Search

Your search keyword '"Bianco, Ar"' showing total 413 results
Start Over Author "Bianco, Ar"
413 results on '"Bianco, Ar"'

1. Sub-acute physical and mental decline associated with abnormally hypercalcemia: the case report of an oldest-old woman saved by surgery

Author

Monacelli M, Patrizia Mecocci, Boccardi, Puma F, Luca Parretti, Messina S, Marta Baroni, Carmelinda Ruggiero, and Bianco Ar

Subjects
medicine.medical_specialty, Hyperparathyroidism, Calcimimetic, medicine.drug_class, business.industry, Anorexia, Loop diuretic, medicine.disease, Surgery, medicine, Medical history, medicine.symptom, business, Primary hyperparathyroidism, Depression (differential diagnoses), Parathyroid adenoma
Abstract

Background: the case of an oldest-old woman with severe hypercalcemia and hyperparathyroidism due to left parathyroid adenoma. Case presentation: An 85-year-old woman, hospitalized for rapid loss of functional abilities, mental confusion, worsening of depression, anorexia and incontinence. In the medical history, she had depression, hypertension, osteopenia and osteoarthritis. Blood examinations showed high levels of calcium and intact parathyroid hormone (PTHi), severe renal failure with hyperphosphoremia. After hydration and loop diuretic administration, renal function improved and pamidronate and calcimimetic treatments were followed by reduction of calcium levels. The ultrasound of neck identified a possible parathyroid adenoma; 99Tc-sestamibi scintigraphy and CT scan with contrast confirmed the diagnosis. The surgical left hemithyroidectomy was the treatment of choice and the PTHi and calcium reached normal circulating levels immediately post-surgery. At the 3-month clinical follow-up from surgery, the functional, psychological and cognitive functions improved substantially, although mood disorder secondary to disability persisted. Conclusions: Hypercalcemia due to primary hyperparathyroidism is a low prevalence condition among older adults. However, we should keep in mind whenever we find ourselves facing a sudden and unjustified physical, psychological and cognitive deterioration in such a clinical condition old and oldest-old persons.

Published
2019
Full Text
View/download PDF

3. Cancro del colon-retto

Author

CARLOMAGNO, Chiara, DE PLACIDO, SABINO, Bianco AR, Bianco AR, Carlomagno, Chiara, DE PLACIDO, Sabino, and Bianco, Ar

Subjects
tumore del colon-retto, tumori del colon-retto, timori del colon-retto
Abstract

epidemiologia, eziologia, prevenzione, presentazione clinica, diagnosi, stadiazione, trattamento e follow up delle neoplasia del grosso intestino

Published
2003

4. Raltitrexed versus standard leucovorin-modulated 5Fluorouracil: results form the randomized phase III Pan-European Trial in Adjuvant Colon Cancer 01 (PETACC-1)

Author

Popov I, Carrato A, Sobrero A, Vincent M, Kerr D, Labianca R, Bianco AR, El Serafi M, Bedenne L, Paillot B, Mini E, Sanches E, Welch J, Colette L, Praet M, Wils J, CARLOMAGNO, Chiara, Popov, I, Carrato, A, Sobrero, A, Vincent, M, Kerr, D, Labianca, R, Bianco, Ar, El Serafi, M, Bedenne, L, Paillot, B, Mini, E, Sanches, E, Welch, J, Colette, L, Praet, M, Wils, J, and Carlomagno, Chiara

Subjects
adjuvant chemotherapy, colon
Abstract

the aim of the study was the non-inferiority of raltitrexed as compared with standard 5fluorouracil-folinic acid as adjuvant chemotherapy for radically resected colon cancer patients. 993 patinets have been randomized; the enrollement was prematurely closed when 17 raltitrexed-related deaths were recorded. The toxicity was higher in patinets treated with raltitrexed. RSF and OAS were slight inferion in patinets treated with raltitrexed. In conclusion, the study failed to demonstrate the non-inferiority of raltitrexed.

Published
2008

5. Novel TLR9 agonist induces EGFR inhibition and synergistic antitumor activity with EGFR inhibitors

Author

DAMIANO, VINCENZO, BIANCO, ROBERTO, D'ARMIENTO, FRANCESCO PAOLO, LEONARDI, ANTONIO, DE PLACIDO, SABINO, TORTORA, GIAMPAOLO, CAPUTO R, BIANCO AR, AGRAWAL S, CIARDIELLO F, Damiano, Vincenzo, Caputo, R, Bianco, Roberto, D'Armiento, FRANCESCO PAOLO, Leonardi, Antonio, DE PLACIDO, Sabino, Bianco, Ar, Agrawal, S, Ciardiello, F, and Tortora, Giampaolo

Subjects
TLR9, EGFR, cetuximab
Abstract

Immunostimulating Toll-like receptor 9 (TLR9) agonists cause antitumor activity interfering also with cancer proliferation and angiogenesis by mechanisms still incompletely understood. We hypothesized that modified TLR9 agonists could impair epidermal growth factor receptor (EGFR) signaling and, by this means, greatly enhance EGFR inhibitors effect, acting on both the receptor targeting and the immunologic arm. EXPERIMENTAL DESIGN: We used a novel second-generation, modified, immunomodulatory TLR9 agonist (IMO), alone and in combination with the anti-EGFR monoclonal antibody cetuximab or tyrosine kinase inhibitor gefitinib, on the growth of GEO and cetuximab-resistant derivatives GEO-CR colon cancer xenografts. We have also evaluated the expression of several proteins critical for cell proliferation, apoptosis, and angiogenesis, including EGFR, mitogen-activated protein kinase, Akt, bcl-2, cyclooxygenase-2, vascular endothelial growth factor, and nuclear factor-kappaB. RESULTS: IMO inhibited GEO growth and signaling by EGFR and the other proteins critical for cell proliferation and angiogenesis. IMO plus the anti-EGFR antibody cetuximab synergistically inhibited tumor growth, signaling proteins, and microvessel formation. EGFR signaling inhibition by IMO is relevant because IMO cooperated also with EGFR tyrosine kinase inhibitor gefitinib in GEO tumors, while it was inactive against GEO-CR xenografts. On the other hand, IMO boosted the non-EGFR-dependent cetuximab activity, causing a cooperative antitumor effect in GEO-CR cells. Finally, combination of IMO, cetuximab and chemotherapeutic irinotecan eradicated the tumors in 90% of mice. CONCLUSION: IMO interferes with EGFR-related signaling and angiogenesis and has a synergistic antitumor effect with EGFR inhibitors, especially with cetuximab, boosting both the EGFR dependent and independent activity of this agent. Moreover, this therapeutic strategy could be translated in patients affected by colorectal cancer.

