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1. Chatni SS, Sainani RS, Mehta SA, Mohandas KM: Infusion chemotherapy with cisplatinum and fluorouracil in the treatment of locally-advanced and metastatic gallbladder cancer. J Cancer Res Ther; 2008 Oct-Dec;4(4):151-5
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  • [Title] Infusion chemotherapy with cisplatinum and fluorouracil in the treatment of locally-advanced and metastatic gallbladder cancer.
  • BACKGROUND: Gallbladder cancer (GBC) has a poor prognosis.
  • Chemotherapy is traditionally considered to be ineffective.
  • MATERIALS AND METHODS: A total of 65 patients with inoperable GBC received palliative chemotherapy with CDDP and 5-FU.
  • Response was assessed after three cycles of chemotherapy.
  • RESULTS: A total of 19 patients had locally advanced unresectable cancer and 46 patients had metastatic cancer.
  • A total of 212 chemotherapy cycles were administered to the patients.
  • Response evaluation after three cycles of chemotherapy revealed complete response in five patients [7.69%; 95% confidence interval (95% CI): 2.87-16.22], partial response in 17 patients (26.15%; 95% CI: 16.57-37.81), stabilization of disease in 9 patients (13.85%; 95% CI: 6.96-23.88), and progression in 21 patients (32.30%; 95% CI: 21.80-44.35).
  • The median overall survival was 5.7 months and the median time to disease progression was 3.1 months.
  • This chemotherapy combination was well tolerated.
  • There were no chemotherapy-related deaths.
  • CONCLUSIONS: Infusion chemotherapy with CDDP and 5-FU appears to have a fair amount of activity in patients of inoperable GBC, with acceptable toxicity.
  • Tumor shrinkage following treatment with this regimen enabled surgical resection in two patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Fluorouracil / administration & dosage. Gallbladder Neoplasms / drug therapy. Gallbladder Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Prognosis. Prospective Studies. Treatment Outcome

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  • (PMID = 19052386.001).
  • [ISSN] 1998-4138
  • [Journal-full-title] Journal of cancer research and therapeutics
  • [ISO-abbreviation] J Cancer Res Ther
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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2. Thivat E, Thérondel S, Lapirot O, Abrial C, Gimbergues P, Gadéa E, Planchat E, Kwiatkowski F, Mouret-Reynier MA, Chollet P, Durando X: Weight change during chemotherapy changes the prognosis in non metastatic breast cancer for the worse. BMC Cancer; 2010;10:648
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  • [Title] Weight change during chemotherapy changes the prognosis in non metastatic breast cancer for the worse.
  • BACKGROUND: Weight change during chemotherapy is reported to be associated with a worse prognosis in breast cancer patients, both with weight gain and weight loss.
  • However, most studies were conducted prior to the common use of anthracycline-base chemotherapy and on North American populations with a mean BMI classified as overweight.
  • Our study was aimed to evaluate the prognostic value of weight change during anthracycline-based chemotherapy on non metastatic breast cancer (European population) with a long term follow-up.
  • METHODS: Patients included 111 women diagnosed with early stage breast cancer and locally advanced breast cancer who have been treated by anthracycline-based chemotherapy regimen between 1976 and 1989.
  • The relative percent weight variation (WV) between baseline and postchemotherapy treatment was calculated and categorized into either weight change (WV > 5%) or stable (WV < 5%).
  • Cox proportional hazard models were used to evaluate any potential association of weight change and known prognostic factors with the time to recurrence and overall survival.
  • During chemotherapy treatment, 31% of patients presented a notable weight variation which was greater than 5% of their initial weight.In multivariate analyses, weight change (> 5%) was positively associated with an increased risk of both recurrence (RR 2.28; 95% CI: 1.29-4.03) and death (RR 2.11; 95% CI: 1.21-3.66).
  • CONCLUSIONS: Our results suggest that weight change during breast-cancer chemotherapy treatment may be related to poorer prognosis with higher recurrence and higher mortality in comparison to women who maintained their weight.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Weight Gain. Weight Loss
  • [MeSH-minor] Adult. Anthracyclines / administration & dosage. Body Mass Index. Chi-Square Distribution. Disease-Free Survival. Female. France. Humans. Kaplan-Meier Estimate. Middle Aged. Neoplasm Invasiveness. Neoplasm Recurrence, Local. Neoplasm Staging. Proportional Hazards Models. Retrospective Studies. Risk Assessment. Risk Factors. Survival Rate. Time Factors. Treatment Outcome

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  • (PMID = 21108799.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines
  • [Other-IDs] NLM/ PMC3006393
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3. Couluris M, Mayer JL, Freyer DR, Sandler E, Xu P, Krischer JP: The effect of cyproheptadine hydrochloride (periactin) and megestrol acetate (megace) on weight in children with cancer/treatment-related cachexia. J Pediatr Hematol Oncol; 2008 Nov;30(11):791-7
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  • [Title] The effect of cyproheptadine hydrochloride (periactin) and megestrol acetate (megace) on weight in children with cancer/treatment-related cachexia.
  • BACKGROUND: Children with cancer frequently have associated cachexia and malnutrition.
  • Appetite stimulation and increased food intake is 1 approach to combat cancer-related cachexia.
  • MATERIALS AND METHODS: Cyproheptadine hydrochloride (CH), an appetite stimulant, was administered to children with cancer-associated cachexia to prevent further weight loss.
  • One patient on MA developed low cortisol levels and hyperlipidemia.
  • CONCLUSIONS: This study demonstrates that CH is a safe and effective way to promote weight gain in children with cancer/treatment-related cachexia.

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  • (PMID = 18989154.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / U10 CA81920; United States / NCI NIH HHS / CA / U10 CA081920; United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098543-06
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Appetite Stimulants; 0 / Gastrointestinal Agents; 2YHB6175DO / Cyproheptadine; TJ2M0FR8ES / Megestrol Acetate
  • [Other-IDs] NLM/ NIHMS184870; NLM/ PMC2917791
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4. Schmelz EM, Xu H, Sengupta R, Du J, Banerjee S, Sarkar FH, Rishi AK, Majumdar AP: Regression of early and intermediate stages of colon cancer by targeting multiple members of the EGFR family with EGFR-related protein. Cancer Res; 2007 Jun 1;67(11):5389-96
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  • [Title] Regression of early and intermediate stages of colon cancer by targeting multiple members of the EGFR family with EGFR-related protein.
  • A role of the epidermal growth factor receptor (EGFR) family has been suggested in colon cancer etiology, progression, and/or severity.
  • Our recently identified pan-erbB inhibitor EGFR-related protein (ERRP) targets EGFRs by attenuating their activation and subsequent signaling leading to cellular growth inhibition.
  • In the present study, we evaluated the therapeutic effectiveness of ERRP on early and intermediate stages of colon cancer by examining regression of chemically induced aberrant crypt foci (ACF) in the colon of CF1 mice and intestinal adenomas in APC(Min+/-) (Min) mice.
  • This treatment significantly reduced the number of ACF from 25.0 +/- 3.0 (controls) to 14.9 +/- 1.6 (ERRP-treated; P = 0.011) and also reduced their size (P < 0.01).
  • In conclusion, our data show that ERRP is effective in regressing both early and intermediate intestinal lesions and could be an effective therapeutic agent for colon cancer.
  • [MeSH-major] Colonic Neoplasms / drug therapy. Drosophila Proteins / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] 1,2-Dimethylhydrazine. Adenoma / chemically induced. Adenoma / drug therapy. Adenoma / metabolism. Adenoma / pathology. Animals. Apoptosis / drug effects. Carcinogens. Cell Growth Processes / drug effects. Female. Intestinal Mucosa / drug effects. Intestinal Mucosa / metabolism. Male. Mice. Mice, Inbred C57BL. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Neoplasm Staging. Precancerous Conditions / chemically induced. Precancerous Conditions / drug therapy. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Receptors, Estrogen / genetics. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / pharmacology. Transforming Growth Factor alpha / metabolism

