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1. Schor NF: New approaches to pharmacotherapy of tumors of the nervous system during childhood and adolescence. Pharmacol Ther; 2009 Apr;122(1):44-55
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  • [Title] New approaches to pharmacotherapy of tumors of the nervous system during childhood and adolescence.
  • Malignant tumors of the brain collectively account for 21% of all cancers and 24% of all cancer-related deaths in this age group.
  • Neuroblastoma, a peripheral nervous system tumor, is the most common extracranial solid tumor of childhood, and 65% of children with this tumor have only a 10 or 15% chance of living 5 years beyond the time of initial diagnosis.
  • Novel pharmacological approaches to nervous system tumors are urgently needed.
  • This review presents the role of and current challenges to pharmacotherapy of malignant tumors of the nervous system during childhood and adolescence and discusses novel approaches aimed at overcoming these challenges.

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  • [Cites] Spine (Phila Pa 1976). 2002 Jun 1;27(11):E284-7 [12045531.001]
  • [Cites] Pediatr Hematol Oncol. 2002 Jul-Aug;19(5):337-45 [12078865.001]
  • [Cites] Cancer Chemother Pharmacol. 2002 Jun;49(6):438-44 [12107547.001]
  • [Cites] Cancer Lett. 2002 Aug 8;182(1):53-9 [12175523.001]
  • [Cites] Bone Marrow Transplant. 2002 Aug;30(3):135-40 [12189530.001]
  • [Cites] Oncogene. 2002 Sep 5;21(39):6132-7 [12203125.001]
  • [Cites] Cancer Res. 2002 Sep 1;62(17):4867-75 [12208732.001]
  • [Cites] Neurochem Res. 2002 Aug;27(7-8):665-74 [12374201.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6462-6 [12438236.001]
  • [Cites] Acta Paediatr Suppl. 2004 May;93(445):6-11 [15176712.001]
  • [Cites] J Pediatr Hematol Oncol. 2005 Nov;27(11):604-6 [16282892.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10183-7 [16288004.001]
  • [Cites] Neurobiol Dis. 2005 Dec;20(3):969-85 [16006137.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11735-42 [16357186.001]
  • [Cites] Curr Opin Investig Drugs. 2005 Dec;6(12):1200-14 [16370386.001]
  • [Cites] Cancer Chemother Pharmacol. 2006 Feb;57(3):357-67 [16001169.001]
  • [Cites] Int J Cancer. 2006 May 15;118(10):2584-93 [16353135.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):3238-47 [16540676.001]
  • [Cites] Mol Cancer Ther. 2006 Mar;5(3):593-601 [16546973.001]
  • [Cites] Clin Cancer Res. 2006 Mar 15;12(6):1750-9 [16551859.001]
  • [Cites] Cancer Lett. 2007 May 18;250(1):107-16 [17084521.001]
  • [Cites] Cancer Lett. 2007 May 18;250(1):17-24 [17141950.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 May;66(5):714-22 [17388794.001]
  • [Cites] J Bioenerg Biomembr. 2007 Feb;39(1):35-41 [17549641.001]
  • [Cites] J Neurooncol. 2007 Sep;84(2):119-29 [17361331.001]
  • [Cites] Lancet Oncol. 2007 Aug;8(8):685-95 [17644483.001]
  • [Cites] Cancer Res. 2007 Nov 1;67(21):10351-60 [17974978.001]
  • [Cites] Pediatr Neurosurg. 2008;44(2):97-103 [18230922.001]
  • [Cites] Pediatr Endocrinol Rev. 2008 Feb;5 Suppl 2:720-6 [18317443.001]
  • [Cites] Oncologist. 2008 Jun;13(6):690-9 [18586924.001]
  • [Cites] Pediatr Neurosurg. 2008;44(4):304-12 [18504417.001]
  • [Cites] Pediatr Neurosurg. 2008;44(4):324-8 [18504420.001]
  • [Cites] Cancer Chemother Pharmacol. 2008 Sep;62(4):699-706 [18338171.001]
  • [Cites] Neuro Oncol. 2008 Aug;10(4):599-607 [18577561.001]
  • [Cites] Neurology. 2008 Jul 29;71(5):365-73 [18663182.001]
  • [Cites] Arch Pathol Lab Med. 2008 Aug;132(8):1350-4 [18684041.001]
  • [Cites] J Neurooncol. 2008 Oct;90(1):99-103 [18566744.001]
  • [Cites] J Neurooncol. 2008 Oct;90(1):57-61 [18587536.001]
  • [Cites] Arch Med Res. 2008 Oct;39(7):655-62 [18760193.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6756-63 [12438277.001]
  • [Cites] Int J Cancer. 2003 Jan 20;103(3):387-92 [12471622.001]
  • [Cites] Cancer Detect Prev. 2002;26(6):444-53 [12507229.001]
  • [Cites] Cancer Res. 2003 Mar 1;63(5):1122-9 [12615731.001]
  • [Cites] Methods Mol Biol. 2003;218:71-83 [12616713.001]
  • [Cites] Am J Pathol. 2003 Jul;163(1):321-31 [12819037.001]
  • [Cites] Cancer Lett. 2003 Jul 18;197(1-2):131-5 [12880972.001]
  • [Cites] Cancer Lett. 2003 Jul 18;197(1-2):225-30 [12880986.001]
  • [Cites] Paediatr Drugs. 2003;5(8):533-43 [12895136.001]
  • [Cites] J Pediatr Hematol Oncol. 2003 Aug;25(8):601-5 [12902911.001]
  • [Cites] Cancer Genet Cytogenet. 2003 Oct 1;146(1):41-7 [14499695.001]
  • [Cites] Eur J Cancer. 2003 Oct;39(15):2234-8 [14522384.001]
  • [Cites] Mol Cancer Ther. 2003 Sep;2(9):911-7 [14555710.001]
  • [Cites] Clin Cancer Res. 2004 Jan 1;10(1 Pt 1):84-7 [14734455.001]
  • [Cites] Cancer Res. 2004 Mar 1;64(5):1773-80 [14996739.001]
  • [Cites] Neurosci Lett. 2007 Mar 6;414(2):110-4 [17293044.001]
  • [Cites] Pediatr Blood Cancer. 2007 Apr;48(4):403-7 [16609952.001]
  • [Cites] Cancer Chemother Pharmacol. 2000;45(1):1-8 [10647494.001]
  • [Cites] Pediatr Neurosurg. 2000 Jan;32(1):30-6 [10765136.001]
  • [Cites] J Clin Neurosci. 2000 Jan;7(1):20-3 [10847645.001]
  • [Cites] Drugs. 2000 Jun;59(6):1261-77 [10882162.001]
  • [Cites] Med Pediatr Oncol. 2000 Dec;35(6):597-602 [11107126.001]
  • [Cites] Med Pediatr Oncol. 2000 Dec;35(6):619-22 [11107131.001]
  • [Cites] Cancer Treat Rev. 2000 Dec;26(6):449-62 [11139374.001]
  • [Cites] Eur J Cancer. 2001 May;37(7):930-8 [11313183.001]
  • [Cites] Anticancer Drugs. 2001 Jun;12(5):467-73 [11395575.001]
  • [Cites] Mol Med. 2001 Jun;7(6):393-400 [11474132.001]
  • [Cites] Cancer Res. 2001 Aug 15;61(16):6185-93 [11507071.001]
  • [Cites] J Mol Med (Berl). 2001 Aug;79(8):428-36 [11511973.001]
  • [Cites] Cell Signal. 2001 Jul;13(7):499-505 [11516625.001]
  • [Cites] Oncogene. 2001 Sep 13;20(41):5865-77 [11593392.001]
  • [Cites] Mol Pharmacol. 2002 Jan;61(1):142-9 [11752215.001]
  • [Cites] Int J Cancer. 2002 Mar 1;98(1):128-33 [11857396.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Nov;23(8):500-5 [11878777.001]
  • [Cites] Mol Pharmacol. 2002 Apr;61(4):710-9 [11901208.001]
  • [Cites] Cancer Res. 1996 May 15;56(10):2336-42 [8625308.001]
  • [Cites] J Neurosci. 1996 Jun 15;16(12):3895-9 [8656283.001]
  • [Cites] Arch Biochem Biophys. 1997 Aug 15;344(2):413-23 [9264556.001]
  • [Cites] Curr Pharm Biotechnol. 2004 Oct;5(5):471-80 [15544495.001]
  • [Cites] Ann N Y Acad Sci. 2004 Dec;1028:81-9 [15650234.001]
  • [Cites] J Neurooncol. 2005 Jan;71(2):181-7 [15690136.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Feb 8;102(6):1933-8 [15671173.001]
  • [Cites] Proteomics. 2005 Feb;5(3):796-804 [15682461.001]
  • [Cites] Mol Cell Biol. 2005 Mar;25(6):2320-30 [15743827.001]
  • [Cites] Clin Cancer Res. 2005 Apr 1;11(7):2747-55 [15814657.001]
  • [Cites] Mol Cancer Ther. 2005 Apr;4(4):547-53 [15827327.001]
  • [Cites] Methods Mol Med. 2005;111:267-81 [15911985.001]
  • [Cites] J Clin Pathol. 2005 Jul;58(7):695-9 [15976334.001]
  • [Cites] Mol Cancer Ther. 2005 Jul;4(7):1128-35 [16020671.001]
  • [Cites] Oncogene. 2005 Jul 21;24(31):4965-74 [15897897.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7267-75 [16103078.001]
  • [Cites] J Neurochem. 2005 Sep;94(5):1448-56 [16001965.001]
  • [Cites] Br J Cancer. 2005 Sep 5;93(5):529-37 [16136028.001]
  • [Cites] Neurosci Lett. 2005 Dec 2;389(2):77-82 [16125842.001]
  • [Cites] Neoplasia. 2004 Jan-Feb;6(1):29-40 [15068669.001]
  • [Cites] BMC Cancer. 2003 Mar 26;3:10 [12697075.001]
  • [Cites] Brain Res. 2004 Jun 25;1012(1-2):13-21 [15158156.001]
  • [Cites] J Clin Oncol. 2006 Apr 1;24(10):1546-53 [16575006.001]
  • [Cites] Oncogene. 2006 May 25;25(22):3150-9 [16501609.001]
  • [Cites] Clin Cancer Res. 2006 Jun 1;12(11 Pt 1):3485-93 [16740774.001]
  • [Cites] Hong Kong Med J. 2006 Jun;12(3):222-4 [16760552.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2885-90 [16682723.001]
  • [Cites] Cancer Invest. 2006 Apr-May;24(3):310-7 [16809160.001]
  • [Cites] Inorg Chem. 2006 Aug 7;45(16):6263-8 [16878935.001]
  • [Cites] Mol Cancer Ther. 2006 Sep;5(9):2241-50 [16985058.001]
  • [Cites] Int J Oncol. 2006 Nov;29(5):1295-301 [17016664.001]
  • [Cites] Health Phys. 2007 Jan;92(1):33-9 [17164597.001]
  • [Cites] Pediatr Blood Cancer. 2007 Mar;48(3):311-7 [16609945.001]
  • [Cites] Neoplasia. 2006 Nov;8(11):964-74 [17215959.001]
  • [Cites] BMC Cancer. 2006;6:294 [17181871.001]
  • [Cites] J Clin Oncol. 2007 Feb 1;25(4):376-83 [17264333.001]
  • [Cites] Biochem Pharmacol. 2007 Mar 1;73(5):643-55 [17150196.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1019-29 [17283134.001]
  • [Cites] J Neuropathol Exp Neurol. 2008 Sep;67(9):911-20 [18716553.001]
  • [Cites] Pediatr Blood Cancer. 2008 Nov;51(5):675-8 [18623206.001]
  • [Cites] J Cell Physiol. 2008 Dec;217(3):584-9 [18651562.001]
  • [Cites] J Neurosurg Pediatr. 2008 Oct;2(4):269-72 [18831662.001]
  • [Cites] Ann N Y Acad Sci. 2008 Sep;1138:22-31 [18837879.001]
  • [Cites] Neuro Oncol. 2008 Oct;10(5):675-89 [18701711.001]
  • [Cites] J Child Neurol. 2008 Oct;23(10):1149-59 [18952581.001]
  • [Cites] J Child Neurol. 2008 Oct;23(10):1179-85 [18952584.001]
  • [Cites] Childs Nerv Syst. 2009 Jan;25(1):39-45 [18946672.001]
  • [Cites] Neuro Oncol. 2008 Dec;10(6):1040-60 [18676356.001]
  • [Cites] Curr Cancer Drug Targets. 2004 Jun;4(4):313-26 [15180497.001]
  • [Cites] Oncol Rep. 2004 Aug;12(2):403-9 [15254709.001]
  • [Cites] Chemotherapy. 2004 Jun;50(3):119-26 [15272226.001]
  • [Cites] Br J Cancer. 2004 Aug 2;91(3):425-9 [15266331.001]
  • [Cites] Neurosurg Focus. 2003 Nov 15;15(5):E13 [15323470.001]
  • [Cites] Mol Cancer Ther. 2004 Sep;3(9):1137-46 [15367708.001]
  • [Cites] J Natl Cancer Inst. 2004 Oct 6;96(19):1457-66 [15467035.001]
  • [Cites] Cancer. 1971 Feb;27(2):374-8 [5100400.001]
  • [Cites] Natl Cancer Inst Monogr. 1976 Nov;44:49-54 [1030781.001]
  • [Cites] Cancer Res. 1987 Oct 15;47(20):5411-4 [2820568.001]
  • [Cites] Biochem Pharmacol. 1988 Feb 1;37(3):562-3 [2827689.001]
  • [Cites] J Clin Invest. 1992 Mar;89(3):774-81 [1531835.001]
  • [Cites] Cancer Res. 1994 Jun 15;54(12):3253-9 [8205548.001]
  • [Cites] Cancer Res. 1995 Jun 15;55(12):2576-82 [7780971.001]
  • [Cites] Cancer Res. 1996 Mar 15;56(6):1199-203 [8640797.001]
  • [Cites] Cancer Detect Prev. 2005;29(5):456-63 [16185816.001]
  • (PMID = 19318043.001).
  • [ISSN] 1879-016X
  • [Journal-full-title] Pharmacology & therapeutics
  • [ISO-abbreviation] Pharmacol. Ther.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS038569; United States / NINDS NIH HHS / NS / NS038569-10; United States / NCI NIH HHS / CA / CA074289-09; United States / NCI NIH HHS / CA / R01 CA074289-09; United States / NCI NIH HHS / CA / R01 CA074289; United States / NINDS NIH HHS / NS / R01 NS038569-10
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 141
  • [Other-IDs] NLM/ NIHMS112040; NLM/ PMC2699440
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2. Solomayer EF, Feuerer M, Bai L, Umansky V, Beckhove P, Meyberg GC, Bastert G, Schirrmacher V, Diel IJ: Influence of adjuvant hormone therapy and chemotherapy on the immune system analysed in the bone marrow of patients with breast cancer. Clin Cancer Res; 2003 Jan;9(1):174-80
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  • [Title] Influence of adjuvant hormone therapy and chemotherapy on the immune system analysed in the bone marrow of patients with breast cancer.
  • PURPOSE: Bone marrow is a special compartment for antitumor immunological memory in patients with breastcancer.
  • Until now, the influence of adjuvant systemic therapy on the immune system has only been investigated in peripheral blood and not in bone marrow.
  • In this study, we analyzed the effect of hormone therapy and chemotherapy on the immune activation status in bone marrow.
  • EXPERIMENTAL DESIGN: In 34 patients with breast cancer, bone marrow was aspirated 24 months after primary surgery and adjuvant systemic therapy.
  • The immune system of these patients was compared with that of patients at the time of primary surgery (n = 90).
  • RESULTS: The proportion of all T cells was significantly lower in patients after adjuvant systemic therapy than in patients with primary breast cancer or normal healthy donors.
  • Chemotherapy apparently had a particularly suppressive effect on naïve CD4 T cells and, to a lesser extent, on memory CD4 T cells.
  • Hormone therapy apparently had a significant suppressive effect on both naïve and memory CD8 T cells.
  • The numbers of NK cells (CD56) and of monocytes/macrophages (CD14) recovered rapidly after adjuvant chemotherapy.
  • However, subpopulations with potential antitumor reactivity, such as activated NK and NK T cells, were reduced per long term after chemotherapy.
  • CONCLUSIONS: These findings suggest profound and long-lasting negative effects on the bone marrow immune system by present day adjuvant therapy in breast cancer.
  • [MeSH-major] Bone Marrow Cells / drug effects. Bone Marrow Cells / immunology. Breast Neoplasms / therapy
  • [MeSH-minor] Antigens, CD56 / biosynthesis. Antigens, CD8 / biosynthesis. CD4-Positive T-Lymphocytes / immunology. Female. Hormones / therapeutic use. Humans. Immunophenotyping. Intercellular Adhesion Molecule-1 / biosynthesis. Killer Cells, Natural / drug effects. Killer Cells, Natural / metabolism. Macrophages / drug effects. Monocytes / drug effects. Phenotype. Prognosis. T-Lymphocytes / drug effects. T-Lymphocytes / metabolism

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  • (PMID = 12538466.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antigens, CD8; 0 / Hormones; 126547-89-5 / Intercellular Adhesion Molecule-1
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3. Finlay JL, Dhall G, Boyett JM, Dunkel IJ, Gardner SL, Goldman S, Yates AJ, Rosenblum MK, Stanley P, Zimmerman RA, Wallace D, Pollack IF, Packer RJ, Children's Cancer Group: Myeloablative chemotherapy with autologous bone marrow rescue in children and adolescents with recurrent malignant astrocytoma: outcome compared with conventional chemotherapy: a report from the Children's Oncology Group. Pediatr Blood Cancer; 2008 Dec;51(6):806-11
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  • [Title] Myeloablative chemotherapy with autologous bone marrow rescue in children and adolescents with recurrent malignant astrocytoma: outcome compared with conventional chemotherapy: a report from the Children's Oncology Group.
  • PURPOSE: Children and adolescents with malignant astrocytomas recurring after initial treatment have a dismal prognosis, with only rare patients surviving 1-year beyond recurrence.
  • METHODS: Twenty-seven children and adolescents with malignant astrocytomas [17 glioblastoma multiforme and 10 anaplastic astrocytoma (AA)] following initial tumor progression, received myeloablative chemotherapy followed by autologous marrow rescue with one of three thiotepa and etoposide-based chemotherapy regimens, administered alone (n = 11) or combined with carmustine (n = 5) or carboplatin (n = 11).
  • Time to progression and death following myeloablative chemotherapy for these patients was compared non-randomly with outcome of a contemporaneously treated cohort of similar patients who received only conventional chemotherapy following initial tumor progression.
  • The two cohorts were compared for age, histology, prior therapies, extent of surgical resection at progression, and time from initial diagnosis to progression.
  • RESULTS: Five of 27 children (two with glioblastoma multiforme and three with AA) survive event-free from 8.3 to 13.3 years (median of 11.1 years) following myeloablative chemotherapy.
  • Of 56 children with recurrent malignant astrocytoma who received conventional chemotherapy following initial progression, no patient survives.
  • CONCLUSIONS: Myeloablative chemotherapy with autologous marrow rescue can produce durable remissions in children and young adults with recurrent malignant gliomas, in the setting of minimal residual tumor burden achieved surgically.

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  • [Cites] Anticancer Res. 1999 Jul-Aug;19(4C):3569-74 [10629654.001]
  • [Cites] J Neurooncol. 2006 Mar;77(1):89-94 [16292488.001]
  • [Cites] Clin Cancer Res. 2001 Jan;7(1):32-7 [11205914.001]
  • [Cites] Acta Neurochir (Wien). 2002 Dec;144(12):1265-70; discussion 1270 [12478337.001]
  • [Cites] Cancer Chemother Rep. 1966 Mar;50(3):163-70 [5910392.001]
  • [Cites] J Neurosurg. 1981 Apr;54(4):455-60 [6259300.001]
  • [Cites] J Clin Oncol. 1984 May;2(5):432-7 [6726296.001]
  • [Cites] J Clin Oncol. 1986 May;4(5):639-45 [3009725.001]
  • [Cites] J Clin Oncol. 1987 May;5(5):783-9 [3553437.001]
  • [Cites] J Clin Oncol. 1987 Aug;5(8):1221-31 [3040919.001]
  • [Cites] Br J Cancer. 1988 Dec;58(6):779-82 [2852028.001]
  • [Cites] J Neurooncol. 1989 May;7(1):5-11 [2754456.001]
  • [Cites] J Neurooncol. 1989 Jul;7(2):165-77 [2550594.001]
  • [Cites] J Clin Oncol. 1989 Nov;7(11):1748-56 [2681557.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1990 Feb;18(2):321-4 [2154418.001]
  • [Cites] Cancer. 1990 Dec 15;66(12):2465-9 [2249186.001]
  • [Cites] J Neurooncol. 1990 Dec;9(3):239-48 [1964962.001]
  • [Cites] J Neurooncol. 1991 Apr;10(2):139-44 [1654401.001]
  • [Cites] Med Pediatr Oncol. 1993;21(1):49-53 [8381203.001]
  • [Cites] Cancer. 1993 Jul 1;72(1):271-5 [8508417.001]
  • [Cites] J Clin Oncol. 1995 Jan;13(1):112-23 [7799011.001]
  • [Cites] J Neurooncol. 1994;19(1):69-74 [7815106.001]
  • [Cites] Bone Marrow Transplant. 1996 Mar;17(3):389-94 [8704692.001]
  • [Cites] J Clin Oncol. 1996 Sep;14(9):2495-503 [8823328.001]
  • [Cites] Cancer. 1998 Aug 15;83(4):813-6 [9708950.001]
  • [Cites] J Neurooncol. 1999 May;43(1):43-7 [10448870.001]
  • [Cites] Bone Marrow Transplant. 2000 Jul;26(2):153-60 [10918425.001]
  • (PMID = 18802947.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA013539; United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / CA013539-30; United States / NCI NIH HHS / CA / U10 CA013539-30; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA021765-259003; United States / NCI NIH HHS / CA / P30 CA021765-259003; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / CA 21765
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myeloablative Agonists; 6PLQ3CP4P3 / Etoposide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; U68WG3173Y / Carmustine
  • [Other-IDs] NLM/ NIHMS65899; NLM/ PMC2844080
  • [Investigator] Bleyer A; Khayat A; Sather H; Krailo M; Buckley J; Stram D; Sposto R; Hutchinson R; Matthay K; Gaynon P; Geyer JR; Shurin S; Reaman G; Ortega J; Ruymann F; Weiner M; Blatt J; Lukens J; Wolff L; Neglia J; Lange B; Steinherz P; Breitfeld P; O'Brien R; Cohen H; Fryer C; Wells R; Finklestein J; Feig S; Tannous R; Odom L; Gilchrist G; Barnard D; Wiley J; Ettinger L; Hetherington M; Coccia P; Norris D; Nachman J; Raney B; Baker D; Sanders J; Rausen A; Cairo M
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4. Gérard J, Berdin B, Portier G, Godon A, Tessier-Marteau A, Geneviève F, Zandecki M: [Bone marrow necrosis in two patients with neoplastic disorders]. Ann Biol Clin (Paris); 2007 Nov-Dec;65(6):636-42
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  • [Title] [Bone marrow necrosis in two patients with neoplastic disorders].
  • Bone marrow necrosis is defined by extensive necrosis of the myeloid tissue and bone marrow stroma.
  • Diagnosis is done on characteristic cytological pattern of the bone marrow aspiration and/or biopsy.
  • An haematological malignancy was suspected after observation of a few peripheral blood blast cells, but necrosis was found on the bone marrow aspiration and could not lead to further haematological diagnosis.
  • Within next days, the white blood cell count and the number of blasts increased, leading to the diagnosis of acute monoblastic leukaemia.
  • A chemotherapy was started but the patient died 20 days after admission.
  • The second patient, aged 28, has been hospitalized for severe bleeding a few days after the diagnosis of a metastatic gastric tumour.
  • The bone marrow aspiration, made for the evaluation of a thrombocytopenia, showed a massive necrosis.
  • According to literature, bone marrow necrosis is in most instances secondary to either an haematological malignancy (60%) or to a solid tumour (30%), but only at times observed with a non-malignant disorder.
  • Bone pain, fever, cytopenias and elevated serum lactic dehydrogenase and alkaline phosphatase are frequently reported, but are mostly non specific of the diagnosis in these malignant conditions.
  • Examination of the bone marrow leads to the diagnosis: cells are pycnotic, scarcely recognizable in a background of amorphous extracellular eosinophilic proteinaceous material, and histology shows disappearance of fat spaces with preservation of the bone tissue.
  • Tissue hypoxemia due to microcirculation failure may be the main mechanism leading to the necrosis, whatever the related disorder.
  • Supportive care together with specific therapy of the causal disease must be started promptly.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Monocytic, Acute / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Biopsy. Humans. Male. Necrosis. Neoplasm Metastasis