Published
2006

8. ANTITUMOR ACTIVITY OF ZD6474, A VEGFR-2 AND EGFR SMALL MOLECULE TYROSINE KINASE INHIBITOR, IN COMBINATION WITH SC-236, A CYCLOOXYGENASE-2 INHIBITOR

Author

TUCCILLO C, ROMANO M, TROIANI T, MARTINELLI E, MORGILLO F, DE VITA F, FONTANINI G, BIANCO AR, AND CIARDIELLO F., BIANCO, ROBERTO, TORTORA, GIAMPAOLO, Tuccillo, C, Romano, M, Troiani, T, Martinelli, E, Morgillo, F, DE VITA, F, Bianco, Roberto, Fontanini, G, Bianco, Ar, Tortora, Giampaolo, and AND CIARDIELLO, F.

Subjects
VEGFR-2, EGFR, COX-2, ZD6474, SC-236
Published
2005

9. A meta-analysis on the interactionbetween HER-2 expression and response to endocrine treatment in advanced breastcancer

Author

De Laurentiis M, Arpino G, Massarelli E, Ruggiero A, Carlomagno C, Tortora G, D'Agostino D, Caputo F, Cancello G, Montagna E, Malorni L, Zinno L, Lauria R, Bianco AR, De Placido S., CIARDIELLO, Fortunato, De Laurentiis, M, Arpino, G, Massarelli, E, Ruggiero, A, Carlomagno, C, Ciardiello, Fortunato, Tortora, G, D'Agostino, D, Caputo, F, Cancello, G, Montagna, E, Malorni, L, Zinno, L, Lauria, R, Bianco, Ar, and De Placido, S.

Published
2005

10. A randomised factorial trial of sequential doxorubicin and CMF vs CMF and chemotherapy alone vs chemotherapy followed by goserelin plus tamoxifen as adjuvant treatment of node-positive breast cancer

Author

DE PLACIDO, SABINO, DE LAURENTIIS, MICHELINO, LAURIA, ROSSELLA, PETRELLA, GIUSEPPE, LIMITE, GENNARO, COSTANZO, RAFFAELE, DE LENA M, LORUSSO V, PARADISO A, D'APRILE M, PISTILLUCCI G, FARRIS A, SAROBBA MG, PALAZZO S, MANZIONE L, ADAMO V, PALMERI S, FERRAU F, PAGLIARULO C, BIANCO AR, GOCSI COOPERATIVE G.R.O.U.P., DE PLACIDO, Sabino, DE LAURENTIIS, Michelino, DE LENA, M, Lorusso, V, Paradiso, A, D'Aprile, M, Pistillucci, G, Farris, A, Sarobba, Mg, Palazzo, S, Manzione, L, Adamo, V, Palmeri, S, Ferrau, F, Lauria, Rossella, Pagliarulo, C, Petrella, Giuseppe, Limite, Gennaro, Costanzo, Raffaele, Bianco, Ar, and GOCSI COOPERATIVE, G. R. O. U. P.

Abstract

The sequential doxorubicin --> CMF (CMF=cyclophosphamide, methotrexate, fluorouracil) regimen has never been compared to CMF in a randomised trial. The role of adding goserelin and tamoxifen after chemotherapy is unclear. In all, 466 premenopausal node-positive patients were randomised to: (a) CMF x 6 cycles (CMF); (b) doxorubicin x 4 cycles followed by CMF x 6 cycles (A --> CMF); (c) CMF x 6 cycles followed by goserelin plus tamoxifen x 2 years (CMF --> GT); and (d) doxorubicin x 4 cycles followed by CMF x 6 cycles followed by goserelin plus tamoxifen x 2 years (A --> CMF --> GT). The study used a 2 x 2 factorial experimental design to assess: (1) the effect of the chemotherapy regimens (CMF vs A --> CMF or arms a+c vs b+d) and (2) the effect of adding GT after chemotherapy (arms a+b vs c+d). At a median follow-up of 72 months, A --> CMF as compared to CMF significantly improved disease-free survival (DFS) with a multivariate hazard ratio (HR)=0.740 (95\% confidence interval (CI): 0.556-0.986; P=0.040) and produced a nonsignificant improvement of overall survival (OS) (HR=0.764; 95\% CI: 0.489-1.193). The addition of GT after chemotherapy significantly improved DFS (HR=0.74; 95\% CI: 0.555-0.987; P=0.040), with a nonsignificant improvement of OS (HR=0.84; 95\% CI: 0.54-1.32). A --> CMF is superior to CMF. Adding GT after chemotherapy is beneficial for premenopausal node-positive patients..

Published
2005

11. Antitumor activity ofZD6126, a novel vascular-targeting agent, is enhanced when combined with ZD1839, an epidermal growth factor receptor tyrosine kinase inhibitor, and potentiatesthe effects of radiation in a human non-small cell lung cancer xenograft model

Author

Raben D, Bianco C, Damiano V, Bianco R, Melisi D, Mignogna C, D'Armiento FP, Cionini L, Bianco AR, Tortora G, Bunn P., CIARDIELLO, Fortunato, Raben, D, Bianco, C, Damiano, V, Bianco, R, Melisi, D, Mignogna, C, D'Armiento, Fp, Cionini, L, Bianco, Ar, Tortora, G, Ciardiello, Fortunato, and Bunn, P.

