BioMedLib Search Engine [ goto HOMEPAGE ]

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The results from our model much more closely approximate the experimental values than the former model built up by Datskos, Rajic and Datskou [1](APL, Vol.73 (1998) No.16, pp 3219-2321), represented by the reduction of the error between calculation and measurement from 25 times to 0.85 times.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 28903192.001).

[ISSN] 1424-8220

[Journal-full-title] Sensors (Basel, Switzerland)

[ISO-abbreviation] Sensors (Basel)

[Language] eng

[Publication-type] Journal Article

[Publication-country] Switzerland

[Keywords] NOTNLM ; Photostriction / deformation / microcantilever / silicon

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Abductor pollicis longus (APL) muscle is known to exhibit different variations with respect to its attachments.

Various studies have reported the splitting of the APL muscle.

Comparative anatomical findings of split insertion of APL is commonly found in chimpanzees, gorillas and gibbons.

In the present study, we describe an anomalous APL muscle, which originated from the posterior surface of the shaft of the radius and ulna and traversed a course deep to the extensor retinaculum.

Interestingly, immediately after emerging form the deeper aspect of extensor retinaculum, the thin tendon of the APL muscle continued again as a muscular belly in relation to the dorsolateral part of the 1st metacarpal bone, to end as a tendon with its attachment to the base of the proximal phalanx.

Such an unusual variation of APL with its attachment into proximal phalanx is a rare finding and may be of importance in altering the mechanics of the thumb during abduction.

The clinical significance of such an anatomical variation of APL may be important during reconstructive surgeries involving thumb and also of academic interest.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 28795947.001).

[ISSN] 1211-4286

[Journal-full-title] Acta medica (Hradec Kralove)

[ISO-abbreviation] Acta Medica (Hradec Kralove)

[Language] eng

[Publication-type] Journal Article

[Publication-country] Czech Republic

[Keywords] NOTNLM ; Abductor pollicis longus / Anomaly / Attachment / Muscle / Tendon / Variation

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute promyelocytic leukemia: from highly fatal to highly curable.

Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia.

Morphologically, it is identified as the M3 subtype of acute myeloid leukemia by the French-American-British classification and cytogenetically is characterized by a balanced reciprocal translocation between chromosomes 15 and 17, which results in the fusion between promyelocytic leukemia (PML) gene and retinoic acid receptor alpha (RARalpha).

It seems that the disease is the most malignant form of acute leukemia with a severe bleeding tendency and a fatal course of only weeks.

Chemotherapy (CT; daunorubicin, idarubicin and cytosine arabinoside) was the front-line treatment of APL with a complete remission (CR) rate of 75% to 80% in newly diagnosed patients.

Since the introduction of all-trans retinoic acid (ATRA) in the treatment and optimization of the ATRA-based regimens, the CR rate was raised up to 90% to 95% and 5-year disease free survival (DFS) to 74%.

The use of arsenic trioxide (ATO) since early 1990s further improved the clinical outcome of refractory or relapsed as well as newly diagnosed APL.

In this article, we review the history of introduction of ATRA and ATO into clinical use and the mechanistic studies in understanding this model of cancer targeted therapy.

[MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

Hazardous Substances Data Bank. ARSENIC TRIOXIDE .

Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18299451.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Historical Article; Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide

[Number-of-references] 111

   

Advertisement

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Antiphospholipid antibodies and acute-phase response in non-metastatic colorectal cancer patients.

AIM: To investigate the plasma levels and prevalence of the most common antiphospholipid antibodies, as well as their relationships with several plasma markers of inflammation, in order to characterize some aspects of cancer thrombophilia.

MATERIALS AND METHODS: Eighty-three cancer patients with non-metastatic colorectal solid tumors and 94 control subjects were tested for the presence of IgG/IgM/IgA anti-cardiolipin and anti-Beta2-glycoprotein I antibodies and of several acutephase reactants, i.e., fibrinogen, factor VIII:C and C4b-binding protein.

RESULTS: In cancer patients the plasma levels of the acute-phase reactants and the IgA/IgG anti-cardiolipin and IgA anti-Beta2- glycoprotein I antibodies were significantly higher; the acute-phase reactants were significantly correlated with anti-cardiolipin antibodies; the prevalence of antiphospholipid antibodies was not significantly higher.

CONCLUSIONS: In patients with non-metastatic colorectal cancer the acute-phase response is associated with antiphospholipid generation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 28207104.001).

[ISSN] 1724-6008

[Journal-full-title] The International journal of biological markers

[ISO-abbreviation] Int. J. Biol. Markers

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cell-cycle regulation and dynamics of cytoplasmic compartments containing the promyelocytic leukemia protein and nucleoporins.

Nucleoporins and the promyelocytic leukemia protein (PML) represent structural entities of nuclear pore complexes and PML nuclear bodies, respectively.

In addition, these proteins might function in a common biological mechanism, because at least two different nucleoporins, Nup98 and Nup214, as well as PML, can become aberrantly expressed as oncogenic fusion proteins in acute myeloid leukemia (AML) cells.

Here we show that PML and nucleoporins become directed to common cytoplasmic compartments during the mitosis-to-G1 transition of the cell cycle.

These protein assemblies, which we have termed CyPNs (cytoplasmic assemblies of PML and nucleoporins), move on the microtubular network and become stably connected to the nuclear membrane once contact with the nucleus has been made.

The ability of PML to target CyPNs depends on its nuclear localization signal, and loss of PML causes an increase in cytoplasmic-bound versus nuclear-membrane-bound nucleoporins.

CyPNs are also targeted by the acute promyelocytic leukemia (APL) fusion protein PML-RARalpha and can be readily detected within the APL cell line NB4.

These results provide insight into a dynamic pool of cytoplasmic nucleoporins that form a complex with the tumor suppressor protein PML during the G1 phase of the cell cycle.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19339552.001).

[ISSN] 0021-9533

[Journal-full-title] Journal of cell science

[ISO-abbreviation] J. Cell. Sci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / CREBBP protein, human; 0 / Nuclear Localization Signals; 0 / Nuclear Pore Complex Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 0 / Tubulin Modulators; 0 / Tumor Suppressor Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 143220-95-5 / PML protein, human; EC 2.3.1.48 / CREB-Binding Protein; SH1WY3R615 / Nocodazole

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Rituximab effectively reverses papilledema associated with cerebral venous sinus thrombosis in antiphospholipid antibody syndrome.

PURPOSE: A case of bilateral papilledema secondary to cerebral venous sinus thrombosis treated with Rituximab, an anti-CD20 monoclonal antibody.

METHODS: A 23 year old obese female with a one week history of blurred vision, headaches and vomiting presented with bilateral papilledema.

Laboratory investigations revealed thrombocytopenia, prolonged prothrombin time (not reversed when mixed with normal plasma) and anticardiolipin antibodies.

The patient to have anti phospholipid antibody syndrome and treated with rituximab I.V.

CONCLUSIONS: Rituximab was effective in reversing papilledema and cerebral sinus thrombosis, while preserving the vision in patient with antiphospholipid antibody syndrome.

It is efficacious in treating papilledema in patients refractory to treatment with systemic steroids and immunoglobulin, with better clinical compliance and no side effects.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 28221537.001).

[ISSN] 1724-6016

[Journal-full-title] European journal of ophthalmology

[ISO-abbreviation] Eur J Ophthalmol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Impact of international collaboration on the prognosis of childhood acute promyelocytic leukemia in Iraq.

As a consequence of a collaborative project between the Al Mansour Hospital for Pediatrics in Baghdad and the Pediatric Unit of Hematology of "La Sapienza" University, in Rome, in October 2003 a specific all-trans-retinoic acid-based protocol was designed in order to offer a modern therapeutic program for the management of Iraqi children with acute promyelocytic leukemia, adapted to the severe local difficulties.

The preliminary encouraging results represent a substantial improvement over the earlier experience in childhood acute promyelocytic leukemia in Iraq.

[MeSH-major] Leukemia, Promyelocytic, Acute / therapy. Tretinoin / administration & dosage

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16533724.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] Italy

[Chemical-registry-number] 5688UTC01R / Tretinoin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Relapse in acute promyelocytic leukemia and the role of hematopoietic stem cell transplantation in the treatment of APL].

[Transliterated title] Relaps akutní promyelocytárni leukemie a role transplantace krvetvorných kmenových bunek v terapii APL.

The authors focused on relapses and transplantation treatment in APL.

Considering treatment of relapses in APL, arsenic trioxide is now the standard treatment of APL relapse, however, treatment with gentuzumab ozogamicin should be considered when only a molecular relapse is detected.

The following part of the issue is focused on the current status of hematopoietic stem cell transplantation in APL and on indications of transplantations from a modern APL therapy point of view.

[MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Promyelocytic, Acute / therapy

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

Genetic Alliance. consumer health - Transplantation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18780574.001).

[ISSN] 0042-773X

[Journal-full-title] Vnitr̆ní lékar̆ství

[ISO-abbreviation] Vnitr Lek

[Language] cze

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Czech Republic

[Number-of-references] 36

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Incidence rates of acute promyelocytic leukemia among Hispanics, blacks, Asians, and non-Hispanic whites in the United States.

Despite significant improvements in the prognosis of acute promyelocytic leukemia brought about by therapeutic advances, understanding of the epidemiology of acute promyelocytic leukemia remains limited.

Earlier reports have suggested that Hispanics may have an increased incidence of acute promyelocytic leukemia, but no systematic analysis of national data has yet been reported.

We performed a retrospective cohort study, using data from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute from 1992-2001 in order to compare leukemia incidence rates as a function of race and ethnicity.

We identified 709 cases of acute promyelocytic leukemia and analyzed incidence rates by race and sex.

Hispanics were not found to have greater lifetime incidence rates than whites, with an incidence relative rate (IRR) of 0.86 that of whites (P=0.17).

Blacks had lower lifetime incidence rates than non-Hispanic whites (IRR=0.75, P=0.04), Hispanics (IRR=0.64, P=0.007), and Asians (IRR=0.67, P=0.03).

These results indicate that while US Hispanics do not have greater lifetime incidence rates of acute promyelocytic leukemia, blacks have lower incidence rates of acute promyelocytic leukemia than Hispanics, non-Hispanic whites, and Asians.

[MeSH-major] African Americans / statistics & numerical data. Asian Continental Ancestry Group / statistics & numerical data. European Continental Ancestry Group / statistics & numerical data. Hispanic Americans / statistics & numerical data. Leukemia, Promyelocytic, Acute / epidemiology. Leukemia, Promyelocytic, Acute / ethnology

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

MedlinePlus Health Information. consumer health - African American Health.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16835508.001).

[ISSN] 0959-8278

[Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)

[ISO-abbreviation] Eur. J. Cancer Prev.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / K05 CA89155; United States / NCI NIH HHS / CA / T-32 CA09529; United States / NCI NIH HHS / CA / U54 CA101388

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Diagnosis and monitoring of PML-RARA-positive acute promyelocytic leukemia by qualitative RT-PCR.

The t(15;17) is the diagnostic hallmark of acute promyelocytic leukemia (APL).

As a result, the RARA and the promyelocytic leukemia (PML) genes are fused.

The use of reverse-transcription polymerase chain reaction (RT-PCR) for the detection of the PML-RARA and RARA-PML fusion genes is the only technique that defines the PML breakpoint type and that allows the definition of a correct strategy for subsequent minimal residual disease (MRD) monitoring.