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  • (PMID = 18039608.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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5. Coutts MA, Borthwick NJ, Hungerford JL, Cree IA: Post-menopausal bleeding: a rare presentation of metastatic uveal melanoma. Pathol Oncol Res; 2006;12(3):184-7
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  • Uveal melanoma differs from cutaneous melanoma in many ways, including its pattern of metastasis, and exhibits latency with clinical evidence of metastasis sometimes appearing many years after primary diagnosis.
  • Further investigation revealed widespread metastatic disease and the patient was not fit for chemotherapy.
  • She died two months after presentation: autopsy revealed metastases in many sites, including the uterus, right ovarian fibroma, kidney, mesentery, liver, lung, thyroid, bone marrow and skin.
  • The immediate cause of death was cardiac tamponade due to a malignant effusion secondary to cardiac metastasis.
  • This case illustrates the widespread metastatic potential of uveal melanoma and highlights the potential for unusual presentation of metastatic disease from this eye tumor.
  • [MeSH-minor] Aged, 80 and over. Endometrial Neoplasms / secondary. Female. Heart Neoplasms / secondary. Humans. Liver Neoplasms / secondary. Neoplasm Metastasis. Postmenopause

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  • [Cites] Acta Ophthalmol (Copenh). 1970;48(6):1113-28 [5537253.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Nov;44(11):4651-9 [14578381.001]
  • [Cites] Am J Ophthalmol. 1985 Nov 15;100(5):666-8 [4061546.001]
  • [Cites] Retina. 1981;1(2):100-6 [7348822.001]
  • [Cites] Gynecol Oncol. 2004 Apr;93(1):252-6 [15047246.001]
  • [Cites] Am J Ophthalmol. 1978 Oct;86(4):557-64 [707604.001]
  • [Cites] Cancer. 1982 Nov 15;50(10):2163-9 [7127256.001]
  • [Cites] J Thorac Cardiovasc Surg. 2005 Dec;130(6):1727-8 [16308029.001]
  • [Cites] Acta Ophthalmol (Copenh). 1963;43:SUPPL 75:1-220 [14050563.001]
  • [Cites] J Med Ethics. 2005 Jun;31(6):360-1 [15923487.001]
  • [Cites] J Med Ethics. 2004 Dec;30(6):561-4 [15574445.001]
  • [Cites] Ophthalmology. 1980 Jun;87(6):549-56 [7413144.001]
  • [Cites] Acta Ophthalmol (Copenh). 1982 Apr;60(2):161-82 [7136531.001]
  • [Cites] Int Ophthalmol. 1985 Mar;7(3-4):175-81 [3997359.001]
  • [Cites] Br J Ophthalmol. 1999 May;83(5):588-94 [10216060.001]
  • [Cites] Arch Ophthalmol. 1999 Nov;117(11):1558-9 [10565531.001]
  • [Cites] Cancer Invest. 1997;15(2):98-105 [9095204.001]
  • [Cites] Acta Cytol. 1978 Nov-Dec;22(6):503-6 [282750.001]
  • [Cites] Chest. 2001 Dec;120(6):2115 [11742953.001]
  • [Cites] APMIS. 1989 Nov;97(11):1018-24 [2590533.001]
  • [Cites] Cancer. 1974 Mar;33(3):729-31 [4815575.001]
  • (PMID = 16998600.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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6. Momiyama N, Kameda K, Mochizuki Y, Natori S, Takekawa Y, Kubo A: [A case of breast cancer with bone marrow and liver metastases responding completely to low-dose weekly paclitaxel combined with toremifene]. Gan To Kagaku Ryoho; 2001 Sep;28(9):1287-9
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  • [Title] [A case of breast cancer with bone marrow and liver metastases responding completely to low-dose weekly paclitaxel combined with toremifene].
  • She was diagnosed with bilateral breast cancer with bone marrow and liver metastases.
  • Myelofunction was recovered after 2 weeks of chemotherapy (CT), and the primary tumors and cervical/axillary lymphadenopathy disappeared after 4 weeks of CT.
  • Bone marrow and liver metastases was no longer detected after 16 weeks of CT, and the case was evaluated as a complete response (CR).
  • The same therapy has been performed for eight months and no evidence of recurrence has been observed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Neoplasms / secondary. Breast Neoplasms / drug therapy. Liver Neoplasms / secondary
  • [MeSH-minor] Adult. Drug Administration Schedule. Female. Humans. Paclitaxel / administration & dosage. Remission Induction. Toremifene / administration & dosage


7. Danet-Desnoyers GA, Luongo JL, Bonnet DA, Domchek SM, Vonderheide RH: Telomerase vaccination has no detectable effect on SCID-repopulating and colony-forming activities in the bone marrow of cancer patients. Exp Hematol; 2005 Nov;33(11):1275-80
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  • [Title] Telomerase vaccination has no detectable effect on SCID-repopulating and colony-forming activities in the bone marrow of cancer patients.
  • OBJECTIVES: The telomerase reverse transcriptase hTERT is a widely expressed tumor-associated antigen recognized by cytotoxic T lymphocytes (CTL).
  • We have previously shown that vaccination of cancer patients against hTERT induces functional anti-tumor CTL in vivo, but it is not known whether hTERT vaccination harms normal cells expressing the enzyme, especially hematopoietic stem cells and progenitors.
  • PATIENTS AND METHODS: We employed colony-forming cell (CFC) assays, long-term in vitro cultures, and nonobese diabetic/severe combined immunodeficient (NOD/SCID) repopulation studies to evaluate the effects of hTERT vaccination on hematopoietic progenitors and stem cells in cancer patients following treatment.
  • RESULTS: Using bone marrow samples obtained from cancer patients before and after vaccination, we found that there was no significant decline in the frequency of granulocyte, macrophage or erythroid CFCs using CFC assays or long-term in vitro cultures.
  • CONCLUSION: These findings suggest that induction of tumor-lytic hTERT-specific T cells in vivo by vaccination does not result in a detectable decline in hematopoietic potential despite the expression of hTERT and major histocompatibility complex class I in bone marrow progenitors and stem cells.
  • Thus, even for self-antigens such as telomerase, tumor immunity does not necessarily involve autoimmunity in normal tissues that share the target.
  • [MeSH-major] Cancer Vaccines / pharmacology. Stem Cells / drug effects. Telomerase / therapeutic use. Vaccination / methods
  • [MeSH-minor] Animals. Antigens, Neoplasm / immunology. Antigens, Neoplasm / therapeutic use. Bone Marrow / drug effects. Breast Neoplasms / therapy. Cells, Cultured. Female. Hematopoietic Stem Cells / drug effects. Histocompatibility Antigens Class I / drug effects. Humans. Male. Mice. Mice, Inbred NOD. Mice, SCID. Prostatic Neoplasms / therapy. T-Lymphocytes, Cytotoxic / drug effects. Treatment Outcome

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  • (PMID = 16263411.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA84050
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Histocompatibility Antigens Class I; EC 2.7.7.49 / Telomerase
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8. Ledzewicz U, Schättler H: Optimal controls for a model with pharmacokinetics maximizing bone marrow in cancer chemotherapy. Math Biosci; 2007 Apr;206(2):320-42
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  • [Title] Optimal controls for a model with pharmacokinetics maximizing bone marrow in cancer chemotherapy.
  • A mathematical model for the depletion of bone marrow under cancer chemotherapy is analyzed as an optimal control problem.
  • The control represents the drug dosage of a single chemotherapeutic agent and pharmacokinetic equations which model its plasma concentration are included.
  • The drug dosages enter the objective linearly.
  • It is shown that optimal controls are bang-bang, i.e. alternate the drug dosages at full dose with rest-periods in between, and that singular controls which correspond to treatment schedules with varying dosages at less than maximum rate are not optimal.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Bone Marrow / drug effects. Models, Biological. Neoplasms / drug therapy
  • [MeSH-minor] Algorithms. Bone Marrow Cells / drug effects. Bone Marrow Cells / pathology. Cell Proliferation / drug effects. Computer Simulation. Humans

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  • (PMID = 16197967.001).
  • [ISSN] 0025-5564
  • [Journal-full-title] Mathematical biosciences
  • [ISO-abbreviation] Math Biosci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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9. Milosevic DP, Kreacic M, Despotovic N, Erceg P, Milanovic P, Mihajlovic G, Mitic S, Davidovic M: The principles of chemotherapy of colorectal cancer in elderly. Adv Gerontol; 2007;20(4):75-8
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  • [Title] The principles of chemotherapy of colorectal cancer in elderly.
  • The prevalence of colorectal cancer (CRC) increases significantly with age, with 40% of patients in Europe being older than 74 years of age at the time of initial diagnosis.
  • The individualized management of the older-aged patient with cancer is based on the answers to the following questions:.
  • 1) will the patient die of cancer or with cancer;.
  • 2) will the patient suffer cancer-related morbidity; and 3) is the patient able to handle the toxicity of treatment?
  • More than chronological age, the following parameters are important when elderly patients are to be treated with antineoplastic agents: general condition, liver function, kidney function and bone marrow status.
  • Frail elderly with malignant disease should not be treated with cytostatic therapy.
  • In the case of fit elderly, the standard chemotherapy (i.e.
  • In elderly ineligible for combination chemotherapy, the capecitabine used orally, as a single-agent therapy, is an important therapeutic option for colorectal cancer.

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  • (PMID = 18383715.001).
  • [ISSN] 1561-9125
  • [Journal-full-title] Advances in gerontology = Uspekhi gerontologii
  • [ISO-abbreviation] Adv Gerontol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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10. Tsangaris GT, Vamvoukakis J, Politis I, Kattamis AC, Tzortzatou-Stathopoulou F: Metallothionein expression prevents apoptosis. II: Evaluation of the role of metallothionein expression on the chemotherapy-induced apoptosis during the treatment of acute leukemia. Anticancer Res; 2000 Nov-Dec;20(6B):4407-11
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  • [Title] Metallothionein expression prevents apoptosis. II: Evaluation of the role of metallothionein expression on the chemotherapy-induced apoptosis during the treatment of acute leukemia.
  • In the present study, the apoptosis preventing effect of hMTs is evaluated in vivo, in order to correlate the apoptotic effect of chemotherapy during the treatment of acute leukemia with the expression of hMTs.
  • The expression of hMTs was studied immunocytochemically in bone marrow smears and peripheral blood cytocentrifugations of 47 children with acute leukemia at diagnosis and during treatment.
  • Apoptosis was quantitatively studied in peripheral blood samples during the induction therapy.
  • Eighteen cases were found to be positive for hMTs expression at diagnosis and the mean apoptosis curve of these cases showed maximal effect on the second day of treatment, the apoptotic action of chemotherapy being completed on the tenth day.
  • The mean apoptosis curve of the hMTs negative cases (29 cases) showed maximal effect on the first day of treatment and the apoptotic action of chemotherapy was completed on the sixth day.
  • When considering the day on which the maximal apoptotic effect appeared and the day on which the apoptotic action of treatment was completed, the results indicated retardation of the chemotherapy-induced apoptosis dependent on hMTs expression, as a result of resistance to treatment.
  • Furthermore, the study of hMTs expression during treatment, showed that although the apoptotic action of chemotherapy eliminates blast cells, a cell population positive for hMTs survived and increased during treatment, since they were able to escape apoptotic cell death.
  • These findings, indicated that in vivo, hMTs constitute a cellular protective mechanism preventing chemotherapy-induced apoptosis, thus regulating the response of patients to treatment.
  • [MeSH-major] Apoptosis / physiology. Bone Marrow / metabolism. Leukemia / metabolism. Metallothionein / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / therapeutic use. Child. Drug Resistance, Neoplasm. Humans. Time Factors

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  • (PMID = 11205280.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 9038-94-2 / Metallothionein
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11. Laughton SJ, Ashton LJ, Kwan E, Norris MD, Haber M, Marshall GM: Early responses to chemotherapy of normal and malignant hematologic cells are prognostic in children with acute lymphoblastic leukemia. J Clin Oncol; 2005 Apr 1;23(10):2264-71
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  • [Title] Early responses to chemotherapy of normal and malignant hematologic cells are prognostic in children with acute lymphoblastic leukemia.
  • PURPOSE: Improved cure rates for children with acute lymphoblastic leukemia (ALL) have resulted from better relapse prediction, using clinical and laboratory features at diagnosis, and more intensive therapy in high-risk patients.
  • More recently, measurements of the variation in the response of malignant lymphoblasts to chemotherapy in vivo have further improved relapse prediction.
  • It is unknown whether the variation in the response of nonmalignant hematologic cells after chemotherapy correlates with the response of lymphoblasts or risk of relapse.
  • PATIENTS AND METHODS: We retrospectively evaluated myelosuppression during induction and consolidation chemotherapy in 227 children uniformly treated for ALL on consecutive Australian and New Zealand Children's Cancer Study Group protocols.
  • The early response to treatment was assessed in a representative subset (n = 62) by determining minimal residual disease (MRD) level by molecular techniques on the end-of-induction bone marrow sample.
  • RESULTS: We found that a slow rate of myeloid recovery at the end of induction chemotherapy, reflected in a low absolute neutrophil count (ANC), was highly predictive of relapse (P < .0001).
  • Multivariate analysis confirmed the independent prognostic significance of MRD and ANC at the end of induction chemotherapy (P < .05).
  • CONCLUSION: We conclude that the responses of normal myeloid cells and malignant lymphoblasts to chemotherapy predict outcome by distinct mechanisms.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neutropenia / chemically induced. Neutropenia / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cohort Studies. Female. Humans. Infant. Male. Multivariate Analysis. Neoplasm, Residual. Predictive Value of Tests. Prognosis. Recurrence. Retrospective Studies. Risk Factors. Treatment Outcome

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  • [ErratumIn] J Clin Oncol. 2005 Aug 1;23(22):5277
  • (PMID = 15800317.001).
  • [ISSN] 0732-183X
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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12. Miser JS, Goldsby RE, Chen Z, Krailo MD, Tarbell NJ, Link MP, Fryer CJ, Pritchard DJ, Gebhardt MC, Dickman PS, Perlman EJ, Meyers PA, Donaldson SS, Moore SG, Rausen AR, Vietti TJ, Grier HE: Treatment of metastatic Ewing sarcoma/primitive neuroectodermal tumor of bone: evaluation of increasing the dose intensity of chemotherapy--a report from the Children's Oncology Group. Pediatr Blood Cancer; 2007 Dec;49(7):894-900
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  • [Title] Treatment of metastatic Ewing sarcoma/primitive neuroectodermal tumor of bone: evaluation of increasing the dose intensity of chemotherapy--a report from the Children's Oncology Group.
  • BACKGROUND: The outcome for patients with Ewing sarcoma family of tumors (ESFTs) of bone with metastases at diagnosis remains poor despite new approaches to treatment.
  • We evaluated whether a dose-intensity chemotherapy regimen improved survival for patients with ESFTs of bone with metastases at diagnosis.
  • METHODS: We entered 60 patients with metastatic ESFTs of bone onto a single arm trial of a new intensive therapy.
  • Treatment consisted of 51-weeks of chemotherapy and local control of the primary with radiation, surgery, or both.
  • RESULTS: Of the 60 patients with metastatic ESFTs of bone enrolled onto this single arm trial, 12 had metastasis to lung only, 7 to bone marrow or bone only, 38 to multiple sites, 2 in other sites and 3 not specified.
  • Six patients (6-year cumulative incidence: 9%) developed second malignant neoplasms and died.
  • The 6-year overall event-free survival (EFS) was 28% (standard error (SE) 6%) and survival (S) was 29% (SE 6%).
  • CONCLUSION: An intensified treatment regimen using higher doses of cyclophosphamide, ifosfamide, and doxorubicin increased toxicity and risk of second malignancy without improving EFS and S.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Neoplasms / therapy. Neoplasm Recurrence, Local / therapy. Neoplasms, Second Primary / chemically induced. Neuroectodermal Tumors, Primitive / therapy. Sarcoma, Ewing / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Critical Care. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Infant. Injections, Subcutaneous. Male. Risk Factors. Survival Rate. Treatment Outcome

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  • [Copyright] 2007 Wiley-Liss, Inc
  • (PMID = 17584910.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA 13539; United States / NCI NIH HHS / CA / U10 CA 30969; United States / NCI NIH HHS / CA / U10 CA 98543
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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13. García-Sanz R: Thalidomide in multiple myeloma. Expert Opin Pharmacother; 2006 Feb;7(2):195-213
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  • Multiple myeloma is an incurable bone marrow cancer, the treatment of which is notoriously difficult.
  • Only modest advances have been achieved using complex polychemotherapeutic regimens, transplant strategies and supportive therapy.
  • In 1999, when new drugs for myeloma were urgently needed, thalidomide was introduced and opened up a completely new line of therapy for the disease.
  • This article reviews the current knowledge of thalidomide in myeloma treatment, focusing especially on the possible mechanisms of action, clinical results and adverse events of this drug.
  • [MeSH-major] Multiple Myeloma / drug therapy. Thalidomide / therapeutic use

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  • (PMID = 16433584.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 4Z8R6ORS6L / Thalidomide
  • [Number-of-references] 186
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14. Smit E, Oberholzer HM, Pretorius E: A review of immunomodulators with reference to Canova. Homeopathy; 2009 Jul;98(3):169-76
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  • The immune response and the function of the immune response regulation process are described, with special reference to cancer and autoimmune disease.
  • Its role in cancer, bone marrow and haematopoiesis as well as macrophage and monocyte activation is reviewed.
  • [MeSH-major] Acquired Immunodeficiency Syndrome / drug therapy. Crotalid Venoms / therapeutic use. Homeopathy / methods. Immunologic Factors / therapeutic use. Plant Extracts / therapeutic use
  • [MeSH-minor] Anti-HIV Agents / therapeutic use. Blood Platelets / drug effects. Bone Marrow Cells / drug effects. Humans. Lymphocytes / drug effects

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  • (PMID = 19647212.001).
  • [ISSN] 1476-4245
  • [Journal-full-title] Homeopathy : the journal of the Faculty of Homeopathy
  • [ISO-abbreviation] Homeopathy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Canova medication; 0 / Crotalid Venoms; 0 / Immunologic Factors; 0 / Plant Extracts
  • [Number-of-references] 43
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15. Cirstea D, Vallet S, Raje N: Future novel single agent and combination therapies. Cancer J; 2009 Nov-Dec;15(6):511-8
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  • [Title] Future novel single agent and combination therapies.
  • Although multiple myeloma (MM) remains an incurable bone marrow cancer, survival rates have dramatically improved over the past decade, most notably in the younger patient population.
  • An understanding of MM biology and improvement in stem-cell transplantation, better supportive care, and novel therapies with higher efficacy and lower toxicity are all responsible for this improvement.
  • Current novel agents targeting tumor and stromal compartments can be conceptualized as those that target membrane-bound receptors (insulin-like growth factor-1, vascular endothelial growth factor, CD40, etc.
  • ), intracellular signaling kinases (Janus kinase/signal transducers and activators of transcription, phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin, mitogen-activated protein kinase pathways), cell cycle molecular machinery (cyclin-dependent kinases inhibitors), epigenetic abnormalities (DNA methyltransferase and histyone deacetylase), protein dynamics (heat-shock protein 90, ubiquitin-proteasome system), and tumor vasculature and microenvironment (angiogenesis, integrins).
  • This review highlights some of these novel agents tested either alone or in combination for the treatment of MM.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Multiple Myeloma / drug therapy
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Boronic Acids / therapeutic use. Bortezomib. Dexamethasone / therapeutic use. Disease Progression. Humans. Melphalan / therapeutic use. Oligopeptides / therapeutic use. Prednisolone / therapeutic use. Protease Inhibitors / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrazines / therapeutic use


16. Huq A, Singh B, Meeker T, Mascarenhas D: The metal-binding domain of IGFBP-3 selectively delivers therapeutic molecules into cancer cells. Anticancer Drugs; 2009 Jan;20(1):21-31
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  • [Title] The metal-binding domain of IGFBP-3 selectively delivers therapeutic molecules into cancer cells.
  • Conventional chemotherapy for cancer has limited specificity for cancer cells.
  • Here, we investigate the possibility of improving the selectivity of chemotherapy by coadministering targeted biological modifier peptides.
  • We show that the 22-amino acid metal-binding transporter domain (MBD) derived from insulin-like growth factor-binding protein-3 selectively targets cancer cells.
  • The rate of MBD uptake by cells was measured using a panel of 54 human cancer cell lines and correlated with MBD cross-linking to cell surface transferrin receptor, caveolin 1, and integrin beta.
  • Gene array data show that MBD uptake correlates with the expression of genes associated with cellular stress-coping mechanisms commonly upregulated in cancer (nuclear factor-kappaB, Hsp-70B).
  • MBD-tagged peptides designed to inhibit such mechanisms have cytotoxic effects on a broad range of human cancer cell lines.
  • The discriminant validity of these peptides as potential cotherapeutic agents was investigated by comparing their cytotoxicity to cancer cell lines versus normal human cell counterparts.
  • Biodistribution data from in-vivo experiments in mice and rats confirm that MBD-tagged peptides and proteins preferably localize to specific tissues, such as kidney and pancreas.
  • Twenty-five-day subcutaneous administration of a three-peptide cocktail (3 mg/kg) in combination with 5-fluorouracil in Rag-2 mice with established CCRF-CEM leukemia significantly reduces splenomegaly and bone marrow cancer cell burden.
  • In a similar experiment using MDA-MB-435 cells, MBD-tagged peptides reduced human cell burden in bone marrow.
  • Taken together, these data suggest that MBD-tagged molecules can be used as highly selective chemosensitizers in the treatment of hematological and disseminated malignancies.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Carriers. Fluorouracil / administration & dosage. Insulin-Like Growth Factor Binding Protein 3 / administration & dosage. Neoplasms / drug therapy. Peptide Fragments / administration & dosage
  • [MeSH-minor] Animals. Biological Transport. Cell Line, Tumor. Cell Survival / drug effects. DNA-Binding Proteins / deficiency. DNA-Binding Proteins / genetics. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic / drug effects. Humans. Injections, Subcutaneous. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout. Protein Structure, Tertiary. Rats. Tissue Distribution. Xenograft Model Antitumor Assays