Published
2004

12. COMBINED TARGETING OF EGFR AND MDM2 BY GEFITINIB AND ANTISENSE MDM2 COOPERATIVELY INHIBIT HORMONE-INDEPENDENT PROSTATE CANCER

Author

BIANCO, ROBERTO, DE PLACIDO, SABINO, CAPUTO R, DAMIANO V, FICORELLA C, AGRAWAL S, BIANCO AR, CIARDIELLO F, G. TORTORA, Bianco, Roberto, Caputo, R, Damiano, V, DE PLACIDO, Sabino, Ficorella, C, Agrawal, S, Bianco, Ar, Ciardiello, F, and G., Tortora

Subjects
mdm2, EGFR, prostate cancer
Abstract

EGFR) may play a relevant role in the progression, hormone therapy resistance, and prognosis of prostate cancer patients. Also MDM2, a negative p53 regulator that interacts with retinoblastoma (Rb), E2F, p19arf and the rasmitogen- activated protein kinase(MAPK) cascade plays an important role in prostate cancer progression and prognosis. On the basis of the EGFR and MDM2 role in integrating signaling pathways critical for prostate cancer progression, we investigated whether their selective combined blockade may have a cooperative antitumor effect in prostate cancer. For this purpose, we have used the EGFR tyrosine kinase inhibitor gefitinib (ZD1839, Iressa) and a second generation hybrid oligonucleotide antisense MDM2 (AS-MDM2), respectively. Experimental Design: Gefitinib and AS-MDM2 were administered to hormone-refractory and hormone-dependent human prostate cancer cells in vitro and to mice bearing tumor xenografts, evaluating the effects on growth, apoptosis, and protein expression, in vitro and in vivo. Results: We demonstrated that the combination of gefitinib and AS-MDM2 synergistically inhibits the growth of hormone-independent prostate cancer cells in vitro. This effect is accompanied by the inhibition of MDM2, phosphorylated Akt (pAkt), phosphorylated MAPK (pMAPK), and vascular endothelial growth factor (VEGF) expression and by Rb hypophosphorylation. The combination of the two agents in nude mice bearing the same hormone-independent tumors caused a potent cooperative antitumor effect. Tumor samples analysis confirmed the inhibition of MDM2, pAkt, pMAPK, VEGF, and basic fibroblast growth factor expression. Conclusions: This study shows that EGFR and MDM2 play a critical role in the growth of prostate cancer, especially hormone-dependent, and that their combined blockade by gefitinib and AS-MDM2 causes a cooperative antitumor effect, supporting the clinical development of this therapeutic strategy.

Published
2004

16. Antitumor effects of ZD6474, a small molecule Vascular Endothelial Growth Factor receptor tyrosine kinase inhibitor, with additional activity against Epidermal Growth Factor

Author

Ciardiello, F, Caputo, R, Damiano, V, Troiani, T, Vitagliano, D, Carlomagno, F, Veneziani, Bm, Fontanini, G, Bianco, Ar, Tortora, Giampaolo, Ciardiello, F, Caputo, R, Damiano, Vincenzo, Troiani, T, Vitagliano, D, Carlomagno, F, Veneziani, BIANCA MARIA, Fontanini, G, Bianco, Ar, and Tortora, Giampaolo

Subjects
angiogenesis, ZD6474, EGFR
Published
2003

17. EGF activates an inducible survival response via the RAS-> Erk-1/2 pathway to counteract interferon-alpha-mediated apoptosis in epidermoid cancer cells

Author

CARAGLIA, Michele, TAGLIAFERRI P, MARRA M, GIUBERTI G, BUDILLON A, GENNARO ED, PEPE S, VITALE G, IMPROTA S, TASSONE P, VENUTA S, BIANCO AR, ABBRUZZESE A., Caraglia, Michele, Tagliaferri, P, Marra, M, Giuberti, G, Budillon, A, Gennaro, Ed, Pepe, S, Vitale, G, Improta, S, Tassone, P, Venuta, S, Bianco, Ar, and Abbruzzese, A.

Published
2003

18. External beam radiotherapy in bone metastatic prostate cancer: impact on patients’ pain relief and quality of life

Author

DI LORENZO G, AUTORINO R, CIARDIELLO F, RABEN D, BIANCO C, TROIANI T, PIZZA C, DE LAURENTIIS, MICHELINO, PENSABENE M, D. ARMIENTO M, BIANCO AR, DE PLACIDO, SABINO, DI LORENZO, G, Autorino, R, Ciardiello, F, Raben, D, Bianco, C, Troiani, T, Pizza, C, DE LAURENTIIS, Michelino, Pensabene, M, D., ARMIENTO M, Bianco, Ar, and DE PLACIDO, Sabino

Abstract

Bone metastases are a severe problem in oncology, since they usually are associated with pain. External beam radiation therapy (EBRT) has been, for many years, an important component of the treatment regimen to relieve pain. We have performed a clinical study to evaluate the relationship of response to EBRT in terms of pain relief and improvement in quality of life (QoL). We were also interested in the incidence of acute toxicity with EBRT. We have prospectively evaluated 75 patients (median age 68 years, range 64-79 years) with bone metastases from prostate cancer treated with EBRT, radiographically documented from June 1999 to September 2000. Additional therapies in these patients included: second-line hormonal therapy (HT) in 20 patients, chemotherapy (CT) in 25 patients, biphosphonates in 45 patients. For all patients a pain and narcotic evaluation was done before entering the study. Assessment of response was carried out by evaluating pain relief. QoL was measured by using the EORTC QLQ-C30 questionnaire. Toxicity analysis was based on the ROTG grading system. Survival was calculated by Kaplan-Meier estimate from the start of EBRT treatment until the last follow-up or death. A total of 61 out of 75 patients (81%) experienced some type of pain relief after treatment. The complete response rate was 23%. No significant difference in the response rates was found between the group treated with EBRT alone versus the groups treated with EBRT + CT or EBRT + HT. We noted a significant improvement in some of the scales of the considered EORTC-QLQC30 questionnaire. As expected all treatment-related complications were either grade 1-2 acute or subacute and transitory in nature. The group treated with EBRT + CT experienced slightly higher toxicity rates. There were no treatment-related fatalities. Forteen patients of 61 (23%) responders was alive at 12 months. Our results confirm the ability of EBRT to relieve bony pain in the majority of the cancer patients treated as measured by prospective analysis of pain scales prior to and after EBRT. Minimal side effects were experienced and QoL improved as shown by the results of the specific questionnaire.

