplasms / pathology. Neurocytoma / pathology. Peritoneal Neoplasms / secondary
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Fatal Outcome. Humans. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness. Neoplasm, Residual. Peritoneum. Reoperation. Tomography, X-Ray Computed

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  • (PMID = 14762613.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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27. Silva EG, Gershenson DM, Malpica A, Deavers M: The recurrence and the overall survival rates of ovarian serous borderline neoplasms with noninvasive implants is time dependent. Am J Surg Pathol; 2006 Nov;30(11):1367-71
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  • [Title] The recurrence and the overall survival rates of ovarian serous borderline neoplasms with noninvasive implants is time dependent.
  • Ovarian serous borderline neoplasm with noninvasive implants traditionally have been considered to be nonaggressive tumors associated with an excellent prognosis.
  • Eighty cases of advanced-stage ovarian serous borderline tumor with noninvasive implants were identified; the minimum follow-up period for these cases was 5 years or until the death of the patient.
  • The following cases were excluded: patients treated by cystectomy, patients who died of other causes, patients who developed other tumors, and patients who had as the only positive material after resection of the primary borderline neoplasm a tumor detected on a second look or third look operation.
  • Slides of the recurrent tumor were available in all cases except for 2 in which the diagnosis was established clinically.
  • After surgery, 58 patients were treated with chemotherapy, 7 with radiotherapy, and 1 with hormonal therapy.
  • Thirty-five patients (44%) developed recurrences.
  • Only 10% of the patients had a recurrence in less than 5 years, 19% had their recurrences between 5 and 10 years, 10% between 10 and 15 years, and 5% more than 15 years after resection of the primary neoplasm.
  • Of the 35 patients who had a recurrence, 2 were diagnosed clinically, both are alive with progressive disease at 1 and 5 years after the diagnosis of the recurrence; 6 had recurrent serous borderline tumors, all are without evidence of disease with a follow-up ranging from 7 to 18 years after resection of the ovarian borderline tumor (median 14 y); and 27 patients subsequently developed low-grade serous carcinoma, 7 are alive with progressive disease with a follow-up ranging from 10 to 29 years (median 15 y) and 20 died of disease between 3 to 25 years after resection of the ovarian borderline tumor (median 16 y).
  • In summary, the true recurrence rate of ovarian serous borderline tumors with noninvasive implants can only be obtained through a long follow-up.
  • In this group of patients, 77% and 34% of the subsequent tumors developed 5 years and 10 years after diagnosis of the ovarian tumor, respectively.
  • Histologic examination of the recurrent tumor is important in determining further therapy and prognosis for these patients; all patients who recurred with borderline tumor are without evidence of disease, whereas 74% of the patients who recurred with low-grade serous carcinoma died of disease.
  • [MeSH-major] Cystadenocarcinoma, Serous / mortality. Neoplasm Recurrence, Local / epidemiology. Ovarian Neoplasms / mortality
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Female. Follow-Up Studies. Gynecologic Surgical Procedures. Humans. Middle Aged. Radiotherapy. Survival Rate. Time Factors

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  • (PMID = 17063075.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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