Standardized conditions for RT-PCR analysis of fusion transcripts from chromosome aberrations in acute leukemia, including APL, have recently been reported in the context of the Biomed-1 Concerted Action, and are described in detail in this chapter.

[MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

[MeSH-minor] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Gene Expression Profiling / methods. Humans. Monitoring, Physiologic / methods. Neoplasm, Residual / genetics. Translocation, Genetic

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16502581.001).

[ISSN] 1543-1894

[Journal-full-title] Methods in molecular medicine

[ISO-abbreviation] Methods Mol. Med.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Importance of genetic heterogeneity in curing adult acute leukemia (AL).

Publication of the French-American-British classification 34 years ago resulted in acceptance that morphology and cytochemistry separated AL into two different diseases, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), that required separate treatment.

During the next 15-20 years the importance of cytogenetics in dissecting ALL and AML into entities requiring different therapies became widely accepted, resulting in 2001 in their first incorporation into the World Health Organization (WHO) classification of AL.

The most striking example of increased curability of AL is acute promyelocytic leukemia, in which targeted therapy combined with chemotherapy has increased survival from a 2-week median to an 80% cure rate.

Recognition of increased sensitivity of a genetic subtype of AML to high-dose cytarabine (HiDAC) has increased the cure rate of core-binding factor (CBF) AML from <10%-25% to 55%-60%.

Recent discovery of the adverse impact of KIT mutations in CBF AML may allow the addition of tyrosine kinase inhibitors to HiDAC to substantially further increase cure.

Among adult de novo AML 40%-45% are cytogenetically normal (CN); the striking molecular heterogeneity of CN-AML is now being recognized and promises to allow individualized approaches that improve substantially upon the current cure rate of 40%.

New approaches to studying the leukemia genome and epigenome should improve our understanding of AL heterogeneity, identify new therapeutic targets, and allow the cure of most patients.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 27962366.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] APX3330 inhibition of the redox function of ape-1/ref-1 (Ref-1) in promyelocytic leukemia cells enhances retinoic acid (ATRA) induced myeloid differentiation and limits cell proliferation as an approach to the prevention of the retinoic acid syndrome (RAS).

: e14613 Background: ATRA + chemotherapy has improved the treatment of promyelocytic leukemia(APL).

However, 25% of ATRA treated APL patients experience toxicities that comprise the RAS (life-threatening respiratory distress, edema, renal failure, hypotension, coagulopathy and rising blast count).

One approach to prevent RAS is to limit blast proliferation and enhance myeloid differentiation.

HL60 myeloid leukemia cells are promyeloblasts that respond to ATRA with granulocytic differentiation/growth arrest.

These finding may provide a therapeutic approach for prevention of the RAS.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 27964118.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Detecting PML-RARalpha transcript in acute promyelocytic leukemia using real-time quantitative RT-PCR.

BACKGROUND: Real-time quantitative RT-PCR (RQ-PCR) assay has become a vital tool to monitor residual disease of leukemia.

However, the complexity and standardization of RQ-PCR should never be overlooked and the results should be interpreted cautiously in clinical conditions.

We aimed to assess the methodology of RQ-PCR and its clinical applications in monitoring molecular kinetics of 36 newly diagnosed cases of acute promyelocytic leukemia patients with t (15;.

17) from October 2004 to December 2005.

The quantitation of PML-RARalpha transcripts was represented by the normalized quotient, that is, PML-RARalpha transcript copies divided by ABL transcript copies.

RESULTS: The sensitivity of RQ-PCR was 1 per 10(5) cells and 5 copies of the PML-RARalpha transcript could be reproducibly detected.

No false positive results occurred in 40 non-acute promyelocytic leukemia samples.

Compared with pretreatment, median reduction of the PML-RARalpha transcript before first consolidation therapy differed significantly between group 1 and group 2 (log scale, 3.15 vs 2.31, P = 0.024).

Interestingly, we found that PML-RARalpha transcript levels temporarily increased in bone marrow (7 patients) and peripheral blood (22 patients) samples of patients during induction therapy in both groups.

CONCLUSIONS: The RQ-PCR assay is reliable for the detection of PML-RARalpha transcripts.

Arsenics, all-trans retinoic acid and mitoxantrone triad induction treatment of acute promyelocytic leukemia is superior to two-drug combination induction therapy in terms of the molecular response.

[MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18028775.001).

[ISSN] 0366-6999

[Journal-full-title] Chinese medical journal

[ISO-abbreviation] Chin. Med. J.

[Language] eng

[Publication-type] Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Acute pancreatitis during the treatment of relapsed acute promyelocytic leukemia with As2O3].

A 77-year-old man suffered from acute pancreatitis during the treatment of relapsed acute promyelocytic leukemia with As2O3.

Pancreatic enzyme levels were elevated and the computed tomography scan of the abdomen showed swelling of the pancreas.

As acute pancreatitis due to As2O3 was suspected, As2O3 was discontinued.

Acute pancreatitis should be considered as a possible complication during treatment with As2O3.

[MeSH-major] Antineoplastic Agents / adverse effects. Arsenicals / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / adverse effects. Pancreatitis / chemically induced

[MeSH-minor] Acute Disease. Humans. Male. Recurrence

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

Genetic Alliance. consumer health - Pancreatitis.

MedlinePlus Health Information. consumer health - Pancreatitis.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16479979.001).

[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] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute promyelocytic leukemia with PML-RARA fusion on i(17q) and therapy-related acute myeloid leukemia.

We describe a patient with acute promyelocytic leukemia (APL) and the karyotype 46,XX,i(17)(q10) with PML-RARA fusion gene detected by fluorescence in situ hybridization (FISH) and nested reverse transcriptase-polymerase chain reaction (RT-PCR).

FISH using dual-color translocation probes for PML (promyelocytic leukemia) and RARA (retinoic acid receptor-alpha) showed fusion signal for PML-RARA on both arms of i(17q).

The patient attained complete remission (CR) with all-trans retinoic acid treatment and became PML-RARA negative.

One year later, while PML-RARA negative on FISH and RT-PCR, the patient presented with thrombocytopenia.

Bone marrow examination suggested an acute monoblastic leukemia (AML-M5a) including the karyotype 46,XX,t(8;16) (p11.2;p13.3),inv(11)(p15q22 approximately q23)[11]/47,idem,+i(8)(q10)[9].

The occurrence of therapy related acute leukemia after successful therapy for APL is an emerging problem.

[MeSH-major] Antineoplastic Agents / adverse effects. Chromosomes, Human, Pair 17. Isochromosomes. Leukemia, Monocytic, Acute / chemically induced. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Receptors, Retinoic Acid / genetics. Tretinoin / adverse effects

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

Genetic Alliance. consumer health - Leukemia, Myeloid.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15899384.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / retinoic acid receptor alpha; 143220-95-5 / PML protein, human; 5688UTC01R / Tretinoin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute promyelocytic leukemia in childhood.

Acute promyelocytic leukemia (APL) is a relatively rare form of acute myelogenous leukemia (AML).

In the United States, APL in children constitutes only 5% to 10% of AML.

Molecularly, the disease is characterized by a fusion protein, promyelocytic leukemia (PML)-retinoic acid receptor (RAR)-alpha that results from a balanced reciprocal translocation between the PML gene on chromosome 15 and the RAR-alpha (RARA) gene on chromosome 17.

A major advance in the field of APL treatment has been the use of all-trans-retinoic acid (ATRA).

Advances in the treatment of APL have taken this form of AML from a disease with significant morbidity and mortality to one with an excellent outcome.

Recent trials have shown a role for arsenic trioxide in both newly diagnosed and relapsed APL.

[MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use

[MeSH-minor] Anthracyclines / therapeutic use. Child. Child, Preschool. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Humans. Prognosis. Translocation, Genetic

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

Hazardous Substances Data Bank. ARSENIC TRIOXIDE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Blood. 1992 Nov 1;80(9):2176-81 [1421389.001]

[Cites] Leukemia. 2004 Oct;18(10):1587-90 [15356649.001]

[Cites] Blood. 2009 Feb 26;113(9):1875-91 [18812465.001]

[Cites] Blood. 1998 Aug 1;92(3):784-9 [9680345.001]

[Cites] J Clin Oncol. 1998 Jan;16(1):78-85 [9440726.001]

[Cites] Blood. 1999 Nov 15;94(10):3315-24 [10552940.001]

[Cites] Blood. 1992 Feb 1;79(3):543-53 [1732003.001]

[Cites] Blood. 1999 Nov 1;94(9):3015-21 [10556184.001]

[Cites] J Clin Oncol. 2005 Oct 20;23(30):7632-40 [16234524.001]

[Cites] Blood. 2005 Jul 15;106(2):447-53 [15677559.001]

[Cites] Blood. 1992 Apr 15;79(8):1916-9 [1562718.001]

[Cites] Leukemia. 2003 Aug;17(8):1600-4 [12886249.001]

[Cites] Ann Intern Med. 1985 Oct;103(4):620-5 [3862359.001]

[Cites] Blood. 2005 Dec 1;106(12):3768-76 [16105978.001]

[Cites] Leukemia. 2000 Aug;14(8):1371-7 [10942231.001]

[Cites] Blood. 2004 Feb 15;103(4):1237-43 [14576047.001]

[Cites] N Engl J Med. 1996 May 30;334(22):1428-34 [8618581.001]

[Cites] Pediatr Blood Cancer. 2008 Aug;51(2):210-5 [18428427.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Apr 13;101(15):5328-35 [15044693.001]

[Cites] J Clin Oncol. 2009 Feb 1;27(4):504-10 [19075265.001]

[Cites] Blood. 2006 Apr 1;107(7):2627-32 [16352810.001]

[Cites] Blood. 2010 Oct 28;116(17):3171-9 [20644121.001]

[Cites] Blood. 1990 Nov 1;76(9):1710-7 [2224120.001]

[Cites] Eur J Cancer Prev. 2006 Aug;15(4):367-70 [16835508.001]

[Cites] Am J Pediatr Hematol Oncol. 1994 Nov;16(4):384-6 [7978063.001]

[Cites] Blood. 1999 Aug 15;94(4):1192-200 [10438706.001]

[Cites] J Biol Regul Homeost Agents. 1999 Oct-Dec;13(4):195-200 [10703942.001]

[Cites] Am J Med. 1984 May;76(5):827-41 [6586073.001]

[Cites] J Clin Oncol. 2006 Dec 20;24(36):5703-10 [17116939.001]

[Cites] Pediatr Blood Cancer. 2008 Jul;51(1):133-5 [18293388.001]

[Cites] N Engl J Med. 1998 Nov 5;339(19):1341-8 [9801394.001]

[Cites] Pediatr Blood Cancer. 2009 Jan;52(1):11-3 [18816805.001]

[Cites] Blood. 1999 Jun 15;93(12):4131-43 [10361110.001]

[Cites] Pediatr Blood Cancer. 2008 Oct;51(4):521-4 [18493994.001]

[Cites] Blood. 2000 Aug 15;96(4):1247-53 [10942364.001]

[Cites] Ann Hematol. 2002 Sep;81(9):504-7 [12373350.001]

[Cites] Biol Blood Marrow Transplant. 2008 Jul;14(7):824-30 [18541203.001]

[Cites] Leukemia. 1997 Jul;11(7):921-8 [9204969.001]

[Cites] Br J Haematol. 2005 Jul;130(2):196-202 [16029447.001]

[Cites] Leukemia. 2007 Mar;21(3):446-52 [17205057.001]

[Cites] N Engl J Med. 1997 Oct 9;337(15):1021-8 [9321529.001]

[Cites] Ann Hematol. 2001 Jul;80(7):417-22 [11529468.001]

[Cites] J Clin Oncol. 2004 Apr 15;22(8):1404-12 [15084614.001]

(PMID = 19840521.001).