Published
2003

19. Combined targeted inhibition of Bcl-2, Bcl-xL, EGFR and Protein Kinase A Type I causes potent antitumor, apoptotic and antiangiogenic activity

Author

TORTORA G, CAPUTO R, DAMIANO V, TROIANI T, BIANCO AR, ZANGEMEISTER WITTKE U, CIARDIELLO F., VENEZIANI, BIANCA MARIA, DE PLACIDO, SABINO, Tortora, Giampaolo, Caputo, R, Damiano, Vincenzo, Troiani, T, Veneziani, BIANCA MARIA, DE PLACIDO, Sabino, Bianco, Ar, ZANGEMEISTER WITTKE, U, Ciardiello, F., Tortora, G, and Damiano, V

Subjects
EGFR, bcl-2, Protein Kinase A
Published
2003

22. EXPRESSION OF EPIDERMAL GROWTH FACTOR RECEPTOR (EGFR) CORRELATES WITH DISEASE RELAPSE AND PROGRESSION TO ANDROGEN-INDEPEDENCE IN HUMAN PROSTATE CANCER

Author

DI LORENZO G, D'ARMIENTO, FRANCESCO PAOLO, DE ROSA G, STAIBANO, STEFANIA, AUTORINO R, D'ARMIENTO, MARIA, DE LAURENTIIS, MICHELINO, DE PLACIDO, SABINO, CATALANO G, BIANCO AR, CIARDIELLO F., TORTORA, GIAMPAOLO, DI LORENZO, G, Tortora, G, D'Armiento, FRANCESCO PAOLO, DE ROSA, G, Staibano, Stefania, Autorino, R, D'Armiento, Maria, DE LAURENTIIS, Michelino, DE PLACIDO, Sabino, Catalano, G, Bianco, Ar, Ciardiello, F., and Tortora, Giampaolo

Published
2002

23. Enhancement of antitumor activity of ionizing radiation by combined treatment with the selective EGFR-tyrosine kinase inhibitor ZD1839 (‘Iressa’)

Author

BIANCO C, CAPUTO R, TROIANI T, FONTANINI G, RABEN D, BIANCO AR, TORTORA, GIAMPAOLO, BIANCO, ROBERTO, VENEZIANI, BIANCA MARIA, DAMIANO, VINCENZO, PEPE, STEFANO, Bianco, C, Tortora, Giampaolo, Bianco, Roberto, Caputo, R, Veneziani, BIANCA MARIA, Damiano, Vincenzo, Troiani, T, Fontanini, G, Raben, D, Pepe, Stefano, and Bianco, Ar

Subjects
EGFR, gefitinib, ionizing radiation
Published
2002

24. SECOND-LINE CHEMOTHERAPY WITH A HYBRID-ALTERNATING REGIMEN OF BOLUS FLUOROURACIL MODULATED BY METHOTREXATE AND INFUSIONAL FLUOROURACIL MODULATED BY FOLINIC ACID IN PATIENTS WITH METASTATIC COLORECTAL CANCERPRETREATED WITH FLUOROURACIL. A PHASE II STUDY

Author

CARLOMAGNO C, DE LAURENTIIS, MICHELINO, LAURIA R, ARPINO, GRAZIA, MASSARELLI E, FERRARA C, MILANO A, VERNAGLIA LOMBARDI A, COSTANZO R, CATALANO G, BIANCO AR, DE PLACIDO, SABINO, Carlomagno, C, DE LAURENTIIS, Michelino, Lauria, R, Arpino, Grazia, Massarelli, E, Ferrara, C, Milano, A, VERNAGLIA LOMBARDI, A, Costanzo, R, Catalano, G, Bianco, Ar, and DE PLACIDO, Sabino

Published
2002

31. Resistance to taxanes is induced by c-erbB-2 overexpression in human MCF-10A mammary epithelial cells and is blocked by combined treatment with an antisense oligonucleotide targeting protein kinase A

Author

CIARDIELLO F, CAPUTO R, POMATICO G, BIANCO AR, DE LAURENTIIS, MICHELINO, DE PLACIDO, SABINO, TORTORA, GIAMPAOLO, Ciardiello, F, Caputo, R, Pomatico, G, DE LAURENTIIS, Michelino, DE PLACIDO, Sabino, Bianco, Ar, and Tortora, Giampaolo

Subjects
taxanes resistance, c-erbB-2, protein kinase A
Published
2000

32. Antiangiogenic and antitumor activity of anti-EGFR C225 monoclonal antibody in combination with Vascular Endothelial Growth Factor antisense oligonucleotide in human GEO colon cancer cells

Author

Ciardiello, F, Bianco, R, Damiano, V, Fontanini, G, Caputo, R, Pomatico, G, DE PLACIDO, S, Bianco, Ar, Mendelsohn, J, Tortora, Giampaolo, Ciardiello, F, Bianco, Roberto, Damiano, Vincenzo, Fontanini, G, Caputo, R, Pomatico, G, DE PLACIDO, Sabino, Bianco, Ar, Mendelsohn, J, and Tortora, Giampaolo

Subjects
cetuximab, VEGF, EGFR
Published
2000

33. Interferon-alpha induces apoptosis in human KB cells through a stress-dependent mitogen activated protein kinase pathway that is antagonized by epidermal growth factor

Author

CARAGLIA, Michele, ABBRUZZESE A, LEARDI A, PEPE S, BUDILLON A, BALDASSARE G, SELLERI C, LORENZO SD, FABBROCINI A, GIUBERTI G, VITALE G, LUPOLI G, BIANCO AR, TAGLIAFERRI P., Caraglia, Michele, Abbruzzese, A, Leardi, A, Pepe, S, Budillon, A, Baldassare, G, Selleri, C, Lorenzo, Sd, Fabbrocini, A, Giuberti, G, Vitale, G, Lupoli, G, Bianco, Ar, and Tagliaferri, P.