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  • (PMID = 17545620.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG014343
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Drosophila Proteins; 0 / ERR protein, Drosophila; 0 / NF-kappa B; 0 / Receptors, Estrogen; 0 / Recombinant Fusion Proteins; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; IX068S9745 / 1,2-Dimethylhydrazine
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5. Yamazaki K, Boku N, Shibamoto K, Yasui H, Fukutomi A, Yoshino T, Hironaka S, Onozawa Y, Otake Y, Hasuike N, Matsubayashi H, Inui T, Yamaguchi Y, Ono H: The role of the outpatient clinic in chemotherapy for patients with unresectable or recurrent gastric cancer. Jpn J Clin Oncol; 2007 Feb;37(2):96-101
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  • [Title] The role of the outpatient clinic in chemotherapy for patients with unresectable or recurrent gastric cancer.
  • BACKGROUND: Recently, outpatient chemotherapy centers have become popular in Japan.
  • To clarify the actual conditions of outpatient clinics, we surveyed entire clinical courses of chemotherapy in patients with unresectable or recurrent gastric cancer.
  • METHODS: From the medical records of 64 patients with unresectable or recurrent gastric cancer with no prior chemotherapy, we obtained data on overall survival, non-hospitalized survival, the number of and reasons for attendance at the outpatient clinic and hospitalization, and medical conditions at discharge.
  • RESULTS: The median follow-up time was 520 days, the median survival time was 353 days, and the median non-hospitalized survival time was 282 days.
  • Patients attended the outpatient clinic 1917 times in total; 145 (8%) of these were unplanned visits for accidental disease, disease progression, or toxicity.
  • Patients were hospitalized 291 times in total: 110 (38%) of hospitalizations were unplanned or emergencies because of disease progression or toxicity.
  • Patients were discharged 290 times in total; in 56 of these discharges (19%) unresolved medical problems remained, such as toxicity, total parenteral nutrition, or symptoms related to cancer.
  • Three patients (5%) died from treatment-related leucopenia and thrombocytopenia.
  • CONCLUSIONS: Patients with unresectable and recurrent gastric cancer were treated at outpatient clinics for periods up to 80% longer than the entire clinical course of chemotherapy.
  • The role of the outpatient clinic is very important to chemotherapy for patients with unresectable or recurrent gastric cancer.
  • [MeSH-major] Ambulatory Care Facilities. Antineoplastic Agents / administration & dosage. Cancer Care Facilities. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Emergency Medical Services. Female. Hospitalization / statistics & numerical data. Humans. Japan. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Retrospective Studies. Survival Analysis

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  • (PMID = 17272316.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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6. Senthivinayagam S, Mishra P, Paramasivam SK, Yallapragada S, Chatterjee M, Wong L, Rana A, Rana B: Caspase-mediated cleavage of beta-catenin precedes drug-induced apoptosis in resistant cancer cells. J Biol Chem; 2009 May 15;284(20):13577-88
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  • [Title] Caspase-mediated cleavage of beta-catenin precedes drug-induced apoptosis in resistant cancer cells.
  • Several studies have established a close connection between the Wnt/beta-catenin pathway and tumorigenesis, aberrant activation of which might contribute toward increased cancer cell growth and survival.
  • Extensive research is underway to identify therapeutic agents that can induce apoptosis specifically in cancer cells with minimal collateral damage to normal cells.
  • Although tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis specifically in tumor cells, many cancer cells develop resistance, which can be overcome by combinatorial treatment with other agents: for example, peroxisome proliferator-activated receptor gamma (PPARgamma) ligands.
  • To identify the molecular target mediating combinatorial drug-induced apoptosis, we focused on beta-catenin, a protein implicated in oncogenesis.
  • Our results show that co-treatment of TRAIL-resistant cancer cells with TRAIL and the PPARgamma ligand troglitazone leads to a reduction of beta-catenin expression, coinciding with maximal apoptosis.
  • Modulation of beta-catenin levels via ectopic overexpression or small interference RNA-mediated gene silencing modulates drug-induced apoptosis, indicating involvement of beta-catenin in regulating this pathway.
  • More in-depth studies indicated a post-translational mechanism, independent of glycogen synthase kinase-3beta activity regulating beta-catenin expression following combinatorial drug treatment.
  • These results demonstrate beta-catenin as a promising new target of drug-induced apoptosis, which can be targeted to sensitize apoptosis-resistant cancer cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Drug Resistance, Neoplasm / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Neoplasm Proteins / metabolism. Neoplasms / drug therapy. beta Catenin / metabolism
  • [MeSH-minor] Caspase 3 / metabolism. Caspase 8 / metabolism. Cell Line, Tumor. Chromans / pharmacology. Gene Silencing. Glycogen Synthase Kinase 3 / metabolism. Glycogen Synthase Kinase 3 beta. Humans. PPAR gamma / agonists. PPAR gamma / metabolism. RNA, Small Interfering. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Thiazolidinediones / pharmacology

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  • (PMID = 19289465.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM055835; United States / NCI NIH HHS / CA / R21 CA121221; United States / NCI NIH HHS / CA / CA121221; United States / NIGMS NIH HHS / GM / GM55835
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromans; 0 / Neoplasm Proteins; 0 / PPAR gamma; 0 / RNA, Small Interfering; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Thiazolidinediones; 0 / beta Catenin; EC 2.7.11.1 / GSK3B protein, human; EC 2.7.11.1 / Glycogen Synthase Kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; I66ZZ0ZN0E / troglitazone
  • [Other-IDs] NLM/ PMC2679459
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7. Clouser MC, Roe DJ, Foote JA, Harris RB, Alberts DS: Dose response of retinol and isotretinoin in the prevention of nonmelanoma skin cancer recurrence. Nutr Cancer; 2010;62(8):1058-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dose response of retinol and isotretinoin in the prevention of nonmelanoma skin cancer recurrence.
  • Using data from a randomized, double blind, study of the efficacy of retinol or isotretinoin vs. placebo on recurrence of nonmelanoma skin cancer in high-risk subjects, a reanalysis of the original intent to treat analysis was performed in a dose-response format.
  • Cox proportional hazards models describe the relationship between dose quartiles of isotretinoin and retinol use and time to first occurrence of squamous cell carcinoma (SCC) or basal cell carcinoma (BCC) in crude and adjusted models.
  • These analyses confirm the results of the original intent to treat analyses and raise an interesting question related to the potential for increased risk for patients in the first quartile of retinol dose.

