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1. Laurie SA, Siu LL, Winquist E, Maksymiuk A, Harnett EL, Walsh W, Tu D, Parulekar WR: A phase 2 study of platinum and gemcitabine in patients with advanced salivary gland cancer: a trial of the NCIC Clinical Trials Group. Cancer; 2010 Jan 15;116(2):362-8
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  • [Title] A phase 2 study of platinum and gemcitabine in patients with advanced salivary gland cancer: a trial of the NCIC Clinical Trials Group.
  • BACKGROUND: Salivary gland cancers are rare, histologically diverse, and varied in their biologic behavior and responsiveness to systemic therapy.
  • To the authors' knowledge, there currently is no standard chemotherapy for these tumors, but cisplatin-based regimens are often used.
  • METHODS: Fit, consenting adult patients had advanced, metastatic, or locoregionally recurrent salivary gland cancer (any histologic subtype) that was not suitable for radiation or surgery.
  • Therapy was comprised of gemcitabine at a dose of 1000 mg/m(2) administered intravenously on Days 1 and 8, and cisplatin at a dose of 70 mg/m(2) on Day 2, of a 21-day cycle.
  • If carboplatin was substituted, it was administered on Day 1, targeted to an area under the concentration-time curve of 5 mg/mL/s.
  • Response was assessed every 2 cycles according to Response Evaluation Criteria In Solid Tumors.
  • CONCLUSIONS: This regimen did not meet the predefined criteria to be declared active in advanced salivary gland cancers.
  • Enrollment of patients with these rare cancers into well-designed clinical trials remains an urgent priority.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Deoxycytidine / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Male. Middle Aged. Survival Rate. Time Factors

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  • (PMID = 19924794.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin
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2. Visa L, Caballero M, Grau JJ: [Response to metronomic chemotherapy in a metastatic adenoid cystic carcinoma of the parotid gland]. Acta Otorrinolaringol Esp; 2010 Nov-Dec;61(6):452-4
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  • [Title] [Response to metronomic chemotherapy in a metastatic adenoid cystic carcinoma of the parotid gland].
  • [Transliterated title] Respuesta a quimioterapia metronómica en un carcinoma adenoide quístico metastásico de parótida.
  • Formerly, salivary gland cancer was considered to be chemoresistant.
  • Chemotherapy is indicated when distant metastases or inoperable locorregional disease are observed, although the chemotherapy schedule is not well defined.
  • Data on chemotherapy treatment for adenoid cystic carcinoma consist of phase II trials.
  • Most of these studies analyze therapies with a combination of agents at full dose, although there is no clear evidence that such treatment improves survival.
  • The administration of cytotoxic agents with low doses at frequent, regular intervals with no drug-free interruptions is known as metronomic chemotherapy.
  • Most head-to-head studies show similar or even superior therapeutic results with metronomic scheduling than with a maximum tolerated dose regime.
  • Our case report shows for first time the clinical activity of low-dose paclitaxel and cisplatin chemotherapy given separately as a single agent in metastatic adenoid cystic carcinoma of the parotid.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carcinoma, Adenoid Cystic / drug therapy. Carcinoma, Adenoid Cystic / secondary. Cisplatin / administration & dosage. Paclitaxel / administration & dosage. Parotid Neoplasms / drug therapy. Parotid Neoplasms / pathology
  • [MeSH-minor] Drug Administration Schedule. Female. Humans. Middle Aged

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  • [Copyright] Copyright © 2009 Elsevier España, S.L. All rights reserved.
  • (PMID = 20152955.001).
  • [ISSN] 1988-3013
  • [Journal-full-title] Acta otorrinolaringológica española
  • [ISO-abbreviation] Acta Otorrinolaringol Esp
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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3. Sharon E, Kelly RJ, Szabo E: Sustained response of carcinoma ex pleomorphic adenoma treated with trastuzumab and capecitabine. Head Neck Oncol; 2010;2:12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Carcinoma ex pleomorphic adenoma is a rare histologic subtype of salivary gland cancer with an overall poor prognosis.
  • Limited histopathologic analyses have shown that some such tumors exhibit significant HER2/neu immunoreactivity, suggesting a potential role for HER2-based therapy.
  • We report here a case of a 58-year old man with metastatic carcinoma ex pleomorphic adenoma who achieved a sustained long term response to combination therapy with trastuzumab and capecitabine.
  • CASE PRESENTATION: A 58 year old man presented with T1N2bM0 carcinoma ex pleomorphic adenoma and underwent surgery followed by adjuvant radiation therapy.
  • Since the original tumor was strongly HER2/neu positive by immunohistochemistry, the patient was treated with trastuzumab, capecitabine, and zoledronic acid.
  • Continued treatment has resulted in maintenance of disease control for over 2 years.
  • CONCLUSION: This case illustrates the successful long term treatment of carcinoma ex pleomorphic adenoma with targeted therapy with trastuzumab in combination with chemotherapy.
  • In the absence of definitive clinical trials which are unlikely to be performed due to the rarity of this tumor, case reports such as this one suggest potential utility for trastuzumab in combination with chemotherapy in the treatment of HER2/neu-overexpressing carcinoma ex pleomorphic adenoma.
  • [MeSH-major] Adenoma, Pleomorphic / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Salivary Gland Neoplasms / drug therapy

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  • (PMID = 20504363.001).
  • [ISSN] 1758-3284
  • [Journal-full-title] Head & neck oncology
  • [ISO-abbreviation] Head Neck Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2889991
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4. Omotehara F, Kawamata H, Uchida D, Hino S, Nakashiro K, Fujimori T: Vesnarinone, a differentiation inducing drug, directly activates p21(waf1) gene promoter via Sp1 sites in a human salivary gland cancer cell line. Br J Cancer; 2002 Oct 21;87(9):1042-6
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  • [Title] Vesnarinone, a differentiation inducing drug, directly activates p21(waf1) gene promoter via Sp1 sites in a human salivary gland cancer cell line.
  • We previously demonstrated that a differentiation inducing drug, vesnarinone induced the growth arrest and p21(waf1) gene expression in a human salivary gland cancer cell line, TYS.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cyclins / genetics. Histone Deacetylases / metabolism. Promoter Regions, Genetic. Quinolines / pharmacology. Sp1 Transcription Factor / metabolism. Tumor Cells, Cultured / drug effects
  • [MeSH-minor] Cell Differentiation / drug effects. Cyclin-Dependent Kinase Inhibitor p21. Electrophoretic Mobility Shift Assay. Gene Deletion. Gene Expression Regulation. Gene Expression Regulation, Neoplastic / drug effects. Humans. Luciferases / metabolism. Plasmids. Salivary Gland Neoplasms / drug therapy. Salivary Gland Neoplasms / genetics. Salivary Gland Neoplasms / metabolism. Transcription, Genetic. Transcriptional Activation. Up-Regulation

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  • (PMID = 12434298.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Quinolines; 0 / Sp1 Transcription Factor; 5COW40EV8M / vesnarinone; EC 1.13.12.- / Luciferases; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ PMC2364327
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5. Hamakawa H, Nakashiro K, Sumida T, Shintani S, Myers JN, Takes RP, Rinaldo A, Ferlito A: Basic evidence of molecular targeted therapy for oral cancer and salivary gland cancer. Head Neck; 2008 Jun;30(6):800-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Basic evidence of molecular targeted therapy for oral cancer and salivary gland cancer.
  • BACKGROUND: Recently, attention has been focused on molecular targeted cancer therapy in various tumors.
  • Although there is no single consistent molecular target specific for oral squamous cell carcinoma (OSCC) and salivary gland cancer (SGC), there are a number of promising candidate proteins.
  • RESULTS: Gefitinib ("Iressa," ZD1839), a small molecule EGFR tyrosine kinase inhibitor, can inhibit the proliferation of OSCC cell lines in a dose- and time-dependent manner and lead to cell cycle arrest with accumulation of cells in the G1 phase, and a decrease of cells in S phase.
  • The agent suppressed tumor metastasis in the animal model.
  • Furthermore, a cooperative antiproliferative effect was obtained when cancer cells were treated with radiation followed by gefitinib.
  • Gefitinib enhanced tumor radioresponsiveness by multiple mechanisms, including the growth inhibition and effects on DNA repair after exposure to radiation.
  • Next, the level of COX-2 expression correlated inversely with increased tumor radiation sensitivity.
  • Treatment with celecoxib, a COX-2 selective inhibitor, enhanced the radioresponsiveness of HSC-2 cells, which constitutively expressed COX-2.
  • Recent studies have demonstrated that PPARgamma ligands induce cellular differentiation and inhibit cell growth in carcinomas of various types.
  • These data suggest that synthetic PPARgamma ligands may be useful for molecular targeting of oral cancer.
  • Finally, the possibility of using molecular targeted therapy directed at hormone receptors in the treatment of advanced SGCs was described.
  • CONCLUSION: The basic data strongly suggested the possibility of tumor suppression by targeting these molecules.
  • Studies of different targeted agents alone or with more conventional treatment modalities are needed to fully determine what role the targeted therapy will play in the management of patients with OSCC and SGC.
  • [MeSH-major] Carcinoma, Squamous Cell / drug therapy. Mouth Neoplasms / drug therapy. Salivary Gland Neoplasms / drug therapy
  • [MeSH-minor] Cyclooxygenase 2 Inhibitors / therapeutic use. Humans. PPAR gamma / antagonists & inhibitors. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptors, Progesterone / antagonists & inhibitors