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  • (PMID = 19342998.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Drug Carriers; 0 / Insulin-Like Growth Factor Binding Protein 3; 0 / Peptide Fragments; 0 / Rag2 protein, mouse; U3P01618RT / Fluorouracil
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17. Kumar L, Verma R, Radhakrishnan VR: Recent advances in the management of multiple myeloma. Natl Med J India; 2010 Jul-Aug;23(4):210-8
MedlinePlus Health Information. consumer health - Multiple Myeloma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Multiple myeloma is a disease of malignant plasma cells in the bone marrow.
  • Interaction of malignant plasma cells with the bone marrow microenvironment plays a key role in the pathogenesis of the disease.
  • Induction therapy with these novel drugs in combination with dexamethasone is associated with higher response rates including complete response in one-fourth of patients with bortezomib combinations.
  • Further consolidation with intensive chemotherapy supported by autologous stem cell transplant in young, eligible patients results in complete response in 50%-70% of patients with improved survival.
  • Simplified criteria for staging, uniform response criteria, more sensitive methods for detection of residual disease (immunofixation and free light chain assay), and recognition of potential adverse cytogenetic and genomic abnormalities have further refined the management of patients with myeloma.
  • Along with earlier diagnosis, improved treatment and better management of complications have resulted in longer disease control and survival with a better quality of life.
  • [MeSH-major] Multiple Myeloma / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic. Cytogenetics. Early Diagnosis. Humans. Neoplasm, Residual / diagnosis. Prognosis. Stem Cell Transplantation

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  • (PMID = 21192514.001).
  • [ISSN] 0970-258X
  • [Journal-full-title] The National medical journal of India
  • [ISO-abbreviation] Natl Med J India
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] India
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18. Chiewvit P, Danchaivijitr N, Sirivitmaitrie K, Chiewvit S, Thephamongkhol K: Does magnetic resonance imaging give value-added than bone scintigraphy in the detection of vertebral metastasis? J Med Assoc Thai; 2009 Jun;92(6):818-29
MedlinePlus Health Information. consumer health - MRI Scans.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does magnetic resonance imaging give value-added than bone scintigraphy in the detection of vertebral metastasis?
  • OBJECTIVE: To determine the role of Magnetic Resonance (MR) imaging for the investigation ofpatients with suspected metastasis to the spine by bone scintigraphy.
  • MATERIAL AND METHOD: Retrospectively reviewed with comparison was made between Technetium-99m Methylene Diphosphonate (99(m)Tc-MDP) bone scintigraphy and corresponding spine MR images in 48 cases of vertebral metastasis at Siriraj Hospital.
  • The intervals between bone scintigraphy and MR images did not exceed 1 month.
  • The authors studied between January 2005 and December 2006 Bone scintigraphy were performed with planar imaging of the entire body and MR imaging was performed with the 1.5 tesla and 3.0 tesla scanner using standard techniques with T1-, T2-weighted images and fat-suppressed T1-weighted images with intravenous administration of gadopentetate dimeglumine.
  • The MR imaging findings were studied: location (cervical or thoracic or lumbar or sacrum spine), number of lesions (solitary or multiple lesions), pattern of enhancement (homogeneous or inhomogeneous), involvement of spinal canal, compression of spinal cord, extradural extension, other incidental findings such as pulmonary metastasis, pleural effusion, lymphadenopathy The final diagnosis was confirmed clinically and followed-up for further management (radiation or surgery) or followed-up by MR imaging (1 month-16 months) and bone scintigraphy (5 months-12 months).
  • Primary neoplasms include breast cancer (n=11), colorectal cancer (n=7), lung cancer (n=6), prostate cancer (n=5), nasopharyngeal cancer (n=5), head and neck cancer (n=3), thyroid cancer (n=2), liver cancer (n=2), esophagus cancer (n=1), bladder cancer (n=1), retroperitoneum cancer (n=1), medulloblastoma (n=1), cervical cancer (n=1), ovarian cancer (n=1), malignant melanoma (n=1).
  • The result of bone scintigraphy and MR imaging is used to evaluate vertebral metastasis: in 44 lesions of bone scintigraphy positive for vertebral metastasis, 40/44 lesions (91%) which MR imaging reveal vertebral metastasis.
  • In 24 lesions of negative of bone scintigraphy for vertebral metastasis, the authors found that 14/24 lesions (58%) showed positive of vertebral metastasis from MR imaging.
  • In this group, the authors recommended a further investigation because 58% of negative bone scintigraphy lesions are depicted by only MR imaging.
  • CONCLUSION: The authors conclude that the MR imaging is more efficient than the bone scintigraphy in detecting vertebral metastasis, especially in the cases that bone scintigraphy are equivocal or negative for vertebral metastasis in high clinical suspicion.
  • Furthermore, MR imaging is important for the further treatment planning such as radiation therapy or systemic chemotherapy.
  • Although MR imaging is useful in the detection of early metastasis that are localized completely in the bone marrow cavity routinely bone scintigraphy remains that most cost-effective method for examination of the entire skeleton.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Diphosphonates. Female. Humans. Male. Middle Aged. Neoplasm Metastasis / radionuclide imaging. Organotechnetium Compounds. Radionuclide Imaging. Retrospective Studies. Spinal Cord Compression. Young Adult

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  • (PMID = 19530588.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Organotechnetium Compounds; 0 / technetium 99m methylene bisphosphonate
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19. Falah M, Schiff D, Burns TM: Neuromuscular complications of cancer diagnosis and treatment. J Support Oncol; 2005 Jul-Aug;3(4):271-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuromuscular complications of cancer diagnosis and treatment.
  • Neuromuscular disorders are a common cause of morbidity in patients with cancer.
  • They can be a direct effect of the primary malignancy, a paraneoplastic effect, or a treatment complication.
  • Malignant neoplasms may infiltrate or compress nerve roots, plexi, and peripheral nerves, causing various sensory and motor symptoms.
  • Electrodiagnostic testing, cerebrospinal fluid analysis, and neuroimaging are helpful in confirming the diagnosis.
  • Treatment for neuropathies of neoplastic origin involves irradiation and chemotherapy, which may improve pain, but usually does not improve neurologic function.
  • Paraneoplastic syndromes are rare and sometimes result from production of autoantibodies directed against neural antigens present in tumor tissues.
  • They commonly precede any symptoms related to the cancer itself, and discovery of such syndromes necessitates a thorough investigation to look for an occult neoplasm.
  • Treatment of the underlying cancer occasionally improves neurologic function.
  • These side effects are a limiting factor in cancer treatment.
  • Other potential neuromuscular problems related to cancer include side effects of steroids and other immunosuppressants, effects secondary to bone marrow transplantation, and infections.
  • [MeSH-major] Neoplasms / complications. Neoplasms / diagnosis. Neuromuscular Diseases / etiology
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Diagnosis, Differential. Electromyography. Humans. Morbidity. Pain / etiology. Paraneoplastic Syndromes / diagnosis. Paraneoplastic Syndromes / etiology. Quality of Life

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  • [CommentIn] J Support Oncol. 2005 Jul-Aug;3(4):287-8 [16092599.001]
  • [CommentIn] J Support Oncol. 2005 Jul-Aug;3(4):285-6 [16092598.001]
  • (PMID = 16092597.001).
  • [ISSN] 1544-6794
  • [Journal-full-title] The journal of supportive oncology
  • [ISO-abbreviation] J Support Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 98
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20. Miser JS, Krailo MD, Tarbell NJ, Link MP, Fryer CJ, Pritchard DJ, Gebhardt MC, Dickman PS, Perlman EJ, Meyers PA, Donaldson SS, Moore S, Rausen AR, Vietti TJ, Grier HE: Treatment of metastatic Ewing's sarcoma or primitive neuroectodermal tumor of bone: evaluation of combination ifosfamide and etoposide--a Children's Cancer Group and Pediatric Oncology Group study. J Clin Oncol; 2004 Jul 15;22(14):2873-6
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  • [Title] Treatment of metastatic Ewing's sarcoma or primitive neuroectodermal tumor of bone: evaluation of combination ifosfamide and etoposide--a Children's Cancer Group and Pediatric Oncology Group study.
  • PURPOSE: One hundred twenty patients with metastatic Ewing's sarcoma or primitive neuroectodermal tumor (PNET) of bone were entered onto a randomized trial evaluating whether the addition of ifosfamide and etoposide to vincristine, doxorubicin, cyclophosphamide, and dactinomycin improved outcomes.
  • METHODS: Thirty-two patients had metastases to lungs only, 12 patients had metastases to bone marrow or bones only, 64 patients had metastases in multiple sites, and five patients had metastases in other sites; seven patients could not be assessed precisely.
  • Treatment comprised 9 weeks of chemotherapy before local control and 42 weeks of chemotherapy; thereafter, regimen A consisted of vincristine 2 mg/m(2), cyclophosphamide 1,200 mg/m(2), and either doxorubicin 75 mg/m(2) or dactinomycin 1.25 mg/m(2).
  • The event-free survival (EFS) and survival (S) at 8 years were 20% (SE, 5%) and 32% (SE, 6%), respectively, for those treated on regimen A and 20% (SE, 6%) and 29% (SE, 6%), respectively, for those treated on regimen B.
  • Patients who had only lung metastases had EFS and S of 32% (SE, 8%) and 41% (SE, 9%), respectively, at 8 years.
  • Two had second malignant neoplasms.
  • CONCLUSION: Adding ifosfamide and etoposide to standard therapy does not improve outcomes of patients with Ewing's sarcoma or PNET of bone with metastases at diagnosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / drug therapy. Neuroectodermal Tumors, Primitive / drug therapy. Sarcoma, Ewing / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Dactinomycin / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Humans. Ifosfamide / administration & dosage. Neoplasm Metastasis. Survival Analysis. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 15254055.001).
  • [ISSN] 0732-183X
  • [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] Clinical Trial; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 1CC1JFE158 / Dactinomycin; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; UM20QQM95Y / Ifosfamide
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21. Burdach S, van Kaick B, Laws HJ, Ahrens S, Haase R, Körholz D, Pape H, Dunst J, Kahn T, Willers R, Engel B, Dirksen U, Kramm C, Nürnberger W, Heyll A, Ladenstein R, Gadner H, Jürgens H, Go el U: Allogeneic and autologous stem-cell transplantation in advanced Ewing tumors. An update after long-term follow-up from two centers of the European Intergroup study EICESS. Stem-Cell Transplant Programs at Düsseldorf University Medical Center, Germany and St. Anna Kinderspital, Vienna, Austria. Ann Oncol; 2000 Nov;11(11):1451-62
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In order to evaluate a possible therapeutic benefit after allogeneic SCT in patients with advanced Ewing tumors (AET), we compared outcome after autologous and allogeneic stem-cell transplantation (SCT).
  • All patients underwent remission induction chemotherapy and local treatment before myeloablative therapy.
  • Seventeen of thirty-six patients had multifocal primary Ewing's tumor, eighteen of thirty-six had early, multiple or multifocal relapse, one of thirty-six patients had unifocal late relapse.
  • We analyzed the following risk factors, that could possibly influence the event-free survival (EFS): number of involved bones, degree of remission at time of SCT, type of graft, indication for SCT, bone marrow infiltration, bone with concomitant lung disease, age at time of diagnosis, pelvic involvement, involved compartment radiation, histopathological diagnosis.
  • Eighteen of thirty-six patients suffered relapse or died of disease, nine of thirty-six died of treatment related toxicity (DOC).
  • Age > or = 17 years at initial diagnosis (P < 0.005) significantly deteriorated outcome.
  • According to the type of graft, EFS was 0.25 +/- 0.08 after autologous and 0.20 +/- 0.13 after allogeneic SCT.
  • CONCLUSIONS: Because of the rather short observation period. secondary malignant neoplasms (SMN) may complicate the future clinical course of some of our patients who are currently viewed as event-free survivors.
  • The patient group was to small to analyze for a possible graft-versus-tumor effect.

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  • (PMID = 11142486.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Interleukin-2
  • [Number-of-references] 56
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22. Fallahi B, Beiki D, Mousavi SA, Gholamrezanezhad A, Eftekhari M, Fard-Esfahani A, Alimoghaddam K, Mirpour S, Eskandarian A, Saghari M: 99mTc-MIBI whole body scintigraphy and P-glycoprotein for the prediction of multiple drug resistance in multiple myeloma patients. Hell J Nucl Med; 2009 Sep-Dec;12(3):255-9
MedlinePlus Health Information. consumer health - Multiple Myeloma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 99mTc-MIBI whole body scintigraphy and P-glycoprotein for the prediction of multiple drug resistance in multiple myeloma patients.
  • Multi-drug resistance (MDR) is a major challenge in the treatment of multiple myeloma (MM).
  • There is low sensitivity of technetium-99m methoxy isobutyl isonitrile ((99m)Tc-MIBI) whole body scan (WBS) in the detection of active MM lesions, because (99m)Tc-MIBI is washed out from malignant cells in the presence of P-glycoprotein (PGP).
  • Thirteen patients had no previous history of treatment and 21 had a history of previous chemo-radiotherapy.
  • The diagnosis and staging of the disease were based upon routine laboratory and clinical criteria like bone marrow plasma cell count, serum M component, calcium, albumin, beta(2)-microglobulin.
  • Measurements of PGP and WBS using (99m)Tc-MIBI were performed before initialization of treatment and the response to treatment was assessed one year later.
  • The baseline (99m)Tc-MIBI WBS were considered positive for the detection of active lesions when at least one area of non-physiologic increased activity was noted.
  • Our results showed that for WBS, the sensitivity, specificity, positive predictive value, negative predictive value and accuracy in active state for the diagnosis of MDR were 38.9%, 62.5%, 70%, 31.2% and 46.1%, respectively.
  • Also the above values for the detection of MDR, using PGP values were 50%, 50%, 69.2%, 30.8% and 50%, respectively.
  • The relative risk of resistant to multiple regimens of chemotherapy after one year follow up in patients with negative to patients with positive (99m)Tc-MIBI WBS was 1.02 (0.60-1.72).
  • In conclusion, we found a low sensitivity of WBS and of PGP in the detection of MDR in patients with active MM.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Multiple Myeloma / diagnosis. Multiple Myeloma / drug therapy. P-Glycoprotein / blood. Radiopharmaceuticals. Technetium Tc 99m Sestamibi. Whole Body Imaging / methods
  • [MeSH-minor] Drug Resistance, Multiple. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Prognosis. Reproducibility of Results. Sensitivity and Specificity. Treatment Outcome

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  • (PMID = 19936339.001).
  • [ISSN] 1790-5427
  • [Journal-full-title] Hellenic journal of nuclear medicine
  • [ISO-abbreviation] Hell J Nucl Med
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / P-Glycoprotein; 0 / Radiopharmaceuticals; 971Z4W1S09 / Technetium Tc 99m Sestamibi
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23. Colovic N, Jurisic V, Colovic M: Malignant histiocytosis with central nervous system involvement and hepatic mucinous cystadenoma in a single patient with review of the literature. J BUON; 2007 Oct-Dec;12(4):539-42
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  • [Title] Malignant histiocytosis with central nervous system involvement and hepatic mucinous cystadenoma in a single patient with review of the literature.
  • Malignant histiocytosis is a rare neoplasm of the reticuloendothelial system characterized by neoplastic proliferation of tissue histiocytes.
  • We report a case of malignant histiocytosis in a 64-year-old female initially operated on for a mucinous cystadenoma of her liver.
  • Histology and immunohistochemistry of the lymph node and bone marrow specimens showed extensive infiltration with atypical cells, resembling malignant histiocytes (CD45, CD45RO, CD11c, CD68, lysozyme, antitrypsin and alpha1-antichymotrypsin positive; CD1, CD35, B-cell and T-cells markers negative).
  • The therapy was switched to CHOP (cyclophosphamide, vincristine, doxorubicin, and prednisone) with disappearance of lymphadenopathy.
  • Bone marrow infiltration by histiocytes was reduced to 20%.
  • Two months after completion of 8 cycles of CHOP she experienced severe headaches, vomiting, loss of consciousness, and developed paraparesis.
  • The patient was then treated with intrathecal methotrexate, prednisolone and cytosine-arabinoside and systemic chemotherapy with etoposide and cyclophosphamide.
  • Her condition improved, she became conscious, her headache diminished, she became mobile but skin and nodal lesions reappeared along with extensive marrow histiocytic infiltration.
  • She finally died 22 months after diagnosis.
  • [MeSH-major] Brain Neoplasms / diagnosis. Histiocytic Sarcoma / diagnosis. Neoplasms, Second Primary / diagnosis


24. Whitehead RP, Moon J, McCachren SS, Hersh EM, Samlowski WE, Beck JT, Tchekmedyian NS, Sondak VK, Southwest Oncology Group: A Phase II trial of vinorelbine tartrate in patients with disseminated malignant melanoma and one prior systemic therapy: a Southwest Oncology Group study. Cancer; 2004 Apr 15;100(8):1699-704
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  • [Title] A Phase II trial of vinorelbine tartrate in patients with disseminated malignant melanoma and one prior systemic therapy: a Southwest Oncology Group study.
  • BACKGROUND: Single-agent chemotherapy with dacarbazine continues to be the standard of care for the treatment of metastatic melanoma.
  • However, there is a large population of patients who have failed first-line therapy and might benefit from additional treatment.
  • In the current study, the authors evaluated the antitumor effects and toxicity of vinorelbine therapy in patients who had failed one prior systemic therapy.
  • METHODS: Patients were required to have a histologic diagnosis of melanoma and be of Stage IV with measurable disease, a Southwest Oncology Group (SWOG) performance status (PS) of 0-2, no evidence of brain metastases, and adequate bone marrow and liver function.
  • Treatment was comprised of vinorelbine given at a dose of 30 mg/m(2)/week by intravenous bolus.
  • The group of previously treated patients may be used to evaluate new agents for the treatment of disseminated melanoma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Melanoma / drug therapy. Skin Neoplasms / drug therapy. Vinblastine / analogs & derivatives. Vinblastine / therapeutic use
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Drug Resistance, Neoplasm. Female. Humans. Injections, Intravenous. Male. Middle Aged. Neoplasm Metastasis

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  • [Copyright] Copyright 2004 American Cancer Society.
  • (PMID = 15073859.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA13612; United States / NCI NIH HHS / CA / CA20319; United States / NCI NIH HHS / CA / CA22433; United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / CA35176; United States / NCI NIH HHS / CA / CA35431; United States / NCI NIH HHS / CA / CA37981; United States / NCI NIH HHS / CA / CA38926; United States / NCI NIH HHS / CA / CA42777; United States / NCI NIH HHS / CA / CA45807; United States / NCI NIH HHS / CA / CA46441; United States / NCI NIH HHS / CA / CA58348; United States / NCI NIH HHS / CA / CA58861; United States / NCI NIH HHS / CA / CA63850; United States / NCI NIH HHS / CA / CA67575; United States / NCI NIH HHS / CA / CA76132
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 5V9KLZ54CY / Vinblastine; Q6C979R91Y / vinorelbine
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25. Koscielniak E, Morgan M, Treuner J: Soft tissue sarcoma in children: prognosis and management. Paediatr Drugs; 2002;4(1):21-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Soft tissue sarcoma in children: prognosis and management.
  • Soft tissue sarcomas (STS) account for approximately 7% of malignant neoplasms in children.
  • The heterogeneity of STS makes the diagnosis and therapy particularly difficult and should be reserved for specialized centers with expertise in treating cancer in children.
  • Major progress in the accuracy of diagnosis and classification has been made by the identification of specific, recurring genetic alterations t(2;13)(q35;q14) and t(1;13)(p36;q14) in alveolar rhabdomyosarcomas (RMS), t(X;18)(p11;q11) for synovial sarcoma (SS) and t(11;22)(q24;q12) or t(21;22)(q22;q12) for Ewing's tumor family.
  • As a result of large multicenter STS studies, such as the North-American Intergroup Rhabdomyosarcoma Study, the German Pediatric Soft Tissue Sarcoma Study Group (CWS), Italian Gruppo Cooperativo Italiano study and Sociètè Internationale d'Oncologie Pèdiatrique (SIOP) Malignant Mesenchymal Tumors study, the identification of more effective treatment strategies and improvement in prognosis have been made in the last 30 years.
  • Prognostic variables were identified and, by exploring novel therapeutic strategies, criteria were established for the use of preoperative chemotherapy and radiotherapy, and primary and delayed second-look surgery.
  • As a result of evaluation of different drugs active in STS, refinements in the utilization of chemotherapy have been made possible.
  • Clinical trials have also been instrumental in defining the late effects of treatment.
  • In STS the following drugs have proven to be useful: dactinomycin, vincristine, alkylating agents such as cyclophosphamide and ifosfamide, as well as anthracyclines such as doxorubicin (adriamycin) and epi-doxorubicin.
  • In general, with conventional fractionation (1 x 1.8 to 2 Gy/day) radiotherapy doses between 40 and 50 Gy should be administered.
  • The German CWS group explored the effectiveness of 32 Gy when accelerated and hyperfractionated, and given simultaneously to chemotherapy, and found it adequate for local tumor control in patients with selected favorable prognostic factors.
  • When treated with a combination of chemotherapy and local therapy, STS showed an event-free survival between 50 and 80% [RMS 70%, extraskeletal Ewing sarcoma (EES) and peripheral neuroectodermal tumor (PNET) circa 50%, and SS 70 to 80%].
  • Age (>10 years), bone, and/or bone marrow metastases are associated with a very poor prognosis (survival rate of about 5%).
  • The value of high dose chemotherapy with hematopoietic stem cell rescue in patients with poor prognostic STS remains unclear and should be performed in controlled studies only.
  • [MeSH-major] Sarcoma / diagnosis. Soft Tissue Neoplasms / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols. Child. Combined Modality Therapy. Humans. Neoplasm Staging. Prognosis. Radiotherapy. Rhabdomyosarcoma / diagnosis. Rhabdomyosarcoma / surgery. Rhabdomyosarcoma / therapy