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  • (PMID = 21058193.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA027502; United States / NCI NIH HHS / CA / CA-27502; United States / NCI NIH HHS / CA / CA-34256
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 11103-57-4 / Vitamin A; EH28UP18IF / Isotretinoin
  • [Other-IDs] NLM/ NIHMS583867; NLM/ PMC4104190
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8. Kim SC: [Surgical management of pancreatic cancer]. Korean J Gastroenterol; 2008 Feb;51(2):89-100
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  • [Title] [Surgical management of pancreatic cancer].
  • Pancreatic cancer is a major problematic concern among all forms of gastrointestinal malignancies because of its poor prognosis.
  • Although significant progress has been made in the surgical treatment in terms of increased resection rate and decreased treatment-related morbidity and mortality, the true survival rate still remains below 5% today.
  • Surgical options for pancreatic cancer are based on the its unique anatomy and physiology, catastrophic tumor biology, experience of surgeon, and status of patients.
  • Four main options exist for the surgical treatment of pancreatic cancer.
  • These include standard "Whipple" pancreaticoduodenectomy (PD), pylorus preserving PD (PPPD), distal pancreatectomy (left-side pancreatectomy), and total pancreatectomy according to the location of tumor.
  • Portal vein involvement by tumor is regarded as an anatomical extension of disease, and en bloc resection of portal vein with tumor is recommended if technically feasible, which is stated in 2002 AJCC tumor staging for pancreatic cancer.
  • In comparison of the survival rates between standard and extended resection of pancreatic head cancer, no significant survival benefit was demonstrated from the prospective reports.
  • PPPD may be superior to standard PD in respect to nutrition and quality of life without any deleterious effect upon long term survival or tumor recurrence.
  • New surgical treatment modalities including modified extended pancreatectomy, neoadjuvant chemotherapy, and radical antegrade modular distal pancreatectomy have been tried to improve the patients' survival.
  • However, early diagnosis and treatment remain as key factors for the cure of pancreatic cancer irrespective of various surgical trials.
  • [MeSH-minor] Humans. Neoplasm Staging. Pancreaticoduodenectomy. Portal Vein / pathology. Portal Vein / surgery. Prognosis. Survival Rate

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  • (PMID = 18349571.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Number-of-references] 57
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9. Brard L, Weitzen S, Strubel-Lagan SL, Swamy N, Gordinier ME, Moore RG, Granai CO: The effect of total parenteral nutrition on the survival of terminally ill ovarian cancer patients. Gynecol Oncol; 2006 Oct;103(1):176-80
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  • [Title] The effect of total parenteral nutrition on the survival of terminally ill ovarian cancer patients.
  • OBJECTIVES: Total parenteral nutrition (TPN) for terminal ovarian cancer patients remains controversial.
  • In this study, we compared survival from time of terminal intestinal obstruction (TIO) diagnosis in patients who received TPN versus those who did not.
  • METHODS: A historical cohort of 55 patients with stage IIIC/IV epithelial ovarian cancer hospitalized for TIO between 1994 and 2002 was studied.
  • Number of chemotherapy cycles completed after TIO diagnosis, major complications of TPN, and demographics were measured.
  • RESULTS: The median survival from time of TIO diagnosis was 72 days (range 16-485) for patients receiving TPN and 41.0 days (range 4-133) for those not receiving TPN (P = 0.05), but no difference in survival was observed when adjusting for chemotherapy.
  • Patients receiving TPN after obstruction were more likely to undergo concurrent chemotherapy (64 vs. 26%, P = 0.004).
  • One major TPN-related complication was found.
  • CONCLUSIONS: Ovarian cancer patients with TIO receiving TPN had a median survival benefit of 4 weeks.
  • This benefit decreased when patients were treated with concurrent chemotherapy.
  • [MeSH-major] Intestinal Obstruction / therapy. Ovarian Neoplasms / therapy. Parenteral Nutrition, Total
  • [MeSH-minor] Cohort Studies. Epithelial Cells / pathology. Female. Humans. Middle Aged. Neoplasm Staging. Retrospective Studies. Survival Rate. Terminal Care

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  • (PMID = 16564074.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / K12 HD043447
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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10. Theobald S: [Nutrition and prostate cancer--what is the scientific evidence?]. Med Monatsschr Pharm; 2006 Oct;29(10):371-7
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  • [Title] [Nutrition and prostate cancer--what is the scientific evidence?].
  • Prostate cancer is the most frequently occurring form of cancer in German men with an incidence of 49.000 in the year 2002.
  • Among individual food groups/nutrients a high consumption of total fat, saturated fats, meat, dairy, and calcium are related to an increased risk.
  • Tomato products, soy, lycopene, selenium, marine omega-3-fatty acids and vitamin E in smokers may inversely be associated with prostate cancer.
  • Evidence from experimental studies and clinical experience suggest that application of selenium during chemotherapy and/or radiotherapy may decrease therapy related toxicities and increases the effect of the standard therapy on cancer cells.
  • For expert patients it is essential to participate in decisions concerning their standard as well as complementary therapy by developing individual self-help concepts.
  • Physicians should consider these needs when they counsel cancer patients.
  • [MeSH-minor] Diet. Humans. Male. Neoplasm Recurrence, Local / prevention & control. Selenium / therapeutic use

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  • (PMID = 17058896.001).
  • [ISSN] 0342-9601
  • [Journal-full-title] Medizinische Monatsschrift für Pharmazeuten
  • [ISO-abbreviation] Med Monatsschr Pharm
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] H6241UJ22B / Selenium
  • [Number-of-references] 0
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11. Ramos S: Cancer chemoprevention and chemotherapy: dietary polyphenols and signalling pathways. Mol Nutr Food Res; 2008 May;52(5):507-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer chemoprevention and chemotherapy: dietary polyphenols and signalling pathways.
  • Prevention of cancer through dietary intervention recently has received an increasing interest, and dietary polyphenols have become not only important potential chemopreventive, but also therapeutic, natural agents.
  • Polyphenols have been reported to interfere at the initiation, promotion and progression of cancer.
  • They might lead to the modulation of proteins in diverse pathways and require the integration of different signals for the final chemopreventive or therapeutic effect.
  • Polyphenols have been demonstrated to act on multiple key elements in signal transduction pathways related to cellular proliferation, differentiation, apoptosis, inflammation, angiogenesis and metastasis; however, these molecular mechanisms of action are not completely characterized and many features remain to be elucidated.
  • The aim of this review is to provide insights into the molecular basis of potential chemopreventive and therapeutic activities of dietary polyphenols with emphasis in their ability to control intracellular signalling cascades considered as relevant targets in a cancer preventive approach.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Antineoplastic Agents / therapeutic use. Chemoprevention / methods. Flavonoids / therapeutic use. Neoplasms / drug therapy. Phenols / therapeutic use
  • [MeSH-minor] Apoptosis / drug effects. Diet. Fruit. Humans. Neoplasm Metastasis / prevention & control. Polyphenols. Signal Transduction. Vegetables