6. Burris HA 3rd, Taylor CW, Jones SF, Koch KM, Versola MJ, Arya N, Fleming RA, Smith DA, Pandite L, Spector N, Wilding G: A phase I and pharmacokinetic study of oral lapatinib administered once or twice daily in patients with solid malignancies. Clin Cancer Res; 2009 Nov 1;15(21):6702-8
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  • EXPERIMENTAL DESIGN: Cancer patients (n = 81) received oral doses of lapatinib ranging from 175 to 1,800 mg once daily or 500 to 900 mg twice daily.
  • One patient with head and neck cancer achieved a confirmed complete response and 22 patients had stable disease of >or=8 weeks including three patients with stable disease of >10 months (renal, lung, and salivary gland cancers).

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  • (PMID = 19825948.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] None / None / / P30 CA014520-36; United States / NCI NIH HHS / CA / P30 CA014520-36; United States / NCI NIH HHS / CA / P30 CA014520; United States / NCI NIH HHS / CA / P30 CA014520-38; United States / NCI NIH HHS / CA / P30 CA014520-37
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0VUA21238F / lapatinib; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ NIHMS340777; NLM/ PMC3232441
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7. Harada K, Kawaguchi S, Supriatno, Onoue T, Yoshida H, Sato M: Enhancement of apoptosis in salivary gland cancer cells by the combination of oral fluoropyrimidine anticancer agent (S-1) and radiation. Int J Oncol; 2004 Oct;25(4):905-11
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  • [Title] Enhancement of apoptosis in salivary gland cancer cells by the combination of oral fluoropyrimidine anticancer agent (S-1) and radiation.
  • S-1 is a new oral antineoplastic agent which can inhibit cell growth and induces apoptosis in certain types of cancer cells including gastric carcinomas, colorectal cancers and salivary gland cancers, but its effect on response of tumor cells to radiation has not been clarified yet.
  • We have reported that S-1 can sensitize human oral cancer cells to radiation, and that S-1 in combination with radiation can exert remarkable effects on decreasing clonogenic survival and in vivo tumor growth.
  • Here, we demonstrate the mechanism of apoptosis enhancing activity by the combination treatment of S-1 and radiation in salivary gland cancer cells.
  • In addition, the combined treatment of S-1 and radiation resulted in an increased DNA fragmentation by detecting Hoechst 33258 staining.
  • Moreover, apoptosis of the cells by combined treatment of S-1 and radiation was associated with reactive oxygen/nitrogen species generation and the activation of caspase-8, -9 and -3.
  • These results indicate that S-1 in combination with radiation can markedly enhance apoptosis of salivary gland cancer cells, and the combined therapy of S-1 and radiation are currently leading to the design of clinical studies.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Apoptosis. Oxonic Acid / pharmacology. Pyridines / pharmacology. Salivary Gland Neoplasms / therapy. Tegafur / pharmacology
  • [MeSH-minor] Administration, Oral. Caspases / metabolism. Cell Division / drug effects. Cell Division / radiation effects. Cell Line, Tumor. Combined Modality Therapy. Drug Combinations. Humans. Reactive Nitrogen Species. Reactive Oxygen Species

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  • (PMID = 15375539.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0 / Pyridines; 0 / Reactive Nitrogen Species; 0 / Reactive Oxygen Species; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; EC 3.4.22.- / Caspases
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8. Fukuda M, Kusama K, Sakashita H: Cimetidine inhibits salivary gland tumor cell adhesion to neural cells and induces apoptosis by blocking NCAM expression. BMC Cancer; 2008;8:376
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  • [Title] Cimetidine inhibits salivary gland tumor cell adhesion to neural cells and induces apoptosis by blocking NCAM expression.
  • BACKGROUND: Cimetidine, a histamine type-2 receptor antagonist, has been reported to inhibit the growth of glandular tumors such as colorectal cancer, however the mechanism of action underlying this effect is unknown.
  • Adenoid cystic carcinoma is well known as a malignant salivary gland tumor which preferentially invades neural tissues.
  • We demonstrated previously that human salivary gland tumor (HSG) cells spontaneously express neural cell adhesion molecule (NCAM), that HSG cell proliferation may be controlled via a homophilic (NCAM-NCAM) binding mechanism and that NCAM may be associated with perineural invasion by malignant salivary gland tumors.
  • Here, we investigated the effects of cimetidine on growth and perineural/neural invasion of salivary gland tumor cells.
  • METHODS: In this study, we have examined the effect of cimetidine on cancer cell adhesion to neural cells in vitro, one of the critical steps of cancer invasion and metastasis.
  • RESULTS: We have demonstrated for the first time that cimetidine can block the adhesion of HSG cells to neural cell monolayers and that it can also induce significant apoptosis in the tumor mass in a nude mouse model.
  • CONCLUSION: These findings suggest that growth and perineural/neural invasion of salivary gland tumors can be blocked by administration of cimetidine via induction of apoptosis and in which NCAM plays a role.
  • [MeSH-major] Cell Adhesion / drug effects. Cimetidine / pharmacology. Histamine H2 Antagonists / pharmacology. Neoplasm Invasiveness / physiopathology. Neural Cell Adhesion Molecules / metabolism. Salivary Gland Neoplasms / drug therapy. Salivary Gland Neoplasms / physiopathology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Dose-Response Relationship, Drug. Down-Regulation. Gene Expression / drug effects. Humans. Mice. Mice, Nude. NF-kappa B / drug effects. Neurons / pathology. Tumor Cells, Cultured

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  • (PMID = 19091137.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histamine H2 Antagonists; 0 / NF-kappa B; 0 / Neural Cell Adhesion Molecules; 80061L1WGD / Cimetidine
  • [Other-IDs] NLM/ PMC2635382
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9. Kawamata H, Fujimori T, Imai Y: TSC-22 (TGF-beta stimulated clone-22): a novel molecular target for differentiation-inducing therapy in salivary gland cancer. Curr Cancer Drug Targets; 2004 Sep;4(6):521-9
MedlinePlus Health Information. consumer health - Salivary Gland Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TSC-22 (TGF-beta stimulated clone-22): a novel molecular target for differentiation-inducing therapy in salivary gland cancer.
  • Separately, we identified TSC-22 cDNA as an anti-cancer drug (vesnarinone)-inducible gene in a human salivary gland cancer cell line, TYS.
  • Vesnarinone is known to have a differentiation-inducing activity in several cell types.
  • We showed that TSC-22 negatively regulated the growth of TYS cells, and that down-regulation of TSC-22 played a major role in the salivary gland tumorigenesis.
  • Thus, because TSC-22 is a key molecule for differentiation of several cells, it can be used as a molecular target for cancer differentiation therapy in salivary gland cancer.
  • [MeSH-major] Cell Differentiation. Drug Delivery Systems / methods. Repressor Proteins / genetics. Salivary Gland Neoplasms / pathology