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  • [Cites] J Clin Oncol. 1997 May;15(5):1831-6 [9164192.001]
  • [Cites] J Pediatr Hematol Oncol. 1997 Nov-Dec;19(6):483-91 [9407933.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 May;23(4):215-20 [11846299.001]
  • [Cites] Pediatr Transplant. 1999;3 Suppl 1:52-8 [10587972.001]
  • [Cites] Med Pediatr Oncol. 1998 May;30(5):269-75 [9544222.001]
  • [Cites] J Clin Oncol. 2001 Jun 1;19(11):2812-20 [11387352.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1052-6 [11287975.001]
  • [Cites] Acta Orthop Scand Suppl. 1999 Jun;285:8-10 [10429615.001]
  • [Cites] Cancer. 1995 Sep 15;76(6):1073-85 [8625211.001]
  • [Cites] J Clin Oncol. 1997 Apr;15(4):1544-52 [9193351.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):945-52 [9508177.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3706-19 [10577842.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(1):204-13 [10623711.001]
  • [Cites] N Engl J Med. 1991 Mar 21;324(12):808-15 [1997853.001]
  • [Cites] J Clin Oncol. 1999 Sep;17(9):2796-803 [10561355.001]
  • [Cites] N Engl J Med. 1999 Jul 29;341(5):342-52 [10423470.001]
  • [Cites] J Clin Oncol. 1993 Feb;11(2):262-70 [8426203.001]
  • [Cites] J Pediatr Hematol Oncol. 2000 Mar-Apr;22(2):112-8 [10779023.001]
  • [Cites] Bone Marrow Transplant. 1997 Feb;19(3):227-31 [9028550.001]
  • [Cites] N Engl J Med. 2000 Sep 14;343(11):750-8 [10984562.001]
  • [Cites] J Clin Oncol. 1990 Mar;8(3):443-52 [2407808.001]
  • [Cites] J Clin Oncol. 1996 Oct;14(10):2653-65 [8874324.001]
  • [Cites] Curr Opin Oncol. 1994 Jul;6(4):397-402 [7803541.001]
  • [Cites] Eur J Cancer. 1998 Jun;34(7):1050-62 [9849454.001]
  • [Cites] J Clin Oncol. 2001 Jun 15;19(12):3091-102 [11408506.001]
  • [Cites] J Clin Oncol. 1995 Mar;13(3):610-30 [7884423.001]
  • [Cites] Med Pediatr Oncol. 1991;19(2):89-95 [2011101.001]
  • [Cites] Acta Orthop Scand Suppl. 1999 Jun;285:30-40 [10429619.001]
  • [Cites] Cancer. 1992 Nov 15;70(10):2557-67 [1482503.001]
  • [Cites] Arch Orthop Trauma Surg. 2000;120(1-2):65-9 [10653107.001]
  • [Cites] Klin Padiatr. 1999 Jul-Aug;211(4):291-5 [10472564.001]
  • (PMID = 11817983.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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26. Amare PS, Baisane C, Saikia T, Nair R, Gawade H, Advani S: Fluorescence in situ hybridization: a highly efficient technique of molecular diagnosis and predication for disease course in patients with myeloid leukemias. Cancer Genet Cytogenet; 2001 Dec;131(2):125-34
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  • [Title] Fluorescence in situ hybridization: a highly efficient technique of molecular diagnosis and predication for disease course in patients with myeloid leukemias.
  • The accuracy of cytogenetic diagnosis in the management of hematological malignancies has improved significantly over the past 10 years.
  • Fluorescence in situ hybridization (FISH), a technique of molecular cytogenetics, has played a pivotal role in the detection of unique sub-microscopic chromosomal rearrangements that helped in the identification of chromosomal loci, which contain genes involved in leukemogenesis.
  • We studied the feasibility and sensitivity of the FISH technique for molecular analysis of translocations markers, t(9;22) and t(15;17) for accurate molecular diagnosis and for monitoring the disease in 21 patients with chronic myeloid leukemia (CML) who received interferon-alpha and/or chemotherapy (7 patients), bone marrow transplantation (14 patients), and 14 patients with acute promyelocytic leukemia (APL) who received all-trans-retinoic acid (ATRA) and/or chemotherapy.
  • We also applied conventional karyotyping (CK) for identification of t(9;22) and t(15;17) at diagnosis.
  • Evaluation of Ph positive status of CML marrow at diagnosis by CK (100% Ph+ cells) and FISH (80-92% BCR-ABL fusion) pointed the existence of dormant clone of normal residual hematopoietic cells along with actively proliferating clones of Ph positive cells.
  • Since the time of FISH analysis, 5 to 7 patients with higher fraction of leukemic cells (5-11%) relapsed within a short period (1-7 months).
  • Our data show that FISH has a potential to detect and measure the fraction of aberrant malignant cells in remission marrows, induced by BMT in CML and chemotherapy in APL.
  • In the present studies, FISH on interphase cells also demonstrated its efficiency in the molecular diagnosis by its ability to detect BCR-ABL and PML-RARA fusion in CML with masked/variant Ph and t(15;17) negative APL, respectively.
  • The efficiency of technique in molecular diagnosis was also proved in one of the CML patients who progressed to myeloid blastic phase where interphase FISH could identify an extra BCR-ABL fusion on both chromosomes 9 indicating insertion of BCR into ABL and its duplication.
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Fusion Proteins, bcr-abl / genetics. Humans. Karyotyping. Male. Middle Aged. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Predictive Value of Tests. Sensitivity and Specificity

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  • (PMID = 11750052.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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27. Quilon JM, Gaskin TA, Ludwig AS, Alley C: Collision tumor: invasive ductal carcinoma in association with mucosa-associated lymphoid tissue (MALT) lymphoma in the same breast. South Med J; 2006 Feb;99(2):164-7
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  • [Title] Collision tumor: invasive ductal carcinoma in association with mucosa-associated lymphoid tissue (MALT) lymphoma in the same breast.
  • Synchronous occurrence of multiple neoplastic processes is uncommon and the relationship between breast cancer with lymphoproliferative diseases is unusual as well.
  • Furthermore, breast involvement by malignant lymphoma is a rare event and primary breast mucosa-associated lymphoid tissue (MALT) lymphoma is even rarer.
  • We report a patient with synchronous occurrence of malignant lymphoma of MALT type and ductal carcinoma of the breast, presenting as "collision tumor," invading each other and occurring as a single mass in the breast.
  • Staging bone marrow biopsy did not show involvement by malignant lymphoma or carcinoma.
  • Our patient was treated with chemotherapy for the lymphoma.
  • She also received radiotherapy and aromatase inhibitor as adjuvant therapy for the breast carcinoma.
  • [MeSH-minor] Biopsy. Bone Marrow / pathology. Diagnosis, Differential. Female. Humans. Mastectomy. Middle Aged. Neoplasm Invasiveness

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  • [CommentIn] South Med J. 2006 Feb;99(2):108-10 [16509544.001]
  • (PMID = 16509555.001).
  • [ISSN] 0038-4348
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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28. McIlwain L, Sokol L, Moscinski LC, Saba HI: Acute myeloid leukemia mimicking primary testicular neoplasm. Presentation of a case with review of literature. Eur J Haematol; 2003 Apr;70(4):242-5
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  • [Title] Acute myeloid leukemia mimicking primary testicular neoplasm. Presentation of a case with review of literature.
  • Further work-up with computed tomography of the chest, abdomen and pelvis revealed massive retroperitoneal, peripancreatic and mediastinal lymphadenopathy, suggesting primary testicular neoplasm.
  • The patient was subjected to right orchiectomy that showed infiltration of testicular tissue with malignant cells, originally misinterpreted as undifferentiated carcinoma.
  • Bone marrow (BM) aspirate and biopsy demonstrated replacement of marrow with immature myeloid cells.
  • Both the morphology and immunophenotype of the blast cells were consistent with AML type M4 (acute myelo-monocytic leukemia), using French-American-British (FAB) classification.
  • The patient received standard induction chemotherapy with cytosine arabinoside (ARA-C) and daunorubicin followed with two cycles of consolidation therapy with high dose ARA-C, which resulted in remission of BM disease and resolution of lymphadenopathy and left testicular masses.
  • After the second cycle of consolidation therapy, the patient developed sepsis that was complicated by refractory disseminated intravascular coagulopathy.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / diagnosis. Leukemic Infiltration / diagnosis. Testicular Neoplasms / diagnosis. Testis / pathology
  • [MeSH-minor] Abdominal Pain / etiology. Adult. Antigens, CD / analysis. Antigens, Neoplasm / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Diagnosis, Differential. Diagnostic Errors. Disseminated Intravascular Coagulation / etiology. Estradiol / blood. Fatal Outcome. Gynecomastia / etiology. Humans. Immunophenotyping. Karyotyping. Male. Multiple Organ Failure / etiology. Neoplasm Proteins / analysis. Neoplastic Stem Cells / chemistry. Neoplastic Stem Cells / pathology. Peroxidase / analysis

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  • (PMID = 12656749.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 04079A1RDZ / Cytarabine; 4TI98Z838E / Estradiol; EC 1.11.1.7 / Peroxidase; ZS7284E0ZP / Daunorubicin
  • [Number-of-references] 19
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29. Mimeault M, Batra SK: Targeting of cancer stem/progenitor cells plus stem cell-based therapies: the ultimate hope for treating and curing aggressive and recurrent cancers. Panminerva Med; 2008 Mar;50(1):3-18
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  • [Title] Targeting of cancer stem/progenitor cells plus stem cell-based therapies: the ultimate hope for treating and curing aggressive and recurrent cancers.
  • The rapid progression from aggressive primary cancers into locally advanced and invasive and/or metastatic diseases remains a big obstacle for an early diagnosis and curative therapeutic intervention for cancer patients.
  • The late-stage leukemias and disseminated and metastatic sarcomas, melanomas, brain tumors and epithelial cancers are the devastating diseases associated with a high rate of recurrence after treatment with the conventional clinical therapies including surgery, ionizing radiation, hormonal therapy and systemic chemotherapy, which generally lead to the death of patients.
  • Therefore, the establishment of the molecular events underlying cancer initiation and progression into locally invasive and metastatic diseases is of major interest in basic cancer research as well as for the development of new effective clinical therapeutic options against the recurrent and lethal cancers.
  • Recent advances have led to the identification of specific oncogenic products that are implicated in the malignant transformation of adult stem/progenitor cells into leukemic or tumorigenic and migrating cancer stem/progenitor cells during cancer progression.
  • Of therapeutic interest, the molecular targeting of deregulated signaling elements in cancer stem/progenitor cells and their local microenvironment represents a new potential strategy for the development of more effective clinical treatments against aggressive cancers.
  • Particularly, the combined use of chemotherapeutic drugs to eradicate cancer-initiating cells with hematopoietic stem cell or genetically-modified stem cell transplant is emerging as potential cancer treatments that hold great promise in the area of clinical cancer research.
  • These targeting and stem cell-based therapies may offer the ultimate hope for treating and even curing the patients diagnosed with locally advanced cancers at high risk of recurrence, metastatic and/or relapsed cancers in the clinics.

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  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:82-101 [14633778.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15178-83 [14645703.001]
  • [Cites] Blood. 2004 Feb 1;103(3):1166-70 [14512297.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2332-6 [14630803.001]
  • [Cites] Cancer Lett. 2004 Feb 20;204(2):213-24 [15013220.001]
  • [Cites] Blood Rev. 2004 Sep;18(3):167-79 [15183901.001]
  • [Cites] Eur J Cancer. 2004 Jul;40(10):1522-9 [15196536.001]
  • [Cites] Crit Rev Oncol Hematol. 2004 Jul;51(1):1-28 [15207251.001]
  • [Cites] Nat Immunol. 2004 Jul;5(7):738-43 [15170211.001]
  • [Cites] Transfusion. 2004 Jul;44(7):1087-97 [15225252.001]
  • [Cites] Panminerva Med. 2004 Mar;46(1):49-59 [15238881.001]
  • [Cites] Skin Pharmacol Physiol. 2004 Jul-Aug;17(4):153-66 [15258446.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] N Engl J Med. 2004 Sep 2;351(10):998-1012 [15342808.001]
  • [Cites] Oncogene. 2004 Sep 20;23(43):7274-82 [15378087.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 28;101(39):14228-33 [15381773.001]
  • [Cites] Am J Pathol. 2006 Dec;169(6):2223-35 [17148683.001]
  • [Cites] Expert Opin Biol Ther. 2007 Jan;7(1):41-51 [17150018.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Neurobiol Dis. 2007 Feb;25(2):217-29 [17141509.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1030-7 [17283135.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1113-20 [17283145.001]
  • [Cites] Stem Cells. 2007 Feb;25(2):371-9 [17038675.001]
  • [Cites] J BUON. 2006 Oct-Dec;11(4):433-8 [17309174.001]
  • [Cites] Nature. 2007 Feb 22;445(7130):851-7 [17314971.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):2187-96 [17332349.001]
  • [Cites] Best Pract Res Clin Haematol. 2007 Mar;20(1):57-65 [17336255.001]
  • [Cites] J Natl Compr Canc Netw. 2007 Feb;5(2):203-15 [17335689.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4635-40 [17299092.001]
  • [Cites] Genes Dev. 2007 Jun 1;21(11):1382-95 [17510286.001]
  • [Cites] Pediatr Blood Cancer. 2007 Aug;49(2):196-8 [17417796.001]
  • [Cites] Mol Vis. 2007;13:823-32 [17615543.001]
  • [Cites] Carcinogenesis. 2007 Jul;28(7):1379-86 [17341655.001]
  • [Cites] Clin Exp Metastasis. 2007;24(5):353-62 [17487557.001]
  • [Cites] Clin Pharmacol Ther. 2007 Sep;82(3):252-64 [17671448.001]
  • [Cites] Stem Cells Dev. 2007 Aug;16(4):637-48 [17784837.001]
  • [Cites] Stem Cells. 2007 Sep;25(9):2302-11 [17569791.001]
  • [Cites] Ann Oncol. 2007 Oct;18(10):1605-19 [17355951.001]
  • [Cites] Carcinogenesis. 2007 Sep;28(9):2053-8 [17434930.001]
  • [Cites] Int J Cancer. 2007 Nov 15;121(10):2125-31 [17565741.001]
  • [Cites] Clin Exp Metastasis. 2007;24(7):485-93 [17653825.001]
  • [Cites] Pigment Cell Res. 2007 Dec;20(6):458-65 [17935489.001]
  • [Cites] Cancer Treat Rev. 2008 May;34(3):247-58 [18226859.001]
  • [Cites] Stem Cell Rev. 2008 Spring;4(1):27-49 [18288619.001]
  • [Cites] Blood. 2000 Feb 1;95(3):1007-13 [10648416.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1166-73 [11493466.001]
  • [Cites] Lancet Oncol. 2002 Jan;3(1):35-43 [11905603.001]
  • [Cites] Nat Immunol. 2002 Jul;3(7):687-94 [12068293.001]
  • [Cites] Nat Rev Cancer. 2002 Jun;2(6):442-54 [12189386.001]
  • [Cites] Cancer Cell. 2002 Sep;2(3):175-8 [12242149.001]
  • [Cites] Cancer Res. 2002 Oct 15;62(20):5657-63 [12384520.001]
  • [Cites] Nat Rev Cancer. 2002 Nov;2(11):826-35 [12415253.001]
  • [Cites] Cancer Res. 2002 Dec 15;62(24):7170-4 [12499252.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] Pathol Oncol Res. 2003;9(1):13-9 [12704441.001]
  • [Cites] Growth Factors. 2003 Mar;21(1):1-14 [12795332.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):685-94 [12951587.001]
  • [Cites] Cell Mol Life Sci. 2005 Aug;62(16):1863-70 [16003493.001]
  • [Cites] Nat Rev Cancer. 2005 Sep;5(9):744-9 [16148886.001]
  • [Cites] Mini Rev Med Chem. 2005 Sep;5(9):805-24 [16178723.001]
  • [Cites] Ernst Schering Found Symp Proc. 2006;(5):155-79 [17939301.001]
  • [Cites] Oncologist. 2007 Oct;12(10):1237-46 [17962617.001]
  • [Cites] Front Biosci. 2008;13:1887-91 [17981676.001]
  • [Cites] J Cell Mol Med. 2007 Sep-Oct;11(5):981-1011 [17979879.001]
  • [Cites] Med Princ Pract. 2008;17(1):84-5 [18059108.001]
  • [Cites] Br J Hosp Med (Lond). 2007 Nov;68(11):589-93 [18087845.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Feb;49(2):636-43 [18235009.001]
  • [Cites] J Clin Oncol. 2008 Feb 1;26(4):626-32 [18235122.001]
  • [Cites] Nat Clin Pract Oncol. 2008 Feb;5(2):102-11 [18235442.001]
  • [Cites] Nat Rev Cancer. 2006 Jun;6(6):425-36 [16723989.001]
  • [Cites] Mol Cancer Ther. 2006 May;5(5):1299-308 [16731763.001]
  • [Cites] Eur J Cancer. 2006 Jun;42(9):1309-15 [16682183.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6063-71 [16778178.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2891-6 [16782928.001]
  • [Cites] J Cell Biochem. 2006 Jul 1;98(4):757-69 [16598744.001]
  • [Cites] Hepatology. 2006 Jul;44(1):240-51 [16799977.001]
  • [Cites] Curr Drug Targets. 2006 Jul;7(7):861-79 [16842217.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 25;103(30):11154-9 [16849428.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7011-21 [15466194.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7445-52 [16885340.001]
  • [Cites] Leukemia. 2006 Sep;20(9):1533-8 [16871285.001]
  • [Cites] Cell Cycle. 2006 Aug;5(15):1597-601 [16880743.001]
  • [Cites] Pediatr Blood Cancer. 2006 Oct 15;47(5):560-6 [16395684.001]
  • [Cites] Leuk Lymphoma. 2006 Aug;47(8):1545-52 [16966265.001]
  • [Cites] Mol Cancer Res. 2006 Sep;4(9):607-19 [16966431.001]
  • [Cites] Bone Marrow Transplant. 2006 Oct;38(7):493-9 [16980997.001]
  • [Cites] Hum Mol Genet. 2006 Oct 15;15 Spec No 2:R210-9 [16987886.001]
  • [Cites] Ann Oncol. 2006 Nov;17(11):1620-4 [16600978.001]
  • [Cites] Stem Cells. 2006 Nov;24(11):2319-45 [16794264.001]
  • [Cites] Klin Padiatr. 2006 Nov-Dec;218(6):321-6 [17080334.001]
  • [Cites] Int J Cancer. 2007 Jan 1;120(1):160-9 [17013895.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 7;103(45):16870-5 [17077147.001]
  • [Cites] Panminerva Med. 2006 Sep;48(3):165-74 [17122752.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:219-25 [17124064.001]
  • [Cites] J Cell Mol Med. 2006 Oct-Dec;10(4):857-65 [17125590.001]
  • [Cites] J Cell Mol Med. 2006 Oct-Dec;10(4):995-1013 [17125601.001]
  • [Cites] Clin Invest Med. 2006 Oct;29(5):301-11 [17144440.001]
  • [Cites] Exp Cell Res. 2006 Nov 15;312(19):3701-10 [17046749.001]
  • [Cites] Mol Vis. 2005;11:729-37 [16179903.001]
  • [Cites] Hematology. 2005 Oct;10(5):349-59 [16203604.001]
  • [Cites] Expert Rev Anticancer Ther. 2005 Oct;5(5):835-46 [16221053.001]
  • [Cites] Expert Rev Vaccines. 2005 Oct;4(5):699-710 [16221071.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):323-35 [16226707.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9328-37 [16230395.001]
  • [Cites] Chest. 2005 Oct;128(4):2268-73 [16236883.001]
  • [Cites] Pancreas. 2005 Nov;31(4):301-16 [16258363.001]
  • [Cites] Curr Opin Neurol. 2005 Dec;18(6):639-44 [16280674.001]
  • [Cites] Cancer Lett. 2005 Dec 18;230(2):199-210 [16297706.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2304-12 [16193083.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10946-51 [16322242.001]
  • [Cites] Haematologica. 2007 Mar;92(3):323-31 [17339181.001]
  • [Cites] PLoS One. 2007;2(3):e293 [17356702.001]
  • [Cites] Br J Haematol. 2007 Apr;137(1):20-35 [17359369.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):967-78 [17363490.001]
  • [Cites] Semin Cancer Biol. 2007 Jun;17(3):241-7 [16839774.001]
  • [Cites] Bone Marrow Transplant. 2007 Apr;39(7):397-400 [17322933.001]
  • [Cites] Cancer Metastasis Rev. 2007 Mar;26(1):203-14 [17273942.001]
  • [Cites] J Thorac Oncol. 2007 Apr;2(4):327-43 [17409807.001]
  • [Cites] Adv Cancer Res. 2007;97:25-60 [17419940.001]
  • [Cites] Exp Clin Endocrinol Diabetes. 2007 Mar;115(3):160-5 [17427103.001]
  • [Cites] Oncology. 2006;71(1-2):32-9 [17344669.001]
  • [Cites] Exp Gerontol. 2007 May;42(5):385-90 [17275237.001]
  • [Cites] Curr Eye Res. 2007 Mar;32(3):281-90 [17453948.001]
  • [Cites] Leukemia. 2007 May;21(5):926-35 [17330101.001]
  • [Cites] Nat Rev Drug Discov. 2006 Aug;5(8):649-59 [16883303.001]
  • [Cites] Leukemia. 2007 May;21(5):949-55 [17361218.001]
  • [Cites] Cancer Cell. 2007 May;11(5):421-9 [17482132.001]
  • [Cites] Crit Rev Oncol Hematol. 2007 Jun;62(3):214-26 [17368038.001]
  • [Cites] Philos Trans R Soc Lond B Biol Sci. 2007 Jun 29;362(1482):959-71 [17317642.001]
  • [Cites] Trends Mol Med. 2007 May;13(5):192-9 [17383232.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Jun 15;357(4):1084-9 [17466949.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4807-15 [17510410.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4827-33 [17510412.001]
  • [Cites] J Cell Sci. 2007 Feb 1;120(Pt 3):468-77 [17227796.001]
  • [Cites] Nature. 2004 Oct 7;431(7009):707-12 [15361885.001]
  • [Cites] Nature. 1984 Feb 2-8;307(5950):471-3 [6694739.001]
  • [Cites] J Clin Oncol. 1998 Jan;16(1):165-72 [9440739.001]
  • [Cites] Nat Med. 1998 Sep;4(9):1038-45 [9734397.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):324-31 [15549094.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):396-401 [15549107.001]
  • [Cites] Springer Semin Immunopathol. 2004 Nov;26(1-2):95-108 [15378271.001]
  • [Cites] Oncogene. 2004 Dec 16;23(58):9392-400 [15558011.001]
  • [Cites] J Clin Oncol. 2005 Jan 10;23(2):293-300 [15637392.001]
  • [Cites] Carcinogenesis. 2005 Feb;26(2):495-502 [15513931.001]
  • [Cites] Cell Cycle. 2004 Dec;3(12):1502-5 [15611623.001]
  • [Cites] Nat Rev Cancer. 2005 Feb;5(2):91-101 [15685194.001]
  • [Cites] J Neurooncol. 2005 Jan;71(1):33-8 [15719272.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):275-84 [15803154.001]
  • [Cites] Bone Marrow Transplant. 2005 Apr;35(8):763-6 [15750608.001]
  • [Cites] Med Hypotheses. 2005;64(6):1182-7 [15823713.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3025-9 [15833827.001]
  • [Cites] Am J Clin Oncol. 2005 Jun;28(3):281-8 [15923802.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4490-5 [15930263.001]
  • [Cites] Breast Cancer Res. 2005;7(3):86-95 [15987436.001]
  • [Cites] J Pediatr Surg. 2005 Jun;40(6):936-41; discussion 941 [15991174.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5506-11 [15994920.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6207-19 [16024622.001]
  • [Cites] Neoplasia. 2005 Jun;7(6):623-9 [16036113.001]
  • [Cites] Lancet. 2005 Jul 23-29;366(9482):318-20 [16039336.001]
  • [Cites] Br J Haematol. 2005 Aug;130(3):373-81 [16042686.001]
  • [Cites] Cancer Cell. 2005 Aug;8(2):119-30 [16098465.001]
  • [Cites] N Engl J Med. 2005 Aug 25;353(8):811-22 [16120861.001]
  • [Cites] Cancer Cell. 2008 Feb;13(2):153-66 [18242515.001]
  • [Cites] Cell Death Differ. 2008 Mar;15(3):504-14 [18049477.001]
  • [Cites] J Cell Physiol. 2008 May;215(2):287-91 [18205182.001]
  • [Cites] BMC Cancer. 2008;8:48 [18261235.001]
  • [Cites] Growth Factors. 2007 Dec;25(6):400-16 [18365871.001]
  • [Cites] Cell Stem Cell. 2007 Sep 13;1(3):313-23 [18371365.001]
  • [Cites] Endocr Rev. 2008 Apr;29(2):234-52 [18292464.001]
  • [Cites] Clin Pharmacol Ther. 2008 May;83(5):673-91 [17786164.001]
  • [Cites] Breast Cancer Res. 2008;10(1):R10 [18241344.001]
  • [Cites] Semin Oncol. 2005 Dec;32(6 Suppl 9):S78-81 [16399438.001]
  • [Cites] J Invest Dermatol. 2006 Jan;126(1):142-53 [16417230.001]
  • [Cites] J Exp Med. 2006 Jan 23;203(1):73-85 [16380511.001]
  • [Cites] Int J Cancer. 2006 Feb 15;118(4):1022-31 [16108016.001]
  • [Cites] Cancer. 2006 Feb 15;106(4):859-66 [16419074.001]
  • [Cites] Nat Rev Drug Discov. 2006 Feb;5(2):147-59 [16424916.001]
  • [Cites] Cell Cycle. 2006 Feb;5(4):452-6 [16479164.001]
  • [Cites] Oncogene. 2006 Mar 16;25(12):1696-708 [16449977.001]
  • [Cites] J Pediatr Surg. 2006 Apr;41(4):624-32; discussion 624-32 [16567167.001]
  • [Cites] Stem Cells. 2006 Mar;24(3):506-13 [16239320.001]
  • [Cites] J Clin Oncol. 2006 Apr 20;24(12):1924-31 [16567768.001]
  • [Cites] Hum Cell. 2006 Feb;19(1):24-9 [16643604.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4553-7 [16651403.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4532-9 [16469872.001]
  • [Cites] Leuk Lymphoma. 2006 Jan;47(1):1-7 [16321820.001]
  • [Cites] Neoplasia. 2005 Nov;7(11):967-76 [16331882.001]
  • [Cites] Nature. 2005 Dec 8;438(7069):820-7 [16341007.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11459-68 [16357154.001]
  • [Cites] Carcinogenesis. 2006 Jan;27(1):1-22 [16195239.001]
  • [Cites] Nat Rev Neurosci. 2006 Jan;7(1):75-84 [16371952.001]
  • [Cites] Adv Cancer Res. 2007;96:23-50 [17161675.001]
  • [Cites] Mol Cancer. 2006;5:67 [17140455.001]
  • [Cites] Mod Pathol. 2007 Jan;20(1):102-7 [17143262.001]
  • [Cites] Semin Diagn Pathol. 2006 May;23(2):63-9 [17193819.001]
  • [Cites] PLoS Med. 2006 Dec;3(12):e482 [17194186.001]
  • [Cites] Nature. 2007 Jan 4;445(7123):111-5 [17122771.001]
  • [Cites] PLoS One. 2006;1:e23 [17183650.001]
  • [Cites] Pediatr Blood Cancer. 2007 Mar;48(3):349-53 [16302216.001]
  • [Cites] Annu Rev Med. 2007;58:267-84 [17002552.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):69-82 [17222791.001]
  • [Cites] Expert Opin Biol Ther. 2006 Dec;6(12):1255-62 [17223735.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):973-8 [17210912.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Curr Biol. 2007 Jan 23;17(2):165-72 [17196391.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Feb;13(2):235-44 [17241929.001]
  • [Cites] Neurosurg Clin N Am. 2007 Jan;18(1):59-69, viii-ix [17244554.001]
  • [Cites] Neurosurg Clin N Am. 2007 Jan;18(1):71-80, ix [17244555.001]
  • (PMID = 18427384.001).
  • [ISSN] 0031-0808
  • [Journal-full-title] Panminerva medica
  • [ISO-abbreviation] Panminerva Med
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA078590; United States / NCI NIH HHS / CA / U01 CA111294; United States / NCI NIH HHS / CA / CA111294; United States / NCI NIH HHS / CA / CA78590
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Italy
  • [Number-of-references] 210
  • [Other-IDs] NLM/ NIHMS526856; NLM/ PMC3828640
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30. Bruland OS, Høifødt H, Saeter G, Smeland S, Fodstad O: Hematogenous micrometastases in osteosarcoma patients. Clin Cancer Res; 2005 Jul 1;11(13):4666-73
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bone marrow and peripheral blood samples from 60 patients with suspected bone sarcoma were examined for the presence and number of micrometastatic osteosarcoma cells by a sensitive immunomagnetic detection assay, using in parallel two osteosarcoma-associated antibodies.
  • Forty-nine of the patients had osteosarcoma, and of these, as many as 31 (63%) had tumor cells in bone marrow, in many cases with a high number of cells.
  • None of 38 control bone marrow samples were positive, including 11 from patients with suspected bone sarcoma at time of sampling who later were found not to have osteosarcoma.
  • Fifteen of 28 patients without overt metastases at primary diagnosis (54%) were positive, 12 of whom had localized high-grade primary tumors in the extremity.
  • In the group of 22 patients with extremity localized nonmetastatic osteosarcoma, information was available on the histologic response to preoperative chemotherapy in 15 patients.
  • None of the three patients in the bone marrow-negative group who had a poor response to chemotherapy have relapsed, whereas two of the four poor responders in the bone marrow-positive cohort are dead of disease.
  • Among 12 patients with overt metastasis at primary diagnosis, 11 (92%) were positive in bone marrow with a very high number of osteosarcoma cells.
  • Moreover, in cases with numerous osteosarcoma cells in bone marrow attempts to grow the selected cells in vitro were successful in two of eight attempts, and in two of five cases, isolated cells produced tumors with osteosarcoma characteristics in nude mice.
  • In conclusion, already at primary diagnosis, a very high fraction of osteosarcoma patients had malignant cells in bone marrow, and a correlation between the presence of tumor cells, clinical stage, and disease progression was found.
  • Attempts to subgroup osteosarcoma patients for more individualized treatment based on the presence of micrometastatic cells should be studied in a larger cohort of patients.
  • [MeSH-major] Bone Marrow Neoplasms / diagnosis. Bone Neoplasms / pathology. Osteosarcoma / pathology
  • [MeSH-minor] Adolescent. Adult. Animals. Bone Marrow Examination. Child. Female. Humans. Immunomagnetic Separation. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Neoplasm Transplantation. Neoplasms, Experimental / pathology. Survival Analysis. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 16000559.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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31. van der Reijden BA, Simons A, Luiten E, van der Poel SC, Hogenbirk PE, Tönnissen E, Valk PJ, Löwenberg B, De Greef GE, Breuning MH, Jansen JH: Minimal residual disease quantification in patients with acute myeloid leukaemia and inv(16)/CBFB-MYH11 gene fusion. Br J Haematol; 2002 Aug;118(2):411-8