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  • (PMID = 18435439.001).
  • [ISSN] 1613-4133
  • [Journal-full-title] Molecular nutrition & food research
  • [ISO-abbreviation] Mol Nutr Food Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents; 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols
  • [Number-of-references] 179
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12. Lee WY, Huang SC, Tzeng CC, Chang TL, Hsu KF: Alterations of metastasis-related genes identified using an oligonucleotide microarray of genistein-treated HCC1395 breast cancer cells. Nutr Cancer; 2007;58(2):239-46
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  • [Title] Alterations of metastasis-related genes identified using an oligonucleotide microarray of genistein-treated HCC1395 breast cancer cells.
  • Genistein, one of the major isoflavones, potently inhibits the growth and metastasis of breast cancer.
  • We investigated the effect of genistein in HCC1395 cells, a cell line derived from an early-stage primary breast cancer.
  • We used human oligonucleotide microarrays to determine the gene expression profile altered by genistein treatment.
  • We used quantitative real-time polymerase chain reaction to verify the microarray data at the mRNA level.
  • We conclude that genistein-induced alternations of gene expression involving metastasis may be exploited for devising chemopreventive and therapeutic strategies, particularly for early-stage breast cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Breast Neoplasms / drug therapy. Gene Expression Regulation, Neoplastic / drug effects. Genistein / pharmacology. Oligonucleotide Array Sequence Analysis / methods
  • [MeSH-minor] Cell Survival / drug effects. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Female. Flow Cytometry. Gene Expression Profiling. Humans. Neoplasm Invasiveness. Neoplasm Metastasis / drug therapy. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 17640171.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; DH2M523P0H / Genistein
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13. Kieback DG, Einzmann T, Labinsky E, Fischer DC, Niebergall H, Hasenburg A: Aggressive management of recurrent ovarian cancer--the challenge of individualizing cancer therapy illustrated by a case report. Onkologie; 2004 Aug;27(4):393-7
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  • [Title] Aggressive management of recurrent ovarian cancer--the challenge of individualizing cancer therapy illustrated by a case report.
  • BACKGROUND: In clinical practice, treatment recommendations and the patient's wishes often diverge, facing the physician with difficult choices.
  • CASE REPORT: The clinical course of a 36-year-old patient with 'platinum-refractory' ovarian cancer is reported.
  • The patient experienced a symptomatic relapse 7 months after debulking surgery and completion of platinum-based first-line chemotherapy.
  • Her husband supported her, and both asked for maximal therapy, including intensive care treatment for recurrent respiratory tract infections and total parenteral nutrition (TPN).
  • Problems related to TPN and progression of disease affected her individual perception of quality of life to a much lower extent than expected and perceived by her caretakers.
  • All professional health care providers were more than once very reluctant to continue treatment and only after extensive counseling gave in to the demand of the patient for further treatment, considering the effort futile - only to be surprised by treatment response and recovery.
  • After 3 years of palliation, the tumor was resistant to all cytotoxic regimens and the patient died 2 months after withdrawal of chemotherapy.
  • CONCLUSION: This case report illustrates that also in the age of evidence-based medicine individualized treatment beyond proven strategies can offer patient benefit.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carcinoma, Papillary / drug therapy. Neoplasm Recurrence, Local / drug therapy. Ovarian Neoplasms / drug therapy. Palliative Care / methods. Patient Participation. Puerperal Disorders / drug therapy
  • [MeSH-minor] Adult. Critical Care / psychology. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Resistance, Neoplasm. Female. Humans. Medical Futility. Motivation. Parenteral Nutrition, Total / psychology. Quality of Life / psychology

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  • (PMID = 15347897.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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14. Chen J, Power KA, Mann J, Cheng A, Thompson LU: Dietary flaxseed interaction with tamoxifen induced tumor regression in athymic mice with MCF-7 xenografts by downregulating the expression of estrogen related gene products and signal transduction pathways. Nutr Cancer; 2007;58(2):162-70
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  • [Title] Dietary flaxseed interaction with tamoxifen induced tumor regression in athymic mice with MCF-7 xenografts by downregulating the expression of estrogen related gene products and signal transduction pathways.
  • At sacrifice, the tumors were analyzed by immunohistochemistry for cell proliferation, apoptosis, and expression of estrogen-related genes and signal transduction pathways.
  • In conclusion, after long-term treatment, FS did not stimulate tumor growth and combined with TAM, regressed tumor size in part due to downregulation of the expression of estrogen-related gene products and signal transduction pathways.
  • [MeSH-major] Antineoplastic Agents, Hormonal / pharmacology. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Estrogens / metabolism. Flax. Tamoxifen / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Down-Regulation. Drug Synergism. Humans. Immunohistochemistry. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Random Allocation. Receptors, Estrogen / metabolism. Signal Transduction. Transplantation, Heterologous

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  • (PMID = 17640162.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R21 CA100639-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Estrogens; 0 / Receptors, Estrogen; 094ZI81Y45 / Tamoxifen
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15. Jenkinson AD, Lim J, Agrawal N, Menzies D: Laparoscopic feeding jejunostomy in esophagogastric cancer. Surg Endosc; 2007 Feb;21(2):299-302

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laparoscopic feeding jejunostomy in esophagogastric cancer.
  • BACKGROUND: Patients with esophagogastric malignancies often require nutritional supplementation in the perioperative period, especially in the setting where neoadjuvant therapy may delay tumor resection.
  • A simple technique is described here that can be performed at the time of staging laparoscopy and that has not been described before.
  • RESULTS: Forty-three patients treated over a 4-year period who had a laparoscopic feeding jejunostomy placed at the time of staging laparoscopy were reviewed.
  • Of these, 35 had preoperative chemotherapy according to a modified MRC OEO2 protocol.
  • The mean time to surgery was 10 weeks.
  • There were no conversions to an open procedure, nor were there any laparotomies for tube-related complications.
  • Mean time in the operating room for each procedure was 44 minutes.
  • It facilitates optimization of nutrition in the perioperative period for these patients, especially in those receiving preoperative chemotherapy.
  • [MeSH-major] Enteral Nutrition / methods. Jejunostomy / methods. Laparoscopy / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chi-Square Distribution. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Esophagectomy / methods. Female. Follow-Up Studies. Gastrectomy / methods. Humans. Male. Middle Aged. Neoplasm Staging. Nutritional Status. Probability. Retrospective Studies. Risk Assessment. Stomach Neoplasms / pathology. Stomach Neoplasms / surgery. Treatment Outcome. Weight Gain