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  • [Copyright] Copyright 2004 Bentham Science Publishers Ltd.
  • (PMID = 15379637.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Repressor Proteins; 0 / TSC22D1 protein, human; 0 / Tgfb1i4 protein, mouse
  • [Number-of-references] 37
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10. Stennert E, Kisner D, Jungehuelsing M, Guntinas-Lichius O, Schröder U, Eckel HE, Klussmann JP: High incidence of lymph node metastasis in major salivary gland cancer. Arch Otolaryngol Head Neck Surg; 2003 Jul;129(7):720-3
MedlinePlus Health Information. consumer health - Salivary Gland Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High incidence of lymph node metastasis in major salivary gland cancer.
  • OBJECTIVE: To analyze the incidence and risk factors for clinically apparent and occult lymph node metastases in patients with major salivary gland cancers.
  • Patients were treated with surgery alone (55%); surgery and radiation therapy (43%); or a combination of surgery, radiation, and chemotherapy (2%).
  • Histologic diagnosis was significantly related to the incidence of lymph node metastasis: 89% (16/18) for undifferentiated carcinomas.
  • However, so-called low-risk tumors had incidence rates of 22% to 47%.
  • Neck metastasis was found in 29% (10/34) of T1, 54% (38/70) of T2, 65% (20/31) of T3, and 54% (16/25) of T4 tumors.
  • CONCLUSIONS: We found a high incidence of lymph node metastasis from major salivary gland cancers.
  • Neck dissections should be considered as an integral part of the surgical approach in patients with major salivary gland cancer, especially if no postoperative radiation therapy is planned.
  • [MeSH-major] Salivary Gland Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adolescent. Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / pathology. Child. Disease-Free Survival. Female. Humans. Lymph Node Excision. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Risk Factors

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  • (PMID = 12874071.001).
  • [ISSN] 0886-4470
  • [Journal-full-title] Archives of otolaryngology--head & neck surgery
  • [ISO-abbreviation] Arch. Otolaryngol. Head Neck Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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11. Hocwald E, Korkmaz H, Yoo GH, Adsay V, Shibuya TY, Abrams J, Jacobs JR: Prognostic factors in major salivary gland cancer. Laryngoscope; 2001 Aug;111(8):1434-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic factors in major salivary gland cancer.
  • OBJECTIVE: To identify features of major salivary gland cancers that are prognostic for disease-free survival.
  • STUDY DESIGN: A retrospective study of 78 patients with major salivary gland cancer (64 parotid and 14 submandibular gland) who underwent surgery for definitive treatment from 1976 to 1996.
  • A select group of patients also received adjuvant radiation (56%) and/or chemotherapy (13%).
  • Age, gender, tumor site, T-stage, facial paralysis, histologic neck involvement, perineural invasion, and cancer grade were analyzed with respect to disease-free survival.
  • The role of adjuvant treatment in terms of clinical outcome was also investigated.
  • Examining clinical and histologic features one at a time, we found poorer prognosis was associated with submandibular tumors compared with parotid (P =.02), higher T-stage (P =.001), positive cervical nodes (P <.001), perineural invasion (P =.002), and high-grade or adenoid cystic tumors (P =.002).
  • Receipt of both adjuvant radiation and cisplatin-based chemotherapy (P =.05) was an independent predictor of longer disease-free survival.
  • Our limited data also suggest that adjuvant chemotherapy and radiation therapy may improve disease-free survival.
  • [MeSH-major] Parotid Neoplasms / mortality. Submandibular Gland Neoplasms / mortality
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Child. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Prognosis. Proportional Hazards Models. Radiotherapy, Adjuvant. Retrospective Studies

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  • (PMID = 11568581.001).
  • [ISSN] 0023-852X
  • [Journal-full-title] The Laryngoscope
  • [ISO-abbreviation] Laryngoscope
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Ruzich JC, Ciesla MC, Clark JI: Response to paclitaxel and carboplatin in metastatic salivary gland cancer: a case report. Head Neck; 2002 Apr;24(4):406-10
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  • [Title] Response to paclitaxel and carboplatin in metastatic salivary gland cancer: a case report.
  • BACKGROUND: Malignant tumors of the salivary gland are rare entities that are treated primarily by surgical resection.
  • For patients with recurrent or unresectable disease, options include radiation therapy or chemotherapy; however, responses are few and of short duration.
  • Patients with metastatic disease have been treated with chemotherapy, but, again, response rates have been low and of short duration.
  • A biopsy revealed adenocarcinoma of a minor salivary gland.
  • Ten months after surgical resection, neck dissection, and radiation therapy, the patient was found to have metastatic disease to the lung.
  • Chemotherapy was initiated with carboplatin and paclitaxel.
  • CONCLUSIONS: The use of carboplatin and paclitaxel in the setting of metastatic salivary gland cancer is a viable option.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / therapeutic use. Paclitaxel / therapeutic use. Salivary Gland Neoplasms / drug therapy
  • [MeSH-minor] Humans. Male. Middle Aged. Treatment Outcome

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  • [Copyright] Copyright 2002 Wiley Periodicals, Inc.
  • (PMID = 11933184.001).
  • [ISSN] 1043-3074
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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13. Woo HJ, Bai CH, Kim YD, Song SY: Mucoepidermoid carcinoma of the submandibular gland after chemotherapy in a child. Auris Nasus Larynx; 2009 Apr;36(2):244-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mucoepidermoid carcinoma of the submandibular gland after chemotherapy in a child.
  • Second malignant neoplasms (SMNs) have become a concern in survivors of childhood malignancy.
  • Although there are many reports describing SMN in patients treated for childhood cancer, salivary gland tumors rarely appear in these reports.
  • Radiotherapy is a well-known risk factor for the development of secondary salivary gland malignancies after the treatment of childhood cancer.
  • However, it is not well known whether chemotherapy itself treatment increases the risk of salivary gland malignancies.
  • We report a child case with mucoepidermoid carcinoma of the submandibular gland as a SMN after chemotherapy alone for acute myeloid leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Carcinoma, Mucoepidermoid / chemically induced. Leukemia, Myeloid, Acute / drug therapy. Neoplasms, Second Primary / chemically induced. Submandibular Gland Neoplasms / chemically induced
  • [MeSH-minor] Adolescent. Biopsy. Busulfan / adverse effects. Busulfan / therapeutic use. Child. Child, Preschool. Cyclophosphamide / adverse effects. Cyclophosphamide / therapeutic use. Cytarabine / adverse effects. Cytarabine / therapeutic use. Daunorubicin / adverse effects. Daunorubicin / therapeutic use. Dexamethasone / adverse effects. Dexamethasone / therapeutic use. Disease-Free Survival. Etoposide / adverse effects. Etoposide / therapeutic use. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Image Processing, Computer-Assisted. Male. Neck Dissection. Positron-Emission Tomography. Thioguanine / adverse effects. Thioguanine / therapeutic use. Tomography, X-Ray Computed. Transplantation Conditioning

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  • (PMID = 18602781.001).
  • [ISSN] 1879-1476
  • [Journal-full-title] Auris, nasus, larynx
  • [ISO-abbreviation] Auris Nasus Larynx
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; FTK8U1GZNX / Thioguanine; G1LN9045DK / Busulfan; ZS7284E0ZP / Daunorubicin; DCTER protocol
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14. Omotehara F, Nakashiro K, Uchida D, Hino S, Fujimori T, Kawamata H: Transcriptional activation of cyclin-dependent kinase inhibitor, p21waf1 gene by treatment with a differentiation inducing agent, vesnarinone in a human salivary gland cancer cell line. J Exp Clin Cancer Res; 2003 Mar;22(1):57-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional activation of cyclin-dependent kinase inhibitor, p21waf1 gene by treatment with a differentiation inducing agent, vesnarinone in a human salivary gland cancer cell line.
  • Recently, a new concept for cancer therapy termed "tumor dormancy therapy" has been proposed.
  • The concept of this therapy is to prolong the survival time of cancer patients while maintaining their quality of life.
  • We have been developing a differentiation-inducing therapy, which is included in the tumor dormancy therapy, for salivary gland cancer.
  • In this study, we examined the effect of a differentiation-inducing drug, Vesnarinone on the growth of several cancer cells, and examined the molecular mechanism by which Vesnarinone induces the cyclin dependent kinase inhibitor, p21waf1 in the cancer cells.
  • Vesnarinone significantly suppressed the growth of TYS (salivary gland cancer cells), PC3 (prostate cancer cells), and A431 (squamous cell cancer cells).
  • Thus, analyzing the molecular mechanisms of differentiation inducing drugs may lead to the development of a new therapeutic strategy for several human malignancies, including salivary gland cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cyclins / genetics. Gene Expression Regulation, Neoplastic / drug effects. Quinolines / therapeutic use. Salivary Gland Neoplasms / pathology. Transcriptional Activation
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Division / drug effects. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / genetics. Enzyme Inhibitors. Humans. Plasmids. RNA, Messenger / genetics. Tumor Cells, Cultured

