Claudia Lanari

ORCID: 0000-0003-0555-2309
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About
Contact & Profiles
Research Areas
  • Estrogen and related hormone effects
  • Cancer Cells and Metastasis
  • Fibroblast Growth Factor Research
  • HER2/EGFR in Cancer Research
  • Cytokine Signaling Pathways and Interactions
  • Breast Cancer Treatment Studies
  • Cancer Immunotherapy and Biomarkers
  • Metastasis and carcinoma case studies
  • PI3K/AKT/mTOR signaling in cancer
  • Advanced Breast Cancer Therapies
  • Cancer, Hypoxia, and Metabolism
  • Lung Cancer Research Studies
  • Immunotherapy and Immune Responses
  • Bioactive Compounds and Antitumor Agents
  • Cancer, Stress, Anesthesia, and Immune Response
  • Immune cells in cancer
  • Cancer-related Molecular Pathways
  • Cancer Research and Treatments
  • Cancer Risks and Factors
  • Endometrial and Cervical Cancer Treatments
  • Reproductive System and Pregnancy
  • Growth Hormone and Insulin-like Growth Factors
  • Epigenetics and DNA Methylation
  • Wnt/β-catenin signaling in development and cancer
  • Kruppel-like factors research

Experimental Medicine and Biology Institute
2016-2025

Consejo Nacional de Investigaciones Científicas y Técnicas
2016-2025

Magdalena Villegas de Martínez el Hospital
2018

Sanatorio Otamendi y Miroli
2018

Virginia Commonwealth University
2018

Vanderbilt University
2018

Broad Institute
2018

Weizmann Institute of Science
2018

Moores Cancer Center
2018

University of California, San Diego
2016

Abstract It has been proposed that progesterone (P4) induces the suppression of immune responses, particularly during pregnancy. However, knowledge about mechanisms involved remained largely elusive. We demonstrate herein peripheral blood NK (PBNK) cells express both classical receptor (PR) isoforms and are specifically affected by actions P4 through two apparently independent mechanisms. Progesterone caspase-dependent PBNK cell death, which is reversed different anti-progestins, ZK 98.299...

10.4049/jimmunol.180.8.5746 article EN The Journal of Immunology 2008-04-15

Abstract The purpose of this study was to elucidate the mechanisms associated with specific effects AKT1 and AKT2 isoforms in breast cancer progression. We modulated abundance AKT IBH-6 T47D human cell lines showed that promoted proliferation, through S6 cyclin D1 upregulation, but it inhibited migration invasion β1-integrin focal adhesion kinase (FAK) downregulation. In contrast, F-actin vimentin induction. Thus, while overexpression local tumor growth, downregulation or peritumoral lung...

10.1038/srep44244 article EN cc-by Scientific Reports 2017-03-13

Synthetic progesterone used in contraception drugs (progestins) can promote breast cancer growth, but the mechanisms involved are unknown. Moreover, it remains unclear whether cytoplasmic interactions between receptor (PR) and estrogen alpha (ERα) required for PR activation. In this study, we a murine progestin-dependent tumor to investigate role of ERα progestin-induced cell proliferation. We found that treatment with progestin medroxyprogesterone acetate (MPA) induced expression activation...

10.1158/0008-5472.can-11-3290 article EN Cancer Research 2012-03-07

Abstract Fibroblast growth factor (FGF) receptor 2 (FGFR-2) polymorphisms have been associated with an increase in estrogen and progesterone (PR)-positive breast cancer risk; however, a clear mechanistic association between FGFR-2 steroid hormone receptors remains elusive. In previous works, we shown cross talk FGF2 progestins mouse mammary carcinomas. To investigate the mechanisms underlying these interactions to validate our findings human setting, used T47D cells tissue samples. We showed...

10.1158/0008-5472.can-10-3074 article EN Cancer Research 2011-04-05

Progression to hormone‐independent growth leading endocrine therapy resistance occurs in a high proportion of patients with estrogen receptor alpha (ERα) and progesterone receptors (PR) positive breast cancer. We others have previously shown that estrogen‐ progestin‐induced tumor requires ERα PR interaction at their target genes. Here, we show fibroblast factor 2 (FGF2)‐induces cell proliferation through activation the MYC enhancer proximal promoter. inhibitors, antiestrogens or...

10.1002/ijc.32252 article EN International Journal of Cancer 2019-03-07

Abstract The mechanisms by which mammary carcinomas acquire hormone independence are still unknown. To study the role of cancer‐associated fibroblasts (CAF) in acquisition hormone‐independence we used a hormone‐dependent (HD) mouse tumor and its hormone‐independent (HI) variant, grows vivo without supply. HI tumors express higher levels FGFR‐2 than HD tumors. In spite their differences, both have same requirement primary cultures. We demonstrated that CAF from (CAF‐HI) growing vitro , FGF‐2...