Published
1999

34. Synergistic growth inhibition and induction of apoptosis by a novel mixed backbone antisense oligonuclotide targeting CRIPTO in combination with C225 anti-EGFR monoclonal antibody and 8-Cl-cAMP in human GEO colon cancer cells

Author

Normanno, N, Tortora, Giampaolo, DE LUCA, A, Pomatico, G, Casamassimi, A, Agrawal, S, Mendelsohn, J, Bianco, Ar, Ciardiello, F., Normanno, N, Tortora, Giampaolo, DE LUCA, A, Pomatico, G, Casamassimi, A, Agrawal, S, Mendelsohn, J, Bianco, Ar, and Ciardiello, F.

Subjects
cetuximab, colon cancer cells, CRIPTO
Published
1999

35. Desferioxamine increases iron depletion and apoptosis induced by ara-C of human myeloid leukaemic cells

Author

LEARDI A, SELLERI C, PEPE S, PIZZI C, NOTARO R, FABBROCINI A, DE LORENZO S, MUSICÒ M, ABBRUZZESE A, BIANCO AR, TAGLIAFERRI P., CARAGLIA, Michele, A., Leardi, M., Caraglia, Selleri, Carmine, Pepe, Stefano, Pizzi, Claudia, R., Notaro, Fabbrocini, Antonietta, DE LORENZO, Sonya, M., Musico, A., Abbruzzese, Bianco, ANGELO RAFFAELE, P. T. a. g. l. i. a. f. e. r. r., I., Leardi, A, Caraglia, Michele, Selleri, C, Pepe, S, Pizzi, C, Notaro, R, Fabbrocini, A, DE LORENZO, S, Musicò, M, Abbruzzese, A, Bianco, Ar, and Tagliaferri, P.

Subjects
Antimetabolites, Antineoplastic, flow cytometry, Iron, Antidotes, Cytarabine, desferioxamine, Apoptosis, Drug Synergism, HL-60 Cells, Deferoxamine, apoptosi, HL60 and U937 cell, Leukemia, Myeloid, Acute Disease, Receptors, Transferrin, Tumor Cells, Cultured, Humans, Drug Interactions, Ara C, cell growth inhibition, Cell Division
Abstract

We investigated whether changes in iron metabolism and the transferrin receptor (TRF-R) expression were involved in the antileukaemic effects of arabinoside cytosine (ara-C). Treatment with 100 nM ara-C for 48h reduced thymidine uptake and increased the surface expression of the TRF-R on leukaemic blasts derived from 13/16 (81%) patients and on the HL-60 and U-937 cell lines. Whereas intracellular non-haem iron was strongly depleted 24 h after ara-C addition, TRF-R up-regulation and recovery of intracellular non-haem iron concentration occurred together after a longer exposure of the cultured cells to the drug. Since iron is an essential regulator of cell proliferation we have evaluated the effects of the combination between ara-C and the iron chelator desferioxamine (DSF) on the growth of HL-60 and U-937 cells. We found that desferioxamine strongly potentiated the effects of ara-C on leukaemic cell growth inhibition and apoptosis. This is the first report of a positive interaction between ara-C and an iron chelator in terms of antileukaemic effects.

Published
1998

36. Carboplatin plus Vinorelbine, a new well tolerated and active regimen for the treatment of extensive-stage small-cell lung cancer: a phase II study

Author

GRIDELLI C, PERRONE F, IANNIELLO GP, BRANCACCIO L, IAFFAIOLI RV, CURCIO C, D'APRILE M, CIOFFI R, CIGOLARI S, ROSSI A, PALAZZOLO G, VELTRI E, PERGOLA M, DE PLACIDO S, MONFARDINI S, BIANCO AR, GALLO, Ciro, Gridelli, C, Perrone, F, Ianniello, Gp, Brancaccio, L, Iaffaioli, Rv, Curcio, C, D'Aprile, M, Cioffi, R, Cigolari, S, Rossi, A, Palazzolo, G, Veltri, E, Pergola, M, DE PLACIDO, S, Gallo, Ciro, Monfardini, S, and Bianco, Ar

Published
1998

40. Differential immunohistochemical detection of transforming growth factor alpha, amphiregulin and CRIPTO in human normal and malignant breast tissues

Author

PANICO L, D'ANTONIO A, SALVATORE G, MEZZA E, TORTORA G, DE LAURENTIIS M, DE PLACIDO S, GIORDANO T, MERINO M, SALOMON DS, MULLICK WJ, PETTINATO G, SCHNITT SJ, BIANCO AR, CIARDIELLO, Fortunato, Panico, L, D'Antonio, A, Salvatore, G, Mezza, E, Tortora, G, DE LAURENTIIS, M, DE PLACIDO, S, Giordano, T, Merino, M, Salomon, D, Mullick, Wj, Pettinato, G, Schnitt, Sj, Bianco, Ar, and Ciardiello, Fortunato

Subjects
Adult, EGF Family of Proteins, Membrane Glycoproteins, Epidermal Growth Factor, Breast Neoplasms, Middle Aged, Transforming Growth Factor alpha, GPI-Linked Proteins, Amphiregulin, Epithelium, Neoplasm Proteins, Immunoenzyme Techniques, Receptors, Estrogen, Lymphatic Metastasis, Humans, Intercellular Signaling Peptides and Proteins, Female, Breast, Growth Substances, Receptors, Progesterone, Carcinoma in Situ, Glycoproteins
Abstract