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  • (PMID = 12725323.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / Quinolines; 0 / RNA, Messenger; 5COW40EV8M / vesnarinone; EC 2.7.11.22 / Cyclin-Dependent Kinases
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15. Agulnik M, Siu LL: An update on the systemic therapy of malignant salivary gland cancers: role of chemotherapy and molecular targeted agents. Curr Med Chem Anticancer Agents; 2004 Nov;4(6):543-51
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  • [Title] An update on the systemic therapy of malignant salivary gland cancers: role of chemotherapy and molecular targeted agents.
  • Salivary gland cancers are a rare malignancy accounting for less than 1% of all cancers and 3-6% of cancers of the head and neck region.
  • The classification of salivary gland tumors is traditionally based on morphology and the different subtypes exhibit various clinical behaviors.
  • The low grade and biologically indolent cell types include the adenoid cystic, acinic cell and adenocarcinoma while the salivary duct, squamous and mucoepidermoid are more active and high grade.
  • The initial management of salivary gland malignancies is to assess resectability and possible adjuvant radiation therapy.
  • Those with locoregional recurrence or metastatic disease are treated with systemic therapy.
  • Both single agent and combination chemotherapy have been used for the treatment of this disease.
  • Clinicopathological data have demonstrated correlations between poor clinical outcomes and the expression of molecular markers such as mutated p53 protein and vascular endothelial growth factor (VEGF) in salivary gland cancers.
  • Recent studies have also evaluated the epidermal growth factor receptor family including erbB1/EGFR and erbB2/HER2 as potential therapeutic targets.
  • Given the suboptimal response rates, duration of response, and toxicity of conventional chemotherapy, a better understanding of the biology of salivary gland malignancies will lead to improved prognostication and treatment.
  • With the emergence of molecular targeted therapy, these tumors become an optimal candidate for trials of investigational drugs and established drugs for new indications.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Delivery Systems / methods. Salivary Gland Neoplasms / drug therapy


16. Laurie SA, Licitra L: Systemic therapy in the palliative management of advanced salivary gland cancers. J Clin Oncol; 2006 Jun 10;24(17):2673-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systemic therapy in the palliative management of advanced salivary gland cancers.
  • Cancers of the salivary glands are unusual lesions that vary widely in their histologic appearance and molecular characteristics.
  • Likewise, there is a wide spectrum of biologic behavior, ranging from low-grade, minimally invasive tumors, to highly lethal malignancies.
  • There are few data on the role of systemic therapies in the management of these cancers, and chemotherapy is generally reserved for the palliative management of advanced disease that is not amenable to local therapies such as surgery and/or radiation.
  • The majority of patients for whom systemic therapy is considered will have either adenoid cystic carcinoma, mucoepidermoid carcinoma, or high-grade adenocarcinoma.
  • This article will review the available literature regarding the use of palliative chemotherapy for patients with advanced salivary gland cancer of these histologies, with an emphasis on the potential role of targeted agents.
  • There is a need for a determined, coordinated effort to conduct high-quality clinical trials in patients with these rare cancers.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / therapeutic use. Carcinoma, Adenoid Cystic / drug therapy. Carcinoma, Mucoepidermoid / drug therapy. Neoplasm Recurrence, Local / drug therapy. Palliative Care. Salivary Ducts. Salivary Gland Neoplasms / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Boronic Acids / therapeutic use. Bortezomib. Clinical Trials as Topic. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Humans. Neoplasm Metastasis. Pyrazines / therapeutic use. Quinazolines / therapeutic use. Receptor, ErbB-2 / metabolism. Receptors, Androgen / metabolism. Trastuzumab

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  • (PMID = 16763282.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 0 / Quinazolines; 0 / Receptors, Androgen; 0VUA21238F / lapatinib; 0W860991D6 / Deoxycytidine; 69G8BD63PP / Bortezomib; B76N6SBZ8R / gemcitabine; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab
  • [Number-of-references] 87
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17. Omotehara F, Uchida D, Hino S, Begum NM, Yoshida H, Sato M, Kawamata H: In vivo enhancement of chemosensitivity of human salivary gland cancer cells by overexpression of TGF-beta stimulated clone-22. Oncol Rep; 2000 Jul-Aug;7(4):737-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vivo enhancement of chemosensitivity of human salivary gland cancer cells by overexpression of TGF-beta stimulated clone-22.
  • We have isolated transforming growth factor-beta-stimulated clone-22 (TSC-22) cDNA as an anti-cancer drug-inducible gene in a human salivary gland cancer cell line, TYS.
  • TSC-22-expressing TYS cells formed tumors in nude mice, but tumors formed by TSC-22-expressing TYS cells were significantly smaller than tumors formed by control cells (p<0.001, one way ANOVA).
  • Furthermore, intraperitoneal injection of 5-fluorouracil (5-FU) markedly inhibited the growth of the TSC-22-expressing TYS tumors, but did not affect the growth of control tumors.
  • It was found by TUNEL assay that TSC-22-expressing TYS tumors were induced to undergo apoptosis by 5-FU treatment.
  • [MeSH-major] Fluorouracil / therapeutic use. Repressor Proteins / physiology. Salivary Gland Neoplasms / drug therapy
  • [MeSH-minor] Analysis of Variance. Animals. Antineoplastic Agents / therapeutic use. Antineoplastic Agents / toxicity. Apoptosis / drug effects. Cell Survival / drug effects. Clone Cells. Humans. Mice. Mice, Nude. Recombinant Fusion Proteins / analysis. Recombinant Proteins / biosynthesis. Transfection. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 10854535.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] GREECE
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Recombinant Fusion Proteins; 0 / Recombinant Proteins; 0 / Repressor Proteins; 0 / TSC22D1 protein, human; 0 / Tgfb1i4 protein, mouse; U3P01618RT / Fluorouracil
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18. Prenen H, Kimpe M, Nuyts S: Salivary gland carcinomas: molecular abnormalities as potential therapeutic targets. Curr Opin Oncol; 2008 May;20(3):270-4
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  • [Title] Salivary gland carcinomas: molecular abnormalities as potential therapeutic targets.
  • PURPOSE OF REVIEW: Salivary gland neoplasms are composed of histopathologically and clinically diverse entities.
  • The reported response rates of salivary gland tumors to chemotherapy are generally poor.
  • Molecular studies have provided some information on their biology and have identified new targets with therapeutic potential.
  • RECENT FINDINGS: Several agents are currently being tested that target molecular signaling and cancer cell biology.
  • Novel treatments under evaluation include tyrosine kinase inhibitors, antibodies, angiogenesis inhibitors, demethylating agents, and proteasome inhibitors.
  • SUMMARY: Some of these new targeted approaches hold promise for our future ability to treat patients with salivary gland cancer unresponsive to traditional therapy, but others were disappointing.
  • The presence of the molecular target alone is not sufficient to guarantee an antitumor effect with targeted therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Salivary Gland Neoplasms / metabolism. Salivary Gland Neoplasms / therapy
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Benzamides. Boronic Acids / therapeutic use. Bortezomib. Humans. Imatinib Mesylate. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrazines / therapeutic use. Pyrimidines / therapeutic use. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / drug effects