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  • We have designed a real-time CBFB-MYH11 reverse transcription polymerase chain reaction (RT-PCR) assay to quantify minimal residual disease (MRD) in patients with inv(16)-positive acute myeloid leukaemia (AML).
  • Six patients were followed for a median of 17.5 months after diagnosis during which 120 evaluable samples were analysed.
  • The CBFB-MYH11 expression at diagnosis varied only fourfold between the six patients and was virtually identical to that observed in the CBFB-MYH11-positive cell line ME-1.
  • For two cases, a patient-specific real-time PCR for CBFB-MYH11 quantification at genomic DNA level was designed.
  • Similar disease levels were found at the RNA and genomic DNA level during and after treatment, indicating that CBFB-MYH11 gene expression was unaltered during treatment and that the percentage of malignant cells can be accurately quantified at the RNA level.
  • Following successive courses of chemotherapy, the reduction of malignant cells was found to be significantly more pronounced (80-250-fold greater) in peripheral blood compared with bone marrow in five out of six cases tested.
  • Treatment with gemtuzumab ozogamicin as sole agent at relapse did not result in a selective decrease of tumour cells in three cases analysed.
  • We conclude that real-time PCR is a powerful method of monitoring MRD levels and quantifying the antileukaemic effect of separate (experimental) courses of chemotherapy.
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Male. Middle Aged. Neoplasm, Residual. Oncogene Proteins, Fusion / genetics. Prospective Studies. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 12139724.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Oncogene Proteins, Fusion
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32. Van der Woude HJ, Egmont-Petersen M: Contrast-enhanced magnetic resonance imaging of bone marrow. Semin Musculoskelet Radiol; 2001;5(1):21-33
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  • [Title] Contrast-enhanced magnetic resonance imaging of bone marrow.
  • In the assessment with magnetic resonance (MR) imaging of bone marrow disorders, the use of contrast agents is usually not critical because T1-weighted spin-echo and fat-suppressed sequences (STIR or fat-sat intermediate weighted) are robust and largely available techniques for depiction of neoplastic and non-neoplastic lesions of the bone marrow.
  • This article discusses the characteristics of dynamic contrast-enhanced MR imaging of bone marrow edema, ischemia, and neoplasm.
  • It emphasizes its value in staging and in monitoring of response to chemotherapy of several bone tumors.
  • These fast dynamic contrast-enhanced techniques do not allow differentiation between benign and malignant primary osseous tumors because the biologic behavior rather than the malignant potential of these lesions is reflected.
  • [MeSH-major] Bone Marrow / pathology. Bone Marrow Diseases / diagnosis. Contrast Media. Magnetic Resonance Imaging
  • [MeSH-minor] Bone Marrow Neoplasms / diagnosis. Bone Marrow Neoplasms / drug therapy. Bone Neoplasms / diagnosis. Bone Neoplasms / pathology. Edema / diagnosis. Gadolinium DTPA. Humans. Ischemia / diagnosis

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  • (PMID = 11371333.001).
  • [ISSN] 1089-7860
  • [Journal-full-title] Seminars in musculoskeletal radiology
  • [ISO-abbreviation] Semin Musculoskelet Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; K2I13DR72L / Gadolinium DTPA
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33. Widmer S, Tinguely M, Egli F, Thiel MA: Lethal Epstein-Barr virus associated NK/T-cell lymphoma with primary manifestation in the conjunctiva. Klin Monbl Augenheilkd; 2005 Mar;222(3):255-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The lesion had increased over a period of 2 months despite topical corticosteroid treatment.
  • Conjunctival biopsy revealed a highly malignant, CD3 + and BCL2 + extranodal T-cell lymphoma with features of an NK/T-cell origin (CD56 +, TIA + TCR-rearrangement: germline).
  • THERAPY AND OUTCOME: Systemic 1 (st) cycle chemotherapy with cyclophosphamide, doxorubicin, vincristin and prednisone resulted in a complete remission of the swelling within 4 days.
  • The patient died within a month because of untreatable pancytopenia due to malignant bone marrow infiltration.
  • CONCLUSIONS: LMG is a rare but highly malignant Epstein-Barr virus associated NK/T-cell lymphoma that can occur in healthy, immune competent Caucasians.
  • The LMG has a high mortality rate despite systemic treatment and can be lethal within a few months or even weeks.
  • [MeSH-major] Conjunctival Neoplasms / diagnosis. Epstein-Barr Virus Infections / diagnosis. Eyelid Neoplasms / diagnosis. Granuloma, Lethal Midline / diagnosis. Killer Cells, Natural / pathology. Lymphoma, T-Cell, Peripheral / diagnosis. T-Lymphocytes / pathology
  • [MeSH-minor] Antigens, CD3 / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Conjunctiva / pathology. Eyelids / pathology. Fatal Outcome. Humans. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / radiotherapy. Proto-Oncogene Proteins c-bcl-2 / analysis. Radiotherapy, Adjuvant

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  • (PMID = 15785994.001).
  • [ISSN] 0023-2165
  • [Journal-full-title] Klinische Monatsblätter für Augenheilkunde
  • [ISO-abbreviation] Klin Monbl Augenheilkd
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Proto-Oncogene Proteins c-bcl-2
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34. Müller HL, Marx A, Trusen M, Schneider P, Kühl J: Disseminated malignant ectomesenchymoma (MEM): case report and review of the literature. Pediatr Hematol Oncol; 2002 Jan-Feb;19(1):9-17

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disseminated malignant ectomesenchymoma (MEM): case report and review of the literature.
  • Malignant ectomesenchymoma (MEM) is a rare soft tissue tumor believed to arise from a pluripotent migratory neural crest cell and composed fo both a mesenchymal element and a neuroectodermal element.
  • The authors report the case of an 11-month-old male who presented with a local abdominal MEM and systemic metastases into lungs, liver, bones, and bone marrow.
  • This is the first reported case of an MEM with initial bone marrow dissemination.
  • The tumor consisted of a neuroblastoma component and a mesenchymal component with sarcomatous features.
  • Diagnosis and therapy were complicated by the histological heterogeneity of the tumor, which also influenced the clinical appearance and course in this case.
  • A literature search revealed 15 other evaluated cases that arose in soft tissue and had adequate clinicopathologic data.
  • Complete surgical resection was the mainstay of treatment, and chemotherapy also appeared to be important.
  • In all reported patients (n = 3) with initial metastases or bone marrow dissemination, as in this case, no cure could be achieved.
  • In patients with disseminated MEM, new therapeutic approaches such as high-dose chemotherapy followed by stem cell rescue should be considered, similar to the current strategy in patients with stage VI neuroblastoma or soft tissue sarcoma.
  • [MeSH-minor] 3-Iodobenzylguanidine. Bone Marrow Neoplasms / radionuclide imaging. Bone Marrow Neoplasms / secondary. Bone Marrow Neoplasms / therapy. Fatal Outcome. Humans. Infant. Magnetic Resonance Imaging. Male. Neoplasm Metastasis / pathology. Neoplasm Recurrence, Local / therapy

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  • (PMID = 11787870.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 35MRW7B4AD / 3-Iodobenzylguanidine
  • [Number-of-references] 13
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35. Andersson PO, Brune M, Ekman T: Remission inversion and no transplant-related mortality--a single centre experience of autologous stem cell transplantation in malignant lymphoma. Acta Oncol; 2000;39(7):849-56
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  • [Title] Remission inversion and no transplant-related mortality--a single centre experience of autologous stem cell transplantation in malignant lymphoma.
  • Between 1989 and 1998 93 patients with malignant lymphoma were treated, in our centre, with high-dose chemotherapy and autologous stem cell transplantation.
  • Diagnosis according to the REAL-classification were: 38 patients with high-grade lymphoma (diffuse large B-cell lymphoma (DLCL) (n = 26), anaplastic T-cell (n = 5), lymfoblastic (n = 3) and others (n = 4)), 31 patients with low-grade lymphoma (follicular (n = 18), mantle cell (n = 4), B-CLL (n = 3) and others (n = 6)) and, finally, 24 patients with Hodgkin's disease.
  • The source of stem cells was bone marrow (14 patients), peripheral blood stem cells (64 patients) or a combination of both sources (15 patients).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Lymphoma / mortality. Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Transplantation, Autologous

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  • (PMID = 11145444.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
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36. Oechsle K, Lange-Brock V, Kruell A, Bokemeyer C, de Wit M: Prognostic factors and treatment options in patients with leptomeningeal metastases of different primary tumors: a retrospective analysis. J Cancer Res Clin Oncol; 2010 Nov;136(11):1729-35

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic factors and treatment options in patients with leptomeningeal metastases of different primary tumors: a retrospective analysis.
  • We evaluated prognostic factors and treatment options in patients (pts) with LM of different malignancies in a single center experience.
  • METHODS: Single center data on characteristics, treatment and outcome of 135 consecutive pts (73 solid tumors and 62 hematologic malignancies) with LM between 1989 and 2005 were retrospectively analyzed.
  • RESULTS: Treatment consisted of systemic chemotherapy (SC) plus intrathecal chemotherapy (ITC) in 28%, ITC alone in 22%, radiotherapy (RT) plus ITC in 12% and other modalities (SC, RT, SC + RT) in 7%.
  • Thirteen percent of pts received supportive care only (4% not evaluable on treatment).
  • Median survival from diagnosis of LM was 2.5 months.
  • Univariate analysis revealed age >50, interval between diagnosis of primary tumor and LM ≤12 months, lung cancer and malignant melanoma, and Karnofsky performance status ≤70 as significant negative predictors for overall survival.
  • CONCLUSIONS: In patients with LM an age >50, performance status ≤70%, interval between diagnosis of primary tumor and LM ≤12 months, primary tumor (lung cancer, malignant melanoma) and lack of cytologic response present negative prognostic factors.
  • Systemic chemotherapy is significantly associated with longer survival time than local treatment modalities.
  • [MeSH-major] Meningeal Carcinomatosis / pathology. Neoplasm Metastasis / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Combined Modality Therapy. Female. Hematologic Neoplasms / drug therapy. Hematologic Neoplasms / mortality. Hematologic Neoplasms / pathology. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / mortality. Lung Neoplasms / pathology. Lung Neoplasms / radiotherapy. Male. Melanoma / drug therapy. Melanoma / mortality. Melanoma / pathology. Melanoma / radiotherapy. Middle Aged. Neoplasms / drug therapy. Neoplasms / mortality. Neoplasms / pathology. Prognosis. Proportional Hazards Models. Retrospective Studies. Survival Analysis

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  • [Cites] J Neurol Sci. 2004 Aug 30;223(2):167-78 [15337619.001]
  • [Cites] Eur J Cancer. 2004 Dec;40(18):2726-33 [15571954.001]
  • [Cites] Curr Opin Oncol. 2006 Nov;18(6):637-43 [16988587.001]
  • [Cites] Cancer. 1996 Apr 1;77(7):1315-23 [8608509.001]
  • [Cites] J Clin Oncol. 1993 Mar;11(3):561-9 [8445432.001]
  • [Cites] Cancer Invest. 2005;23(2):145-54 [15813508.001]
  • [Cites] Neurology. 1994 Aug;44(8):1463-9 [8058150.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):255-60 [16344918.001]
  • [Cites] Expert Opin Pharmacother. 2005 Jun;6(7):1115-25 [15957966.001]
  • [Cites] Cancer. 2007 Dec 15;110(12):2640-7 [17960791.001]
  • [Cites] J Neurooncol. 1997 Oct;35(1):55-64 [9266441.001]
  • [Cites] Jpn J Clin Oncol. 2003 Dec;33(12):608-12 [14769837.001]
  • [Cites] J Clin Oncol. 1998 Apr;16(4):1561-7 [9552066.001]
  • [Cites] J Neurooncol. 2007 Aug;84(1):107-17 [17332946.001]
  • [Cites] Neuro Oncol. 2008 Apr;10(2):199-207 [18287337.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3110-6 [10506606.001]
  • [Cites] J Neurooncol. 2007 Aug;84(1):57-62 [17310266.001]
  • [Cites] Cancer. 1998 May 1;82(9):1756-63 [9576299.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3605-13 [15908671.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Mar 1;37(4):745-51 [9128946.001]
  • (PMID = 20204406.001).
  • [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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37. Cohen Y, Amir G, Schibi G, Amariglio N, Polliack A: Rapidly progressive diffuse large B-cell lymphoma with initial clinical presentation mimicking seronegative Wegener's granulomatosis. Eur J Haematol; 2004 Aug;73(2):134-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Thereafter he developed skin and lung lesions which on biopsy consisted of mixed 'inflammatory' infiltrates with granulomatous vasculitis.
  • A diagnosis of seronegative Wegener's granulomatosis was made and the patient received a combination of prednisone and cyclophosphamide with clinical improvement and clearance of the radiological lesions in the lungs.
  • The patient was now completely asymptomatic for 1 yr, but then generalized lymphadenopathy appeared, which was shown by histopathology to be large B-cell lymphoma, also involving the bone marrow.
  • Despite intensive chemotherapy, his disease could not be controlled because of primary chemoresistance, which was perhaps in some way related to exposure to the suboptimal doses of chemotherapy given during the 'inflammatory' period before the diagnosis of lymphoma was established.
  • It also shows the possible risk of 'masking' a true lymphoma by treating non-malignant diseases with immunosuppressive agents, which may eventually contribute to the development of chemoresistant lymphoma.
  • [MeSH-major] Granulomatosis with Polyangiitis / diagnosis. Lymphoma, B-Cell / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis
  • [MeSH-minor] Adult. Biopsy. Complementarity Determining Regions / genetics. Cyclophosphamide / adverse effects. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Disease Progression. Drug Resistance, Neoplasm / drug effects. Humans. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Male. Prednisone / adverse effects. Prednisone / therapeutic use


38. Marcucci G, Caligiuri MA, Bloomfield CD: Molecular and clinical advances in core binding factor primary acute myeloid leukemia: a paradigm for translational research in malignant hematology. Cancer Invest; 2000;18(8):768-80
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  • [Title] Molecular and clinical advances in core binding factor primary acute myeloid leukemia: a paradigm for translational research in malignant hematology.
  • Detection of t(8;21)(q22;q22) or inv(16)(p13q22) in adult patients with primary AML is a favorable independent prognostic indicator for achievement of cure after intensive chemotherapy or bone marrow transplantation and may serve as a paradigm for risk-adapted treatment in AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Cytarabine / therapeutic use. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Transcription Factors / genetics
  • [MeSH-minor] Animals. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor alpha Subunits. Diagnosis, Differential. Humans. Neoplasm, Residual. Prognosis. Randomized Controlled Trials as Topic. Remission Induction. Retrospective Studies. Survival Analysis. Transcription Factor AP-2. Translocation, Genetic. Treatment Outcome

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  • (PMID = 11107447.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P30CA16058
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Core Binding Factor alpha Subunits; 0 / DNA-Binding Proteins; 0 / Transcription Factor AP-2; 0 / Transcription Factors; 0 / core binding factor alpha; 04079A1RDZ / Cytarabine
  • [Number-of-references] 96
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39. Bessenyei B, Urbán L, Takács I, Zeher M, Szegedi G, Semsei I: [Detection and diagnostic value of t(14;18) translocation in minimal residual disease of follicular lymphoma]. Orv Hetil; 2000 Jul 30;141(31):1715-9
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  • [Title] [Detection and diagnostic value of t(14;18) translocation in minimal residual disease of follicular lymphoma].
  • The minimal residual disease is important in several malignant diseases, such as in hematopoietic malignancies (e.g. in follicular lymphoma) or in solid tumors, due to the presence of a tumor burden following a treatment of these diseases.
  • It is inevitable to learn the results of radio- and/or chemotherapy, i.e. whether the translocation-bearing cells disappeared from the lymphocytes of peripheral blood as well as from that of bone marrow, or we have to take into account the minimal residual disease.
  • Using nested-PCR one can detect the translocation in 1 out of 10(5) cells, this way the results of the treatments can be controlled: one can establish the emergence of remissions; and the relapses could also be detected earlier than by using conventional diagnostic methods.
  • Our experience, yielded by the follow up studies of follicular lymphoma patients, shows that the results of PCR detection correlate excellently with the conclusions of other diagnostic techniques.
  • Nevertheless, the t(14;18) translocation-bearing cells can also be detected in peripheral lymphocytes of healthy donors as well as in that of different diseases of other types than lymphoma, but not in bone marrow.
  • Therefore we emphasize the importance of the translocation-detection in the bone marrow of the patients of follicular lymphoma.
  • More and more advanced techniques have made it possible to detect the minimal residual disease, this way it will be easier to diagnose and to predict the outcome of different malignant diseases.
  • [MeSH-major] Bone Marrow Neoplasms / genetics. Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 18 / genetics. Lymphoma, Follicular / genetics. Translocation, Genetic
  • [MeSH-minor] Diagnosis, Differential. Humans. Neoplasm, Residual / genetics. Polymerase Chain Reaction. Predictive Value of Tests

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  • (PMID = 10976195.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] HUNGARY
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40. Gupta P, Singh U, Singh SK, Kapoor R, Gupta V, Das A: Bilateral symmetrical metastasis to all extraocular muscles from distant rhabdomyosarcoma. Orbit; 2010 Jun;29(3):146-8
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  • The common sites for spread from inguinal region include regional lymph nodes, lungs, bone marrow and bone cortex.
  • After 2 weeks of initial surgery the patient developed bilateral axial proptosis and radiological imaging revealed bilateral extraocular muscle thickening involving all the extraocular muscles.
  • COMMENT: Although rhabdomyosarcoma is the commonest primary orbital malignant mass developing in young patients, it is an uncommon metastasis.
  • The present report describes one such patient with favorable initial response to chemotherapy and muscle thickness reverting to normal.
  • Metastasis from a distant site should be considered in differential diagnosis when evaluating a patient with bilateral enlargement of all extraocular muscles.
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease Progression. Follow-Up Studies. Humans. Male. Neoplasm Invasiveness / pathology. Neoplasm Staging. Oculomotor Muscles. Orbital Neoplasms / drug therapy. Orbital Neoplasms / secondary. Orchiectomy / methods. Risk Assessment