[ISSN] 1534-6269

[Journal-full-title] Current oncology reports

[ISO-abbreviation] Curr Oncol Rep

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Anthracyclines; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide

[Number-of-references] 47

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [A case of acute promyelocytic leukemia with double ider (17q-)].

This study reported a relapsed case of acute promyelocytic leukemia with complex chromosomal aberrations of double ider (17q-) and explored its laboratory and clinical features.

In conclusion, double ider (17q-) is a rare additional abnormality in APL patients; combination of FISH with M-FISH techniques is a reliable way to identify such complicated chromosomal aberrations.

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18088491.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Acute promyelocytic leukemia with CD59 deficiency].

The study was aimed to investigate whether CD59 is deficient in acute promyelocytic leukemia (APL) blast cells.

Expression of CD59 on APL blast cells was analysed by flow cytometry.

The results showed that the deficiency of CD59 expression in 12 out of 19 APL samples was found, its incidence was significantly higher than that in other acute myeloid leukemia (AML) samples (deficiency of CD59 expression in 14 of 40 non-APL AML samples, p=0.042).

The expression of CD59 became normal after the patients achieved complete remission (CR), which indicated that the deficient of CD59 expression was only found in APL blast cells, but also found in APL cell line NB4 cells.

Sequencing pig-A gene coding region of NB4 cells and one APL patient with deficiency of CD59 displayed that the mutation of pig-A gene was not observed, therefore the deficiency of CD59 expression in APL cells did not result from mutation of pig-A gene.

It is concluded that the deficiency of CD59 expression exists in APL blast cells more probably.

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

Genetic Alliance. consumer health - Cd59 deficiency.

Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 21129240.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD59; 0 / Membrane Proteins; 0 / phosphatidylinositol glycan-class A protein; 5688UTC01R / Tretinoin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute promyelocytic leukemia during pregnancy.

OBJECTIVE: To report our experience about a woman with acute promyelocytic leukemia (APL) during pregnancy.

PATIENT(S): A 32-year-old-woman, gravida 2, para 1, at the 25th week of pregnancy with a diagnosis of APL.

The mother is now undergoing the third and last consolidation step with good results, and APL is in remission.

CONCLUSION(S): In cases of APL during the second and third trimesters, the modern chemotherapy associated with close monitoring of maternal and fetal well-being could ensure a good outcome for both the mother and the baby.

[MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Pregnancy Complications, Neoplastic / diagnosis

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

Genetic Alliance. consumer health - Pregnancy.

MedlinePlus Health Information. consumer health - Tumors and Pregnancy.

Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright © 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.

(PMID = 20447623.001).

[ISSN] 1556-5653

[Journal-full-title] Fertility and sterility

[ISO-abbreviation] Fertil. Steril.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 5688UTC01R / Tretinoin; 7S5I7G3JQL / Dexamethasone; ZRP63D75JW / Idarubicin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Presentation of acute promyelocytic leukemia as granulocytic sarcoma.

Granulocytic sarcoma (GS) is a localized tumor composed of immature myeloid cells.

This extramedullary tumor can present before, concurrent with or after the diagnosis of acute myeloid leukemia.

GS is extremely uncommon in acute promyelocytic leukemia (APL).

As a proportion of patients never develop systemic disease, correct and timely diagnosis may be rather difficult, but is a prerequisite for optimal outcome.

GS should be considered in the differential diagnosis of children with unusual bone lesions.

We describe a patient with GS who presented with symptoms mimicking osteomyelytis or rheumatoid disease.

[MeSH-major] Diagnostic Errors. Leukemia, Promyelocytic, Acute / complications. Sarcoma, Myeloid / etiology

[MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arthritis, Psoriatic / diagnosis. Biomarkers, Tumor / analysis. Female. Humans. Oncogene Proteins, Fusion / analysis. Osteolysis / etiology. Osteomyelitis / diagnosis. Remission Induction. Shoulder Pain / etiology. Tretinoin / administration & dosage

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2007 Wiley-Liss, Inc.

(PMID = 17437290.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Expression of survivin gene in NB4 cell line and cells of acute promyelocytic leukemia and its anti-apoptosis and clinical significance].

The study was aimed to detect expression rate of survivin gene in APL cell and to explore the relationship between its expression and clinical manifestation.

PML/RARalpha and survivin mRNA expression were analyzed by using reverse transcriptase polymerase chain reaction (RT-PCR) technique.

By treatment with ATRA, survivin mRNA expression in NB4 cell gradually decreased along with time delay and almost could not be detected at the 72th hour. (2) the positive and negative rate of survivin mRNA expression was 67% and 33% respectively, while in all 36 cases of de novo and relapse APL patients, the PML/RAR(alpha) fusion gene expression was positive.

In 22 cases at remission stage, the PML/RARalpha fusion gene expression was negative, and the positive and negative rate of survivin mRNA expression was 36% and 64% respectively.

The survivin mRNA expression positive rates in the de novo group, relapse group and PML/RARalpha fusion gene L-type positive group were obviously higher than those in remission period group (P < 0.05) and were significantly lower than those in acute leukemia group (P < 0.05, < 0.001). (3) whether the survivin mRNA expression was positive or negative in 36 cases of de novo and relapse APL patients, all the 36 cases could obtain complete remission.

4 APL patients with positive expression of survivin mRNA had DIC and serious infection (one patient died).

The clinical symptom showed slight skin or mucosa bleeding, fever and asthenic in the patients with negative expression of survivin mRNA.

When 2 APL patients with positive expression of survivin mRNA had been treated with ATRA, induction differentiation sign in their peripheral blood and bone marrow figures was not obvious.

It is concluded that the survivin gene positive expression rate is lower in acute promyelocytic leukemia than that in any other types of leukemia and is related to clinical manifestation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16638209.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / Receptors, Retinoic Acid; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] CD2+ acute promyelocytic leukemia is associated with leukocytosis, variant morphology and poorer prognosis.

The T cell-lineage marker CD2 is sometimes expressed in acute promyelocytic leukemia (APL), and CD2 expression is reported to correlate with some clinical characteristics.

However, the significance of CD2 expression in APL has not been fully elucidated.

We evaluated CD2 expression in APL treated by the same treatment strategy in a single institute, and whether it had any special characteristics.

Among 29 APL, 6 were positive for CD2.

Patients with CD2+ APL tended to have a higher leukocyte count than CD2- APL (34.5 +/- 13.1/l vs. 6.8 +/- 2.1/l), morphological characteristics as variant-APL (50 vs. 0%).

They also showed poor clinical prognosis.

The CR rate of CD2- APL was 87.0% while that of CD2+ APL was 50 %.

The mortality was 13.0 and 66.7%, respectively, and the survival rate was significantly lower in CD2+ APL.

CD2 expression was proven to be a risk factor associated with death in addition to the morphological characteristics of variant-APL and leukocytosis.

These results indicated that CD2 expression might have a significant impact on the prognosis of APL.

Whether CD2+ APL should be characterized as a special clinical entity should be discussed in a larger patient population.

[MeSH-major] Antigens, CD2 / analysis. Leukemia, Promyelocytic, Acute / pathology

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16178910.001).

[ISSN] 0141-9854

[Journal-full-title] Clinical and laboratory haematology

[ISO-abbreviation] Clin Lab Haematol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD2; 0 / Antigens, Neoplasm

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Treatment of newly diagnosed patients with acute promyelocytic leukemia with modified spanish treatment protocol.

The results of treatment of acute promyelocytic leukemia, when combination ATRA + chemotherapy is used in induction and maintainance therapy and risk adapted strategy applied in consolidation, improved at present time.

Enhanced supportive therapy also contribute to improved outcome of APL patients.

3 - year relapse free, overall survival and clinical and biological presenting features of APL patients were evaluated.

29 (90.6%) patients achieved complete hematologic remission, 2 (6.3 %) molecular relapses were observed, death was observed in 4 patients (12.5%).

Survival results correspond with other published clinical studies.

Current recommendations for treatment with risk-adapted strategy for patients with newly diagnosed acute promyelocytic leukemia resulted in our patients group to comparable outcome and good compliance like in other published studies.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20353280.001).

[ISSN] 0028-2685

[Journal-full-title] Neoplasma

[ISO-abbreviation] Neoplasma

[Language] eng

[Publication-type] Journal Article

[Publication-country] Slovakia

[Chemical-registry-number] 5688UTC01R / Tretinoin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Mutant transcription factors and tyrosine kinases as therapeutic targets for leukemias: from acute promyelocytic leukemia to chronic myeloid leukemia and beyond.

Mutations in transcription factors (TFs) and protein tyrosine kinases (PTKs), which result in inhibition of differentiation/apoptosis or enhanced proliferative/survival advantage of hematopoietic stem/progenitor cells, are two classes of the most frequently detected genetic abnormalities in leukemias.

The great success of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) in treating acute promyelocytic leukemia through modulation of the causative PML-RARalpha oncoprotein represents the first two paradigms of mutant TFs-targeting therapeutic strategies for leukemia.

More recently, tyrosine kinase inhibitor STI-571/Imatinib mesylate/Gleevec in the treatment of Breakpoint Cluster Region-Abelson (BCR-ABL) positive leukemia elicits paradigm of mutant PTKs as ideal antileukemia targets.

Thus to further improve clinical outcome of leukemia patients, elucidation of pathogenesis of leukemia, screening for oncoprotein-targeting small molecules, as well as rationally designed combination of drugs with potential synergy are of importance.

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Mutation / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Transcription Factors / antagonists & inhibitors

Genetic Alliance. consumer health - Chronic Myeloid Leukemia.

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17433911.001).

[ISSN] 0065-230X

[Journal-full-title] Advances in cancer research

[ISO-abbreviation] Adv. Cancer Res.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Transcription Factors; EC 2.7.10.1 / Protein-Tyrosine Kinases

[Number-of-references] 142

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Case report: acute promyelocytic leukemia with +der(17)t(15;17) detected by fluorescence in situ hybridization (FISH).

We describe an unusual case of acute promyelocytic leukemia with +der(17)t(15;17) as the additional cytogenetic abnormality and with t(15;17) defined by fluorescence in situ hybridization (FISH) using a PML/RARA dual color, dual fusion translocation probe.

By performing a step-by-step, complementary approach to evaluate unusual chromosomal abnormalities, we detected RARA/PML fusion on a marker chromosome similar to chromosome 17.

[MeSH-major] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Leukemia, Promyelocytic, Acute / diagnosis

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15943185.001).

[ISSN] 0091-7370

[Journal-full-title] Annals of clinical and laboratory science

[ISO-abbreviation] Ann. Clin. Lab. Sci.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cryptic insertion of PML-RARA into the 3p25 locus in an acute promyelocytic leukemia with t(3;17)(p25;q21).