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  • (PMID = 18391625.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Boronic Acids; 0 / Piperazines; 0 / Pyrazines; 0 / Pyrimidines; 0 / Quinazolines; 0 / Vascular Endothelial Growth Factor A; 69G8BD63PP / Bortezomib; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Number-of-references] 35
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19. Guntinas-Lichius O, Wendt T, Buentzel J, Esser D, Lochner P, Mueller A, Schultze-Mosgau S, Altendorf-Hofmann A: Head and neck cancer in Germany: a site-specific analysis of survival of the Thuringian cancer registration database. J Cancer Res Clin Oncol; 2010 Jan;136(1):55-63
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  • [Title] Head and neck cancer in Germany: a site-specific analysis of survival of the Thuringian cancer registration database.
  • OBJECTIVE: To describe epidemiology and prognosis of head and neck cancer in Germany.
  • METHODS: We analyzed the Thuringian cancer registry database from 1996 to 2005.
  • 3,821 cases with primary head and neck cancer were evaluated for patient's characteristics, tumor stage, incidence, treatment, and trends in overall survival.
  • RESULTS: During the period 1996-2005, the incidence of oropharynx, hypopharynx, larynx, and salivary gland cancer increased significantly for males, and of oral cavity and hypopharynx cancer for females.
  • There was a significant trend using more multimodal therapy combining surgery, radiotherapy, and chemotherapy, and to use less radiotherapy as a single modality.
  • The median follow-up time of patients alive was 42 months.
  • The site-specific 5-year OS for lip, oral cavity, nasopharynx, oropharynx, hypopharynx, larynx, salivary gland, and nose/paranasal sinus cancer was 75.7, 42.6, 43.5, 45.9, 27.2, 57.3, 61.0, and 34.9%, respectively.
  • The multivariate analysis showed that male gender, age ≥ 60 years, therapy without surgery, higher T classification, N classification, and M classification were independent significant negative risk factors for OS (p < 0.0001).
  • Cancer of the oral cavity and of the hypopharynx had a significant lower OS than lip cancer (p = 0.012 and p = 0.044, respectively).
  • CONCLUSIONS: Many subsites of head and neck cancer have changing incidence.
  • Although treatment strategies have changed, outcome has not improved significantly from 1995 to 2006.
  • [MeSH-major] Databases, Factual / statistics & numerical data. Head and Neck Neoplasms / epidemiology. Head and Neck Neoplasms / therapy. Registries / statistics & numerical data
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Female. Germany / epidemiology. Humans. Incidence. Male. Middle Aged. Neoplasm Staging. Survival Analysis. Young Adult

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  • [Cites] BMC Public Health. 2006 Jun 06;6:146 [16756650.001]
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  • (PMID = 19568769.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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20. Milano A, Longo F, Basile M, Iaffaioli RV, Caponigro F: Recent advances in the treatment of salivary gland cancers: emphasis on molecular targeted therapy. Oral Oncol; 2007 Sep;43(8):729-34
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  • [Title] Recent advances in the treatment of salivary gland cancers: emphasis on molecular targeted therapy.
  • Salivary gland cancers include tumors of different histologic characteristics and biological behavior.
  • Radical surgery, followed or not by radiation therapy, represents the main treatment approach for this disease.
  • The role of systemic chemotherapy is less clearly defined since trials of single-agent chemotherapy have consistently shown low response rates.
  • The determination of the molecular abnormalities underlying the different subtypes of salivary gland cancers might lead to more active targeted therapies.
  • C-kit is overexpressed in a wide percentage of salivary gland carcinomas, but clinical trials with single-agent imatinib have been negative.
  • ErbB1 and ErbB2 are also frequently overexpressed in salivary gland cancers and this has provided the rationale for clinical trials with trastuzumab, cetuximab, gefitinib, lapatinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasm Proteins / antagonists & inhibitors. Salivary Gland Neoplasms / drug therapy

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  • (PMID = 17350323.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
  • [Number-of-references] 60
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21. Chandana SR, Conley BA: Salivary gland cancers: current treatments, molecular characteristics and new therapies. Expert Rev Anticancer Ther; 2008 Apr;8(4):645-52
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  • [Title] Salivary gland cancers: current treatments, molecular characteristics and new therapies.
  • Salivary gland cancers are relatively rare and quite diverse.
  • Current therapy relies on local ablation.
  • There are few large clinical trials or randomized trials to guide treatment, especially for metastatic disease.
  • This article reviews the epidemiology, staging, molecular characteristics, and treatment evidence for the most common types of salivary cancers and suggests potential future diagnostic and treatment directions.
  • Progress in understanding the molecular and cell biology of salivary gland cancers may lead to the development of targeted therapies in these rare tumors.
  • Multidisciplinary and multi-institutional collaborative studies are needed to help improve survival in salivary gland cancers.
  • [MeSH-major] Adenocarcinoma. Salivary Gland Neoplasms
  • [MeSH-minor] Carcinoma, Adenoid Cystic / drug therapy. Carcinoma, Adenoid Cystic / genetics. Carcinoma, Adenoid Cystic / radiography. Carcinoma, Adenoid Cystic / surgery. Carcinoma, Mucoepidermoid / drug therapy. Carcinoma, Mucoepidermoid / genetics. Carcinoma, Mucoepidermoid / radiography. Carcinoma, Mucoepidermoid / surgery. Humans. Mutation. Prognosis. Radiotherapy, Adjuvant

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  • (PMID = 18402531.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 81
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22. Pederson AW, Haraf DJ, Blair EA, Stenson KM, Witt ME, Vokes EE, Salama JK: Chemoreirradiation for recurrent salivary gland malignancies. Radiother Oncol; 2010 Jun;95(3):308-11
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  • [Title] Chemoreirradiation for recurrent salivary gland malignancies.
  • BACKGROUND AND PURPOSE: To report our experience in treating recurrent salivary gland malignancies using concurrent chemotherapy and reirradiation.
  • MATERIALS AND METHODS: Between 1986 and 2007, 14 patients with locoregionally recurrent salivary gland cancer underwent maximal surgical resection followed by adjuvant 5-fluorouracil and hydroxyurea-based chemotherapy concurrently with 1.5Gy twice daily or 2Gy daily reirradiation.
  • The median reirradiation dose was 66Gy (R 30-72Gy) after a mean radiation treatment interval of 48 months.
  • The parotid gland (n=6) and minor salivary glands (n=6) were involved more commonly than the submandibular gland (n=2).
  • CONCLUSIONS: Concurrent chemotherapy and reirradiation for recurrent salivary malignancies result in promising locoregional control for patients with recurrent salivary gland malignancies.
  • [MeSH-major] Salivary Gland Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Radiotherapy Dosage. Treatment Failure

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20385414.001).
  • [ISSN] 1879-0887
  • [Journal-full-title] Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
  • [ISO-abbreviation] Radiother Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
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23. Védrine PO, Coffinet L, Temam S, Montagne K, Lapeyre M, Oberlin O, Orbach D, Simon C, Sommelet D: Mucoepidermoid carcinoma of salivary glands in the pediatric age group: 18 clinical cases, including 11 second malignant neoplasms. Head Neck; 2006 Sep;28(9):827-33
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  • [Title] Mucoepidermoid carcinoma of salivary glands in the pediatric age group: 18 clinical cases, including 11 second malignant neoplasms.
  • BACKGROUND: Salivary gland tumors represent 1% of head and neck tumors, with only 5% of these occurring in patients younger than 20 years.
  • Mucoepidermoid carcinoma (MEC) is one of the most frequent salivary gland cancers among adults and children.
  • RESULTS: Treatment included surgery or radiotherapy, or both.
  • Eleven patients had been previously treated by radiotherapy and/or chemotherapy for a first malignant tumor, specifically, lymphoid leukemia (n = 4), lymphoma (n = 3), brain tumor (n = 2), sarcoma (n = 1), and retinoblastoma (n = 1).
  • Treatment involves surgical removal of the tumor plus radiotherapy, according to histologic staging.
  • The survival rate does not differ in the subgroup of patients with MEC as a secondary tumor.
  • [MeSH-major] Carcinoma, Mucoepidermoid / pathology. Salivary Gland Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Lymphoma / pathology. Male. Neoplasms, Neuroepithelial / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Rhabdomyosarcoma / pathology