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  • (PMID = 20497080.001).
  • [ISSN] 1744-5108
  • [Journal-full-title] Orbit (Amsterdam, Netherlands)
  • [ISO-abbreviation] Orbit
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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41. Lee SG, Choi JR, Kim JS, Park TS, Lee KA, Song J: Therapy-related acute lymphoblastic leukemia with t(9;22)(q34;q11.2):a case study and review of the literature. Cancer Genet Cytogenet; 2009 May;191(1):51-4
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  • [Title] Therapy-related acute lymphoblastic leukemia with t(9;22)(q34;q11.2):a case study and review of the literature.
  • Therapy-related acute lymphoblastic leukemia (t-ALL) with t(9;22)(q34;q11.2) is rarely reported as a secondary malignant neoplasm.
  • We present a novel case of t-ALL with t(9;22) in a patient with primary breast cancer.
  • The interval between diagnosis of breast cancer and the appearance of ALL was 4 years.
  • The patient was treated with partial mastectomy and axillary lymph node dissection followed by six cycles of CMF (cyclophosphamide, methotrexate, 5-fluorouracil) chemotherapy and radiation therapy.
  • Bone metastases were found 3 years after surgery, and she was treated with epirubicin and paclitaxel.
  • This case has the following unique features: BCR/ABL gene rearrangement in t-ALL, and two types of malignant cells (leukemic lymphoblasts and metastatic breast cancer cells) coexisted in the bone marrow.
  • [MeSH-major] Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Biopsy, Fine-Needle. Bone Marrow / pathology. Female. Humans. Karyotyping. Middle Aged

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  • (PMID = 19389510.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
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42. Brück P, Mousset S, Bühme A, Hoelzer D, Atta J: Nonsecretory primary plasma cell leukemia with good response to thalidomide-based treatment. Int J Hematol; 2007 Jul;86(1):66-8
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  • [Title] Nonsecretory primary plasma cell leukemia with good response to thalidomide-based treatment.
  • The criterion for the diagnosis of PCL is based on the finding of malignant plasma cells in the peripheral blood (more than 2 x 10(9)/L or more than 20% of white blood cells).
  • Examination of blood smears led to the diagnosis of PCL, which was confirmed by bone marrow biopsy.
  • Due to the patient's impaired general condition, intensive chemotherapy could not be administered.
  • After an oral induction chemotherapy consisting of cyclophosphamide and high dose dexamethasone followed by one cycle of high-dose dexamethasone and thalidomide no evidence of the disease in the peripheral blood was detectable.
  • Consequently, the patient was put on a thalidomide maintenance therapy.
  • Six months after first diagnosis, the patient was found to have bone marrow and peripheral blood relapse with anemia and neutropenia in the clinical context of acute on chronic renal failure.
  • After a limited response to further chemotherapy, the patient died 14 months after the first diagnosis while on dexamethasone maintenance.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Plasma Cell / drug therapy. Thalidomide / therapeutic use
  • [MeSH-minor] Aged. Fatal Outcome. Humans. Male. Neoplasm Recurrence, Local

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  • [Cites] Bone Marrow Transplant. 1997 Nov;20(10):901-4 [9404934.001]
  • [Cites] Blood. 1999 Feb 1;93(3):1032-7 [9920853.001]
  • [Cites] Leuk Lymphoma. 2002 Feb;43(2):351-4 [11999568.001]
  • [Cites] Leuk Lymphoma. 2002 May;43(5):1067-73 [12148888.001]
  • [Cites] Am J Hematol. 1994 Mar;45(3):262-4 [8296801.001]
  • [Cites] Semin Oncol. 2001 Dec;28(6):607-12 [11740818.001]
  • [Cites] Eur J Haematol. 2001 Jul;67(1):51-3 [11553267.001]
  • [Cites] Leukemia. 1998 Dec;12(12):1977-82 [9844928.001]
  • [Cites] Hematol Oncol Clin North Am. 1999 Dec;13(6):1259-72 [10626149.001]
  • [Cites] Transplant Proc. 2002 Nov;34(7):2929-30 [12431661.001]
  • [Cites] Ann Hematol. 2002 Feb;81(2):119-23 [11907796.001]
  • [Cites] Semin Hematol. 1987 Jul;24(3):202-8 [3116673.001]
  • [Cites] Leuk Res. 2001 Feb;25(2):103-7 [11166824.001]
  • [Cites] Ann Hematol. 2002 Jul;81(7):362-7 [12185504.001]
  • [Cites] Ann Hematol. 1999 Jan;78(1):25-7 [10037265.001]
  • (PMID = 17675269.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 4Z8R6ORS6L / Thalidomide
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43. Dieleman FJ, Dekker AW: [Kahler's disease. Multiple myeloma]. Ned Tijdschr Tandheelkd; 2007 May;114(5):228-30
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  • Kahler's disease, multiple myeloma, is a malignant condition of unbridled multiplication of plasma cells in bone marrow.
  • Clinical features are anaemia, pain in the affected bones, spontaneous bone fractures and increased infection susceptibility.
  • With the present chemotherapy a good response is seen in 50-70% of patients, but complete response occurs only in a minority of patients.
  • Radiotherapy is often used in addition to chemotherapy.
  • In order to minimize the risk of complications, it is advocated to be in touch with the patients haematologist before starting an invasive oral treatment.
  • [MeSH-major] Mandibular Neoplasms / diagnosis. Multiple Myeloma / diagnosis
  • [MeSH-minor] Bone Resorption. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Remission Induction. Treatment Outcome

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  • (PMID = 17552301.001).
  • [ISSN] 0028-2200
  • [Journal-full-title] Nederlands tijdschrift voor tandheelkunde
  • [ISO-abbreviation] Ned Tijdschr Tandheelkd
  • [Language] dut
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Netherlands
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44. Jain KK: Use of bacteria as anticancer agents. Expert Opin Biol Ther; 2001 Mar;1(2):291-300
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  • Historically, bacteria were used as oncolytic agents for malignant brain tumours.
  • Advances in bacteriology and molecular biology have widened the scope of bacterial approaches to cancer therapy and various possibilities include the use of bacteria as sensitising agents for chemotherapy, as delivery agents for anticancer drugs, and as vectors for gene therapy.
  • Bacterial toxins can be used for tumour destruction and cancer vaccines can be based on immunotoxins of bacterial origin.
  • The most promising approaches are the use of genetically modified bacteria for selective destruction of tumours, and bacterial gene-directed enzyme prodrug therapy.
  • TAPET (Tumour Amplified Protein Expression Therapy) uses a genetically altered strain of Salmonella as a bacterial vector, or vehicle, for preferentially delivering anticancer drugs to solid tumours.
  • Verotoxin 1 (VT1) of Escherichia coli has been used for ex vivo purging of human bone marrow of cancer cells before autologous bone marrow transplant. E. coli genes and enzymes have become part of well-known prodrug approaches to cancer in which inert prodrugs can be converted in vivo to highly active species.
  • IL-4 fused with Pseudomonas exotoxin has been administered directly into malignant brain tumours and binds with high affinity to IL-4 receptors, which do not exist on normal brain cells, thus destroying a major part of the tumour without harming the normal brain tissue.
  • No ideal anticancer agent of bacterial origin that is applicable to all types of cancers has been discovered yet.
  • The most promising approach to malignant brain tumours appears to be the use of genetically engineered bacteria that destroy the tumour selectively while sparing the normal brain tissue.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bacteria / genetics. Bacteria / immunology. Genetic Therapy / methods

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  • (PMID = 11727536.001).
  • [ISSN] 1471-2598
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bacterial Toxins; 0 / Escherichia coli Proteins; 0 / Prodrugs; 0 / Recombinant Fusion Proteins; 207137-56-2 / Interleukin-4; EC 1.7.- / Nitroreductases; EC 2.4.2.1 / Purine-Nucleoside Phosphorylase; EC 2.4.2.8 / Hypoxanthine Phosphoribosyltransferase; EC 3.5.4.- / Nucleoside Deaminases; EC 3.5.4.1 / Cytosine Deaminase
  • [Number-of-references] 33
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45. Mittal R, Al Awadi S, Sahar O, Behbehani AM: Ewing's sarcoma as second malignant neoplasm after retinoblastoma: a case report. Med Princ Pract; 2008;17(1):84-5
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  • [Title] Ewing's sarcoma as second malignant neoplasm after retinoblastoma: a case report.
  • OBJECTIVES: To report a case of a child with the hereditary form of unilateral retinoblastoma (RB), who developed Ewing's sarcoma of the right fibula 3 years after the enucleation of the right eye.
  • He was fully investigated and found to have locally advanced RB with bone marrow involvement (Reese-Ellsworth stage IVA).
  • The patient received chemotherapy and diode laser thermotherapy in Kuwait and the UK.
  • He was treated with chemotherapy, surgery (complete excision of the fibula) and high-dose chemotherapy followed by autologous stem cell transplantation.
  • The child is now nearly 2 years after completing the treatment and is disease free.
  • CONCLUSIONS: This case confirms the increased risk of a second malignant neoplasm (SMN) in children with hereditary RB.
  • These children need a very close follow-up for the early diagnosis of SMNs or even subsequent malignancies.
  • [MeSH-major] Bone Neoplasms / diagnosis. Fibula. Neoplasms, Second Primary / diagnosis. Retinal Neoplasms / diagnosis. Retinoblastoma / diagnosis. Sarcoma, Ewing / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child, Preschool. Diagnosis, Differential. Eye Enucleation. Humans. Infant. Male. Stem Cell Transplantation. Treatment Outcome

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  • [Copyright] (c) 2007 S. Karger AG, Basel.
  • (PMID = 18059108.001).
  • [ISSN] 1423-0151
  • [Journal-full-title] Medical principles and practice : international journal of the Kuwait University, Health Science Centre
  • [ISO-abbreviation] Med Princ Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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46. Machet L, De Muret A, Wiezberka E, Bernez A, Abdallah-Lotf M, Linassier C, Petrella T: [Agranular CD4+ CD56+ CD123+ hematodermic neoplasm (blastic NK-cell lymphoma) revealed by cutaneous localization: 2 cases]. Ann Dermatol Venereol; 2004 Nov;131(11):969-73
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  • [Title] [Agranular CD4+ CD56+ CD123+ hematodermic neoplasm (blastic NK-cell lymphoma) revealed by cutaneous localization: 2 cases].
  • BACKGROUND: Agranular CD4+ CD56+ hematodermic neoplasm (blastic NK-cell lymphoma) has been recently described.
  • Preliminary histological examination of cutaneous biopsy taken in both patients showed a malignant proliferation suggesting a cutaneous lymphoma, and the patients were referred.
  • No rearrangement of the T-cell receptor gene or the immunoglobulin heavy chain gene were evidenced.
  • The first patient was treated with chemotherapy, with complete remission.
  • A cutaneous relapse promptly occurred, followed by bone and cerebral localizations.
  • The patient died one year after the diagnosis of the disease, in spite of intensification of the treatment.
  • Treatment is still ongoing in the second patient.
  • COMMENTS: The histological presentation of these two patients was very similar with an unusual phenotype of tumor cells expressing CD4, CD56, CD123, but not expressing CD3 and CD20.
  • However, the tumor cells derive from the dendritic plasmacytoid cells, also called type 2 dendritic cells, and perhaps from a common precursor to lymphocyte T and dendritic plasmacytoid cells.
  • This justifies attempting aggressive protocols, with bone marrow allograft in the younger patients.
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fatal Outcome. Humans. Interleukin-3 Receptor alpha Subunit. Male. Phenotype

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  • (PMID = 15602384.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD56; 0 / IL3RA protein, human; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Receptors, Interleukin-3
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47. Buchner AM, Sonnenberg A: Medical diagnoses and procedures associated with clostridium difficile colitis. Am J Gastroenterol; 2001 Mar;96(3):766-72
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  • METHODS: The Patient Treatment File of the Department of Veterans Affairs contains the computerized records of all inpatients treated in 172 Veterans Affairs hospitals distributed throughout the United States.
  • The computerized medical records of 15,091 cases with C. difficile colitis and 61,931 controls without the diagnosis were extracted from the annual files between 1993 and 1998.
  • The numbers of procedures were 75,479 and 129,612, respectively. C. difficile colitis was significantly associated with HIV infection, candidiasis, malignant neoplasm and chemotherapy, malnutrition, pneumonia, aspiration pneumonitis, intestinal obstruction, diverticulitis, renal failure, urinary tract infection, decubitus, and osteomyelitis.
  • Interventional procedures involving the respiratory tract, bone marrow biopsy, arterial and venous catheterization, urinary catheterization, dialysis, gastrostomy tube, and physical therapy were also frequently associated with the development of C. difficile colitis.
  • CONCLUSIONS: These associations reflect the influence of causal relationships (such as the use of antibiotics and chemotherapy), an increased risk of exposure to C. difficile among immobilized bedridden patients with chronic disease states, or a general system failure in patients with end-stage disease.

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  • (PMID = 11280548.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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48. Wu H, Wasik MA, Przybylski G, Finan J, Haynes B, Moore H, Leonard DG, Montone KT, Naji A, Nowell PC, Kamoun M, Tomaszewski JE, Salhany KE: Hepatosplenic gamma-delta T-cell lymphoma as a late-onset posttransplant lymphoproliferative disorder in renal transplant recipients. Am J Clin Pathol; 2000 Apr;113(4):487-96
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  • We report 2 cases of renal transplant recipients in whom hepatosplenic gamma-delta T-cell lymphoma (gamma-delta HSTCL) developed 5 and 10 years after transplantation.
  • Markedly atypical lymphoid infiltrate of intermediate to large cells was observed in the spleen, liver, and bone marrow.
  • The malignant cells showed typical immunophenotype of gamma-delta T cells (CD2+, CD3+, CD4-, CD8-, CD7+, gamma-delta T-cell receptor-positive, and alpha-beta T-cell receptor-negative) with clonal T-cell receptor gene rearrangement and were of the V-delta-1 subset.
  • The malignant T cells in both cases were of host tissue origin.
  • Despite initial response to chemotherapy, both patients died within 6 months of diagnosis.
  • [MeSH-minor] Adult. DNA, Neoplasm / analysis. Fas Ligand Protein. Fatal Outcome. Female. Gene Rearrangement, delta-Chain T-Cell Antigen Receptor / genetics. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Membrane Glycoproteins / metabolism. Membrane Proteins / metabolism. Middle Aged. Poly(A)-Binding Proteins. Polymerase Chain Reaction. RNA-Binding Proteins / metabolism. Receptors, Interleukin-2 / blood

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  • (PMID = 10761449.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Membrane Proteins; 0 / Poly(A)-Binding Proteins; 0 / Proteins; 0 / RNA-Binding Proteins; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / Receptors, Interleukin-2; 0 / TIA1 protein, human
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49. Blanco JG, Dervieux T, Edick MJ, Mehta PK, Rubnitz JE, Shurtleff S, Raimondi SC, Behm FG, Pui CH, Relling MV: Molecular emergence of acute myeloid leukemia during treatment for acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2001 Aug 28;98(18):10338-43
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  • [Title] Molecular emergence of acute myeloid leukemia during treatment for acute lymphoblastic leukemia.
  • Therapy-related acute myeloid leukemias (t-AML) with translocations of the MLL gene are associated with the use of topoisomerase II inhibitors.
  • We established the emergence of the malignant clone in a child who developed t-AML with a t(11;19) (q23;p13.3) during treatment for acute lymphoblastic leukemia (ALL).
  • The MLL-ENL and the reciprocal ENL-MLL genomic fusions and their chimeric transcripts were characterized from samples collected at the time of t-AML diagnosis.
  • The MLL-ENL fusion was not detectable in bone marrow at the time of ALL diagnosis or after 2 months of chemotherapy (frequency <8.3 x 10(-7) cells(-1)).
  • The genomic fusion was first detected in bone marrow after 6 months of treatment at a frequency of one in 4,000 mononuclear bone marrow cells; the frequency was one in 70 cells after 20 months of therapy.
  • At the first detection of MLL-ENL, the only topoisomerase II inhibitors the patient had received were one dose of daunorubicin and two doses of etoposide.
  • The MLL-ENL fusion was not detectable in blood at the time of ALL diagnosis or after 0.7, 2, 8, 10, and 12 months of therapy but was detectable in blood at 16 months (one in 2.3 x 10(4) cells).
  • These data indicate that the malignant clone was not present before therapy, arose early during chemotherapy, and was able to proliferate even during exposure to antileukemic therapy.

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  • [Cites] Cancer Res. 2001 Jan 1;61(1):59-63 [11196198.001]
  • [Cites] Blood. 1999 Jul 15;94(2):803-7 [10397748.001]
  • [Cites] Biochemistry. 1988 Nov 1;27(22):8369-79 [2853964.001]
  • [Cites] N Engl J Med. 1989 Jul 20;321(3):136-42 [2787477.001]
  • [Cites] Lancet. 1991 Aug 10;338(8763):359-63 [1713639.001]
  • [Cites] N Engl J Med. 1991 Dec 12;325(24):1682-7 [1944468.001]
  • [Cites] Cancer Res. 1992 Feb 15;52(4):797-802 [1737339.001]
  • [Cites] BMJ. 1992 Apr 11;304(6832):951-8 [1581717.001]
  • [Cites] Biotechniques. 1992 Sep;13(3):444-9 [1389177.001]
  • [Cites] J Clin Oncol. 1993 Feb;11(2):271-8 [8426204.001]
  • [Cites] Clin Pharmacol Ther. 1994 Jan;55(1):15-20 [8299312.001]
  • [Cites] Blood. 1994 May 15;83(10):2780-6 [8180374.001]
  • [Cites] Cancer Res. 1994 Aug 15;54(16):4277-80 [8044771.001]
  • [Cites] Blood. 1994 Sep 15;84(6):1747-52 [8080983.001]
  • [Cites] Leukemia. 1994 Oct;8(10):1646-8 [7934159.001]
  • [Cites] Blood. 1995 Feb 15;85(4):902-11 [7531515.001]
  • [Cites] Nucleic Acids Res. 1995 Jan 25;23(2):256-60 [7862530.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1680-4 [7564509.001]
  • [Cites] Nature. 1995 Nov 30;378(6556):505-8 [7477409.001]
  • [Cites] Leukemia. 1995 Dec;9(12):1990-6 [8609707.001]
  • [Cites] Blood. 1996 Feb 1;87(3):1134-9 [8562939.001]
  • [Cites] J Natl Cancer Inst. 1996 Apr 3;88(7):407-18 [8618232.001]
  • [Cites] Blood. 1996 Jun 1;87(11):4804-8 [8639852.001]
  • [Cites] Cell. 1996 Jun 14;85(6):853-61 [8681380.001]
  • [Cites] Comput Chem. 1996 Mar;20(1):119-21 [8867843.001]
  • [Cites] Cancer Res. 1997 Jan 1;57(1):117-22 [8988051.001]
  • [Cites] Semin Hematol. 1999 Oct;36(4 Suppl 7):59-72 [10595755.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2814-9 [10706619.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4790-5 [10758153.001]
  • [Cites] Br J Haematol. 2000 Apr;109(1):13-23 [10848777.001]
  • [Cites] Blood. 1997 Apr 1;89(7):2369-75 [9116280.001]
  • [Cites] Ann Intern Med. 1997 Apr 15;126(8):608-14 [9103127.001]
  • [Cites] J Clin Oncol. 1997 Apr;15(4):1583-6 [9193356.001]
  • [Cites] Genes Chromosomes Cancer. 1997 Oct;20(2):185-95 [9331569.001]
  • [Cites] Leukemia. 1998 Mar;12(3):346-52 [9529129.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • [Cites] J Clin Oncol. 1998 Sep;16(9):3016-20 [9738570.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13176-81 [9789061.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3793-803 [9808573.001]
  • [Cites] Leukemia. 1998 Dec;12(12):1994-2005 [9844930.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):569-77 [10080601.001]
  • [Cites] Leukemia. 1999 Mar;13(3):335-42 [10086723.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):4075-82 [10463610.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):4095-9 [10463613.001]
  • [Cites] Cancer. 1999 Sep 15;86(6):1080-6 [10491537.001]
  • [Cites] Science. 1999 Oct 15;286(5439):487-91 [10521338.001]
  • [Cites] Lancet. 2001 Jan 6;357(9249):43-4 [11197365.001]
  • (PMID = 11526240.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Databank-accession-numbers] GENBANK/ AF373585/ AF373586/ AF373587
  • [Grant] United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / CA36401; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA051001; United States / NCI NIH HHS / CA / R01 CA036401; United States / NCI NIH HHS / CA / CA51001
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Neoplasm; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 0 / Topoisomerase II Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC56962
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50. Yel L, Liao O, Lin F, Gupta S: Severe T- and B-cell immune deficiency associated with malignant thymoma. Ann Allergy Asthma Immunol; 2003 Nov;91(5):501-5
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  • [Title] Severe T- and B-cell immune deficiency associated with malignant thymoma.
  • OBJECTIVE: To report the case of a 32-year-old, white man with an invasive malignant thymoma and profound combined T- and B-cell immunodeficiency associated with a normal CD4+/CD8+ T-cell ratio, absence of circulating B cells, and infection with an unusual organism.
  • METHODS: The patient presented with a superior vena cava syndrome caused by a malignant thymoma.
  • During chemotherapy and radiotherapy, he experienced recurrent episodes of pulmonary infections due to Haemophilus influenza and Serratia marcescens and persistent oral thrush.
  • RESULTS: Sixteen months after the diagnosis of thymoma, the immunological evaluation revealed profound lymphopenia, eosinopenia, very low counts of both CD4+ T cells and CD8+ T cells, and a normal CD4+/CD8+ ratio with negative delayed-type hypersensitivity skin test results.
  • Despite treatment with intravenous immunoglobulin, the patient died of respiratory insufficiency and sepsis secondary to a chronic pulmonary infection.
  • CONCLUSIONS: Malignant thymoma may be associated with severe combined immunodeficiency.
  • A normal CD4+/CD8+ ratio and the absence of peripheral B cells suggest a bone marrow defect that affects both T and B cells in the pathogenesis of this syndrome.
  • Comprehensive immunological evaluation should be performed when thymoma is diagnosed to initiate an early and effective treatment to prevent life-threatening complications.
  • [MeSH-minor] Adult. Antibody Formation / immunology. Antibody Specificity / immunology. CD4-CD8 Ratio. Humans. Immunoglobulin G / blood. Immunoglobulin G / immunology. Lymphocyte Count. Magnetic Resonance Imaging. Male. Neoplasm Invasiveness. Serratia Infections / diagnosis. Serratia Infections / immunology. Serratia Infections / microbiology. Serratia marcescens / immunology. Severity of Illness Index. Tomography, X-Ray Computed

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  • (PMID = 14692437.001).
  • [ISSN] 1081-1206
  • [Journal-full-title] Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
  • [ISO-abbreviation] Ann. Allergy Asthma Immunol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin G
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51. Bhatia P, Das R, Ahluwalia J, Malhotra P, Varma N, Varma S, Sharma SC, Garewal G: Acute leukemia/myelodysplastic syndrome as a sequelae of carcinoma breast: a report of five cases from north India. Indian J Pathol Microbiol; 2009 Apr-Jun;52(2):167-70
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  • A second malignant neoplasm has been found to be more frequent than might be expected from the general population rates.
  • Therapy-related myelodysplastic syndrome and acute leukemia are dreaded long-term complications of five cases of hematological malignancies following treatment for successful breast cancer therapy (therapeutic drugs or radiotherapy).
  • The patients presented 2-5 years after treatment of breast carcinoma.
  • One patient received chemotherapy after surgery.
  • One patient underwent only surgery and after 3 years presented with acute myeloid leukemia and bone marrow metastasis of carcinoma of the breast.
  • At the time of presentation, all the patients had either bicytopenia or pancytopenia.
  • A close follow-up with complete blood cell counts of the patients who previously had carcinoma of the breast is suggested for early detection of hematological abnormalities.
  • However, the poor prognosis, limited financial resources and poor health insurance coverage results in few patients and their family members opting for treatment.
  • [MeSH-major] Breast Neoplasms / complications. Breast Neoplasms / therapy. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adult. Aged. Drug-Related Side Effects and Adverse Reactions. Female. Humans. India. Middle Aged. Pancytopenia / diagnosis. Radiotherapy / adverse effects


