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1. Giacomazzi J, Selistre S, Duarte J, Ribeiro JP, Vieira PJ, de Souza Macedo G, Rossi C, Czepielewski M, Netto CB, Hainaut P, Ashton-Prolla P: TP53 p.R337H is a conditional cancer-predisposing mutation: further evidence from a homozygous patient. BMC Cancer; 2013;13:187
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  • [Title] TP53 p.R337H is a conditional cancer-predisposing mutation: further evidence from a homozygous patient.
  • BACKGROUND: Adrenocortical carcinomas (ACCs) are among the most common childhood cancers occurring in infants affected with the Li-Fraumeni and Li- Fraumeni-like (LFS/LFL) syndromes, which are caused by dominant germline mutations in the TP53 gene.
  • CASE PRESENTATION: At age 11 months, the patient was diagnosed with a virilising anaplastic adrenal cortical tumour, which was completely excised without disturbing the adrenal capsule.
  • Family history was consistent with an LFL tumour pattern, and genotyping identified the TP53 p.R337H mutation in both alleles in genomic DNA from lymphocytes and fibroblasts.
  • Patients with the homozygous TP53 p.R337H genotype will require careful surveillance for lifetime cancer risk and for effects on metabolic capacity later in life.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Carcinoma / genetics. Genetic Predisposition to Disease. Germ-Line Mutation / genetics. Li-Fraumeni Syndrome / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 23570263.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC3637265
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2. Poli G, Ceni E, Armignacco R, Ercolino T, Canu L, Baroni G, Nesi G, Galli A, Mannelli M, Luconi M: 2D-DIGE proteomic analysis identifies new potential therapeutic targets for adrenocortical carcinoma. Oncotarget; 2015 Mar 20;6(8):5695-706
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  • [Title] 2D-DIGE proteomic analysis identifies new potential therapeutic targets for adrenocortical carcinoma.
  • Adrenocortical carcinoma (ACC) is a rare aggressive tumor with poor prognosis when metastatic at diagnosis.
  • The tumor biology is still mostly unclear, justifying the limited specificity and efficacy of the anti-cancer drugs currently available.
  • This study reports the first proteomic analysis of ACC by using two-dimensional-differential-in-gel-electrophoresis (2D-DIGE) to evaluate a differential protein expression profile between adrenocortical carcinoma and normal adrenal.
  • Gene ontology analysis revealed that most of the proteins concurs towards a metabolic shift, called the Warburg effect, in adrenocortical cancer.
  • Moreover, immunohistochemistry performed on paraffin-embedded ACC and normal adrenal specimens confirmed marked positive staining for all 6 proteins diffusely expressed by neoplastic cells, compared with normal adrenal cortex.In conclusion, our preliminary findings reveal a different proteomic profile in adrenocortical carcinoma compared with normal adrenal cortex characterized by overexpression of mainly metabolic enzymes, thus suggesting the Warburg effect also occurs in ACC.
  • [MeSH-major] Adrenal Cortex Neoplasms / chemistry. Adrenocortical Carcinoma / chemistry. Biomarkers, Tumor / analysis. Two-Dimensional Difference Gel Electrophoresis / methods

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  • (PMID = 25691058.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC4467395
  • [Keywords] NOTNLM ; biomarkers / cancer metabolism / proteomics
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3. Dawoodji A, Chen JL, Shepherd D, Dalin F, Tarlton A, Alimohammadi M, Penna-Martinez M, Meyer G, Mitchell AL, Gan EH, Bratland E, Bensing S, Husebye ES, Pearce SH, Badenhoop K, Kämpe O, Cerundolo V: High frequency of cytolytic 21-hydroxylase-specific CD8+ T cells in autoimmune Addison's disease patients. J Immunol; 2014 Sep 01;193(5):2118-26
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  • The mechanisms behind destruction of the adrenal glands in autoimmune Addison's disease remain unclear.
  • Autoantibodies against steroid 21-hydroxylase, an intracellular key enzyme of the adrenal cortex, are found in >90% of patients, but these autoantibodies are not thought to mediate the disease.
  • Using overlapping 18-aa peptides spanning the full length of 21-hydroxylase, we identified immunodominant CD8(+) and CD4(+) T cell responses in a large proportion of Addison's patients both ex vivo and after in vitro culture of PBLs ≤20 y after diagnosis.
  • These results have implications for earlier diagnosis of adrenal failure and ultimately a potential target for therapeutic intervention and induction of immunity against adrenal cortex cancer.
  • [MeSH-minor] Adolescent. Adrenal Cortex Neoplasms / immunology. Adrenal Cortex Neoplasms / pathology. Adult. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / pathology. Humans. Middle Aged