10.1002/ijc.23802 article EN International Journal of Cancer 2008-09-02

Breast cancer, the most common cancer in women countries, is a highly stressful disease. Catecholamines released during stress bind to adrenoceptors and we have recently described alpha(2)-adrenoceptors human breast cell lines, linked enhanced proliferation. The purpose was assess vivo effects of compounds acting on reliable model cancer.The expression confirmed by immunocytochemistry, immunofluorescence reverse transcription-PCR mouse mammary tumour line MC4-L5. Proliferation assessed...

10.1038/bjp.2008.278 article EN British Journal of Pharmacology 2008-07-07

Background: Compelling evidence shows that progestins regulate breast cancer growth. Using preclinical models, we demonstrated antiprogestins are inhibitory when the level of progesterone receptor isoform A (PR-A) is higher than B (PR-B) and they might stimulate growth PR-B predominant. The aims this study were to investigate ex vivo responses mifepristone (MFP) in carcinomas with different PR ratios examine their clinical molecular characteristics. Methods: We performed human tissue culture...

10.1093/jnci/djw317 article EN JNCI Journal of the National Cancer Institute 2016-12-03

Abstract Purpose: Preclinical data suggest that antiprogestins inhibit the growth of luminal breast carcinomas express higher levels progesterone receptor isoform A (PRA) than B (PRB). Thus, we designed a presurgical window opportunity trial to determine therapeutic effects mifepristone in patients with cancer, based on their high PRA/PRB ratio (MIPRA; NCT02651844). Patients and Methods: Twenty > 1.5 (determined by Western blots), PR ≥ 50%, naïve from previous treatment, were included...

10.1158/1078-0432.ccr-22-2060 article EN cc-by-nc-nd Clinical Cancer Research 2022-10-21

The second edition of the Buenos Aires Breast Cancer Symposium (BA-BCS), first held in person, took place from September 3rd to 6th Aires, Argentina. This report provides an overview talks delivered as individual lectures or part mini-symposia illustrating diversity and complexity topics discussed throughout meeting. event brought together leading scientists clinical experts dedicated advancing breast cancer research improving therapeutic strategies patient care. contributions both speakers...

10.1007/s10911-025-09577-5 article EN cc-by-nc-nd Journal of Mammary Gland Biology and Neoplasia 2025-03-15

Using a model of medroxyprogesterone acetate (MPA)-induced mouse mammary tumors that transit through different stages hormone dependence, we previously reported the activation phosphatidylinositol 3-kinase (PI3K)/AKT (protein kinase B) pathway is critical for growth hormone-independent (HI) carcinomas but not hormone-dependent (HD) carcinomas. The objective this work was to explore whether PI3K/AKT responsible changes in tumor phenotype and transition autonomous growth. We found inhibition...

10.1093/carcin/bgr303 article EN Carcinogenesis 2011-12-17

We have previously described enhanced human breast cancer cell proliferation and mouse mammary tumor growth induced by α(2)-adrenoceptor (α(2)-AR) expression in epithelial cells. The aim of the present work was to assess if stromal fibroblasts can contribute this effect. α(2)-AR assessed immunocytochemistry immunohistochemistry, [(3)H]-Thymidine incorporation measuring with caliper. All tested expressed at least two subtypes α(2)-adrenergic agonists fibroblast proliferation. In vivo, agonist...

10.2174/156800911796191051 article EN Current Cancer Drug Targets 2011-06-28

There is emerging interest in understanding the role of progesterone receptors (PRs) breast cancer. The aim this study was to investigate proliferative effect progestins and antiprogestins depending on relative expression A (PRA) B (PRB) isoforms PR. In mifepristone (MFP)‐resistant murine carcinomas antiprogestin responsiveness restored by re‐expressing PRA using demethylating agents histone deacetylase inhibitors. Consistently, two human cancer xenograft models, one manipulated overexpress...

10.1002/ijc.29304 article EN International Journal of Cancer 2014-11-01

There is a consensus that progestins and thus their cognate receptor molecules, the progesterone receptors (PR), are essential in development of adult mammary gland regulators proliferation lactation. However, role for natural breast carcinogenesis remains poorly understood. A hint to possible came from studies which synthetic progestin medroxyprogesterone acetate was associated with an increased cancer risk women under hormone replacement therapy. have been also used treatment inhibit...

10.1530/erc-18-0179 article EN Endocrine Related Cancer 2018-07-10
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