52. Szynglarewicz B, Matkowski R, Smorag Z, Forgacz J, Pudelko M, Kornafel J: Hepatitis C virus infection and locally advanced splenic marginal zone lymphoma. Pathol Oncol Res; 2007;13(4):382-4
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  • Splenic marginal zone lymphoma (SMZL) is a rare malignant B-cell neoplasm, usually with an indolent clinical course and favorable prognosis.
  • Treatment options include chemotherapy, surgery, radiation and immunotherapy.
  • A 66-year-old woman with twelve-year history of HCV infection was admitted due to locally advanced abdominal tumor involving the spleen and the left part of the diaphragm.
  • Neither peripheral lymphadenopathy nor bone marrow pathology was found.
  • Following surgery, chemotherapy (CHOP regimen) and immunotherapy (anti-CD20 antibody) were given.
  • Surgical resection of even locally advanced SMZL with involvement of adjacent tissues can be performed as a diagnostic and therapeutic procedure.
  • Because of possible lymphoma regression following anti-viral therapy, a systematic screening for HCV in patients with SMZL seems to be valuable and helpful for treatment planning.
  • [MeSH-major] Hepatitis C / complications. Lymphoma, B-Cell, Marginal Zone / diagnosis. Lymphoma, B-Cell, Marginal Zone / virology. Splenic Neoplasms / diagnosis. Splenic Neoplasms / virology

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  • [Cites] Cancer. 2004 Nov 1;101(9):2050-7 [15389479.001]
  • [Cites] Cancer. 2004 Jan 1;100(1):107-15 [14692030.001]
  • [Cites] Leuk Lymphoma. 2005 Sep;46(9):1365-8 [16109616.001]
  • [Cites] J Immunol. 2005 May 15;174(10 ):6532-9 [15879157.001]
  • [Cites] Leuk Lymphoma. 2003 Jul;44(7):1113-20 [12916862.001]
  • [Cites] N Engl J Med. 2002 Jul 11;347(2):89-94 [12110736.001]
  • [Cites] Leukemia. 2004 Oct;18(10):1711-6 [15284859.001]
  • [Cites] Blood Rev. 2005 Jan;19(1):39-51 [15572216.001]
  • [Cites] Am J Pathol. 2001 Jul;159(1):253-61 [11438472.001]
  • [Cites] Br J Haematol. 2004 Jan;124(2):252-3 [14687039.001]
  • (PMID = 18158578.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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53. van Rhenen A, Moshaver B, Kelder A, Feller N, Nieuwint AW, Zweegman S, Ossenkoppele GJ, Schuurhuis GJ: Aberrant marker expression patterns on the CD34+CD38- stem cell compartment in acute myeloid leukemia allows to distinguish the malignant from the normal stem cell compartment both at diagnosis and in remission. Leukemia; 2007 Aug;21(8):1700-7
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  • [Title] Aberrant marker expression patterns on the CD34+CD38- stem cell compartment in acute myeloid leukemia allows to distinguish the malignant from the normal stem cell compartment both at diagnosis and in remission.
  • This CD34+CD38- population survives chemotherapy and is most probable the cause of minimal residual disease (MRD).
  • Various markers were identified to be aberrantly expressed on the CD34+CD38- population in AML and high-risk MDS samples at diagnosis, including C-type lectin-like molecule-1 and several lineage markers/marker-combinations.
  • Fluorescent in situ hybridization analysis revealed that marker-positive cells were indeed of malignant origin.
  • The markers were neither expressed on normal CD34+CD38- cells in steady-state bone marrow (BM) nor in BM after chemotherapy.
  • We found that these markers were indeed expressed in part of the patients on malignant CD34+CD38- cells in complete remission, indicating the presence of malignant CD34+CD38- cells.
  • Thus, by identifying residual malignant CD34+CD38- cells after chemotherapy, MRD detection at the stem cell level turned out to be possible.
  • This might facilitate characterization of these chemotherapy-resistant leukemogenic cells, thereby being of help to identify new targets for therapy.
  • [MeSH-major] Antigens, CD34 / metabolism. Antigens, CD38 / metabolism. Biomarkers, Tumor / metabolism. Hematopoietic Stem Cells / metabolism. Leukemia, Myeloid / diagnosis. Neoplasm, Residual / diagnosis. Neoplastic Stem Cells / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Bone Marrow / metabolism. Bone Marrow / pathology. Female. Flow Cytometry. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Middle Aged. Prognosis. Remission Induction. Risk Factors. Survival Rate

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  • (PMID = 17525725.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor; EC 3.2.2.5 / Antigens, CD38
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54. Hoshino A, Funato T, Munakata Y, Ishii T, Abe S, Ishizawa K, Ichinohasama R, Kameoka J, Meguro K, Sasaki T: Detection of clone-specific immunoglobulin heavy chain genes in the bone marrow of B-cell-lineage lymphoma after treatment. Tohoku J Exp Med; 2004 Jul;203(3):155-64
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  • [Title] Detection of clone-specific immunoglobulin heavy chain genes in the bone marrow of B-cell-lineage lymphoma after treatment.
  • In order to determine the appropriate treatment of malignant lymphoma, it is important to know the degree to which extra-nodal invasion of lymphoma cells has occurred.
  • By using a clone-specific CDR III probe in each patient, we were able to detect minimal residual disease (MRD) of lymphoma cells in the bone marrow and/or blood in 9 out of 14 cases (64.2%) at the onset of the disease or relapse, whereas abnormal cells in the bone marrow and/or blood were identified by routine morphological analysis in only 4 out of 22 cases (18.2%).
  • This indicates that extranodal invasion of malignant cells may be common in patients with NHL.
  • In some cases, the clone-specific CDR III gene was still expressed in the samples of bone marrow and/or peripheral blood even after chemotherapy, when other markers associated with NHL were no longer expressed.
  • On the other hand, most of the cases whose clone-specific CDR III gene was no longer expressed in the bone marrow and/or in circulation after treatment had a relatively fair prognosis.
  • These results indicate that the detection at molecular level of MRD in extranodal organs may prove useful as a predictor of prognosis for NHL.
  • [MeSH-major] Bone Marrow Cells / metabolism. Genes, Immunoglobulin / genetics. Lymphoma, B-Cell / metabolism
  • [MeSH-minor] Adult. Aged. Complementarity Determining Regions / genetics. DNA / metabolism. Female. Humans. Male. Middle Aged. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Polymerase Chain Reaction. Prognosis. Recurrence. Treatment Outcome

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  • (PMID = 15240924.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Complementarity Determining Regions; 9007-49-2 / DNA
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55. Löffler H, Kosely F, Ho AD, Krämer A: [Blastic plasmacytoid dendritic cell neoplasm - a rare differential diagnosis of neoplastic skin infiltrations associated with systemic symptoms]. Dtsch Med Wochenschr; 2009 Sep;134(39):1927-30
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  • [Title] [Blastic plasmacytoid dendritic cell neoplasm - a rare differential diagnosis of neoplastic skin infiltrations associated with systemic symptoms].
  • [Transliterated title] Blastische plasmozytoide Neoplasie dendritischer Zellen - seltene Differenzialdiagnose neoplastischer Hautinfiltrate mit systemischer Beteiligung.
  • HISTORY AND CLINICAL FINDINGS: A 70-year-old female patient developed a non-pruritic, indolent rash associated with infections and peripheral blood abnormalities.
  • A skin biopsy was suggestive of malignant lymphoma of the skin.
  • Additional immunohistochemistry of the skin specimen as well as cytologic and flow cytometric examination of the bone marrow revealed an immature cell population expressing CD4 and CD56 which infiltrated both the dermis and, with an infiltration grade of about 85 %, the bone marrow.
  • DIAGNOSIS: Blastic plasmacytoid dendritic cell neoplasm (formerly known as blastic NK cell lymphoma).
  • TREATMENT AND COURSE: After the first course of induction chemotherapy with daunorubicin and cytarabin, both the rash and the hematologic findings of bone marrow and peripheral blood showed a complete remission.
  • CONCLUSION: The blastic plasmacytoid dendritic cell neoplasm is a rare, aggressive hematopoietic neoplasm most likely related to acute myeloid leukemia (AML).
  • Since cutaneous involvement is regularly present at diagnosis, the differential diagnosis of unexplained skin lesions should include this disease entity, especially if peripheral blood abnormalities are present.
  • Despite the initial response to cytostatic therapy being mostly excellent, the prognosis is poor.
  • Hence, treatment as high-risk AML seems advisable.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Skin / pathology. Skin Neoplasms / diagnosis
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Biopsy. Bone Marrow / pathology. Diagnosis, Differential. Exanthema. Female. Flow Cytometry. Humans. Immunohistochemistry. Immunophenotyping. Pancytopenia. Prognosis. Remission Induction

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  • [Copyright] Georg Thieme Verlag KG Stuttgart, New York.
  • (PMID = 19760552.001).
  • [ISSN] 1439-4413
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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56. Orsey A, Paessler M, Lange BJ, Nichols KE: Central nervous system juvenile xanthogranuloma with malignant transformation. Pediatr Blood Cancer; 2008 Apr;50(4):927-30
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  • [Title] Central nervous system juvenile xanthogranuloma with malignant transformation.
  • Here, we describe a patient with JXG diffusely involving the central nervous system (CNS), whose disease responded to therapy but subsequently underwent dissemination to the peritoneum and bone marrow.
  • Repeat biopsy at dissemination revealed pleomorphic histiocytes with tetraploidy, suggesting evolution to a clonal histiocytic neoplasm.
  • Despite further chemotherapy, the patient died of disease progression.
  • [MeSH-major] Brain Neoplasms / physiopathology. Brain Neoplasms / therapy. Histiocytic Sarcoma / pathology. Xanthogranuloma, Juvenile / physiopathology. Xanthogranuloma, Juvenile / therapy
  • [MeSH-minor] Anti-Inflammatory Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Diseases / pathology. Child. Cladribine / therapeutic use. Dexamethasone / therapeutic use. Diagnosis, Differential. Disease Progression. Fatal Outcome. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Magnetic Resonance Imaging. Male. Pseudotumor Cerebri / pathology. Radiotherapy


57. Breccia M, Mandelli F, Petti MC, D'Andrea M, Pescarmona E, Pileri SA, Carmosino I, Russo E, De Fabritiis P, Alimena G: Clinico-pathological characteristics of myeloid sarcoma at diagnosis and during follow-up: report of 12 cases from a single institution. Leuk Res; 2004 Nov;28(11):1165-9
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  • [Title] Clinico-pathological characteristics of myeloid sarcoma at diagnosis and during follow-up: report of 12 cases from a single institution.
  • All had been initially misdiagnosed as malignant lymphoma (ML) and a median of 2.9 months (range: 1-6) elapsed between the misdiagnosis and the correct of MS, effectuated in our department.
  • At that time, a bone marrow examination revealed a myelodysplastic condition in seven patients, an infiltration by blast cells >30% in two patients, and normal features in the other three.
  • In the non-leukemic patients a median of 5 months (range: 2-44 months) elapsed between the diagnosis of MS and acute leukemia.
  • In all, 10 patients received intensive treatment.
  • Patients who presented isolated skin localization and received only radiotherapy, obtained a MS-CR, but subsequently developed AML.
  • Only in patients who were treated within 4 months from the initial ML diagnosis we achieved complete remission of both MS and leukemia, whereas in patients who were treated after this time, we obtained a complete disappearance of MS without response at the bone-marrow level, irrespectively of the specific therapy regimen.
  • Median survival time from MS diagnosis was 7 months (range: 1-49 months), and only one patient is still alive, 49 months after bone marrow transplantation.
  • Our data stress the importance of an accurate and prompt identification of this rare form of AML, and suggest that, even in patients with isolated MS, the early administration of AML-like intensive chemotherapy followed by bone marrow transplantation might reduce the risk of subsequently developing systemic disease.
  • [MeSH-major] Bone Marrow Neoplasms / pathology. Sarcoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Humans. Immunophenotyping. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 15380340.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 23
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58. Jacob MC, Chaperot L, Mossuz P, Feuillard J, Valensi F, Leroux D, Béné MC, Bensa JC, Brière F, Plumas J: CD4+ CD56+ lineage negative malignancies: a new entity developed from malignant early plasmacytoid dendritic cells. Haematologica; 2003 Aug;88(8):941-55
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  • [Title] CD4+ CD56+ lineage negative malignancies: a new entity developed from malignant early plasmacytoid dendritic cells.
  • The clinico-biological features of this neoplasm were moreover recently summarized from a large series of 23 patients.
  • INFORMATION SOURCES: The main symptoms at presentation were cutaneous lesions and bone marrow failure, due to invasion by blastic cells, all of which were EBV negative and agranular.
  • Most patients were initially sensitive to chemotherapy regimens, but they rapidly relapsed and died within 3 years.
  • STATE OF THE ART AND PERSPECTIVES: The concordant characteristics led us to confirm that this neoplasm actually represents a new entity, that we propose to rename early pDC leukemia/lymphoma.
  • The diagnosis is primarily based on a characteristic immunophenotypic profile i.e.

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  • (PMID = 12935983.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD56
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59. Al-Mawali A, Gillis D, Lewis I: The role of multiparameter flow cytometry for detection of minimal residual disease in acute myeloid leukemia. Am J Clin Pathol; 2009 Jan;131(1):16-26
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  • [Title] The role of multiparameter flow cytometry for detection of minimal residual disease in acute myeloid leukemia.
  • The presence of minimal residual disease (MRD) in the bone marrow (BM) of patients with acute myeloid leukemia (AML) following chemotherapy has been established by many studies to be strongly associated with relapse of leukemia.
  • In addition, detection of MRD is the major objective of many of the newer diagnostic techniques used in malignant hematology.
  • Because of the wide availability and conceptual straightforwardness of immunophenotyping, flow cytometry is the most accessible method for MRD detection.
  • This review is not an overview of all MRD studies, but rather discusses the possibilities for optimizing MRD detection, the use of multiparameter flow cytometry (MFC) techniques in MRD detection, and the implications for future patient treatment.
  • This review focuses on MRD detection in AML using MFC and discusses the reported correlations of MRD, clinical and biologic features of the disease, and outcome.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis
  • [MeSH-minor] Antigens, CD34 / analysis. Flow Cytometry / methods. Humans. Immunophenotyping / methods. Neoplasm, Residual. Phenotype. Sensitivity and Specificity

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  • (PMID = 19095561.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34
  • [Number-of-references] 65
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60. Barbón García JJ, Viña Escalar C, Menéndez Fernández CL, Fernández Alvarez C, Carballo Fernández C, Villarreal Renedo PM: [Uveal lymphoid infiltration with systemic extension]. Arch Soc Esp Oftalmol; 2003 Mar;78(3):173-6
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  • Ultrasound and computed tomography showed diffuse choroidal thickening.
  • During 6 years of follow-up, he developed a major ocular and orbitary invasion and bone marrow infiltration.
  • He was treated by enucleation and chemotherapy with apparent total remission.
  • This process is regarded as a low malignant condition, but this case of late diagnosis showed a tendency to orbital and systemic extension.
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / pathology. Cyclophosphamide / administration & dosage. Disease Progression. Doxorubicin / administration & dosage. Eye Enucleation. Glaucoma, Neovascular / etiology. Humans. Immunoglobulin kappa-Chains / blood. Male. Neoplasm Invasiveness. Orbital Neoplasms / secondary. Paraproteins. Prednisone / administration & dosage. Remission Induction. Vincristine / administration & dosage

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  • (PMID = 12677496.001).
  • [ISSN] 0365-6691
  • [Journal-full-title] Archivos de la Sociedad Española de Oftalmología
  • [ISO-abbreviation] Arch Soc Esp Oftalmol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Immunoglobulin kappa-Chains; 0 / Paraproteins; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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61. Edinger M, Cao YA, Verneris MR, Bachmann MH, Contag CH, Negrin RS: Revealing lymphoma growth and the efficacy of immune cell therapies using in vivo bioluminescence imaging. Blood; 2003 Jan 15;101(2):640-8
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  • [Title] Revealing lymphoma growth and the efficacy of immune cell therapies using in vivo bioluminescence imaging.
  • Cancer therapeutics have achieved success in the treatment of a variety of malignancies, however, relapse of disease from small numbers of persistent tumor cells remains a major obstacle.
  • Advancement of treatment regimens that effectively control minimal residual disease and prevent relapse would be greatly accelerated if sensitive and noninvasive assays were used to quantitatively assess tumor burden in animal models of minimal residual disease that are predictive of the human response.
  • In vivo bioluminescence imaging (BLI) is an assay for the detection of small numbers of cells noninvasively and enables the quantification of tumor growth within internal organs.
  • We labeled 2 murine lymphoma cell lines with dual function reporter genes and monitored radiation and chemotherapy as well as immune-based strategies that employ the tumorcidal activity of ex vivo-expanded CD8(+) natural killer (NK)-T cells.
  • Using BLI we were able to visualize the entire course of malignant disease including engraftment, expansion, metastasis, response to therapy, and unique patterns of relapse.
  • We also labeled the effector NK-T cells and monitored their homing to the sites of tumor growth followed by tumor eradication.
  • These studies reveal the efficacy of immune cell therapies and the tempo of NK-T cell trafficking in vivo.
  • The complex cellular processes in bone marrow transplantation and antitumor immunotherapy, previously inaccessible to investigation, can now be revealed in real time in living animals.
  • [MeSH-major] Diagnostic Imaging / methods. Immunotherapy, Adoptive / methods. Lymphoma / pathology. Lymphoma / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Division / drug effects. Cell Division / genetics. Cell Division / radiation effects. Female. Genes, Reporter. Killer Cells, Lymphokine-Activated / metabolism. Killer Cells, Lymphokine-Activated / transplantation. Luminescent Measurements. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasm Metastasis / diagnosis. Neoplasm Metastasis / pathology. Radiotherapy. Transduction, Genetic

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  • (PMID = 12393519.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / K08 HL04505-01; United States / NCI NIH HHS / CA / P01 CA49605; United States / NCI NIH HHS / CA / P20 CA86312; United States / NCI NIH HHS / CA / R01 CA80006; United States / NCI NIH HHS / CA / R24 CA92862; United States / NCI NIH HHS / CA / R33 CA88303
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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62. Nihashi T, Hayasaka K, Itou T, Sobajima T, Kato R, Ito K, Ito Y, Ishigaki T, Naganawa S: Usefulness of FDG PET for diagnosis and radiotherapy of the patient with malignant lymphoma involving bone marrow. Radiat Med; 2007 Apr;25(3):130-4
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  • [Title] Usefulness of FDG PET for diagnosis and radiotherapy of the patient with malignant lymphoma involving bone marrow.
  • We experienced a case of relapsed malignant lymphoma with multiple bone marrow or bone lesions.
  • The case was diagnosed as follicular lymphoma by cytological biopsy of the right iliac bone, with (67)Ga scintigraphy showing abnormal, intense uptake in multiple bones.
  • After about 10 months of systemic chemotherapy, a relapse was suspected because of pain in the bilateral legs and a high level of lactate dehydrogenase.
  • Assessment of the lesions in the patient was difficult by computed tomography because the affected sites were localized mainly in the bone marrow. (18)F-Fluorodeoxyglucose (FDG) positron emission tomography (PET) was useful for detecting accurately the relapse sites in the bone marrow and enabled us to determine the field for radiotherapy.
  • There are only a few reports of FDG-PET findings for such bone marrow malignant lymphomas.
  • Therefore, we report the findings of FDG-PET for this case and review some of the literature about bone marrow lymphomas.
  • [MeSH-major] Bone Marrow Neoplasms / diagnostic imaging. Fluorodeoxyglucose F18. Lymphoma / diagnostic imaging. Radiopharmaceuticals. Tomography, Emission-Computed / methods
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Gallium Radioisotopes. Humans. Neoplasm Recurrence, Local

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  • [Cites] N Engl J Med. 1993 Sep 30;329(14 ):987-94 [8141877.001]
  • [Cites] AJR Am J Roentgenol. 2004 Jun;182(6):1579-86 [15150013.001]
  • [Cites] Ann Oncol. 2006 May;17 (5):780-4 [16497824.001]
  • [Cites] Ann Nucl Med. 2005 Dec;19(8):725-8 [16445000.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1258-65 [15126323.001]
  • [Cites] Ann Hematol. 2004 May;83(5):276-8 [15060746.001]
  • [Cites] J Nucl Med. 2003 Jan;44(1):24-9 [12515872.001]
  • [Cites] Semin Nucl Med. 2005 Jul;35(3):160-4 [16098289.001]
  • [Cites] Ann Oncol. 2005 Aug;16(8):1401-2 [15870088.001]
  • [Cites] Radiology. 1998 Feb;206(2):475-81 [9457202.001]
  • [Cites] J Clin Oncol. 1991 May;9(5):762-9 [1707956.001]
  • [Cites] Blood. 1997 Jun 1;89(11):3909-18 [9166827.001]
  • [Cites] Radiology. 2003 May;227(2):353-60 [12637679.001]
  • (PMID = 17450338.001).
  • [ISSN] 0288-2043
  • [Journal-full-title] Radiation medicine
  • [ISO-abbreviation] Radiat Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Gallium Radioisotopes; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
  • [Number-of-references] 14
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63. Moulopoulos LA, Maris TG, Papanikolaou N, Panagi G, Vlahos L, Dimopoulos MA: Detection of malignant bone marrow involvement with dynamic contrast-enhanced magnetic resonance imaging. Ann Oncol; 2003 Jan;14(1):152-8
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  • [Title] Detection of malignant bone marrow involvement with dynamic contrast-enhanced magnetic resonance imaging.
  • BACKGROUND: The purpose of this study was to evaluate the role of dynamic contrast-enhanced magnetic resonance imaging (dMRI) in detecting bone marrow involvement in cancer patients.
  • PATIENTS AND METHODS: We studied 50 consecutive patients with histologically confirmed malignant dissemination to the bone marrow, using dMRI of the lumbosacral spine.
  • Time-signal intensity curves were generated from regions of interest (ROIs) obtained from areas of obvious bone marrow disease (group B).
  • In 16 patients from group B with focal disease, ROIs were also placed on areas with apparently normal bone marrow on static magnetic resonance images (group C).
  • Wash-in (WIN) and wash-out (WOUT) rates, time to peak (TTPK), time to maximum slope (TMSP) values and WIN/TMSP ratios were calculated for each patient.
  • Six patients from group B had follow-up dMRI after chemotherapy: four patients achieved a clinical partial response and two had resistant disease.
  • CONCLUSIONS: dMRI can distinguish normal from malignant bone marrow.
  • It may identify malignant bone marrow infiltration in patients with negative static MRI and serve as both a diagnostic and prognostic tool for patients with bone marrow malignancies.