The expression of growth factors, such as transforming growth factor alpha (TGF alpha), amphiregulin (AR) and CRIPTO, a type-1 tyrosine-kinase growth factor receptor (erbB-2), and a tumor-suppressor gene (p53), that have been implicated in the development and/or the progression of breast cancer, was evaluated by immunohistochemistry in 100 human primary infiltrating breast carcinomas (IBC). AR and CRIPTO immunoreactivity was also assessed in 55 human breast ductal carcinomas in situ (DCIS). Within the 100 IBC, 80, 50, 73, 17, and 34 tumors expressed moderate to high levels of TGF alpha, AR, CRIPTO, erbB-2, and p53 respectively. In addition, AR and CRIPTO immunoreactivity were found in 11 and in 26 out of 55 DCIS respectively. In contrast, only 4, 3, and 2 out of 10 normal mammary-gland samples were weakly positive for TGF alpha, AR, and CRIPTO expression, respectively, whereas none was positive for erbB-2 or p53. Within the 100 IBC, expression of erbB-2 significantly correlated with high histologic and nuclear grading, with high growth fraction, and with estrogen-receptor (ER)- and progesterone-receptor (PgR)-negative tumors. A statistically significant correlation was also observed between p53 expression and high histologic grading, high growth fraction, and PgR-negative tumors. In contrast, no significant correlations were found between TGF alpha, AR, and CRIPTO immunoreactivity and various clinicopathological parameters, with the exception of a positive correlation between TGF alpha and ER expression. These data demonstrate that TGF alpha, AR, and CRIPTO expression are significantly increased in malignant mammary epithelium relative to normal epithelium. In particular, the differential expression of CRIPTO may serve as a potential tumor marker for breast carcinogenesis.

Published
1996

44. Mitimycyn C plus vindesine plus etposide (MEV) versus mitomycin C plus vindesine plus cisplatin (MVP)in stage IV non-small-cell lung cancer: a phase III multicentre randomised trial

Author

GRIDELLI C, PERRONE F, PALMERI S, D'APRILE M, COGNETTI F, ROSSI A, GEBBIA V, PEPE R, VELTRI E, AIROMA G, RUSSO A, INCORONATO P, SCINTO AF, PALAZZOLO G, NATALI M, LEONARDI V, DE PLACIDO S, BIANCO AR, GALLO, Ciro, Gridelli, C, Perrone, F, Palmeri, S, D'Aprile, M, Cognetti, F, Rossi, A, Gebbia, V, Pepe, R, Veltri, E, Airoma, G, Russo, A, Incoronato, P, Scinto, Af, Palazzolo, G, Natali, M, Leonardi, V, Gallo, Ciro, DE PLACIDO, S, and Bianco, Ar

Published
1996

45. Cooperative antiproliferative effects of 8-chloro-cyclic AMP and 528 anti-epidermal growth factor receptor monoclonal antibody on human cancer cells

Author

CIARDIELLO, Fortunato, DAMIANO V, BIANCO C, DI ISERNIA G, RUGGIERO A, CARAGLIA, Michele, TAGLIAFERRI P, BASELGA J, MENDELSOHN J, BIANCO AR, Ciardiello, Fortunato, Damiano, V, Bianco, C, DI ISERNIA, G, Ruggiero, A, Caraglia, Michele, Tagliaferri, P, Baselga, J, Mendelsohn, J, and Bianco, Ar

Subjects
ErbB Receptors, Kinetics, Epidermal Growth Factor, Cell Cycle, Tumor Cells, Cultured, 8-Bromo Cyclic Adenosine Monophosphate, Antibodies, Monoclonal, Humans, Antineoplastic Agents, Breast Neoplasms, Female, DNA Fragmentation, Cell Division
Abstract

8-Chloro-cyclic AMP (8-Cl-cAMP), a site-selective cAMP analogue, is a specific inhibitor of type I cAMP-dependent protein kinase (PKAI) and induces growth inhibition in several human and rodent tumor cell lines. The anti-epidermal growth factor receptor (EGFR) mAb 528 is a blocking antibody able to inhibit the in vitro and in vivo growth of several human cancer cell lines that express functional EGFRs. Since enhanced levels of PKAI are generally found in tumor cells and an increase in PKAI expression is induced by transformation through a transforming growth factor alpha/EGFR autocrine pathway, we have evaluated whether treatment with mAb 528 in combination with 8-Cl-cAMP may have an additive or synergistic growth inhibitory effect on human cancer cells. A dose-dependent inhibition of monolayer cell growth was observed in two human colon cancer cell lines (GEO and CBS) and in a human breast cancer cell line (MDA-468) by treatment with either mAb 528 or 8-Cl-cAMP with 50% inhibitory concentration of 2-10 microgram/ml or 20-25 micrometer, respectively. The combined treatment with low noninhibitory doses of mAb 528 (0.25 microgram/ml) and with 8-Cl-cAMP had a more than additive growth inhibitory effect with a 3- to 5-fold reduction in the 8-Cl-cAMP 50% inhibitory concentration in all cell lines tested. This combined treatment was similarly effective in inhibiting the soft agar cloning efficiency of GEO cells. 8-Cl-cAMP treatment of GEO cells induced a dose-dependent increase in cell membrane-associated EGFRs with a maximum 3- to 4-fold increase within 48-72 h of treatment. These results suggest that a double blockade of the PKAI serine-threonine kinase-dependent and of the EGFR tyrosine kinase-dependent pathways is potentially useful in cancer therapy.