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  • [Copyright] (c) 2006 Wiley Periodicals, Inc.
  • (PMID = 16783829.001).
  • [ISSN] 1043-3074
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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24. Bell RB, Dierks EJ, Homer L, Potter BE: Management and outcome of patients with malignant salivary gland tumors. J Oral Maxillofac Surg; 2005 Jul;63(7):917-28
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  • [Title] Management and outcome of patients with malignant salivary gland tumors.
  • PURPOSE: Refined imaging technology, the use of external beam radiation, neutron beam therapy, and chemotherapy, has altered management strategies for patients with salivary gland malignancies during the past 2 decades.
  • Although treatment remains primarily surgical, optimal therapeutic regimens have yet to be fully realized.
  • The purpose of this investigation is to report our experience with the management of patients with a variety of malignant salivary gland neoplasms that were treated with various combinations of surgery, radiation, and chemotherapy and to review treatment outcome in an effort to identify predictors of survival and locoregional control.
  • MATERIALS AND METHODS: The records of all patients with malignant salivary gland tumors presenting for treatment at our institution between 1992 and 2002 were retrospectively reviewed.
  • The majority of tumors were located in the parotid gland (n = 42), with a significant minority located in the minor salivary glands (n = 29), followed by the submandibular gland (n = 8) and the sublingual gland (n = 6).
  • Mucoepidermoid carcinoma was the most common neoplasm (n = 40).
  • Neck dissection was performed in 29% of patients, and more than half (56%) were treated with adjuvant external beam radiation therapy to a dose of 50 to 70 Gy.
  • Patients were, in general, immediately reconstructed at the time of ablation using composite free tissue transfer when appropriate, local/regional rotational flaps, or maxillary obturators.
  • CONCLUSIONS: The treatment of salivary gland malignancies remains primarily surgical, although adjunctive radiotherapy may play an important role in those patients with advanced-stage disease.
  • The benefits of combined modality therapy awaits prospective clinical trials.
  • [MeSH-major] Carcinoma / therapy. Salivary Gland Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neck Dissection. Neoplasm Invasiveness / prevention & control. Neoplasm Recurrence, Local / prevention & control. Neoplasm Staging. Proportional Hazards Models. Radiotherapy, Adjuvant. Retrospective Studies. Treatment Outcome

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  • (PMID = 16003616.001).
  • [ISSN] 0278-2391
  • [Journal-full-title] Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons
  • [ISO-abbreviation] J. Oral Maxillofac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Gedlicka C, Schüll B, Formanek M, Kornfehl J, Burian M, Knerer B, Selzer E, Scheithauer W, Kornek GV: Mitoxantrone and cisplatin in recurrent and/or metastatic salivary gland malignancies. Anticancer Drugs; 2002 Jun;13(5):491-5
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  • [Title] Mitoxantrone and cisplatin in recurrent and/or metastatic salivary gland malignancies.
  • A phase II study was performed to assess the safety and efficacy of mitoxantrone and cisplatin in locally recurrent and/or metastatic carcinomas of the salivary glands.
  • All of them had previously undergone radical resection and 10 were subsequently treated with adjuvant radiation therapy with (n=3) or without (n=7) concomitant chemotherapy.
  • Therapy according to the study protocol consisted of mitoxantrone given as i.v. bolus on day 1 at a dose of 12 mg/m2 and cisplatin given as 90-min infusion at a dose of 30 mg/m2 on days 1-3.
  • We observed two partial responses (14.3%) and stabilization of disease in nine patients (64.3%); progression during therapy was noted in only three cases (21.4%).
  • The median time to progression was 15 months (range 2-36) and the median survival time was 27 months (range 4-54).
  • Non-hematologic toxicity was in general mild to moderate except for two cases (14%) of grade 3 nausea and vomiting; overall incidence rates were nausea and vomiting (n=14), stomatitis (n=6), diarrhea (n=3), alopecia (n=11), infection (n=7), increase of serum creatinine (n=3), and peripheral neuropathy (n=3).
  • The combination of mitoxantrone and cisplatin seems to be an active and fairly well-tolerated regimen for the treatment of advanced salivary gland cancers.
  • According to the observed high rate of abrogating progressive disease for a long duration, and the resulting promising progression-free and overall survival time, further investigation seems warranted.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lung Neoplasms / drug therapy. Neoplasm Recurrence, Local / drug therapy. Salivary Gland Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Cisplatin / administration & dosage. Disease-Free Survival. Drug Administration Schedule. Humans. Middle Aged. Mitoxantrone / administration & dosage. Nausea / chemically induced. Neutropenia / chemically induced. Palliative Care. Survival Rate. Treatment Outcome

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  • (PMID = 12045460.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] BZ114NVM5P / Mitoxantrone; Q20Q21Q62J / Cisplatin
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26. Agulnik M, Cohen EW, Cohen RB, Chen EX, Vokes EE, Hotte SJ, Winquist E, Laurie S, Hayes DN, Dancey JE, Brown S, Pond GR, Lorimer I, Daneshmand M, Ho J, Tsao MS, Siu LL: Phase II study of lapatinib in recurrent or metastatic epidermal growth factor receptor and/or erbB2 expressing adenoid cystic carcinoma and non adenoid cystic carcinoma malignant tumors of the salivary glands. J Clin Oncol; 2007 Sep 1;25(25):3978-84
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  • [Title] Phase II study of lapatinib in recurrent or metastatic epidermal growth factor receptor and/or erbB2 expressing adenoid cystic carcinoma and non adenoid cystic carcinoma malignant tumors of the salivary glands.
  • PURPOSE: Expression of erbB2 and/or epidermal growth factor receptor (EGFR) is associated with biologic aggressiveness and poor prognosis in malignant salivary gland tumors (MSGTs).
  • Patients with non-ACC MSGTs were treated as a separate single-stage cohort.
  • RESULTS: Of 62 patients screened, 29 of 33 (88%) ACC and 28 of 29 (97%) non-ACC patients expressed EGFR and/or erbB2.
  • For 17 assessable non-ACC patients, there were no objective responses, eight patients (47%) had SD, four patients (24%) had SD > or = 6 months, and nine patients (53%) had PD.
  • Eight paired tumor biopsies for correlative studies were procured; results did not correlate with clinical outcome.
  • CONCLUSION: Although no responses were observed, lapatinib was well tolerated, with prolonged tumor stabilization of > or = 6 months in 36% (95% CI, 21% to 54%) of assessable patients.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Carcinoma, Adenoid Cystic / drug therapy. Carcinoma, Adenoid Cystic / secondary. Epidermal Growth Factor / metabolism. Neoplasm Recurrence, Local / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Quinazolines / therapeutic use. Salivary Gland Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 17761983.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01-CM-57018-16; United States / NCI NIH HHS / CM / N01-CM-62203
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Biomarkers, Tumor; 0 / ERBB2IP protein, human; 0 / Quinazolines; 0VUA21238F / lapatinib; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Protein-Tyrosine Kinases
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27. Razfar A, Heron DE, Branstetter BF 4th, Seethala RR, Ferris RL: Positron emission tomography-computed tomography adds to the management of salivary gland malignancies. Laryngoscope; 2010 Apr;120(4):734-8
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  • [Title] Positron emission tomography-computed tomography adds to the management of salivary gland malignancies.
  • OBJECTIVES/HYPOTHESIS: To evaluate the efficacy of combined positron emission tomography-computed tomography (PET-CT) in identifying salivary gland malignancies and to examine the role of PET-CT in the management of these patients.
  • METHODS: Fifty-five patients with diagnosed salivary gland cancer who had undergone PET-CT scanning were retrospectively reviewed from January 2000 to October 2008.
  • The impact of PET-CT findings on therapeutic management was analyzed.
  • Three patients with recurrence underwent PET-CT scan-directed radiation and/or chemotherapy, whereas nine patients diagnosed with distant disease received palliative treatment.
  • CONCLUSIONS: PET-CT is useful for planning the most appropriate treatment by identifying clinically unrecognized disease.
  • PET-CT shows a high diagnostic accuracy for detecting disease recurrence and distant metastases, thus helping to determine whether patients are candidates for potentially curative or palliative treatment.
  • [MeSH-major] Positron-Emission Tomography / methods. Salivary Gland Neoplasms / radionuclide imaging
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Metastasis / radionuclide imaging. Neoplasm Staging. Prognosis. Reproducibility of Results. Retrospective Studies. Sensitivity and Specificity

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  • (PMID = 20213798.001).
  • [ISSN] 1531-4995
  • [Journal-full-title] The Laryngoscope
  • [ISO-abbreviation] Laryngoscope
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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28. Vidal L, Tsao MS, Pond GR, Cohen EE, Cohen RB, Chen EX, Agulnik M, Hotte S, Winquist E, Laurie S, Hayes DN, Ho J, Dancey J, Siu LL: Fluorescence in situ hybridization gene amplification analysis of EGFR and HER2 in patients with malignant salivary gland tumors treated with lapatinib. Head Neck; 2009 Aug;31(8):1006-12
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  • [Title] Fluorescence in situ hybridization gene amplification analysis of EGFR and HER2 in patients with malignant salivary gland tumors treated with lapatinib.
  • BACKGROUND: Gene amplification status of the epidermal growth factor receptor (EGFR) and the human epidermal growth factor receptor 2 (HER2) were analyzed and correlated with clinical outcome in patients with progressive malignant salivary glands tumors (MSGT) treated with the dual EGFR/Her2 tyrosine kinase inhibitor lapatinib.
  • METHODS: Fluorescence in situ hybridization (FISH) analysis for both EGFR and HER2 gene amplification was performed successfully in the archival tumor specimens of 20 patients with adenoid cystic carcinomas (ACC) and 17 patients with non-ACC, all treated with lapatinib.
  • For non-ACC, no EGFR gene amplifications were detected but 3 patients (18%) were HER2 amplified and all had stained 3+ for both EGFR and HER2 by immunohistochemistry (IHC) in their archival specimens.
  • Two of these patients had time-to-progression (TTP) durations of 8.3 months and 18.4 months, respectively.
  • Interestingly, patients with low and high HER2/chromosome-specific centromeric enumeration probe (CEP) 17 ratio had a prolonged TTP than those with moderate ratios for both ACC and non-AAC subtypes.