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  • (PMID = 12488307.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Contrast Media
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64. Dölken G: Detection of minimal residual disease. Adv Cancer Res; 2001;82:133-85

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of minimal residual disease.
  • A high percentage of patients with leukemia, lymphoma, and solid tumors achieve a complete clinical remission after initial treatment, but the majority of these patients will finally relapse from residual tumor cells detectable in clinical remission only by the most sensitive methods.
  • The in vitro amplification of tumor-specific DNA or RNA sequences by polymerase chain reaction (PCR) allows identification of a few neoplastic cells in 10(4) to 10(6) normal cells.
  • Depending on the underlying malignant disease and therapeutic treatment, the presence of residual tumor cells in an individual patient may herald relapse, but a long-term stable situation or slowly vanishing tumor cells are also possible.
  • Molecular monitoring of residual leukemia and lymphoma cells by quantitative PCR techniques has provided important information about the effectiveness of treatment and the risk of recurrent disease as shown by minimal residual disease (MRD) analysis in patients with various malignant diseases.
  • Such diseases include childhood acute lymphoblastic leukemia, after induction therapy; acute promyelocytic leukemia, during and after chemotherapy; and chronic myelogenous leukemia, during treatment with alpha-interferon and after allogeneic bone marrow transplantation.
  • Evaluation of the predictive value of the detection of MRD has to take into account its evolution and course, the pathogenesis, biology, and natural course of the underlying malignant disease, the molecular genetic lesion, and finally, the type of treatment.
  • Quantification of minimal residual cells by the recently developed real-time quantitative PCR technique will surely have a major impact on our therapeutic strategies for patients with leukemia, lymphomas, and solid tumors.
  • Based on quantitative PCR data, the terms molecular remission and molecular relapse have to be exactly defined and validated in prospective clinical trials to assess the biological and clinical significance of MRD in various types of malignancies.
  • [MeSH-major] Neoplasm, Residual / diagnosis

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  • (PMID = 11447762.001).
  • [ISSN] 0065-230X
  • [Journal-full-title] Advances in cancer research
  • [ISO-abbreviation] Adv. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Number-of-references] 326
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65. Nakazato T, Suzuki K, Mihara A, Sanada Y, Yoshida S, Kakimoto T: [Intravascular large B-cell lymphoma with pontine involvement successfully treated with R-hyper-CVAD/R-MTX-Ara-C regimen]. Rinsho Ketsueki; 2010 Feb;51(2):148-52
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  • Malignant lymphoma was suspected, but histological diagnosis was difficult because superficial lymph nodes could not be palpated.
  • Histological examination of the bone marrow biopsy specimen demonstrated the proliferation of large atypical lymphoid cells positive for CD20 and CD79a in the small capillaries, leading to the diagnosis of intravascular large B-cell lymphoma (IVLBCL).
  • We chose R-hyper-CVAD/R-MTX-Ara-C alternating therapy with MTX intrathecal injection because CNS involvement in IVLBCL was highly suspected, and she responded well.
  • R-hyper-CVAD/R-MTX-Ara-C alternating therapy was effective in an IVLBCL patient with CNS involvement.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Stem Neoplasms / drug therapy. Brain Stem Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / drug therapy. Vascular Neoplasms / drug therapy
  • [MeSH-minor] Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Dexamethasone / administration & dosage. Doxorubicin / administration & dosage. Female. Humans. Methotrexate / administration & dosage. Middle Aged. Neoplasm Invasiveness. Remission Induction. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 20379108.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; YL5FZ2Y5U1 / Methotrexate; CVAD protocol
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66. Bains SN, Hsieh FH: Current approaches to the diagnosis and treatment of systemic mastocytosis. Ann Allergy Asthma Immunol; 2010 Jan;104(1):1-10; quiz 10-2, 41
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  • [Title] Current approaches to the diagnosis and treatment of systemic mastocytosis.
  • OBJECTIVE: To review the clinical manifestations of mastocytosis and examine the recommended diagnostic procedures and therapeutic options available for the treatment of this condition.
  • DATA SOURCES: PubMed searches were performed for articles published regarding presentation and classification of mastocytosis and the diagnostic criteria and treatment options for this condition using the keywords mastocytosis, clinical features, World Health Organization diagnostic criteria, management, pathogenesis, and urticaria pigmentosa.
  • Symptoms are typically limited to the skin in the pediatric population, requiring only symptomatic treatment with spontaneous resolution by puberty.
  • The mainstay of treatment consists of avoidance of triggers of mast cell degranulation and symptom-based therapy.
  • Diagnosis should be established by a bone marrow biopsy in all adults.
  • Patients should be offered symptom-based treatment and cytoreductive therapy only for aggressive systemic mastocytosis or an associated hematologic malignant neoplasm.
  • [MeSH-major] Histamine Antagonists / therapeutic use. Mast Cells / pathology. Mastocytosis, Systemic / diagnosis. Mastocytosis, Systemic / drug therapy
  • [MeSH-minor] Biopsy. Bone Marrow / pathology. Diagnosis, Differential. Glucocorticoids / therapeutic use. Humans. Skin / pathology. Tryptases / metabolism

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  • (PMID = 20143640.001).
  • [ISSN] 1081-1206
  • [Journal-full-title] Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
  • [ISO-abbreviation] Ann. Allergy Asthma Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Histamine Antagonists; EC 3.4.21.59 / Tryptases
  • [Number-of-references] 50
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67. Iversen PO, Sørensen DR, Tronstad KJ, Gudbrandsen OA, Rustan AC, Berge RK, Drevon CA: A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of acute leukemia. Clin Cancer Res; 2006 Jun 1;12(11 Pt 1):3525-31
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  • RESULTS: Whereas TTA prolonged survival (P < 0.05) in both types of rat leukemia, n-3 PUFA had no significant effect compared with controls.
  • Only TTA inhibited (P < 0.05) leukemic infiltration in the bone marrow and spleen, probably due to apoptosis of the leukemic cells.
  • TTA represents a modified fatty acid that exerts unique effects on malignant hematopoietic cells, and the present study indicates that TTA may have a therapeutic potential in patients with acute leukemias.
  • [MeSH-major] Fatty Acids, Unsaturated / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Sulfides / administration & dosage
  • [MeSH-minor] Animals. Apoptosis / drug effects. Diet. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Humans. Leukemic Infiltration / diagnosis. Matrix Metalloproteinases / drug effects. Neoplasm Metastasis. Rats. Structure-Activity Relationship. Survival Rate. Transplantation, Heterologous. Xenograft Model Antitumor Assays

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  • (PMID = 16740779.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids, Unsaturated; 0 / Sulfides; 2921-20-2 / 1-(carboxymethylthio)tetradecane; EC 3.4.24.- / Matrix Metalloproteinases
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68. Tabata M, Satake A, Okura N, Yamazaki Y, Toda A, Nishioka K, Tanaka H, Chin M, Itsukuma T, Yamaguchi M, Misawa M, Kai S, Hara H: Long-term outcome after allogeneic bone marrow transplantation for hematological malignancies with non-remission status. Results of a single-center study of 24 patients. Ann Hematol; 2002 Oct;81(10):582-7
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  • [Title] Long-term outcome after allogeneic bone marrow transplantation for hematological malignancies with non-remission status. Results of a single-center study of 24 patients.
  • To investigate the problem of allogeneic bone marrow transplantation (allo-BMT) for advanced stage patients, we retrospectively analyzed 24 consecutive patients who underwent allo-BMT in the non-remission stage.
  • Twenty-four patients (19 males and 5 females) with acute leukemia, chronic myelogenous leukemia, and malignant lymphoma underwent allo-BMT.
  • The 3-year overall survival rate was 22.5%, with a median survival time of 206 days in AML, 345 days in ALL, and 363 days in CML.
  • In addition, the selection of the source of hematopoietic stem cell transplantation at an optimal time is considered to be another problem to be approached.
  • [MeSH-major] Bone Marrow Transplantation. Drug Resistance, Neoplasm. Hematologic Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Cause of Death. Female. Graft vs Host Disease / diagnosis. Graft vs Host Disease / mortality. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis. Survival Rate. Transplantation Conditioning. Transplantation, Homologous / adverse effects. Transplantation, Homologous / mortality. Treatment Outcome

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  • (PMID = 12424540.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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69. Murota H, Shoda Y, Ishibashi T, Sugahara H, Matsumura I, Katayama I: Improvement of recurrent urticaria in a patient with Schnitzler syndrome associated with B-cell lymphoma with combination rituximab and radiotherapy. J Am Acad Dermatol; 2009 Dec;61(6):1070-5
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  • Schnitzler syndrome is a rare condition defined by chronic urticaria, osteosclerotic bone lesions, and monoclonal IgM gammopathy.
  • We describe a case of intractable chronic urticaria accompanied by a retroperitoneal neoplasm.
  • IgM monoclonal gammopathy, lumber pain, intermittent fever, and elevation of C-reactive protein were the clues for the diagnosis of Schnitzler syndrome.
  • An evaluation for malignancy using systemic computed tomography scan and fluorodeoxyglucose positron emission tomography revealed the retroperitoneal tumor, and a subsequent bone-marrow aspirate confirmed the diagnosis of B-cell lymphoma.
  • This case indicates that a detailed search for malignant neoplasms might be required for the long-term management of Schnitzler syndrome, and that B-cell lymphomas may contribute to the pathogenesis of this condition.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / radiotherapy. Retroperitoneal Neoplasms / radiotherapy. Schnitzler Syndrome / complications. Urticaria / complications
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Murine-Derived. Combined Modality Therapy. Female. Humans. Rituximab

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  • (PMID = 19632739.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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70. Chandwani S, Wentworth C, Burke TA, Patterson TF: Utilization and dosage pattern of echinocandins for treatment of fungal infections in US hospital practice. Curr Med Res Opin; 2009 Feb;25(2):385-93
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  • [Title] Utilization and dosage pattern of echinocandins for treatment of fungal infections in US hospital practice.
  • The purpose of this study was to describe the utilization and dosage pattern of intravenous echinocandins for treatment of fungal infections in US hospitals.
  • Mixed multivariable models were developed to identify factors associated with mean daily dose.
  • Micafungin patients had the highest prevalence of cancer, bone marrow transplant, solid organ transplant, HIV/AIDS, fungal infection, and neutropenia.
  • Mean day 1 dose of echinocandin therapy was 171.2 +/- 85.4 mg, 79.7 +/- 25.6 mg, and 154.3 +/- 67.3 mg; and mean day 2 onwards dose was 98.7 +/- 39.4 mg, 53.1 +/- 12.5 mg, 122.6 +/- 39.4 mg for anidulafungin, caspofungin and micafungin, respectively.
  • The first-day dose of echinocandin therapy (vs. subsequent days) was most strongly associated with mean daily dose.
  • Lack of information on reason for initiating echinocandin therapy was an important study limitation.
  • [MeSH-major] Antifungal Agents / therapeutic use. Drug Utilization Review. Echinocandins / therapeutic use. Hospitals. Mycoses / drug therapy
  • [MeSH-minor] Aged. Cohort Studies. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Retrospective Studies. United States

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  • (PMID = 19192983.001).
  • [ISSN] 1473-4877
  • [Journal-full-title] Current medical research and opinion
  • [ISO-abbreviation] Curr Med Res Opin
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins
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71. Kunisaki Y, Muta T, Yamano Y, Kobayashi Y: Detection of two cell populations corresponding to distinct maturation stages in API-2/MLT-positive mucosa-associated lymphoid tissue lymphoma cells proliferating in pleural effusion. Int J Hematol; 2003 Nov;78(4):357-61

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of two cell populations corresponding to distinct maturation stages in API-2/MLT-positive mucosa-associated lymphoid tissue lymphoma cells proliferating in pleural effusion.
  • A 66-year-old man was admitted to our hospital because of an intra-abdominal tumor and pleural effusion (PE).
  • Abnormal plasmacytoid cells were seen in both the peripheral blood (PB) and the bone marrow (BM).
  • Computed tomography scans showed extensive thickening of the gastric wall and bilateral massive PE without lymph node or pulmonary involvement.
  • The diagnosis was gastric mucosa-associated lymphoid tissue (MALT) lymphoma infiltrating to the PE, PB, and BM.
  • The patient had a good response to fludarabine treatment, which was followed with rituximab therapy.
  • [MeSH-major] Lymphoma, B-Cell, Marginal Zone / pathology. Oncogene Proteins, Fusion / analysis. Pleural Effusion, Malignant / pathology
  • [MeSH-minor] Aged. Antigens, Differentiation, B-Lymphocyte / analysis. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. B-Lymphocytes / pathology. Cell Adhesion Molecules / analysis. Cell Differentiation. Cell Division. Humans. Immunophenotyping. Male. Neoplasm, Residual. Stomach Neoplasms / diagnosis. Stomach Neoplasms / drug therapy. Stomach Neoplasms / pathology

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  • [Cites] Cancer Res. 1997 Sep 15;57(18):3944-8 [9307277.001]
  • [Cites] Blood. 2002 Jan 1;99(1):3-9 [11756145.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • [Cites] Lancet. 1991 Nov 9;338(8776):1175-6 [1682595.001]
  • [Cites] Am J Pathol. 1999 Dec;155(6):2019-27 [10595932.001]
  • [Cites] Mod Pathol. 2001 Aug;14(8):798-805 [11504840.001]
  • [Cites] Int J Hematol. 2002 Dec;76(5):385-93 [12512832.001]
  • [Cites] Blood. 2000 Jul 15;96(2):410-9 [10887100.001]
  • [Cites] Rinsho Ketsueki. 2000 Nov;41(11):1183-8 [11193437.001]
  • [Cites] Br J Haematol. 2001 Dec;115(3):588-94 [11736940.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1 Suppl 2):36-40 [11842387.001]
  • [Cites] Am J Clin Pathol. 2001 Nov;116(5):683-90 [11710684.001]
  • [Cites] Gut. 2001 Oct;49(4):519-25 [11559649.001]
  • [Cites] Am J Clin Pathol. 1999 Jan;111(1 Suppl 1):S8-12 [9894466.001]
  • [Cites] Am J Pathol. 1997 May;150(5):1583-93 [9137085.001]
  • [Cites] Br J Haematol. 1997 Jun;97(3):515-22 [9207392.001]
  • [Cites] Jpn J Cancer Res. 2000 Mar;91(3):301-9 [10760689.001]
  • [Cites] Leuk Res. 1990;14(7):617-22 [2388473.001]
  • [Cites] Acta Otolaryngol Suppl. 1996;523:259-62 [9082801.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Mar;117(2):113-7 [10704680.001]
  • [Cites] Cell. 1993 Jul 16;74(1):185-95 [7687523.001]
  • (PMID = 14686495.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / API2-MALT1 fusion protein, human; 0 / Antigens, Differentiation, B-Lymphocyte; 0 / Cell Adhesion Molecules; 0 / Oncogene Proteins, Fusion
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72. Willmott F, Agarwal N, Heath M, Stevens J, Chakravarti S: Plasma cell myeloma diagnosed in pregnancy. BMJ Case Rep; 2010;2010
MedlinePlus Health Information. consumer health - Tumors and Pregnancy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The clinical picture is one of bone marrow failure, due to infiltration of the marrow by malignant plasma cells; renal failure due to damage to renal tubules by the excess light chains and pain due to lytic lesions of the bones.
  • [MeSH-major] Multiple Myeloma / diagnosis. Pregnancy Complications, Neoplastic / diagnosis
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy, Needle. Bone Marrow / pathology. Cesarean Section. Disease Progression. Female. Fetal Growth Retardation / diagnosis. Hematopoietic Stem Cell Transplantation. Humans. Infant, Newborn. Male. Neoplasm Staging. Pregnancy. Puerperal Disorders / diagnosis. Puerperal Disorders / drug therapy. Puerperal Disorders / pathology. Remission Induction

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  • [Cites] J Bone Joint Surg Am. 2004 Jun;86-A(6):1284-8 [15173303.001]
  • [Cites] Blood. 1966 Jul;28(1):102-11 [5944257.001]
  • [Cites] Obstet Gynecol. 1968 Jun;31(6):811-20 [5742077.001]
  • [Cites] West Indian Med J. 1971 Jun;20(2):97-100 [5110487.001]
  • [Cites] Cancer. 1974 Oct;34(4):1018-22 [4417641.001]
  • [Cites] Arch Pathol Lab Med. 1987 Jan;111(1):38-42 [3800603.001]
  • [Cites] Obstet Gynecol. 1990 Mar;75(3 Pt 2):513-5 [2304725.001]
  • [Cites] Obstet Gynecol. 1990 Mar;75(3 Pt 2):516-8 [2304726.001]
  • [Cites] Int J Gynaecol Obstet. 1991 Aug;35(4):341-2 [1682183.001]
  • [Cites] Am J Obstet Gynecol. 1995 Jan;172(1 Pt 1):217-9 [7847542.001]
  • [Cites] Leuk Res. 1997 Sep;21(9):885-8 [9393604.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3412-20 [15809451.001]
  • [Cites] Am J Clin Pathol. 2005 Jul;124(1):108-12 [15923168.001]
  • [Cites] J Obstet Gynaecol. 2006 Oct;26(7):693-5 [17071446.001]
  • [Cites] Nephrol Dial Transplant. 2007 Dec;22(12):3652-5 [17875572.001]
  • [Cites] Int J Gynaecol Obstet. 2008 Jan;100(1):89-90 [17825829.001]
  • [Cites] Ann Hematol. 2009 Feb;88(2):181-2 [18682949.001]
  • [Cites] Eur J Obstet Gynecol Reprod Biol. 2003 Dec 10;111(2):214-5 [14597255.001]
  • (PMID = 22791481.001).
  • [ISSN] 1757-790X
  • [Journal-full-title] BMJ case reports
  • [ISO-abbreviation] BMJ Case Rep
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3027817
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73. Montillo M, Schinkoethe T, Elter T: Eradication of minimal residual disease with alemtuzumab in B-cell chronic lymphocytic leukemia (B-CLL) patients: the need for a standard method of detection and the potential impact of bone marrow clearance on disease outcome. Cancer Invest; 2005;23(6):488-96
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Eradication of minimal residual disease with alemtuzumab in B-cell chronic lymphocytic leukemia (B-CLL) patients: the need for a standard method of detection and the potential impact of bone marrow clearance on disease outcome.
  • The introduction of new therapeutic agents, such as fludarabine phosphate (Fludara) and alemtuzumab (MabCampath, Campath), has made it possible to treat B-cell chronic lymphocytic leukemia (B-CLL) more effectively, compared with alkylating agents.
  • However, although an increasing number of patients are able to achieve complete remission (CR), relapse is almost inevitable, because of the re-emergence of the malignant clone from small numbers of residual malignant cells.
  • This phenomenon has introduced a need for a more sensitive assessment of low-level disease which, in turn, has encouraged the development of therapies aimed at the eradication of all residual disease in CR patients.
  • Alemtuzumab is the foundation of many eradication-based treatment approaches because of its ability to achieve clinical remissions and to successfully purge minimal residual disease (MRD) from both blood and bone marrow in B-CLL patients.
  • This article describes and compares polymerase chain reaction (PCR) and flow cytometric methodologies for the assessment of MRD, and presents data demonstrating that alemtuzumab can eliminate residual malignant cells from blood and bone marrow (whether assessed by PCR or flow cytometry) at the highest levels of sensitivity currently available.
  • The ability to clear MRD from bone marrow in patients achieving clinical CR using alemtuzumab is a significant step forward in the treatment of B-CLL, and supports treatment strategies in which alemtuzumab is used in combination with other agents.
  • Purging of MRD from both blood and bone marrow also enables patients to proceed to autologous hematopoietic stem cell transplantation, a strategy that is able to achieve long-term remission.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Neoplasm, Residual / diagnosis. Neoplasm, Residual / drug therapy

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  • (PMID = 16203656.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 55
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74. Schmiegelow K: [Individualized cancer treatment. Illustrated by acute lymphoblastic leukemia in children]. Ugeskr Laeger; 2001 Feb 19;163(8):1062-6
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Individualized cancer treatment. Illustrated by acute lymphoblastic leukemia in children].
  • The intensity of treatment in children with acute lymphoblastic leukaemia has conventionally been based on risk group stratification, which reflected the patient's age and white cell count at diagnosis, as well as the immunophenotype and presence of certain high risk chromosomal aberrations.
  • Nevertheless, the risk-adapted and very intensive antileukaemic therapy has been a success, with cure rates as high as 75-80 per cent.
  • A more individualiZed tailoring of the therapy is expected to be available through:.
  • 2) exploration of the in vitro drug sensitivity of the malignant clone;.
  • 3) detailed monitoring of the minimal residual disease down to the level of one leukaemic cell in 10,000-100,000 normal bone marrow cells;.
  • 4) therapeutic drug monitoring and individual dose adjustments; and 5) mapping of the individual patient's risk of serious or even life-threatening side effects.
  • It is likely that these approaches would allow a reduction in the treatment intensity for most patients, thereby reducing the risk of serious toxicity, and concomitantly improve identification of those patients for whom standard therapy is likely to fail and who are thus candidates for stem cell transplantion or experimental therapy in first remission.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Child. Chromosome Aberrations. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Humans. Risk Factors. Tumor Cells, Cultured

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  • (PMID = 11242663.001).
  • [ISSN] 0041-5782
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 41
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75. Manzitti C, Mereu P, Haupt R, Di Blasi A, Bellani FF, Dallorso S: Parotid carcinoma after autologous bone marrow transplantation for relapsed nephroblastoma. J Pediatr Hematol Oncol; 2003 Aug;25(8):672-3
Hazardous Substances Data Bank. DOXORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Parotid carcinoma after autologous bone marrow transplantation for relapsed nephroblastoma.
  • Abdominal irradiation, especially if associated with doxorubicin administration, increases the risk of a secondary malignant neoplasm (SMN) after treatment of nephroblastoma.
  • Secondary malignant salivary tumors are rare and usually occur in patients with previous cranial irradiation.
  • The authors describe the case of a parotid mucoepidermoid carcinoma arising 13 years after diagnosis of nephroblastoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / etiology. Carcinoma / pathology. Liver Neoplasms / drug therapy. Liver Neoplasms / radiotherapy. Neoplasms, Second Primary / etiology. Parotid Neoplasms / etiology. Parotid Neoplasms / pathology. Wilms Tumor / drug therapy. Wilms Tumor / radiotherapy
  • [MeSH-minor] Adult. Doxorubicin / administration & dosage. Humans. Male. Time Factors

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  • (PMID = 12902928.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 80168379AG / Doxorubicin
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76. Rodzaj M, Gałazka K, Majewski M, Zduńczyk A: A diagnostically difficult case of chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA effectively treated with imatinib in accelerated phase: case report. Pol Arch Med Wewn; 2009 Dec;119(12):838-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A diagnostically difficult case of chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA effectively treated with imatinib in accelerated phase: case report.
  • Chronic myeloid neoplasm with eosinophilia and abnormalities of platelet-derived growth factor receptor alpha (PDGFRA), referred to until 2008 as chronic eosinophilic leukemia, is distinguished from hypereosinophilic syndrome (HES), if accompanied by genetic abnormalities that enable to determine eosinophil clonality.
  • In chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA the FIP1L1-PDGFRA fusion gene can be detected.
  • Its product is a protein showing tyrosine kinase activity leading to malignant proliferation of eosinophil precursors.
  • Differential diagnosis of HES is often difficult because hypereosinophilia may also be reactive and may occur in many nonhematological as well as hematological disorders.
  • Traditional treatment of chronic myeloid neoplasm with cytostatic drugs results in a short-term and transient remission or stabilization of the disease.
  • We present the case of a 52-year-old patient with chronic myeloid neoplasm with eosinophilia and abnormalities of PDGFRA, in whom acceleration occurred after a year of cytostatic therapy with hydroxyurea and was successfully treated with imatinib.
  • It was impossible to unequivocally determine the type of bone marrow disease based on histologic criteria, and a wide spectrum of molecular tests differentiating the type of myeloid proliferation were necessary to establish the diagnosis.
  • Further molecular testing showed rearrangement involving the FIP1L1 gene, thus enabling implementation of targeted therapy.
  • [MeSH-major] Hypereosinophilic Syndrome / diagnosis. Hypereosinophilic Syndrome / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Oncogene Proteins, Fusion / metabolism. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha / metabolism. mRNA Cleavage and Polyadenylation Factors / metabolism

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  • (PMID = 20010473.001).
  • [ISSN] 1897-9483
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / FIP1L1-PDGFRA fusion protein, human; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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