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  • (PMID = 17122985.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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16. Feugang JM, Ye F, Zhang DY, Yu Y, Zhong M, Zhang S, Zou C: Cactus pear extracts induce reactive oxygen species production and apoptosis in ovarian cancer cells. Nutr Cancer; 2010;62(5):692-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cactus pear extracts induce reactive oxygen species production and apoptosis in ovarian cancer cells.
  • The protective effect of natural products such as fruits and vegetables against cancer has attracted great attention because of their fewer side effects and therefore, potentially greater safety.
  • We have previously reported that cactus pear mixture aqueous extract (CME) reduces gynecologic cancer cells growth by inducting apoptosis.
  • This study aimed to elucidate the cellular pathway(s) triggered by CME in cancer cells.
  • Normal, immortalized ovarian and ovarian cancer cells (OVCA420, SKOV3) were treated with 5 and 10% CME.
  • After 2 days of treatment, immortalized cells treated with 10% CME accumulated more ROS than untreated cells, whereas cancer cells cultured with 5% and 10% CME exhibited a dramatic increase of reactive oxygen species (ROS).
  • Greater levels of DNA fragmentation, together with a perturbed expression of apoptotic-related (Bax, Bad, caspase 3, Bcl2, p53, and p21) and ROS-sensitive (NF-kappaB, c-jun/c-fos) genes were observed in the treated cancer cells.
  • After three days of treatment, the NF-kappaB and p-/SAPK/JNK expressions were decreased, whereas p-AKT was upregulated.
  • The CME significantly induced apoptosis in cancer cells.
  • The results suggest an inhibitory effect of Arizona CME on cancer cell growth through the accumulation of intracellular ROS, which may activate a cascade of reactions leading to the apoptosis.
  • [MeSH-major] Apoptosis / drug effects. Cactaceae. Ovarian Neoplasms / drug therapy. Plant Extracts / pharmacology. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Female. Fruit. Gene Expression Regulation, Neoplastic / drug effects. Humans. NF-kappa B / antagonists & inhibitors. Neoplasm Proteins / analysis


17. Ramos-De la Medina A, Salgado-Nesme N, Torres-Villalobos G, Medina-Franco H: Clinicopathologic characteristics of gastric cancer in a young patient population. J Gastrointest Surg; 2004 Mar-Apr;8(3):240-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathologic characteristics of gastric cancer in a young patient population.
  • The aim of this study was to analyze the clinicopathologic characteristics of young patients with gastric cancer with special attention to hereditary gastric cancer in a tertiary referral university hospital.
  • Charts from all patients 40 years of age or younger at the time of diagnosis, during the period from January 1, 1987 to December 31, 2001, were retrospectively reviewed.
  • Demographic variables, family history of gastric cancer, clinicopathologic characteristics, and treatment-related variables were analyzed.
  • During the study period, 558 cases of gastric cancer were seen at our institution, 83 (14.8%) were in patients 40 years of age or younger.
  • Fourteen patients (16.9%) had a family history of gastric cancer.
  • Five patients (6%) fulfilled the criteria of hereditary gastric cancer.
  • On univariate analysis, advanced tumor stage, hypoalbuminemia, low performance status, diffuse type, pangastric tumor location, noncurative surgery, and lack of adjuvant chemotherapy had a significant negative impact on survival.
  • On multivariate analysis, advanced tumor stage, pangastric tumor location, and absence of adjuvant chemotherapy were significantly associated with poor prognosis.
  • Family history of gastric cancer or hereditary gastric cancer did not have any impact on prognosis.
  • There is a high frequency of gastric cancer in young patients at our institution.
  • Family history of gastric cancer or hereditary gastric cancer did not have a significant impact on survival.
  • Complete resection and adjuvant chemotherapy appeared to confer the only chance of prolonged survival.
  • [MeSH-minor] Adult. Cadherins / genetics. Female. Humans. Male. Mexico / epidemiology. Multivariate Analysis. Neoplasm Staging. Retrospective Studies. Stomach / pathology. Survival Rate

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  • (PMID = 15019915.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins
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18. Litle VR, Luketich JD, Christie NA, Buenaventura PO, Alvelo-Rivera M, McCaughan JS, Nguyen NT, Fernando HC: Photodynamic therapy as palliation for esophageal cancer: experience in 215 patients. Ann Thorac Surg; 2003 Nov;76(5):1687-92; discussion 1692-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Photodynamic therapy as palliation for esophageal cancer: experience in 215 patients.
  • BACKGROUND: Photodynamic therapy (PDT) utilizes a photosensitizing agent, light, and oxygen to endoscopically ablate cancer cells.
  • This review summarizes our experience with PDT for the palliation of bleeding or obstructing esophageal cancer (EC).
  • After Photofrin II injection, nonthermal light treatment was delivered endoscopically.
  • Dysphagia scores, duration of palliation, reinterventions, complications, and survival after treatment were reviewed.
  • Seventy-five percent of EC were in the distal esophagus.
  • Supplemental nutrition was discontinued after PDT in 8 of 27 patients (30%).
  • PDT complications included perforation (2% of treatment courses), stricture (2%), Candida esophagitis (2%), pleural effusions (4%), and sunburn (6%).
  • The procedure-related mortality rate was 1.8%, and median survival was 4.8 months.
  • CONCLUSIONS: PDT offers effective palliation for patients with obstructing EC in 85% of treatment courses.
  • The ideal EC patient for PDT palliation has an obstructing endoluminal cancer.
  • Patients living more than 2 months may require reintervention to maintain palliation of malignant dysphagia, and a multimodality treatment approach is common.
  • [MeSH-major] Dihematoporphyrin Ether / administration & dosage. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / mortality. Palliative Care / methods. Photochemotherapy / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cohort Studies. Esophagoscopy / methods. Female. Humans. Injections, Intralesional. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Risk Assessment. Survival Rate. Treatment Outcome