Published
1995

46. Adjuvant chemoendocrine therapy for early breast cancer: is it worthwhile?

Author

PERRONE F, DE PLACIDO S, CARLOMAGNO C, LAURIA R, BIANCO AR, GALLO, Ciro, Perrone, F., DE PLACIDO, Sabino, Gallo, C., Carlomagno, Chiara, Lauria, R., Bianco, ANGELO RAFFAELE, Perrone, F, DE PLACIDO, S, Gallo, Ciro, Carlomagno, C, Lauria, R, and Bianco, Ar

Subjects
breast cancer, adjuvant, endocrine therapy, chemotherapy
Published
1995

47. Effects of chemotherapy and hormonal therapy for early breast cancer on recurrence and 15-year survival: an overview of the randomised trials

Author

EBCTCG, Abe, O., Abe, R., Enomoto, K., Kikuchi, K., Koyama, H., Masuda, H., Nomura, Y., Sakai, K., Sugimachi, K., Tominaga, T., Uchino, J., Yoshida, M., Haybittle, Jl, Davies, C., Harvey, Vj, Holdaway, Tm, Kay, Rg, Mason, Bh, Forbes, Jf, Wilcken, N., Gnant, M., Jakesz, R., Ploner, M., Yosef, Hma, Focan, C., Lobelle, Jp, Peek, U., Oates, Gd, Powell, J., Durand, M., Mauriac, L., Di Leo, A., Dolci, S., Piccart, Mj, Masood, Mb, Parker, D., Price, Jj, Hupperets, Psgj, Jackson, S., Ragaz, J., Berry, D., Broadwater, G., Cirrincione, C., Muss, H., Norton, L., Weiss, Rb, Abu-Zahra, Ht, Portnoj, Sm, Baum, M., Cuzick, J., Houghton, J., Riley, D., Gordon, Nh, Davis, Hl, Beatrice, A., Mihura, J., Naja, A., Lehingue, Y., Romestaing, P., Dubois, Jb, Delozier, T., Mace-Lesec H, J., Rambert, P., Andrysek, O., Barkmanova, J., Owen, Jr, Meier, P., Howell, A., Ribeiro, Gc, Swindell, R., Alison, R., Boreham, J., Clarke, M., Collins, R., Darby, S., Elphinstone, P., Evans, V., Godwin, J., Gray, R., Harwood, C., Hicks, C., James, S., Mackinnon, E., Mcgale, P., Mchugh, T., Mead, G., Peto, R., Wang, Y., Albano, J., Oliveira, Cf, Gervasio, H., Gordilho, J., Johansen, H., Mouridsen, Ht, Gelman, Rs, Harris, Jr, Henderson, Ic, Shapiro, Cl, Andersen, Kw, Axelsson, Ck, Blichert-Toft, M., Moller, S., Overgaard, J., Overgaard, M., Rose, C., Cartensen, B., Palshof, T., Trampisch, Hj, Dalesio, O., Vries, Ege, Rodenhuis, S., Tinteren, H., Comis, Rl, Davidson, Ne, Robert, N., Sledge, G., Tormey, Dc, Wood, W., Cameron, D., Chetty, U., Forrest, P., Jack, W., Rossbach, J., Klijn, Jgm, Treurniet-Donker, Ad, Putten, Wlj, Costa, A., Veronesi, U., Bartelink, H., Duchateau, L., Legrand, C., Sylvester, R., Hage, Ja, Velde, Cjh, Cunningham, Mp, Catalano, R., Creech, Rh, Bonneterre, J., Fargeot, P., Fumoleau, P., Kerbrat, P., Namer, M., Jonat, W., Kaufmann, M., Schumacher, M., Minckwitz, G., Bastert, G., Rauschecker, H., Sauer, R., Sauerbrei, W., Schauer, A., Schryver, A., Vakaet, L., Belfiglio, M., Nicolucci, A., Pellegrini, F., Sacco, M., Valentini, M., Mcardle, Cs, Smith, Dc, Galligioni, E., Boccardo, F., Rubagotti, A., Dent, Dm, Gudgeon, Ca, Hacking, A., Erazo, A., Medina, Jy, Izuo, M., Morishita, Y., Takei, H., Fentiman, Is, Hayward, Jl, Rubens, Rd, Skilton, D., Graeff, H., Janicke, F., Meisner, C., Scheurlen, H., Fournier, D., Dafni, U., Fountzilas, G., Klefstrom, P., Blomqvist, C., Saarto, T., Margreiter, R., Asselain, B., Salmon, Rj, Vilcoq, Jr, Rodrigo Arriagada, Hill, C., Laplanche, A., Le, Mg, Spielmann, M., Bruzzi, P., Montanaro, E., Rosso, R., Sertoli, MR, Venturini, M., Amadori, D., Benraadt, J., Kooi, M., Velde, Ao, Dongen, Ja, Vermorken, Jb, Castiglione, M., Cavalli, F., Coates, A., Collins, J., Forbes, J., Gelber, Rd, Goldhirsch, A., Lindtner, J., Price, Kn, Rudenstam, Cm, Senn, Hj, Bliss, Jm, Chilvers, Ced, Coombes, Rc, Hall, E., Marty, M., Borovik, R., Brufman, G., Hayat, H., Robinson, E., Wigler, N., Bonadonna, G., Camerini, T., Palo, G., Del Vecchio, M., Formelli, F., Valagussa, P., Martoni, A., Pannuti, F., Cocconi, G., Colozza, A., Camisa, R., Aogi, K., Takashima, S., Ikeda, T., Inokuchi, K., Sawa, K., Sonoo, H., Korzeniowski, S., Skolyszewski, J., Ogawa, M., Yamashita, J., Bonte, J., Christiaens, R., Paridaens, R., Den Boegart, W., Martin, P., Romain, S., Hakes, T., Hudis, Ca, Wittes, R., Giokas, G., Kondylis, D., Lissaios, B., La Huerta, R., Sainz, Mg, Altemus, R., Cowan, K., Danforth, D., Lichter, A., Lippman, M., O Shaughnessy, J., Pierce, Lj, Steinberg, S., Venzon, D., Zujewski, J., Paradiso, A., Lena, M., Schittulli, F., Myles, Jd, Pater, Jl, Pritchard, Ki, Anderson, S., Bass, G., Brown, A., Bryant, J., Costantino, J., Dignam, J., Fisher, B., Redmond, C., Wieand, S., Wolmark, N., Jackson, Im, Palmer, Mk, Ingle, Jn, Suman, Vj, Bengtsson, No, Jonsson, H., Larsson, Lg, Lythgoe, Jp, Kissin, M., Erikstein, B., Hannisdal, E., Jacobsen, Ab, Varhaug, Je, Gundersen, S., Hauer-Jensen, M., Host, H., Nissen-Meyer, R., Blamey, Rw, Mitchell, Ak, Morgan, Dal, Robertson, Jfr, Di Palma, M., Mathe, G., Misset, Jl, Clark, Rm, Levine, M., Morimoto, K., Takatsuka, Y., Crossley, E., Harris, A., Talbot, D., Taylor, M., Di Blasio, B., Ivanov, V., Semiglazov, V., Brockschmidt, J., Cooper, MR, Ueo, H., Falkson, Ci, A Hern, R., Ashley, S., Powles, Tj, Smith, Ie, Yarnold, Jr, Gazet, Jc, Cocoran, N., Deshpande, N., Di Martino, L., Douglas, P., Lindtner, A., Notter, G., Bryant, Ajs, Ewing, Gh, Firth, La, Krushen-Kosloski, Jl, Foster, L., George, Wd, Stewart, Hj, Stroner, P., Malmstrom, P., Moller, Tr, Ryden, S., Tengrup, I., Tennvall-Nittby, L., Carstenssen, J., Dufmats, M., Hatschek, T., Nordenskjold, B., Soderberg, M., Carpenter, Jt, Albain, K., Crowley, J., Green, S., Martino, S., Osborne, Ck, Ravdin, Pm, Glas, U., Johansson, U., Rutqvist, Le, Singnomklao, T., Wallgren, A., Maibach, R., Thurlimann, B., Brenner, H., Hercbergs, A., Yoshimoto, M., Deboer, G., Paterson, Ahg, Meakin, Jw, Panzarella, T., Shan, Y., Shao, Yf, Wang, X., Zhao, Db, Chen, Zm, Pan, Hc, Bahi, J., Reid, M., Spittle, M., Deutsch, Gp, Senanayake, F., Kwong, Dlw, Bianco, Ar, Carlomagno, C., Laurentiis, M., Placido, S., Buzdar, Au, Smith, T., Bergh, J., Holmberg, L., Liljegren, G., Nilsson, J., Seifert, M., Sevelda, P., Zielinsky, Cc, Buchanan, Rb, Cross, M., Royle, Gt, Dunn, Ja, Hills, Rk, Lee, M., Morrison, Jm, Spooner, D., Litton, A., Chlebowski, Rt, Caffier, H., Faculteit Medische Wetenschappen/UMCG, Guided Treatment in Optimal Selected Cancer Patients (GUTS), Early Breast Cancer Trialists' Collaborative, Group, DE LAURENTIIS, Michelino, and DE PLACIDO, Sabino