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  • [Copyright] Copyright © 2014 by The American Association of Immunologists, Inc.
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  • (PMID = 25063864.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / 11331; United Kingdom / Medical Research Council / / ; United Kingdom / Wellcome Trust / / 084923; United Kingdom / Cancer Research UK / / C399/A2291; United Kingdom / Medical Research Council / / MC/ UU/ 12010/1; United Kingdom / Medical Research Council / / G0900390
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptides; EC 1.14.14.16 / Steroid 21-Hydroxylase
  • [Other-IDs] NLM/ EMS67426; NLM/ PMC4821366
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4. Fay AP, Elfiky A, Teló GH, McKay RR, Kaymakcalan M, Nguyen PL, Vaidya A, Ruan DT, Bellmunt J, Choueiri TK: Adrenocortical carcinoma: the management of metastatic disease. Crit Rev Oncol Hematol; 2014 Nov;92(2):123-32
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  • [Title] Adrenocortical carcinoma: the management of metastatic disease.
  • Adrenocortical cancer is a rare malignancy.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use

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  • [Copyright] Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
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  • (PMID = 24958272.001).
  • [ISSN] 1879-0461
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009172
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal
  • [Other-IDs] NLM/ NIHMS721743; NLM/ PMC4578298
  • [Keywords] NOTNLM ; Adrenocortical carcinoma / Metastatic disease / Targeted therapies / Therapeutics
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5. Millis SZ, Ejadi S, Demeure MJ: Molecular Profiling of Refractory Adrenocortical Cancers and Predictive Biomarkers to Therapy. Biomark Cancer; 2015;7:69-76
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  • [Title] Molecular Profiling of Refractory Adrenocortical Cancers and Predictive Biomarkers to Therapy.
  • PURPOSE: Current first-line chemotherapy for patients with metastatic adrenocortical cancer (ACC) includes doxorubicin, etoposide, cisplatin, and mitotane with a reported response rate of only 23.2%.
  • Other aberrations included overexpression of programmed death-ligand 1 or programmed cell death protein 1 tumor-infiltrating lymphocytes in >40% of cases.

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  • (PMID = 26715866.001).
  • [Journal-full-title] Biomarkers in cancer
  • [ISO-abbreviation] Biomark Cancer
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC4686344
  • [Keywords] NOTNLM ; adrenocortical cancer / molecular profiling / next-generation sequencing / targeted therapy
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6. Livhits M, Li N, Yeh MW, Harari A: Surgery is associated with improved survival for adrenocortical cancer, even in metastatic disease. Surgery; 2014 Dec;156(6):1531-40; discussion 1540-1
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  • [Title] Surgery is associated with improved survival for adrenocortical cancer, even in metastatic disease.
  • BACKGROUND: Adrenocortical carcinoma (ACC) is a rare but lethal tumor.
  • METHODS: ACC cases were abstracted from the California Cancer Registry and Office of Statewide Health Planning and Development (1999-2008).
  • Predictors included patient demographics, comorbidities, tumor size, stage, and treatment (none, surgery, chemotherapy and/or radiation [CRT], and surgery plus CRT).
  • RESULTS: We studied 367 patients with median tumor size of 10 cm.

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  • [Copyright] Copyright © 2014 Elsevier Inc. All rights reserved.
  • [CommentIn] Surgery. 2014 Dec;156(6):1529-30 [25244969.001]
  • (PMID = 25456949.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] ENG
  • [Grant] United States / NCATS NIH HHS / TR / UL1 TR000124; United States / NCATS NIH HHS / TR / UL1TR000124
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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7. Cherradi N: microRNAs as Potential Biomarkers in Adrenocortical Cancer: Progress and Challenges. Front Endocrinol (Lausanne); 2015;6:195
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  • [Title] microRNAs as Potential Biomarkers in Adrenocortical Cancer: Progress and Challenges.
  • Adrenocortical carcinoma (ACC) is a rare malignancy with poor prognosis and limited therapeutic options.
  • Besides the well-known dysfunctional molecular pathways in adrenocortical tumors, such as the IGF2 pathway, the Wnt pathway, and TP53, high-throughput technologies enabled a more comprehensive genomic characterization of adrenocortical cancer.
  • Integration of expression profile data with exome sequencing, SNP array analysis, methylation, and microRNA (miRNA) profiling led to the identification of subgroups of malignant tumors with distinct molecular alterations and clinical outcomes. miRNAs post-transcriptionally silence their target gene expression either by degrading mRNA or by inhibiting translation.
  • In this review, we discuss the current knowledge regarding the deregulation of tumor-associated and circulating miRNAs in ACC patients, while emphasizing their potential significance in pathogenic pathways in light of recent insights into the role of miRNAs in shaping the tumor microenvironment.