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  • (PMID = 14602313.001).
  • [ISSN] 0003-4975
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 97067-70-4 / Dihematoporphyrin Ether
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19. Calviello G, Serini S, Piccioni E: n-3 polyunsaturated fatty acids and the prevention of colorectal cancer: molecular mechanisms involved. Curr Med Chem; 2007;14(29):3059-69
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] n-3 polyunsaturated fatty acids and the prevention of colorectal cancer: molecular mechanisms involved.
  • Increasing evidence supports the hypothesis that nutrition habits play a critical role in the incidence and growth of colorectal cancer.
  • Among dietary factors, fish-derived n-3 polyunsaturated fatty acids (PUFAs) have gained particular interest, since epidemiological studies have shown a reduced incidence of this cancer in populations consuming high levels of fish.
  • Such an anti-neoplastic activity has been related to the regulatory effects exhibited by n-3 PUFAs on cell proliferation and apoptosis.
  • Finally, it has been suggested that they may act as adjuvant therapeutic agents sensitizing tumors, including colon cancer, to different anti-neoplastic drugs.
  • Their inhibitory action has been also recently suggested for the molecular pathways driven by COX-2 and beta-catenin, known to play a major role in the development and progression of colon cancer.
  • The aim of the present review is to analyze the anti-neoplastic effect of n-3 PUFAs towards colon cancer, and examine the molecular mechanisms involved.
  • [MeSH-major] Colorectal Neoplasms / prevention & control. Fatty Acids, Omega-3 / therapeutic use. beta Catenin / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Cell Membrane Structures / physiology. Cyclooxygenase 2 / metabolism. Humans. Inflammatory Bowel Diseases / metabolism. Neoplasm Metastasis / drug therapy. Neoplasm Metastasis / prevention & control. Neovascularization, Pathologic / prevention & control. Oxidative Stress. Vascular Endothelial Growth Factor A / antagonists & inhibitors. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18220742.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Fatty Acids, Omega-3; 0 / Vascular Endothelial Growth Factor A; 0 / beta Catenin; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
  • [Number-of-references] 187
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20. Wang W, Danielsson A, Svanberg E, Lundholm K: Lack of effects by tricyclic antidepressant and serotonin inhibitors on anorexia in MCG 101 tumor-bearing mice with eicosanoid-related cachexia. Nutrition; 2003 Jan;19(1):47-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of effects by tricyclic antidepressant and serotonin inhibitors on anorexia in MCG 101 tumor-bearing mice with eicosanoid-related cachexia.
  • OBJECTIVES: Anorexia is a major clinical problem in large number of patients with advanced cancer disease.
  • Serotonergic mechanisms are assumed to play a role in the process of feeding behavior during normal and pathologic circumstances, which may also involve cancer anorexia according to previous experimental and clinical studies.
  • Also, the treatments did not decrease elevated plasma concentrations of interleukin-6 and prostaglandin E(2) in the tumor-bearing mice.
  • [MeSH-major] Anorexia / drug therapy. Antidepressive Agents, Tricyclic / therapeutic use. Cachexia / drug therapy. Eating / drug effects. Serotonin Uptake Inhibitors / therapeutic use
  • [MeSH-minor] Animals. Body Weight / drug effects. Brain / drug effects. Brain / metabolism. Dinoprostone / blood. Disease Models, Animal. Eicosanoids / blood. Eicosanoids / physiology. Female. Injections, Intraperitoneal. Interleukin-6 / blood. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Nitric Oxide / metabolism. Serotonin / metabolism. Tryptophan / metabolism

  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • Hazardous Substances Data Bank. (L)-Tryptophan .
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  • [CommentIn] Nutrition. 2003 Jan;19(1):67-8 [12507644.001]
  • (PMID = 12507639.001).
  • [ISSN] 0899-9007
  • [Journal-full-title] Nutrition (Burbank, Los Angeles County, Calif.)
  • [ISO-abbreviation] Nutrition
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antidepressive Agents, Tricyclic; 0 / Eicosanoids; 0 / Interleukin-6; 0 / Serotonin Uptake Inhibitors; 31C4KY9ESH / Nitric Oxide; 333DO1RDJY / Serotonin; 8DUH1N11BX / Tryptophan; K7Q1JQR04M / Dinoprostone
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21. Deng G, Lin H, Seidman A, Fornier M, D'Andrea G, Wesa K, Yeung S, Cunningham-Rundles S, Vickers AJ, Cassileth B: A phase I/II trial of a polysaccharide extract from Grifola frondosa (Maitake mushroom) in breast cancer patients: immunological effects. J Cancer Res Clin Oncol; 2009 Sep;135(9):1215-21
MedlinePlus Health Information. consumer health - Breast Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I/II trial of a polysaccharide extract from Grifola frondosa (Maitake mushroom) in breast cancer patients: immunological effects.
  • BACKGROUND: Cancer patients commonly use dietary supplements to "boost immune function".
  • METHODS: In a phase I/II dose escalation trial, 34 postmenopausal breast cancer patients, free of disease after initial treatment, were enrolled sequentially in five cohorts.
  • Two patients withdrew prior to completion of the study due to grade I possibly related side effects: nausea and joint swelling in one patient; rash and pruritus in the second.
  • Cancer patients should be made aware of the fact that botanical agents produce more complex effects than assumed, and may depress as well as enhance immune function.

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  • (PMID = 19253021.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCCIH NIH HHS / AT / P50 AT002779; United States / NCCIH NIH HHS / AT / P50AT002779
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytokines; 0 / Polysaccharides
  • [Other-IDs] NLM/ NIHMS479729; NLM/ PMC3751581
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22. Weyermann P, Dallmann R, Magyar J, Anklin C, Hufschmid M, Dubach-Powell J, Courdier-Fruh I, Henneböhle M, Nordhoff S, Mondadori C: Orally available selective melanocortin-4 receptor antagonists stimulate food intake and reduce cancer-induced cachexia in mice. PLoS One; 2009;4(3):e4774

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Orally available selective melanocortin-4 receptor antagonists stimulate food intake and reduce cancer-induced cachexia in mice.
  • BACKGROUND: Cachexia is among the most debilitating and life-threatening aspects of cancer.
  • It represents a metabolic syndrome affecting essential functional circuits involved in the regulation of homeostasis, and includes anorexia, fat and muscle tissue wasting.
  • It was speculated that blockade of its central physiological target, the melanocortin (MC)-4 receptor, might provide a promising anti-cachexia treatment strategy.
  • This idea is supported by the fact that in animal studies, agouti-related protein (AgRP), the endogenous inverse agonist at the MC-4 receptor, was found to affect two hallmark features of cachexia, i.e. to increase food intake and to reduce energy expenditure.
  • Orally active compounds might offer a considerable advantage for the treatment of cachexia patients.
  • [MeSH-major] Cachexia / drug therapy. Eating / drug effects. Receptor, Melanocortin, Type 4 / antagonists & inhibitors
  • [MeSH-minor] Animals. Body Weight. Brain Chemistry. Cell Line, Tumor. Female. Humans. Kaplan-Meier Estimate. Male. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Random Allocation