Subjects
Oncology, medicine.medical_specialty, Antineoplastic Agents, Hormonal, DEATHS, Ovariectomy, Antineoplastic Agents, Breast Neoplasms, Aged, Anthracyclines, Antineoplastic Combined Chemotherapy Protocols, Cause of Death, Chemotherapy, Adjuvant, Female, Humans, Middle Aged, Neoplasm Metastasis, Neoplasm Recurrence, Local, Ovary, Randomized Controlled Trials as Topic, Receptors, Estrogen, Survival Rate, Tamoxifen, Medicine (all), Breast cancer, MammaPrint, Internal medicine, Receptors, medicine, Chemotherapy, TAMOXIFEN, skin and connective tissue diseases, Survival rate, Adjuvant, Gynecology, Hormonal, medicine.diagnostic_test, Oncotype DX Breast Cancer Assay, business.industry, General Medicine, medicine.disease, Estrogen, Neoplasm Recurrence, Local, Hormonal therapy, Oncotype DX, business, medicine.drug, Epirubicin
Abstract

Background Quinquennial overviews (1985–2000) of the randomised trials in early breast cancer have assessed the 5 year and 10-year effects of various systemic adjuvant therapies on breast cancer recurrence and survival. Here, we report the 10-year and 15-year effects. Methods Collaborative meta-analyses were undertaken of 194 unconfounded randomised trials of adjuvant chemotherapy or hormonal therapy that began by 1995. Many trials involved CMF (cyclophosphamide, methotrexate, fluorouracil), anthracycline-based combinations such as FAC (fluorouracil, doxorubicin, cyclophosphamide) or FEC (fluorouracil, epirubicin, cyclophosphamide), tamoxifen, or ovarian suppression: none involved taxanes, trastuzumab, raloxifene, or modern aromatase inhibitors. Findings Allocation to about 6 months of anthracycline-based polychemotherapy (eg, with FAC or FEC) reduces the annual breast cancer death rate by about 38% (SE 5) for women younger than 50 years of age when diagnosed and by about 20% (SE 4) for those of age 50–69 years when diagnosed, largely irrespective of the use of tamoxifen and of oestrogen receptor (ER) status, nodal status, or other tumour characteristics. Such regimens are significantly (2p=0·0001 for recurrence, 2p For ER-positive disease only, allocation to about 5 years of adjuvant tamoxifen reduces the annual breast cancer death rate by 31% (SE 3), largely irrespective of the use of chemotherapy and of age ( These results combine six meta-analyses: anthracycline-based versus no chemotherapy (8000 women); CMF-based versus no chemotherapy (14 000); anthracycline-based versus CMF-based chemotherapy (14 000); about 5 years of tamoxifen versus none (15 000); about 1–2 years of tamoxifen versus none (33 000); and about 5 years versus 1–2 years of tamoxifen (18 000). Finally, allocation to ovarian ablation or suppression (8000 women) also significantly reduces breast cancer mortality, but appears to do so only in the absence of other systemic treatments. For middle-aged women with ER-positive disease (the commonest type of breast cancer), the breast cancer mortality rate throughout the next 15 years would be approximately halved by 6 months of anthracycline-based chemotherapy (with a combination such as FAC or FEC) followed by 5 years of adjuvant tamoxifen. For, if mortality reductions of 38% (age Interpretation Some of the widely practicable adjuvant drug treatments that were being tested in the 1980s, which substantially reduced 5-year recurrence rates (but had somewhat less effect on 5-year mortality rates), also substantially reduce 15-year mortality rates. Further improvements in long-term survival could well be available from newer drugs, or better use of older drugs.

Published
2005

Catalog

Books, media, physical & digital resources
See catalog results