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  • (PMID = 26834703.001).
  • [ISSN] 1664-2392
  • [Journal-full-title] Frontiers in endocrinology
  • [ISO-abbreviation] Front Endocrinol (Lausanne)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC4719100
  • [Keywords] NOTNLM ; adrenocortical carcinoma / biomarker / circulating miRNA / diagnosis / prognosis / therapeutic targets
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8. Sorrell AD, Espenschied CR, Culver JO, Weitzel JN: Tumor protein p53 (TP53) testing and Li-Fraumeni syndrome : current status of clinical applications and future directions. Mol Diagn Ther; 2013 Feb;17(1):31-47
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  • [Title] Tumor protein p53 (TP53) testing and Li-Fraumeni syndrome : current status of clinical applications and future directions.
  • Prevalent as an acquired abnormality in cancer, the role of tumor protein p53 (TP53) as a germline mutation continues to evolve.
  • The clinical impact of a germline TP53 mutation is often dramatic and affects the full life course, with a propensity to develop rare tumors in childhood and multiple common cancers of unexpectedly early onset in adulthood.
  • In this article, we review the clinical relevance of germline mutations in the TP53 tumor suppressor gene to current healthcare practice, including the optimal ways to identify patients with Li-Fraumeni syndrome (LFS), to recognize the core cancers associated with LFS, and to develop strategies for early detection of LFS-associated tumors.

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  • (PMID = 23355100.001).
  • [ISSN] 1179-2000
  • [Journal-full-title] Molecular diagnosis & therapy
  • [ISO-abbreviation] Mol Diagn Ther
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R25 CA085771; United States / NCI NIH HHS / CA / RC4 CA153828; United States / NCI NIH HHS / CA / R25CA085771; United States / NCI NIH HHS / CA / RC4CA153828
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS459180; NLM/ PMC3627545
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9. Gaujoux S, Hantel C, Launay P, Bonnet S, Perlemoine K, Lefèvre L, Guillaud-Bataille M, Beuschlein F, Tissier F, Bertherat J, Rizk-Rabin M, Ragazzon B: Silencing mutated β-catenin inhibits cell proliferation and stimulates apoptosis in the adrenocortical cancer cell line H295R. PLoS One; 2013;8(2):e55743
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  • [Title] Silencing mutated β-catenin inhibits cell proliferation and stimulates apoptosis in the adrenocortical cancer cell line H295R.
  • CONTEXT: Adrenocortical carcinoma (ACC) is a rare and highly aggressive endocrine neoplasm, with limited therapeutic options.
  • OBJECTIVE: Similar to patient tumor specimen the H295 cell line derived from an ACC harbors a natural activating β-catenin mutation.
  • We herein assess the in vitro and in vivo effect of β-catenin inactivation using a doxycyclin (dox) inducible shRNA plasmid in H295R adrenocortical cancer cells line (clone named shβ).
  • In vivo, on established tumor xenografts in athymic nude mice, 9 days of β-catenin silencing resulted in a significant reduction of CTNNB1 and AXIN2 expression.
  • Moreover, continous β-catenin silencing, starting 3 days after tumor cell inoculation, was associated with a complete absence of tumor growth in the shβ group while tumors were present in all animals of the control group.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Apoptosis / genetics. Gene Silencing. Mutation. beta Catenin / genetics
  • [MeSH-minor] Animals. Cell Cycle / genetics. Cell Line, Tumor. Cell Proliferation. Disease Models, Animal. Female. Humans. Mice. RNA Interference. Signal Transduction. TCF Transcription Factors / metabolism. Transcription, Genetic. Transplantation, Heterologous. Wnt Proteins / metabolism

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  • (PMID = 23409032.001).
  • [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 / TCF Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ PMC3567123
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10. Creemers SG, van Koetsveld PM, van den Dungen ES, Korpershoek E, van Kemenade FJ, Franssen GJ, de Herder WW, Feelders RA, Hofland LJ: Inhibition of Human Adrenocortical Cancer Cell Growth by Temozolomide in Vitro and the Role of the MGMT Gene. J Clin Endocrinol Metab; 2016 Dec;101(12):4574-4584
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of Human Adrenocortical Cancer Cell Growth by Temozolomide in Vitro and the Role of the MGMT Gene.
  • CONTEXT: Treatment of patients with adrenocortical carcinomas (ACC) with mitotane and/or chemotherapy is often associated with toxicity and poor tumor response.
  • OBJECTIVE: The objectives of the study were to evaluate the therapeutic possibilities of temozolomide (TMZ) in ACC cells and to assess the potential predictive role of the DNA repair gene O6-Methylguanine-DNA methyltransferase (MGMT) in adrenocortical tumors.
  • In the cell lines, 11 normal adrenals, 16 adrenocortical adenomas, and 29 ACC, MGMT promoter methylation and expression were determined.
  • In ACC cell lines and adrenal tissues, MGMT promoter methylation was low.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Carcinoma / drug therapy. Antineoplastic Agents, Alkylating / pharmacology. DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Dacarbazine / analogs & derivatives. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / pharmacology. Cell Line, Tumor. Child. DNA Methylation. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Mitotane / pharmacology. Promoter Regions, Genetic. RNA, Messenger / metabolism. Tumor Cells, Cultured. Young Adult

  • Hazardous Substances Data Bank. DACARBAZINE .
  • Hazardous Substances Data Bank. MITOTANE .
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  • (PMID = 27603910.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Hormonal; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 78E4J5IB5J / Mitotane; 7GR28W0FJI / Dacarbazine; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes; YF1K15M17Y / temozolomide
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