We studied a case of a 72-year-old man with acute promyelocytic leukemia and a t(3;17)(p25;q21).

Fluorescence in situ hybridization failed to show rearrangement of the PML (promyelocytic leukemia protein) locus but did demonstrate relocalization of the retinoic acid receptor alpha (RARA) to chromosome 3.

Our analysis indicates that the fusion partner is PML.

This karyotype therefore results in a cryptic PML-RARA fusion inserted into the 3p25 locus.

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.

[Cites] Genet Mol Res. 2009;8(1):1-7 [19224461.001]

[Cites] Cancer Cell. 2009 Jan 6;15(1):7-8 [19111876.001]

[Cites] Blood. 2007 Dec 1;110(12):4073-6 [17712046.001]

[Cites] Leukemia. 2006 Feb;20(2):376-9 [16341036.001]

[Cites] Blood. 1999 May 15;93(10):3167-215 [10233871.001]

[Cites] Blood. 1997 Dec 15;90(12):4876-85 [9389704.001]

[Cites] Blood. 2000 Aug 15;96(4):1297-308 [10942371.001]

[Cites] Proc Natl Acad Sci U S A. 1997 May 13;94(10):5302-7 [9144232.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2551-6 [9122233.001]

[Cites] EMBO J. 1992 Apr;11(4):1397-407 [1314166.001]

[Cites] Gene. 1989 Dec 7;84(1):1-8 [2691331.001]

[Cites] Leukemia. 2002 Oct;16(10):1927-32 [12357344.001]

[Cites] Methods Mol Biol. 2009;538:85-114 [19277575.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11583-8 [9326653.001]

(PMID = 20633765.001).

[ISSN] 1873-4456

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA067346-09; United States / NCI NIH HHS / CA / R01 CA067346; United States / NCI NIH HHS / CA / R01 CA067346-09

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / DNA Primers; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein

[Other-IDs] NLM/ NIHMS205381; NLM/ PMC2925300

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Determinants of oncogenic transformation in acute promyelocytic leukemia: the hetero-union makes the force.

Acute promyelocytic leukemia (APL) is caused by chromosomal translocations that involve the retinoic acid receptor alpha (RAR) and several other genes to yield X-RAR fusion proteins.

Unlike wild-type RARs, which require heterodimerization with the retinoid X receptor (RXR) for their function as DNA-binding transcriptional regulators, X-RAR fusion proteins bind DNA and deregulate transcription as homo-oligomers.

In this issue of Cancer Cell, however, Zeisig et al. and Zhu et al. show that RXR recruitment is a critical determinant for the transforming potential of oligomeric X-RAR fusion proteins and explore the possibility for targeted interventions in APL with either RAR or RXR ligands.

[MeSH-major] Cell Transformation, Neoplastic. Leukemia, Promyelocytic, Acute / pathology

[MeSH-minor] Humans. Ligands. Receptors, Retinoic Acid / metabolism. Retinoid X Receptors / metabolism

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentOn] Cancer Cell. 2007 Jul;12(1):36-51 [17613435.001]

[CommentOn] Cancer Cell. 2007 Jul;12(1):23-35 [17613434.001]

(PMID = 17613430.001).

[ISSN] 1535-6108

[Journal-full-title] Cancer cell

[ISO-abbreviation] Cancer Cell

[Language] eng

[Publication-type] Comment; Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Ligands; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors

[Number-of-references] 10

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Treatment of acute promyelocytic leukemia during pregnancy.

Management of the pregnant patient with acute promyelocytic leukemia (APL) is a challenge.

Immediate treatment of APL is critical, as it is an oncologic emergency, with a high risk of morbidity and mortality associated with disseminated intravascular coagulation.

In addition, complications associated with APL, including retinoic acid syndrome, add to the complexity of management.

To better understand how to manage this complex patient care situation, we searched the PubMed database (January 1972-May 2008) for English-language articles about maternal and fetal outcomes resulting from APL treatment during pregnancy.

A total of 42 cases from 35 articles were identified: 12 first-trimester, 21 second-trimester, and 9 third-trimester cases.

The overall treatment of the pregnant patient with APL should include a discussion about pregnancy termination, especially if APL is diagnosed in the first trimester.

Frequent fetal monitoring, along with aggressive management of potential APL-related complications, is necessary to allow for optimal maternal and fetal outcomes.

[MeSH-major] Antineoplastic Agents / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Pregnancy Complications, Neoplastic / drug therapy. Tretinoin / administration & dosage

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

Genetic Alliance. consumer health - Pregnancy.

MedlinePlus Health Information. consumer health - Tumors and Pregnancy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19476422.001).

[ISSN] 1875-9114

[Journal-full-title] Pharmacotherapy

[ISO-abbreviation] Pharmacotherapy

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin

[Number-of-references] 71

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Treatment of acute promyelocytic leukemia with gemtuzumab ozogamicin.

Acute promyelocytic leukemia (APL) is a form of acute myeloid leukemia characterized by peculiar biologic features and a unique sensitivity to differentiation therapy with all-trans retinoic acid (ATRA).

Modern treatment approaches to APL include simultaneous combination of ATRA and anthracycline-based chemotherapy.

Gemtuzumab ozogamicin is a calicheamicin-conjugated monoclonal antibody directed against CD33, a cell surface antigen highly expressed on APL cells.

A number of preliminary reports have highlighted the sensitivity of APL to gemtuzumab given alone or in combination with other agents.

Several reasons may account for the efficacy of gemtuzumab in APL, including:.

(1) CD33 is detectable in virtually 100% of APL cases;.

(2) calicheamicin belongs to the anthracycline family, a group of chemotherapeutic agents known to be highly effective in APL; and (3) the APL blast cells lack the multidrug resistance glycoprotein 170.

Due to the availability of other highly effective agents (ATRA, arsenic trioxide), relatively few APL patients have been treated thus far with gemtuzumab, and their follow-up is still short.

However, it is conceivable that the use of this agent in APL will increase in the near future in light of its capability to induce molecular remission even in advanced disease.

This review summarizes the mechanism of action and toxicity profile of gemtuzumab as well as the published experience with this compound in patients with newly diagnosed and relapsed APL.

[MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16562371.001).

[ISSN] 1543-0790

[Journal-full-title] Clinical advances in hematology & oncology : H&O

[ISO-abbreviation] Clin Adv Hematol Oncol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / gemtuzumab; S7V92P67HO / arsenic trioxide

[Number-of-references] 53

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute promyelocytic leukemia: an unusual cause of fatal secondary postpartum hemorrhage.

INTRODUCTION: Postpartum haemorrhage can rarely be associated with an underlying coagulation or haematological disorder.

We wish to discuss a case of acute promyelocytic leukemia (APL) presenting as secondary postpartum hemorrhage (PPH), its clinical and pathological features and maternal outcome.

Investigations revealed her to be having APL, a diagnosis not suspected by the referring clinic.

CONCLUSION: The case emphasizes the importance of suspecting, investigating and energetically treating uncommon causes such as acute leukemia when an unusually severe clinical picture in a postpartum setting suggests such a possibility.

This may prove to be life saving, particularly if the leukemia happens to be APL, a cancer with a very high cure rate.

[MeSH-major] Leukemia, Promyelocytic, Acute / complications. Postpartum Hemorrhage / etiology

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16341866.001).

[ISSN] 0932-0067

[Journal-full-title] Archives of gynecology and obstetrics

[ISO-abbreviation] Arch. Gynecol. Obstet.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The promyelocytic leukemia protein PML regulates c-Jun function in response to DNA damage.

The promyelocytic leukemia (PML) gene, a tumor suppressor inactivated in acute promyelocytic leukemia (APL), regulates apoptosis induced by DNA damage.

However, the molecular mechanisms by which PML modulates apoptosis following genotoxic stress are only partially elucidated.

PML is essential for p53-dependent induction of programmed cell death upon gamma-irradiation through PML-nuclear body (NB)-mediated control of p53 acetylation.

Here, we show that PML selectively regulates proapoptotic transcription factors upon different types of DNA damage.

We find that Pml inactivation protects fibroblasts from UV-induced apoptosis in a p53-independent manner.

We demonstrate that c-Jun is required for UV-induced apoptosis and that PML is essential for both c-Jun transcriptional activation and DNA binding upon UV radiation.

We find that PML physically interacts with c-Jun and that upon UV radiation the PML-NBs reorganize into novel nuclear microspeckled structures (UV-NBs), where PML and c-Jun dynamically accumulate.

These data identify a novel PML-dependent pathway for c-Jun transcriptional activation and induction of apoptosis in response to DNA damage and shed new light on the role of PML in tumor suppression.

COS Scholar Universe. author profiles.

Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Nat Cell Biol. 2000 Oct;2(10):730-6 [11025664.001]

[Cites] Cell Mol Life Sci. 2000 Aug;57(8-9):1229-35 [11028915.001]

[Cites] Mutat Res. 2000 Dec 20;457(1-2):113-23 [11106803.001]

[Cites] Cell. 2000 Dec 8;103(6):897-907 [11136975.001]

[Cites] Oncogene. 2001 Apr 30;20(19):2453-64 [11402340.001]

[Cites] Oncogene. 2001 Oct 29;20(49):7223-33 [11704850.001]

[Cites] Mol Cell. 2002 Oct;10(4):843-55 [12419228.001]

[Cites] Oncogene. 2003 Mar 20;22(11):1620-8 [12642865.001]

[Cites] J Natl Cancer Inst. 2004 Feb 18;96(4):269-79 [14970276.001]

[Cites] Blood. 2004 Mar 15;103(6):2358-62 [14630830.001]

[Cites] Oncogene. 1991 Jul;6(7):1285-92 [1650447.001]

[Cites] Cell. 1991 Aug 23;66(4):663-74 [1652368.001]

[Cites] Cell. 1991 Aug 23;66(4):675-84 [1652369.001]

[Cites] Science. 1991 Nov 29;254(5036):1371-4 [1720570.001]

[Cites] EMBO J. 1993 Feb;12(2):479-87 [8382609.001]

[Cites] Nature. 1995 Oct 12;377(6549):552-7 [7566157.001]

[Cites] Nature. 1996 Jun 20;381(6584):713-6 [8649519.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Nov 11;94(23):12255-7 [9356435.001]

[Cites] Science. 1998 Mar 6;279(5356):1547-51 [9488655.001]

[Cites] Oncogene. 1998 Jul 2;16(26):3461-9 [9692554.001]

[Cites] Nat Genet. 1998 Nov;20(3):266-72 [9806545.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Nov 10;95(23):13887-92 [9811896.001]

[Cites] EMBO J. 1999 Jan 4;18(1):188-97 [9878062.001]

[Cites] Nat Genet. 1999 Mar;21(3):326-9 [10080190.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9827-32 [10449779.001]

[Cites] Cell. 2002 Jan 25;108(2):165-70 [11832207.001]

[Cites] Blood. 2000 May 1;95(9):2748-52 [10779416.001]

[Cites] Science. 2000 May 5;288(5467):870-4 [10797012.001]

[Cites] Nat Cell Biol. 2000 May;2(5):E85-90 [10806494.001]

[Cites] Nature. 2000 Jul 13;406(6792):207-10 [10910364.001]

[Cites] Cell. 2000 Oct 13;103(2):239-52 [11057897.001]

(PMID = 15626733.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA-71692; United States / PHS HHS / / T32

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Pml protein, mouse; 0 / Proto-Oncogene Proteins c-jun; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins

[Other-IDs] NLM/ PMC1895009

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Treatment of acute promyelocytic leukemia by retinoids.