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  • (PMID = 19295909.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptor, Melanocortin, Type 4
  • [Other-IDs] NLM/ PMC2654097
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23. Yeh CT, Wu CH, Yen GC: Ursolic acid, a naturally occurring triterpenoid, suppresses migration and invasion of human breast cancer cells by modulating c-Jun N-terminal kinase, Akt and mammalian target of rapamycin signaling. Mol Nutr Food Res; 2010 Sep;54(9):1285-95
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  • [Title] Ursolic acid, a naturally occurring triterpenoid, suppresses migration and invasion of human breast cancer cells by modulating c-Jun N-terminal kinase, Akt and mammalian target of rapamycin signaling.
  • Metastasis is one of the most important factors related to breast cancer therapeutic efficacy.
  • In this study, we first observed that ursolic acid exerted a dose- and time-dependent inhibitory effect on the migration and invasion of highly metastatic breast MDAMB231 cells at non-cytotoxic concentrations.
  • This effect was associated with reduced activities of metalloproteinase-2 (MMP-2) and u-PA, which correlated with enhanced expression of tissue inhibitor of MMP-2 and plasminogen activator inhibitor-1, respectively.
  • A time-dependent inhibition of the protein levels of Rho-like GTPases, growth factor receptor-bound protein 2, Ras and vascular endothelial growth factor in cytosol by ursolic acid treatment was also observed.
  • These results suggest that ursolic acid has potential as a chemopreventive agent for metastatic breast cancer.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Breast Neoplasms / drug therapy. Cell Movement / drug effects. JNK Mitogen-Activated Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. TOR Serine-Threonine Kinases / metabolism. Triterpenes / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cell Proliferation / drug effects. Female. Humans. NF-kappa B / metabolism. Neoplasm Invasiveness / prevention & control. Osmolar Concentration. Phosphorylation / drug effects. Protein Kinase Inhibitors / pharmacology. Protein Transport / drug effects. Signal Transduction / drug effects. Time Factors


24. Meyer F, Bairati I, Jobin E, Gélinas M, Fortin A, Nabid A, Têtu B: Acute adverse effects of radiation therapy and local recurrence in relation to dietary and plasma beta carotene and alpha tocopherol in head and neck cancer patients. Nutr Cancer; 2007;59(1):29-35
Hazardous Substances Data Bank. BETA-CAROTENE .

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  • [Title] Acute adverse effects of radiation therapy and local recurrence in relation to dietary and plasma beta carotene and alpha tocopherol in head and neck cancer patients.
  • There is a debate concerning the effects of antioxidant vitamins during radiation therapy: Can they reduce the adverse effects of therapy without reducing treatment efficacy?
  • We examined whether dietary and plasma beta carotene and alpha tocopherol were related to severe acute adverse effects of radiation therapy and to cancer local recurrence.
  • We conducted a prospective study of 540 head and neck cancer patients treated by radiation therapy.
  • Acute adverse effects of radiation therapy and local recurrence were documented.
  • Alpha tocopherol was not related to severe adverse effects or to cancer recurrence.
  • This study suggests that a higher usual dietary beta carotene intake can reduce the occurrence of severe adverse effects of radiation therapy and decrease local cancer recurrence.
  • [MeSH-major] Head and Neck Neoplasms / drug therapy. Radiation Injuries / prevention & control. alpha-Tocopherol / blood. alpha-Tocopherol / therapeutic use. beta Carotene / blood. beta Carotene / therapeutic use
  • [MeSH-minor] Antioxidants / metabolism. Antioxidants / therapeutic use. Confidence Intervals. Diet. Dietary Supplements. Double-Blind Method. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Odds Ratio. Prospective Studies. Surveys and Questionnaires

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  • (PMID = 17927499.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 01YAE03M7J / beta Carotene; H4N855PNZ1 / alpha-Tocopherol
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25. Lee LT, Schally AV, Liebow C, Lee PP, Lee PH, Lee MT: Dephosphorylation of cancer protein by tyrosine phosphatases in response to analogs of luteinizing hormone-releasing hormone and somatostatin. Anticancer Res; 2008 Sep-Oct;28(5A):2599-605

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  • [Title] Dephosphorylation of cancer protein by tyrosine phosphatases in response to analogs of luteinizing hormone-releasing hormone and somatostatin.
  • The homology of substrate phosphorylation between induced PTK and PTP in the presence of hormones provided evidence that these substrates might be identical or related in tumors.
  • These findings, along with the previous cell culture results, suggest that many solid tumors may respond to treatment with analogues of somatostatin and LHRH.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Neoplasm Proteins / metabolism. Neoplasms / metabolism. Protein Tyrosine Phosphatases / metabolism. Somatostatin / analogs & derivatives. Triptorelin Pamoate / pharmacology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / pharmacology. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Breast Neoplasms / metabolism. Epidermal Growth Factor / pharmacology. Female. Humans. Liver Neoplasms / drug therapy. Liver Neoplasms / enzymology. Liver Neoplasms / metabolism. Male. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / enzymology. Ovarian Neoplasms / metabolism. Phosphorylation. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / metabolism

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  • (PMID = 19035284.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Neoplasm Proteins; 2PK59M9GFF / vapreotide; 51110-01-1 / Somatostatin; 57773-63-4 / Triptorelin Pamoate; 62229-50-9 / Epidermal Growth Factor; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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26. Gerardi MA, Santillan A, Meisner B, Zahurak ML, Diaz Montes TP, Giuntoli RL 2nd, Bristow RE: A clinical pathway for patients undergoing primary cytoreductive surgery with rectosigmoid colectomy for advanced ovarian and primary peritoneal cancers. Gynecol Oncol; 2008 Feb;108(2):282-6
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  • Critical elements of the clinical pathway included: rapid diet advancement, early discontinuance of nasogastric suction, criteria-based utilization of parenteral nutrition, selective laboratory testing, and deferring initiation of chemotherapy until after discharge.
  • The median time to flatus was 6 days for both groups (p=0.95); however, the median time to tolerance of diet was 3 days for Group A and 6 days for Group B (p=0.013).
  • CONCLUSIONS: A critical pathway incorporating rapid diet advancement for patients undergoing primary cytoreductive surgery with rectosigmoid colectomy for ovarian and primary peritoneal cancers is feasible, safe, and associated with a significant reduction in length of hospital stay and hospital-related costs.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Diet. Female. Humans. Intubation, Gastrointestinal. Middle Aged. Neoplasm Staging. Postoperative Care / methods

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  • (PMID = 18023851.001).
  • [ISSN] 1095-6859
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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27. Unek IT, Celtik A, Alacacioğlu A, Cokmert S, Yavuzşen T, Doğan NS, Oztop I, Demirkan B, Yilmaz U: Gastric carcinoma during pregnancy: report of a case. Turk J Gastroenterol; 2007 Mar;18(1):41-3
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  • BACKGROUND/AIMS: Gastric cancer in pregnancy is extremely rare and often diagnosed at advanced stages.
  • Well-recognized pregnancy-related symptoms, such as nausea and epigastric discomfort, can be the first symptoms of gastric cancer.
  • Thus, the diagnosis of gastric cancer in pregnancy is difficult.
  • We herein report a case of gastric cancer in pregnancy to alert clinicians to this rare possibility.
  • Gastroscopy demonstrated a tumor originating from the cardia and invading throughout the distal corpus.
  • An explorative laparotomy revealed an unresectable gastric cancer and multiple peritoneal implants.
  • She was admitted to the medical oncology clinic and received a palliative chemotherapy.
  • A nasogastric tube was inserted for intestinal decompression, and total parenteral nutrition was administered.
  • An adequate pain medication was given.
  • CONCLUSION: Early diagnosis of gastric cancer is very important for a better outcome.
  • [MeSH-minor] Abdominal Pain / etiology. Abortion, Therapeutic. Adult. Antineoplastic Agents / therapeutic use. Ascites. Female. Humans. Neoplasm Invasiveness. Palliative Care. Pregnancy