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  • [Copyright] Copyright 2009 Wiley Periodicals, Inc.
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  • (PMID = 19309723.001).
  • [ISSN] 1097-0347
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CM / CM062203; United States / NCI NIH HHS / CA / U01 CA132123-01; United States / NCI NIH HHS / CA / CA132123-01; United States / NCI NIH HHS / CM / N01-CM-62203; United States / NCI NIH HHS / CM / N01-CM-57018-16; United States / NCI NIH HHS / CA / U01 CA132123; United States / NCI NIH HHS / CA / N01CM62203; United States / NCI NIH HHS / CM / N01 CM062203
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Quinazolines; 0VUA21238F / lapatinib; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ NIHMS95592; NLM/ PMC2711990
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29. Vattemi E, Graiff C, Sava T, Pedersini R, Caldara A, Mandarà M: Systemic therapies for recurrent and/or metastatic salivary gland cancers. Expert Rev Anticancer Ther; 2008 Mar;8(3):393-402
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systemic therapies for recurrent and/or metastatic salivary gland cancers.
  • Salivary gland carcinomas are rare cancers, comprising 1-5% of head and neck cancers.
  • They represent a morphologically and clinically diverse group of tumors.
  • The most commonly histopathologic types are mucoepidermoid cancer, adenoid cystic cancer and adenocarcinomas.
  • Malignant salivary gland tumors generally present as painless, slow-growing tumors that are indistinguishable from benign tumors.
  • Surgery is the principal treatment and is curative in early stage.
  • Radiation therapy should be considered in most patients after surgical resection.
  • Chemotherapy is reserved for palliative treatment of metastatic disease but results are disappointing.
  • Recent studies have investigated the role of targeted therapies in a palliative setting.
  • Multicentre cooperative group clinical trials are required to assess novel therapies to maximize patient resources in this uncommon tumor.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasm Recurrence, Local. Salivary Gland Neoplasms
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Agents, Hormonal / therapeutic use. Benzamides. Boronic Acids / therapeutic use. Bortezomib. Cetuximab. Humans. Imatinib Mesylate. Neoplasm Metastasis. Palliative Care. Piperazines / therapeutic use. Pyrazines / therapeutic use. Pyrimidines / therapeutic use. Quinazolines / therapeutic use. Trastuzumab

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  • (PMID = 18366287.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Benzamides; 0 / Boronic Acids; 0 / Piperazines; 0 / Pyrazines; 0 / Pyrimidines; 0 / Quinazolines; 0VUA21238F / lapatinib; 69G8BD63PP / Bortezomib; 8A1O1M485B / Imatinib Mesylate; P188ANX8CK / Trastuzumab; PQX0D8J21J / Cetuximab; S65743JHBS / gefitinib
  • [Number-of-references] 56
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30. Jensen SB, Pedersen AM, Reibel J, Nauntofte B: Xerostomia and hypofunction of the salivary glands in cancer therapy. Support Care Cancer; 2003 Apr;11(4):207-25
The Lens. Cited by Patents in .

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  • [Title] Xerostomia and hypofunction of the salivary glands in cancer therapy.
  • This review presents data from the literature on oral adverse reactions from the perspectives of subjective feelings of dry mouth (xerostomia) and objective measures of salivary gland hypofunction during and after cancer therapy.
  • Special emphasis is paid to the mechanisms behind xerostomia, impaired saliva secretion and changes in the composition of saliva and to how these relate to radiation therapy involving the salivary glands and to systemic chemotherapy.
  • The oral complications that relate to such iatrogenic changes in salivary gland function are also discussed.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Neoplasms / drug therapy. Neoplasms / radiotherapy. Radiotherapy / adverse effects. Xerostomia / etiology
  • [MeSH-minor] Electrolytes / radiation effects. Humans. Mouth Diseases / etiology. Saliva / drug effects. Saliva / radiation effects. Salivary Glands / drug effects. Salivary Glands / physiology. Salivary Glands / radiation effects. Salivary Proteins and Peptides / drug effects. Salivary Proteins and Peptides / radiation effects. Time

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  • [CommentIn] Support Care Cancer. 2003 Apr;11(4):199-200 [12673457.001]
  • (PMID = 12673459.001).
  • [ISSN] 0941-4355
  • [Journal-full-title] Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer
  • [ISO-abbreviation] Support Care Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Electrolytes; 0 / Salivary Proteins and Peptides
  • [Number-of-references] 184
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31. Yoshimura T, Sumida T, Liu S, Onishi A, Shintani S, Desprez PY, Hamakawa H: Growth inhibition of human salivary gland tumor cells by introduction of progesterone (Pg) receptor and Pg treatment. Endocr Relat Cancer; 2007 Dec;14(4):1107-16
Hazardous Substances Data Bank. PROGESTERONE .

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  • [Title] Growth inhibition of human salivary gland tumor cells by introduction of progesterone (Pg) receptor and Pg treatment.
  • Cancer of the salivary gland is one of the common cancers in the head and the neck regions.
  • This type of cancer develops in the minor and the major salivary glands, and it sometimes metastasizes to other organs, particularly the lung.
  • Morphologic mimicry and similarity in the expression of steroid hormone receptors between salivary gland tumors (SGTs) and breast tumors are well-known phenomena and are occasionally debated in the field of surgical pathology.
  • Progesterone (Pg), one of the female sex steroid hormone, is intimately involved in the development of the mammary gland.
  • Further, it is believed that Pg plays a role in breast cancer progression.
  • In this study, we used ACCM, a human adenoid cystic carcinoma cell line established from the salivary gland, in order to clarify the role of the Pg receptor (PR) on cell proliferation.
  • No effect of Pg on cell proliferation was observed in the PR-deficient aggressive ACCM cells.
  • However, after introducing PR into the ACCM cells, Pg markedly inhibited the proliferative activity of the cells.
  • Moreover, Pg-treated PR transfectants showed significant morphological change; they appeared more flattened and spread out when compared with the ethanol-treated control cells.
  • Our results provided significant insights into the mechanism of suppression of the proliferative property of the cells via the function of PR, and suggested that PR reintroduction therapy might be a viable method of inhibiting human SGT progression.
  • [MeSH-major] Progesterone / therapeutic use. Receptors, Progesterone / physiology. Salivary Gland Neoplasms / drug therapy. Salivary Gland Neoplasms / pathology
  • [MeSH-minor] Breast Neoplasms / pathology. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Female. Flow Cytometry. Humans. Neoplasm Invasiveness. Reverse Transcriptase Polymerase Chain Reaction. Telomerase / genetics. Telomerase / metabolism