We review the role of all-trans retinoic acid (ATRA) in the treatment of acute promyelocytic leukemia (APL).

The combination of ATRA and conventional anthracycline-ARA-C chemotherapy (CT) has clearly demonstrated its superiority over CT alone (in terms of relapse and survival) in newly diagnosed APL.

With those treatments, the relapse risk appears to be only 10%-15%, although it remains greater in patients who initially have high white blood cell counts (often associated with variant M3 morphology, short bcr3 isoform, etc.) and patients with residual disease detectable by RT-PCR at the end of consolidation courses.

ATRA syndrome (now generally called APL differentiation syndrome, as it is also seen with arsenic derivatives) remains the major side effect of ATRA treatment.

It occurs in 10%-15% of patients and is currently fatal in at least 10% of them.

A sizeable proportion of APL patients who relapse after ATRA and CT can be durably salvaged by the same treatment followed by allogeneic or autologous stem cell transplantation, provided the transplant (in the autologous setting) is RT-PCR-negative.

However, in relapsing APL arsenic derivatives (mainly arsenic trioxide) are now considered to be the reference treatment.

Some of the current issues with ATRA treatment in newly diagnosed APL include whether ATRA has a role during consolidation treatment and whether arabinoside (AraC) is required in addition to anthracyclines in the chemotherapy combined to ATRA.

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use

[MeSH-minor] Clinical Trials as Topic. Humans. Treatment Outcome

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17217041.001).

[ISSN] 0070-217X

[Journal-full-title] Current topics in microbiology and immunology

[ISO-abbreviation] Curr. Top. Microbiol. Immunol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Germany

[Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin

[Number-of-references] 132

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute promyelocytic leukemia: an overview with implications for oncology nurses.

Acute promyelocytic leukemia (APL), once described as the form of leukemia with the highest mortality, is now the most potentially curable subtype of adult acute myeloid leukemia.

A brief review of the history of APL will describe the advances in research and clinical practice and their impact on patient outcomes.

Oncology nurses should familiarize themselves with the nuances of APL because of the critical role nurses play in providing support for patients.

This article provides an overview of APL, including the epidemiology and pathophysiology that distinguishes APL from other types of acute leukemia.

Clinical presentation and diagnostic workup for patients suspected of having APL will be reviewed, as will the treatment course.

Nursing implications and management will be provided related to potential treatment complications specific to APL, including coagulopathies, differentiation syndrome, and QT prolongation with the use of arsenic trioxide, as will the side effects and complications that can occur in any patient with leukemia, such as infection, hyperleukocytosis, tumor lysis, and increased intracranial pressure.

[MeSH-major] Leukemia, Promyelocytic, Acute. Oncology Nursing / manpower

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[ReprintIn] ONS Connect. 2010 Dec;25(12):12-3 [21214084.001]

(PMID = 21112852.001).

[ISSN] 1538-067X

[Journal-full-title] Clinical journal of oncology nursing

[ISO-abbreviation] Clin J Oncol Nurs

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Beneficial and adverse effects of molecularly targeted therapies for acute promyelocytic leukemia in central nervous system.

Acute promyelocytic leukemia (APL) is a distinct subset of acute myeloid leukemia characterized by an abnormal fusion protein, PML/RARA.

All-trans retinoic acid (ATRA) and arsenic trioxide, which are the major molecularly targeted therapies in APL, affect or degrade the PML/RARA fusion protein and cause differentiation and apoptosis of APL cells.

These therapies have improved the prognosis of APL patients and are now the main therapeutic options in APL.

In addition, gemtuzumab ozogamicin is another targeted therapy in APL.

On the other hand, the prognosis of patients with central nervous system (CNS) relapses of APL remains poor.

In fact, possible active roles of molecularly targeted therapies in CNS relapses of APL have been suggested, and several new approaches with molecularly targeted therapies for CNS relapses have been examined in APL.

In this review, we discuss three main topics; the relationship between the incidence of CNS relapses and the introduction of molecularly targeted therapies for APL, new approaches with targeted therapies for CNS relapses of APL, and other complications of targeted therapies in CNS such as pseudotumor cerebri induced by ATRA and subarachnoid hemorrhage.

These comprehensive understanding would be helpful for better management of patients with APL.

[MeSH-major] Arsenicals / therapeutic use. Central Nervous System Neoplasms / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

Hazardous Substances Data Bank. ARSENIC TRIOXIDE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19702568.001).

[ISSN] 1996-3181

[Journal-full-title] CNS & neurological disorders drug targets

[ISO-abbreviation] CNS Neurol Disord Drug Targets

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United Arab Emirates

[Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide

[Number-of-references] 46

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Inferior prognostic outcome in acute promyelocytic leukemia with alterations of FLT3 gene.

Alterations of the FLT3 gene, in the form of internal tandem duplications (ITD) and D835 point mutations, occur frequently in acute promyelocytic leukemia (APL).

We therefore evaluated the frequency and clinical relevance of FLT3 aberrations in a series of Korean APL patients.

We assayed FLT3 ITD and D835 mutation status in 75 newly diagnosed APL patients and we correlated the presence of these mutations with clinical parameters and outcomes.

Of the 75 patients, fifteen (20.0%) carried FLT3 mutations, nine (12.0%) with FLT3 ITD, seven (9.3%) with D835 mutations and one with both types.

There was no association between FLT3 aberrations and other clinicohematologic features including age, gender, M3 variant morphology and PML/RARalpha subtype.

Both ITD and D835 mutations were associated with shortened event-free survival (P = 0.048 and P = 0.029, respectively), but there was no correlation between disease-free survival among the 61 patients who achieved complete remission and the presence of FLT3 mutations (P = 0.543 for ITD and P = 0.277 for D835).

FLT3 mutations were less frequent in Korean APL patients than in Western APL patients.

[MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Mutation / genetics. fms-Like Tyrosine Kinase 3 / genetics

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17064989.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Curing APL: differentiation or destruction?

In a recent issue of Nature Medicine, Nasr et al. show that the effectiveness of all-trans retinoic acid and arsenic trioxide in acute promyelocytic leukemia is independent of their ability to cause differentiation.

Targeted destruction of the PML-RARalpha oncoprotein appears key to eliminating the cells from which relapse can arise.

[MeSH-major] Cell Differentiation / drug effects. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / pathology. Oncogene Proteins, Fusion / metabolism

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. ARSENIC TRIOXIDE .

Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentOn] Nat Med. 2008 Dec;14(12):1333-42 [19029980.001]

(PMID = 19111876.001).

[ISSN] 1878-3686

[Journal-full-title] Cancer cell

[ISO-abbreviation] Cancer Cell

[Language] eng

[Publication-type] Comment; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Arsenicals; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Dissection of mechanisms of Chinese medicinal formula Realgar-Indigo naturalis as an effective treatment for promyelocytic leukemia.

To enhance therapeutic efficacy and reduce adverse effects, practitioners of traditional Chinese medicine (TCM) prescribe a combination of plant species/minerals, called formulae, based on clinical experience.

In trying to address the possible beneficial effects of formulae with current biomedical approaches, we use Realgar-Indigo naturalis formula (RIF), which has been proven to be very effective in treating human acute promyelocytic leukemia (APL) as a model.

Here, we report that the ATI combination yields synergy in the treatment of a murine APL model in vivo and in the induction of APL cell differentiation in vitro.

ATI causes intensified ubiquitination/degradation of promyelocytic leukemia (PML)-retinoic acid receptor alpha (RARalpha) oncoprotein, stronger reprogramming of myeloid differentiation regulators, and enhanced G(1)/G(0) arrest in APL cells through hitting multiple targets compared with the effects of mono- or biagents.

Furthermore, ATI intensifies the expression of Aquaglyceroporin 9 and facilitates the transportation of A into APL cells, which in turn enhances A-mediated PML-RARalpha degradation and therapeutic efficacy.

We therefore suggest that dissecting the mode of action of clinically effective formulae at the molecular, cellular, and organism levels may be a good strategy in exploring the value of traditional medicine.

[MeSH-major] Arsenicals / therapeutic use. Drugs, Chinese Herbal / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Medicine, Chinese Traditional. Sulfides / therapeutic use

[MeSH-minor] Animals. Aquaporins / genetics. Aquaporins / metabolism. Cell Differentiation / drug effects. Cell Line, Tumor. Disease Models, Animal. Drug Synergism. G0 Phase / drug effects. G1 Phase / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Oncogene Proteins, Fusion / metabolism. Protein Processing, Post-Translational / drug effects. Transcription, Genetic / drug effects. Ubiquitination / drug effects. Up-Regulation / drug effects

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Nat Cell Biol. 1999 May;1(1):60-7 [10559866.001]

[Cites] Nat Rev Drug Discov. 2007 Jul;6(7):506-7 [17715497.001]

[Cites] Leukemia. 2000 Feb;14(2):255-61 [10673742.001]

[Cites] Clin Cancer Res. 2001 Aug;7(8):2168-81 [11489790.001]

[Cites] Oncogene. 2001 Oct 29;20(49):7146-53 [11704843.001]

[Cites] Nat Rev Cancer. 2002 Sep;2(9):705-13 [12209159.001]

[Cites] Cancer Cell. 2003 Apr;3(4):305-7 [12726855.001]

[Cites] Eur J Biochem. 1981 Mar 16;115(1):207-16 [7227366.001]

[Cites] Blood. 1988 Aug;72(2):567-72 [3165295.001]

[Cites] Nature. 1990 Jan 11;343(6254):177-80 [2153268.001]

[Cites] Blood. 1991 Mar 1;77(5):1080-6 [1995093.001]

[Cites] Biochemistry. 1996 Feb 13;35(6):1761-7 [8639656.001]

[Cites] Blood. 1996 Aug 1;88(3):1052-61 [8704214.001]

[Cites] Blood. 1996 Aug 15;88(4):1248-55 [8695842.001]

[Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11510-5 [8876166.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2551-6 [9122233.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3978-83 [9108090.001]

[Cites] Nature. 1997 May 8;387(6629):188-91 [9144290.001]

[Cites] Nat Rev Cancer. 2005 Jan;5(1):65-72 [15630416.001]

[Cites] Toxicol Appl Pharmacol. 2005 Feb 15;203(1):53-61 [15694464.001]

[Cites] PLoS Med. 2005 Jan;2(1):e12 [15696202.001]

[Cites] Blood. 2007 Jan 15;109(2):740-6 [16968895.001]

[Cites] Blood. 2007 Apr 15;109(8):3441-50 [17197433.001]

[Cites] Blood. 2007 May 15;109(10):4432-40 [17244680.001]

[Cites] Exp Mol Med. 1999 Dec 31;31(4):174-8 [10630370.001]

(PMID = 18344322.001).

[ISSN] 1091-6490

[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

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / AQP9 protein, human; 0 / Aquaporins; 0 / Arsenicals; 0 / Drugs, Chinese Herbal; 0 / Oncogene Proteins, Fusion; 0 / Sulfides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / realgar-indigo naturalis; 56320-22-0 / arsenic disulfide

[Other-IDs] NLM/ PMC2290784

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute promyelocytic leukemia and constitutional trisomy 21.