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  • (PMID = 17450494.001).
  • [ISSN] 2148-5607
  • [Journal-full-title] The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology
  • [ISO-abbreviation] Turk J Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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28. Dupertuis YM, Xiao WH, De Tribolet N, Pichard C, Slosman DO, Bischof Delaloye A, Buchegger F: Unlabelled iododeoxyuridine increases the rate of uptake of [125I]iododeoxyuridine in human xenografted glioblastomas. Eur J Nucl Med Mol Imaging; 2002 Apr;29(4):499-505
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  • 5-Iodo-2'-deoxyuridine (IdUrd), a thymidine (TdR) analogue, can be radiolabelled with iodine-125, an Auger radiation emitter, to provoke double-strand breaks once incorporated into DNA of cancer cells.
  • The rate of uptake of [125I]IdUrd in normal rapidly dividing tissues was also increased by 1.3- to 2.8-fold.
  • TdR completely blocked [125I]IdUrd uptake in tumours and tissues.
  • Analogues of IdUrd, such as deoxyuridine and 5-iodo-1,3-dimethyuracil, did not reproduce the effect of IdUrd on the uptake of [125I]IdUrd, suggesting that it is not related to protection against [125I]IdUrd degradation.
  • It is concluded that combined administration of unlabelled IdUrd may improve the use of radiolabelled IdUrd for cancer diagnosis or therapy.
  • [MeSH-major] DNA, Neoplasm / metabolism. Glioblastoma / metabolism. Idoxuridine / pharmacology. Iodine Radioisotopes / pharmacokinetics. Nucleic Acid Synthesis Inhibitors / pharmacology
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Disease Models, Animal. Humans. In Vitro Techniques. Mice. Mice, Nude. Reference Values. Reproducibility of Results. Sensitivity and Specificity. Tissue Distribution. Transplantation, Heterologous. Tumor Cells, Cultured / metabolism. Xenograft Model Antitumor Assays / methods

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  • (PMID = 11914888.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Iodine Radioisotopes; 0 / Nucleic Acid Synthesis Inhibitors; LGP81V5245 / Idoxuridine
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29. Zikri NN, Riedl KM, Wang LS, Lechner J, Schwartz SJ, Stoner GD: Black raspberry components inhibit proliferation, induce apoptosis, and modulate gene expression in rat esophageal epithelial cells. Nutr Cancer; 2009;61(6):816-26
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  • We have shown that a diet containing freeze-dried black raspberries (BRB) inhibits the development of chemically induced cancer in the rat esophagus.
  • Interestingly, the EtOH extract did not alter cyclooxygenase-2 (COX-2) and nitric oxide synthase (i-NOS) expression in RE-149 DHD cells, whereas both anthocyanins downregulated the expressions of these genes.
  • This differential effect may have been related to the relative amounts of anthocyanins in the extract vs. when they were added individually to the medium.

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  • (PMID = 20155622.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA103180-05; United States / NCI NIH HHS / CA / R01 CA103180; United States / NCI NIH HHS / CA / CA 103180; United States / NCI NIH HHS / CA / R01 CA103180-05
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthocyanins; 0 / Antineoplastic Agents, Phytogenic; 0 / Glucosides; 0 / Plant Extracts; 0 / cyanidin 3-rutinoside; 0 / cyanidin 3-xylosylrutinoside; 7084-24-4 / cyanidin 3-O-glucoside; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, rat; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Ptgs2 protein, rat; EC 3.4.22.- / Caspases, Effector
  • [Other-IDs] NLM/ NIHMS259007; NLM/ PMC3015087
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30. Laubach JP, Mitsiades CS, Roccaro AM, Ghobrial IM, Anderson KC, Richardson PG: Clinical challenges associated with bortezomib therapy in multiple myeloma and Waldenströms Macroglobulinemia. Leuk Lymphoma; 2009 May;50(5):694-702
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  • [Title] Clinical challenges associated with bortezomib therapy in multiple myeloma and Waldenströms Macroglobulinemia.
  • Optimization of bortezomib-based therapy, though, requires an understanding of the various challenges associated with use of the drug.
  • This review highlights the rationale for bortezomib therapy in patients with multiple myeloma and Waldenströms Macroglobulinemia, mechanisms of bortezomib resistance, important therapy-related side effects, and new directions for the use of proteasome inhibitors in these disorders.

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  • [ErratumIn] Leuk Lymphoma. 2009 Jul;50(7):1235
  • (PMID = 19452315.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA126119-02; United States / NCI NIH HHS / CA / R21 CA126119; United States / NCI NIH HHS / CA / R21 CA126119-02
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 68
  • [Other-IDs] NLM/ NIHMS304905; NLM/ PMC3133638
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31. Cabrera R, Nelson DR: Review article: the management of hepatocellular carcinoma. Aliment Pharmacol Ther; 2010 Feb 15;31(4):461-76
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Barcelona Clinic Liver Cancer staging classification system is a clinically useful algorithm for the management of patients with hepatocellular carcinoma.
  • The simultaneous presence of cirrhosis in the patients complicates their management and monitoring for cirrhosis-related complications is important.
  • CONCLUSIONS: Early diagnosis and definitive treatment remains the key to long-term outcome.
  • Studies combining sorafenib with locoregional or other targeted molecular therapies are likely to improve responses and outcome.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Carcinoma, Hepatocellular / diagnosis. Carcinoma, Hepatocellular / therapy. Liver Neoplasms / diagnosis. Liver Neoplasms / therapy. Pyridines / therapeutic use
  • [MeSH-minor] Ablation Techniques. Adult. African Continental Ancestry Group. Asian Continental Ancestry Group. Biopsy. Chemoembolization, Therapeutic. Contrast Media. Drug Eruptions / prevention & control. Female. Health Care Costs. Hepatitis B, Chronic / complications. Hepatitis B, Chronic / epidemiology. Hepatitis C, Chronic / complications. Hepatitis C, Chronic / epidemiology. Humans. Incidence. Liver Cirrhosis / complications. Liver Cirrhosis / mortality. Liver Transplantation. Male. Middle Aged. Neoplasm Staging / methods. Neovascularization, Pathologic / drug therapy. Niacinamide / analogs & derivatives. Phenylurea Compounds. Population Surveillance. Practice Guidelines as Topic. Quality of Life. Randomized Controlled Trials as Topic. Recurrence. Risk Factors. Survival Rate. Tomography, X-Ray Computed. Treatment Outcome. United States / epidemiology. Young Adult

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
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  • [CommentIn] Aliment Pharmacol Ther. 2010 May;31(10):1153-4 [20518755.001]
  • (PMID = 19925500.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Contrast Media; 0 / Phenylurea Compounds; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib
  • [Number-of-references] 96
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