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  • (PMID = 18045962.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Progesterone; 4G7DS2Q64Y / Progesterone; EC 2.7.7.49 / Telomerase
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32. Klubo-Gwiezdzinska J, Van Nostrand D, Burman KD, Vasko V, Chia S, Deng T, Kulkarni K, Wartofsky L: Salivary gland malignancy and radioiodine therapy for thyroid cancer. Thyroid; 2010 Jun;20(6):647-51
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  • [Title] Salivary gland malignancy and radioiodine therapy for thyroid cancer.
  • BACKGROUND: The risk of second primary malignancies in patients with well-differentiated thyroid cancer is of special interest because of the common use of radioactive iodine (RAI) ablation and/or treatment of these patients and the theoretical risk of subsequent nonthyroid malignancies associated with the radiation exposure.
  • This brief report focuses specifically on the occurrence of second primary malignancies of the salivary glands.
  • RAI residency within salivary tissues is known to have both acute and chronic consequences on salivary function, but secondary neoplasia is quite unusual.
  • SUMMARY: We present a very rare case of a patient with papillary thyroid cancer treated with 600 mCi of RAI, who subsequently developed salivary gland cancer.
  • CONCLUSIONS: We recommend salivary gland protection to diminish potential side effects after the exposure to radioiodine.
  • [MeSH-major] Iodine Radioisotopes / adverse effects. Neoplasms, Radiation-Induced. Neoplasms, Second Primary / prevention & control. Salivary Gland Neoplasms / etiology. Thyroid Neoplasms / radiotherapy
  • [MeSH-minor] Female. Humans. Middle Aged. Salivary Glands / drug effects. Salivary Glands / radiation effects

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  • (PMID = 20470209.001).
  • [ISSN] 1557-9077
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes
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33. Maruya S, Namba A, Matsubara A, Kakehata S, Takeda I, Shirasaki T, Hatayama Y, Nagahata M, Yokoyama J, Shinkawa H: Salivary gland carcinoma treated with concomitant chemoradiation with intraarterial cisplatin and docetaxel. Int J Clin Oncol; 2006 Oct;11(5):403-6
Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

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  • [Title] Salivary gland carcinoma treated with concomitant chemoradiation with intraarterial cisplatin and docetaxel.
  • Malignant neoplasms of the salivary gland are uncommon entities in which surgical resection of the primary lesion has been accepted as a standard therapeutic option.
  • The efficacy of radiation and systemic chemotherapy has been limited for patients with recurrent, metastatic, or unresectable disease because of unfavorable response rates and the short duration of the response.
  • We treated one patient with recurrent adenoid cystic carcinoma arising from the sublingual gland and one patient with primary adenocarcinoma arising from the parotid gland with transfemoral intraarterial chemotherapy, based on full-dose cisplatin and docetaxel and concurrent external-beam radiotherapy.
  • The concomitant chemoradiotherapy of cisplatin and docetaxel seemed to be a practicable option for patients with recurrent and unresectable salivary gland carcinomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Parotid Neoplasms / drug therapy. Parotid Neoplasms / radiotherapy. Sublingual Gland Neoplasms / drug therapy. Sublingual Gland Neoplasms / radiotherapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Aged. Carcinoma, Adenoid Cystic / drug therapy. Carcinoma, Adenoid Cystic / radiotherapy. Chemotherapy, Adjuvant. Cisplatin / administration & dosage. Humans. Infusions, Intra-Arterial. Male. Middle Aged. Radiotherapy, Adjuvant. Taxoids / administration & dosage. Treatment Outcome

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  • (PMID = 17058139.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; Q20Q21Q62J / Cisplatin
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34. Locati LD, Bossi P, Perrone F, Potepan P, Crippa F, Mariani L, Casieri P, Orsenigo M, Losa M, Bergamini C, Liberatoscioli C, Quattrone P, Calderone RG, Rinaldi G, Pilotti S, Licitra L: Cetuximab in recurrent and/or metastatic salivary gland carcinomas: A phase II study. Oral Oncol; 2009 Jul;45(7):574-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cetuximab in recurrent and/or metastatic salivary gland carcinomas: A phase II study.
  • EGFR overexpression in salivary gland carcinomas provides the rational for the investigation of anti-EGFR treatments in recurrent and/or metastatic salivary gland cancers (RMSGCs).
  • The activity of cetuximab in terms of clinical benefit rate (CBR) defined as the occurrence of objective response (CR or PR) or stable disease (SD) for >or=6months was investigated.
  • From April to December 2005, 30 patients [23 adenoid cystic carcinoma (ACC) and 7 non-ACC] were treated with cetuximab at 400mg/m(2)/week followed by 250mg/m(2)/week until progression, major toxicity or voluntary discontinuation.
  • None tumor sample showed EGFR gene amplification and an increased EGFR copy number was observed in 12% of samples, all ACC.
  • In RMSGCs further evaluations of EGFR targeting agents are advisable and should take place by appropriate tumor biological selection, differentiating ACC from non-ACC.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Adenoid Cystic / drug therapy. Neoplasm Recurrence, Local / drug therapy. Salivary Gland Neoplasms / drug therapy

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  • (PMID = 18804410.001).
  • [ISSN] 1879-0593
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
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35. Gilbert J, Li Y, Pinto HA, Jennings T, Kies MS, Silverman P, Forastiere AA: Phase II trial of taxol in salivary gland malignancies (E1394): a trial of the Eastern Cooperative Oncology Group. Head Neck; 2006 Mar;28(3):197-204
Hazardous Substances Data Bank. TAXOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of taxol in salivary gland malignancies (E1394): a trial of the Eastern Cooperative Oncology Group.
  • BACKGROUND: Malignant tumors of the salivary glands make up approximately 5% of head and neck cancers.
  • The Eastern Cooperative Oncology Group (ECOG) initiated a phase II evaluation of paclitaxel in patients with locally recurrent or metastatic salivary gland malignancies.
  • METHODS: Chemo-naive patients with histologically confirmed recurrent or metastatic carcinoma of salivary gland origin (mucoepidermoid, adenocarcinoma, or adenoid cystic) were eligible.
  • CONCLUSION: Paclitaxel demonstrates moderate activity in salivary gland tumors of mucoepidermoid and adenocarcinoma histology.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Paclitaxel / therapeutic use. Salivary Gland Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / mortality. Adult. Aged. Aged, 80 and over. Carcinoma, Adenoid Cystic / drug therapy. Carcinoma, Adenoid Cystic / mortality. Carcinoma, Mucoepidermoid / drug therapy. Carcinoma, Mucoepidermoid / mortality. Female. Follow-Up Studies. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / mortality

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  • [Copyright] (c) 2005 Wiley Periodicals, Inc.
  • (PMID = 16470745.001).
  • [ISSN] 1043-3074
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA14548; United States / NCI NIH HHS / CA / CA16116; United States / NCI NIH HHS / CA / CA17145; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / CA23318; United States / NCI NIH HHS / CA / CA66636
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; P88XT4IS4D / Paclitaxel
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36. Nakashiro K, Begum NM, Uchida D, Kawamata H, Shintani S, Sato M, Hamakawa H: Thiazolidinediones inhibit cell growth of human oral squamous cell carcinoma in vitro independent of peroxisome proliferator-activated receptor gamma. Oral Oncol; 2003 Dec;39(8):855-61
Hazardous Substances Data Bank. PIOGLITAZONE .

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  • Recently, we have demonstrated that PPARgamma is expressed in human salivary gland tumors and its ligands inhibit the growth of cultured salivary gland cancer cells.
  • PPARgamma mRNA was detected by RT-PCR in some OSCC tissues and cultured cells, but the PPARgamma protein showed neither expression nor ligand-induced transcriptional activity.
  • Despite loss of PPARgamma function, synthetic PPARgamma ligands caused significant dose-dependent inhibition of cancer cell growth.
  • [MeSH-major] Carcinoma, Squamous Cell / drug therapy. Mouth Neoplasms / drug therapy. Thiazolidinediones / therapeutic use
  • [MeSH-minor] Cell Line, Tumor. Chromans / therapeutic use. DNA Mutational Analysis. Humans. RNA, Messenger / analysis. Receptors, Cytoplasmic and Nuclear / genetics. Receptors, Cytoplasmic and Nuclear / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics. Transcription Factors / metabolism. Transfection / methods

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  • (PMID = 13679209.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromans; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Thiazolidinediones; 0 / Transcription Factors; I66ZZ0ZN0E / troglitazone; X4OV71U42S / pioglitazone
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37. Locati LD, Rinaldi G, Bossi P, Dagrada GP, Quattrone P, Cantú G, Licitra L: Herceptin plus chemotherapy in relapsed and/or metastatic salivary gland cancer. Oral Oncol; 2005 Jan;41(1):97-8
Hazardous Substances Data Bank. Trastuzumab .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Herceptin plus chemotherapy in relapsed and/or metastatic salivary gland cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Salivary Gland Neoplasms / drug therapy

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  • [CommentOn] Oral Oncol. 2003 Oct;39(7):724-7 [12907212.001]
  • (PMID = 15598592.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; P188ANX8CK / Trastuzumab
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