The incidence of acute myelogenous leukemia (AML) in patients with constitutional trisomy 21 is estimated to be 1 in 300; it is usually seen before age four.

Clinical and epidemiological data confirm the improved life expectancy of patients with Down syndrome and their increased susceptibility to the development of leukemia, among other cancers.

The most frequent subtype of AML associated with Down syndrome is acute megakaryoblastic leukemia (FAB: M7).

The description of acute promyelocytic leukemia (APL) in adult patients with Down syndrome is exceedingly rare.

Herein, we describe the unusual presentation, treatment, results, and clinical course of an adult patient with APL and constitutional trisomy 21 and provide a brief review of the literature.

[MeSH-major] Down Syndrome. Leukemia, Promyelocytic, Acute / genetics

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

MedlinePlus Health Information. consumer health - Down Syndrome.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16527614.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [New therapeutic perspectives for arsenic: from acute promyelocytic leukemia to autoimmune diseases].

[Transliterated title] De nouvelles perspectives thérapeutiques pour l'arsenic: De la leucémie aiguë promyélocytaire aux maladies auto-immunes.

Since 1996, arsenic trioxide (As2O3) is used to treat patients with acute promyelocytic leukemia.

This treatment also markedly reduced anti-DNA autoantibodies, rheumatoid factor, IL-18, IFN-gamma, nitric oxide metabolites, TNF-alpha, Fas ligand and IL-10 levels, and immune-complex deposits in glomeruli, leading to significantly prolonged survival rates.

[MeSH-major] Antineoplastic Agents / therapeutic use. Arsenic / therapeutic use. Autoimmune Diseases / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy

[MeSH-minor] Animals. Arsenicals / therapeutic use. Disease Models, Animal. Growth Inhibitors / therapeutic use. Humans. Lupus Erythematosus, Systemic / drug therapy. Lymphoproliferative Disorders / drug therapy. Mice. Oxides / therapeutic use

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

Genetic Alliance. consumer health - Autoimmune Diseases.

MedlinePlus Health Information. consumer health - Arsenic.

MedlinePlus Health Information. consumer health - Autoimmune Diseases.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

Hazardous Substances Data Bank. ARSENIC TRIOXIDE .

Hazardous Substances Data Bank. ARSENIC, ELEMENTAL .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19038100.001).

[ISSN] 0767-0974

[Journal-full-title] Médecine sciences : M/S

[ISO-abbreviation] Med Sci (Paris)

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Growth Inhibitors; 0 / Oxides; N712M78A8G / Arsenic; S7V92P67HO / arsenic trioxide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute promyelocytic leukemia: what are the treatment options?

IMPORTANCE OF THE FIELD: Acute promyelocytic leukemia (APL) represents a paradigm of therapeutic success in clinical hematology.

Notwithstanding, various questions concerning the management of APL remain unanswered.

AREAS COVERED IN THIS REVIEW: The aim of this article is to focus on still controversial issues in the management of APL, such as the role of arsenic trioxide as front-line therapy, the management of older unfit patients, the potential utility of gemtuzumab-ozogamycin and the effectiveness (if any) of maintenance therapy for patients in molecular remission.

WHAT THE READER WILL GAIN: Current and future therapeutic options for the treatment of newly diagnosed and relapsed APL.

TAKE HOME MESSAGE: To date, the therapy of APL is the most successful example of differentiation therapy and its scientific history can serve as a model for subsequent development of similar treatments in other leukemias and cancers.

[MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

Hazardous Substances Data Bank. ARSENIC TRIOXIDE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20163270.001).

[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] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / gemtuzumab; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide

[Number-of-references] 75

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Realgar Nanoparticles Induced Cytotoxicity in Promyelocytic Leukemia HL-60 Cells.

Realgar, one of mineral drugs in Chinese traditional medicines has attracted an increasing attention because of its prominent anti-tumor effect.

Our previous studies have demonstrated that realgar nanoparticles may provide a less toxic agent for anti-neoplasia by suppressing angiogenesis.

In the present study, we improved milling process, prepared raw realgar particles and realgar nanoparticles with the same background As<inf>2</inf>O<inf>3</inf>concentrations and compared their cytoxcity to promyelocytic leukemia HL-60 cells including inhibiting cell growth, inducing oxidative stress.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17282069.001).

[ISSN] 1557-170X

[Journal-full-title] Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference

[ISO-abbreviation] Conf Proc IEEE Eng Med Biol Soc

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Improved outcome of acute promyelocytic leukemia with high WBC counts over the last 15 years: the European APL Group experience.

PURPOSE: Acute promyelocytic leukemia (APL) with pretreatment WBC counts greater than 10,000/microL is still considered to carry a poorer prognosis than APL with WBC lower than 10,000/mL.

PATIENTS AND METHODS: Nine hundred two patients with APL, including 204 patients and 68 patients with WBC counts more than 10,000/microL and more than 50,000/microL, respectively, were enrolled between 1993 and 2005 in two successive randomized trials of the European APL group (APL 93 and APL 2000) that tested, in particular, the modalities of combination of all-trans retinoic acid (ATRA) and chemotherapy, maintenance treatment, escalating doses of cytarabine, early administration of dexamethasone, and CNS prophylaxis.

RESULTS: Between the APL 93 and 2000 trials, the complete response (CR) rate increased from 89.6% to 93%, and the 5-year cumulative incidence of relapse (CIR) decreased from 40% to 9.5% in patients with WBC counts of 10,000 to 50,000/microL.

Whereas in the APL 93 trial, increased WBC counts were significantly associated with higher CIR and shorter survival, this was not the case in the APL 2000 trial.

In patients with increased WBC counts, enrollment onto the APL 2000 trial (v APL 93) and combined maintenance with ATRA and chemotherapy were associated with significantly lower CIR and better survival.

CONCLUSION: Outcome of APL with high WBC count has markedly improved over the years as a result of fewer early deaths and fewer relapses.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Leukocyte Count. Outcome and Process Assessment (Health Care). Quality of Health Care

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Disease-Free Survival. Europe. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Middle Aged. Proportional Hazards Models. Recurrence. Risk Assessment. Risk Factors. Time Factors. Treatment Outcome. Young Adult

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] J Clin Oncol. 2010 Jan 10;28(2):e21; author reply e22-3 [19949004.001]

(PMID = 19414681.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Immunohistochemical expression of promyelocytic leukemia body in soft tissue sarcomas.

BACKGROUND: The function of promyelocytic leukemia (PML) bodies is not well known but plays an important role in controlling cell proliferation, apoptosis and senescence.

This study was undertaken to analyze the clinical significance of PML body expression in primary tumor samples from malignant fibrous histiocytoma (MFH) and liposarcoma patients.

METHODS: We studied MFH and liposarcoma samples from 55 patients for PML bodies.

Fluorescent immunostaining of PML bodies was performed in the paraffin-embedded tumor sections.

RESULTS: PML body immunostaining was identified in 63.9% of MFH and 63.2% of liposarcoma samples.

PML body expression rates of all sarcoma cells were 1.5 +/- 1.8% (range: 0-7.0) in MFH and 1.3 +/- 1.4% (0-5.2) in liposarcoma samples.

PML body expression (p = 0.0053) and a high rate of PML body expression (p = 0.0012) were significantly greater prognostic risk factors for death than the other clinical factors in MFH patients.

All liposarcoma patients without expression of PML were disease free at the end of the study.

CONCLUSION: Our study suggests that the presence of PML bodies may indicate a poor prognosis for MFH and liposarcoma patients.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Nature. 2000 Jul 13;406(6792):207-10 [10910364.001]

[Cites] Cancer Lett. 2003 May 15;194(2):155-62 [12757973.001]

[Cites] Nat Cell Biol. 2000 Oct;2(10):730-6 [11025664.001]

[Cites] Cell Death Differ. 2003 Dec;10(12):1290-9 [12934066.001]

[Cites] Oncogene. 2004 Apr 12;23(16):2819-24 [15077145.001]

[Cites] Am J Pathol. 2004 Aug;165(2):471-80 [15277221.001]

[Cites] Genes Chromosomes Cancer. 2004 Oct;41(2):155-62 [15287028.001]

[Cites] Nature. 1990 Oct 11;347(6293):558-61 [2170850.001]

[Cites] Cell. 1991 Aug 23;66(4):663-74 [1652368.001]

[Cites] Cell. 1991 Aug 23;66(4):675-84 [1652369.001]

[Cites] EMBO J. 1992 Apr;11(4):1397-407 [1314166.001]

[Cites] Proc Natl Acad Sci U S A. 1992 Jun 1;89(11):4840-4 [1317574.001]

[Cites] N Engl J Med. 1993 Jul 15;329(3):177-89 [8515790.001]

[Cites] Blood. 1994 Jan 1;83(1):10-25 [8274729.001]

[Cites] Cancer Res. 1995 Apr 1;55(7):1590-7 [7882370.001]

[Cites] EMBO J. 1995 Sep 1;14(17):4240-8 [7556065.001]

[Cites] J Cancer Res Clin Oncol. 1995;121(9-10):555-63 [7559736.001]

[Cites] J Clin Oncol. 1996 May;14(5):1679-89 [8622088.001]

[Cites] Am J Pathol. 1996 Dec;149(6):2023-35 [8952536.001]

[Cites] J Clin Oncol. 1997 Jan;15(1):350-62 [8996162.001]

[Cites] Nat Med. 1997 Nov;3(11):1271-4 [9359704.001]

[Cites] Oncogene. 1998 Jun 4;16(22):2905-13 [9671411.001]

[Cites] Am J Hum Genet. 1998 Aug;63(2):297-304 [9683622.001]

[Cites] Nat Genet. 1998 Nov;20(3):266-72 [9806545.001]

[Cites] Blood. 1999 May 15;93(10):3167-215 [10233871.001]

[Cites] Clin Cancer Res. 2005 Jan 1;11(1):217-25 [15671549.001]

[Cites] Cancer Res. 2005 Apr 1;65(7):2722-9 [15805271.001]

[Cites] Int J Cancer. 2005 Jul 1;115(4):556-60 [15688424.001]

[Cites] Cancer Lett. 2006 Jan 18;231(2):176-84 [16399222.001]

[Cites] Nature. 2006 Aug 17;442(7104):779-85 [16915281.001]

[Cites] Cell Res. 2008 Jun;18(6):622-40 [18504460.001]

[Cites] EMBO J. 2000 Nov 15;19(22):6185-95 [11080164.001]

[Cites] EMBO J. 2001 Aug 15;20(16):4547-59 [11500381.001]

[Cites] Oncogene. 2001 Oct 29;20(49):7257-65 [11704854.001]

[Cites] Cell. 2002 Jan 25;108(2):165-70 [11832207.001]

[Cites] Differentiation. 2002 Mar;70(1):10-22 [11963652.001]

[Cites] EMBO J. 2002 Jul 1;21(13):3358-69 [12093737.001]

[Cites] Mol Cell Biol. 2002 Aug;22(15):5259-69 [12101223.001]

[Cites] Cancer Cell. 2002 Oct;2(4):257-65 [12398889.001]

[Cites] Cancer Res. 2003 Apr 15;63(8):1759-63 [12702558.001]

[Cites] Genes Dev. 2000 Aug 15;14(16):2015-27 [10950866.001]

(PMID = 19025608.001).

[ISSN] 1756-9966

[Journal-full-title] Journal of experimental & clinical cancer research : CR

[ISO-abbreviation] J. Exp. Clin. Cancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human

[Other-IDs] NLM/ PMC2611968

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Apoptin is modified by SUMO conjugation and targeted to promyelocytic leukemia protein nuclear bodies.

Here, we report for the first time that apoptin interacts directly with the promyelocytic leukemia protein (PML) in tumor cells and accumulates in PML nuclear bodies (NBs), which are involved in apoptosis induction and viral replication.

We also demonstrate that apoptin is sumoylated and that a sumoylation-deficient apoptin mutant is no longer recruited to PML-NBs, but localizes in the nuclear matrix.

This mutant fails to bind PML, but can still induce apoptosis as efficiently as wild-type apoptin.

Moreover, apoptin kills also PML-/- cells and promyelocytic leukemia cells with defective PML expression.

Our results therefore suggest that apoptin kills tumor cells independently of PML and sumoylation, however, the interaction of apoptin with PML and small ubiquitin-like modifier (SUMO) proteins might be relevant for CAV replication.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16924230.001).

[ISSN] 0950-9232

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Capsid Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / SUMO-1 Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / VP3 protein, Chicken anemia virus; 143220-95-5 / PML protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] HLA-DRneg patients without acute promyelocytic leukemia show distinct immunophenotypic, genetic, molecular, and cytomorphologic characteristics compared to acute promyelocytic leukemia.

BACKGROUND: Loss of HLA-DR and CD34 is a well-known characteristic of malignant promyelocytes in acute promyelocytic leukemia (APL).

However, this immunophenotype is not specific for APL.

The purpose of this study was to investigate whether further biological characterization of the HLA-DR(neg) acute myeloid leukemia patients would allow more clearly define criteria to separate APL from non-APL patients.

METHODS: Immunophenotyping, cytogenetics, molecular analyses, and cytomorphology were prospectively performed within routine leukemia diagnostics of 800 patients included in different prospective acute myeloid leukemia multicenter trials.

RESULTS: Beside 60 APL, an additional 62 HLA-DR(neg) non-APL patients were identified.

The main differential characteristics of HLA-DR(neg) non-APL included high CXCR-4 expression in most patients and almost all leukemia cells, a significantly higher proportion of patients presenting with NPM1 mutations as well as the significant association with cup-like nuclear morphology.

The biological distinctness of both leukemia subtypes was further emphasized by the complete absence of aberrant CD2 expression and increased leukocyte and platelet counts in HLA-DR(neg) non-APL patients.

Even in the CD34(pos) subgroup of HLA-DR(neg) non-APL all those features contributed in at least the same way to the separation from APL.

CONCLUSIONS: The results of the present study show that an immunophenotypic, molecular, and cytomorphologic separation of both HLA-DR(neg) leukemia subgroups is possible indicating that both groups are biologically distinct.

[MeSH-major] Flow Cytometry / methods. HLA-DR Antigens / metabolism. Leukemia, Promyelocytic, Acute / metabolism

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2009 Clinical Cytometry Society.

(PMID = 19291801.001).

[ISSN] 1552-4957

[Journal-full-title] Cytometry. Part B, Clinical cytometry

[ISO-abbreviation] Cytometry B Clin Cytom

[Language] eng

[Publication-type] Comparative Study; Journal Article; Multicenter Study

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD34; 0 / CXCR4 protein, human; 0 / DNA, Neoplasm; 0 / HLA-DR Antigens; 0 / Nuclear Proteins; 0 / Receptors, CXCR4; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Increased oxidative DNA products in patients with acute promyelocytic leukemia during arsenic therapy.

Arsenic trioxide (ATO) has been used to treat acute promyelocytic leukemia (APL), but the oxidative DNA damage occurring in patients has not been fully elucidated.

We measured 8-hydroxy-2'-deoxyguanosine (8-OHdG), one of the most abundant oxidative products of DNA, by enzyme-linked immunoassay, and reactive oxidative species (ROS), by luminol- and luminol-H2O2 chemiluminescence, in the plasma of four APL patients treated with ATO.

After six courses of ATO therapy, the plasma 8-OHdG concentration had increased from 45.6+/-22.8 ng/mL to 310.2+/-239.6 ng/mL.

The plasma chemiluminescence level did not change significantly.

These findings suggest that ATO generates intracellular oxidative DNA damage, but this is not correlated with the plasma ROS level.

The clinical significance of 8-OHdG during and after ATO therapy warrants further study.

[MeSH-major] Arsenicals / adverse effects. DNA / blood. Leukemia, Promyelocytic, Acute / blood. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / adverse effects. Reactive Oxygen Species / blood

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17082016.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Comparative Study; Letter

[Publication-country] Italy

[Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 0 / Reactive Oxygen Species; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; 9007-49-2 / DNA; G9481N71RO / Deoxyguanosine; S7V92P67HO / arsenic trioxide

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Isolated central nervous system recurrence of acute promyelocytic leukemia in children.

The incidence of isolated central nervous system (iCNS) relapse in pediatric acute promyelocytic leukemia (APL) is debated.

We analyzed the literature, focusing on clinical trials reported since the advent of ATRA use.

This incidence does not support the use of intrathecal CNS prophylaxis for all children with APL.

[MeSH-major] Central Nervous System Neoplasms / pathology. Leukemia, Promyelocytic, Acute / pathology

[MeSH-minor] Child. Clinical Trials as Topic. Humans. Incidence. Premedication. Recurrence

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Pediatr Blood Cancer. 2009 Aug;53(2):235-6; author reply 237 [19353622.001]

[CommentIn] Pediatr Blood Cancer. 2010 Feb;54(2):336-7; author reply 338 [19847884.001]

(PMID = 18816805.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 27

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute promyelocytic leukemia in patients aged over 60 years: multicenter experience of 34 consecutive unselected patients.

Treatment of acute promyelocytic leukemia (APL) has evolved over recent years, resulting in a cure rate of 75-80%.

However, the prognosis of older patients with APL remains poorer as compared to young adults because of substantial morbidity of either induction or consolidation therapy.

We describe therapeutic results in a series of 34 consecutive APL patients aged over 60 years, with particular emphasis on those patients managed outside of clinical trials because of comorbidities at diagnosis.

Six patients (18%) died within two days of diagnosis; among these, only one was on the AIDA protocol.

Patients accrued into the GIMEMA AIDA protocol achieved longer survival (median not reached vs. 10 months, p=0.03).

In conclusion, our data demonstrate that at least 30% of older APL patients are not eligible to accrual in multicenter trials; furthermore, in this subset, the possibility of early death is substantial.

However, when CR is achieved, a personalized consolidation approach can be adopted with the possibility of achieving long-term disease control.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

[MeSH-minor] Age Factors. Aged. Aged, 80 and over. Clinical Trials as Topic. Female. Humans. Male. Middle Aged. Treatment Outcome

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20393021.001).

[ISSN] 1791-7530

[Journal-full-title] Anticancer research

[ISO-abbreviation] Anticancer Res.

[Language] eng

[Publication-type] Journal Article; Multicenter Study

[Publication-country] Greece

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pharmacological inhibition of BMK1 suppresses tumor growth through promyelocytic leukemia protein.

We found that BMK1 interacted with promyelocytic leukemia protein (PML), and inhibited its tumor-suppressor function through phosphorylation.

Furthermore, activated BMK1 notably inhibited PML-dependent activation of p21.

To further investigate the BMK-mediated inhibition of the tumor suppressor activity of PML in tumor cells, we developed a small-molecule inhibitor of the kinase activity of BMK1, XMD8-92.

COS Scholar Universe. author profiles.

Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

Guide to Pharmacology. gene/protein/disease-specific - ERK subfamily - overview and references .

Guide to Pharmacology. gene/protein/disease-specific - doublecortin like kinase 2 - data and references .

Guide to Pharmacology. gene/protein/disease-specific - mitogen-activated protein kinase 7 - data and references .

Guide to Pharmacology. gene/protein/disease-specific - polo like kinase 4 - data and references .

Guide to Pharmacology. gene/protein/disease-specific - tyrosine kinase non receptor 1 - data and references .

PhosphoSitePlus. gene/protein/disease-specific - PhosphoSitePlus® - comprehensive post-translational modification resource .

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.

[Cites] Oncogene. 2001 Oct 29;20(49):7250-6 [11704853.001]

[Cites] FEBS Lett. 2001 Jul 27;502(1-2):21-4 [11478941.001]

[Cites] Cell. 2002 Jan 25;108(2):165-70 [11832207.001]

[Cites] Nat Rev Cancer. 2001 Dec;1(3):181-93 [11902573.001]

[Cites] Surgery. 2002 Aug;132(2):293-301 [12219026.001]

[Cites] Science. 2002 Dec 6;298(5600):1911-2 [12471242.001]

[Cites] Oncogene. 2003 Mar 6;22(9):1381-9 [12618764.001]

[Cites] J Clin Invest. 2004 Apr;113(8):1138-48 [15085193.001]

[Cites] Cancer Cell. 2004 Apr;5(4):389-401 [15093545.001]

[Cites] Nat Cell Biol. 2004 Jul;6(7):665-72 [15195100.001]

[Cites] Biochem Biophys Res Commun. 1995 Aug 15;213(2):715-24 [7646528.001]

[Cites] J Biol Chem. 1996 Jul 12;271(28):16586-90 [8663194.001]

[Cites] EMBO J. 1997 Dec 1;16(23):7054-66 [9384584.001]

[Cites] Nature. 1998 Oct 15;395(6703):713-6 [9790194.001]

[Cites] J Biol Chem. 1999 Sep 10;274(37):26563-71 [10473620.001]

[Cites] Cancer Res. 2004 Nov 1;64(21):7732-9 [15520177.001]

[Cites] J Mol Med (Berl). 2004 Dec;82(12):800-8 [15517128.001]

[Cites] Nat Biotechnol. 2005 Mar;23(3):329-36 [15711537.001]

[Cites] Circ Res. 2005 Jun 10;96(11):1145-51 [15879308.001]

[Cites] Cancer Res. 2005 Sep 1;65(17):7699-706 [16140937.001]

[Cites] Mol Cell Biol. 2006 Mar;26(5):1679-90 [16478989.001]

[Cites] Nature. 2006 May 25;441(7092):523-7 [16680151.001]

[Cites] Cell. 2006 Jul 28;126(2):269-83 [16873060.001]

[Cites] Nature. 2006 Aug 17;442(7104):779-85 [16915281.001]

[Cites] Biochemistry. 2007 Jan 16;46(2):350-8 [17209545.001]

[Cites] Curr Biol. 2007 Feb 20;17(4):316-22 [17291758.001]

[Cites] Oncogene. 2007 May 14;26(22):3100-12 [17496909.001]

[Cites] Nat Rev Mol Cell Biol. 2007 Dec;8(12):1006-16 [17928811.001]

[Cites] Nat Biotechnol. 2008 Jan;26(1):127-32 [18183025.001]

[Cites] Nat Rev Drug Discov. 2008 May;7(5):391-7 [18404149.001]

[Cites] Neoplasia. 2008 May;10(5):462-70 [18472963.001]

[Cites] J Cell Physiol. 2009 Apr;219(1):152-61 [19089993.001]

[Cites] Breast Cancer Res. 2008;10(6):R105 [19087274.001]

[Cites] Front Biosci (Landmark Ed). 2009;14:497-509 [19273081.001]

[Cites] Mol Cell Biol. 2002 Jan;22(1):270-85 [11739740.001]

[Cites] J Biol Chem. 2000 Jun 16;275(24):18534-40 [10849446.001]

[Cites] Nature. 2000 Jul 13;406(6792):207-10 [10910364.001]

[Cites] Nat Cell Biol. 2000 Oct;2(10):730-6 [11025664.001]

[Cites] EMBO J. 2000 Nov 15;19(22):6185-95 [11080164.001]

[Cites] Nature. 2001 Mar 1;410(6824):37-40 [11242034.001]

[Cites] J Biol Chem. 2001 Mar 23;276(12):8631-4 [11254654.001]

[Cites] J Biol Chem. 2001 Apr 6;276(14):10870-8 [11139578.001]

[Cites] Endocr Rev. 2001 Apr;22(2):153-83 [11294822.001]

[ErratumIn] Cancer Cell. 2010 Oct 19;18(4):396

(PMID = 20832753.001).

[ISSN] 1878-3686

[Journal-full-title] Cancer cell

[ISO-abbreviation] Cancer Cell

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA079871-10; United States / NCI NIH HHS / CA / R01 CA114059-03; United States / NCI NIH HHS / CA / R01 CA079871-08; United States / NCI NIH HHS / CA / R01 CA079871-09; United States / NCI NIH HHS / CA / CA114059; United States / NCI NIH HHS / CA / R01 CA114059-05; United States / NCI NIH HHS / CA / CA079871; United States / NCI NIH HHS / CA / R01 CA114059; United States / NCI NIH HHS / CA / R01 CA114059-04; United States / NCI NIH HHS / CA / R01 CA079871

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Nuclear Proteins; 0 / Protein Kinase Inhibitors; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 7

[Other-IDs] NLM/ NIHMS231387; NLM/ PMC2939729

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Leukemogenesis and therapy of acute promyelocytic leukemia: from the worse to the most favorable subtype of acute myeloid leukemia].

[Transliterated title] Leukemogeneza a lécba akutní promyelocytární leukemie: cesta od nejhorsího k nejpríznivejsímu typu akutní myeloidní leukemie.

The evolution of therapy of acute promyelocytic leukemia (APL) from 1964 to present is reviewed.

The paper is focused on the main findings and key studies which formed current and almost standard therapeutic approach to APL.

The first important development was the use of anthracyclines for the initial therapy of APL in 1967.

The first clinical study which brought information about the effect of ATRA in APL started in China in 1986.

A number of the most important subsequent studies focused on pathogenesis and therapy of APL are analyzed and reviewed.

The additional considerable finding was the discovery of arsenic trioxide (ATO) therapeutic efficacy in APL and ATO is now in particular used for a therapy of relapsed APL.

The publication gives also a recent insight into a leukemogenesis of APL and development of a resistance to ATRA.

At the conclusion, the authors emphasize the need of early diagnosis as a one of the main conditions for successful treatment of APL.

[MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18780571.001).

[ISSN] 0042-773X

[Journal-full-title] Vnitr̆ní lékar̆ství

[ISO-abbreviation] Vnitr Lek

[Language] cze

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Czech Republic

[Number-of-references] 166

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Mouse models of acute promyelocytic leukemia.

Mouse models of acute promyelocytic leukemia have been generated through transgenic, knock-in, retroviral, and xenograft strategies.

Among the areas investigated are the role of reciprocal fusions; effects of target cells, expression levels, and mouse strains; cooperating events; and restrictive and permissive factors.

Furthermore, preclinical studies utilizing these mice have advanced therapy for myeloid leukemia.

[MeSH-major] Antineoplastic Agents / therapeutic use. Disease Models, Animal. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / physiopathology

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17217036.001).

[ISSN] 0070-217X

[Journal-full-title] Current topics in microbiology and immunology

[ISO-abbreviation] Curr. Top. Microbiol. Immunol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Germany

[Chemical-registry-number] 0 / Antineoplastic Agents

[Number-of-references] 70

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Retinoic acid in treating acute promyelocytic leukemia with hyperleukocytosis and its therapeutic strategy].

In order to investigate the occurrence of hyperleukocytosis in treating acute promyelocytic leukemia (APL) patients with all trans retinoic acid (ATRA) and to explore the influence of the level of leucocyte on curative effect of ATRA, the APL patients were divided into three different groups according to the count of leucocyte in peripheral blood.

It is concluded that the ATRA in combination with cytotoxic drugs can efficiently control the occurrence of hyperleukocytosis during ATRA-treating APL and reduce the early mortality.

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18426682.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Does acute promyelocytic leukemia in Indian patients have biology different from the West?

Acute promyelocytic leukemia (APML) is a well-characterized malignancy with typical clinico-hematological and molecular features.

This study was conducted to determine the clinico-hematological profile of APML in India.

Thirty-five patients with APML presenting to Hematology Department, AIIMS, New Delhi, between July 2003 and June 2005 were evaluated for presenting clinical features, hemogram, peripheral smear, bone marrow morphology and cytochemistry.

Reverse transcriptase PCR (RT-PCR) for PML-RARalpha was done in all cases.

Male-to-female ratio was 0.9:1 (males--17 and females--18) with median age 25 years (range 11-57 years).

RT-PCR showed PML-RARalpha in 33/35 cases with the bcr3 isoform being present in 24/33 positive cases (72.7%).

The two cases negative for PML-RARalpha showed typical morphology and responded to ATRA.

APML in India has certain unusual features, which may reflect a different biology.

[MeSH-major] Leukemia, Promyelocytic, Acute / pathology

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18723985.001).

[ISSN] 0377-4929

[Journal-full-title] Indian journal of pathology & microbiology

[ISO-abbreviation] Indian J Pathol Microbiol

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

[Chemical-registry-number] 0 / Azo Compounds; 0 / Naphthalenes; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.- / Esterases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Treatment outcome of acute promyelocytic leukemia with modified aida protocol.

We analyzed the outcome of a series of 19 newly diagnosed patients with acute promyelocytic leukemia treated with AIDA modified protocol, using mitoxantrone in place of idarubicin.

Eleven patients achieved morphologic CR (58%).

The 4-year disease-free survival is 82%.

The study showed the antileukemic efficacy of mitoxantrone and that it could be used as a reasonable option in anthracycline-based strategies in APL.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Blood. 2008 Oct 15;112(8):3130-4 [18664623.001]

[Cites] Semin Oncol. 2008 Aug;35(4):401-9 [18692690.001]

[Cites] Haematologica. 2007 Oct;92(10):1431-2 [18024380.001]

[Cites] Leukemia. 2000 Aug;14(8):1371-7 [10942231.001]

[Cites] Blood. 1996 Aug 15;88(4):1390-8 [8695858.001]

[Cites] Blood. 1993 Sep 15;82(6):1689-94 [8400225.001]

[Cites] Blood. 1998 Aug 1;92(3):784-9 [9680345.001]

(PMID = 20490274.001).

[ISSN] 1687-9112

[Journal-full-title] Advances in hematology

[ISO-abbreviation] Adv Hematol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Egypt

[Other-IDs] NLM/ PMC2871550

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Loss of promyelocytic leukemia protein in human gastric cancers.

To clarify the clinical implications of promyelocytic leukemia (PML) expression in gastric carcinomas, the expression of PML was analyzed in large series of gastric carcinoma by immunohistochemistry, western blotting and reverse transcription-PCR.

PML protein expression was reduced or abolished in gastric carcinomas (31.7 and 10.6%, respectively) by immunohistochemistry.

PML protein loss was associated with more lymphatic invasion, higher pTNM stage, and worse patient survival.

Only one gastric carcinoma cell line showed loss of PML, and the PML protein re-appeared after the treatment of proteasome inhibitor in this cell line.

We conclude that PML protein loss occurs in a minority of gastric carcinomas during carcinogenesis and progression, and suggest the proteasome-dependent pathway as a mechanism of PML protein loss.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16713073.001).

[ISSN] 0304-3835

[Journal-full-title] Cancer letters

[ISO-abbreviation] Cancer Lett.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Down syndrome with microgranular variant of acute promyelocytic leukemia in a child: a case report.

BACKGROUND: Acute promyelocytic leukemia (APL) accounts for less than 10% of pediatric AML.

Cases of APL in Down syndrome (DS) have been described in the literature rarely and it is rarer still to find the microgranular variant (M3v) of APL in trisomy 21 patients.

CASE PRESENTATION: We present a case of a five-year-old female with Down syndrome diagnosed with acute promyelocytic leukemia (APL).

Based on this morphology and cytochemistry, a diagnosis of APL microgranular variant (M3v) was made.

CONCLUSION: This case report emphasizes the importance of a high index of suspicion in the diagnosis of acute promyelocytic leukemia microgranular variant in Down syndrome.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Tumori. 1987 Aug 31;73(4):403-6 [2958963.001]

[Cites] Leukemia. 1994 Aug;8(8):1264-8 [8057659.001]

[Cites] Cancer Genet Cytogenet. 2006 Mar;165(2):176-9 [16527614.001]

[Cites] Am J Hematol. 1997 Nov;56(3):131-42 [9371524.001]

[Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]

[Cites] Blood. 1998 Jan 15;91(2):608-15 [9427716.001]

[Cites] Cancer Genet Cytogenet. 2002 Jan 1;132(1):74-6 [11801315.001]

(PMID = 18036234.001).

[ISSN] 1752-1947

[Journal-full-title] Journal of medical case reports

[ISO-abbreviation] J Med Case Rep

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2211491

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Functional interactions between the Epstein-Barr virus BZLF1 protein and the promyelocytic leukemia protein.

The Epstein-Barr virus immediate-early protein BZLF1 (Z) has been shown to alter the cellular localization of the promyelocytic leukemia (PML) protein.

PML has important implications for growth control, apoptosis, anti-viral effects and many more processes.

Here we further examined the relationship between PML and the Epstein-Barr virus Z protein.

We examined the effect of Z expression on PML protein levels, and the effect of increased PML protein levels on Z-mediated dispersion of PML bodies.

We found that increased levels of PML protein, such as through interferon treatment, were able to suppress Z-mediated PML body dispersion.

We also studied the consequences of PML dispersion by Z, by examining p21 transactivation, A20 transactivation, and MHC Class I presentation levels in Z-expressing cells.

We found that, while Z-mediated dispersion of PML did not affect MHC Class I presentation, it did alter p21 and A20 expression.

In addition, we found that increased levels of PML were able to prevent Z protein binding to mitotic chromosomes.

Our work implies that the balance of PML and Z levels in cells may affect how each protein functions.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16307818.001).

[ISSN] 0168-1702

[Journal-full-title] Virus research

[ISO-abbreviation] Virus Res.

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] Netherlands

[Chemical-registry-number] 0 / BZLF1 protein, Herpesvirus 4, Human; 0 / DNA-Binding Proteins; 0 / Histocompatibility Antigens Class I; 0 / Intracellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Viral Proteins; 143220-95-5 / PML protein, human; EC 1.13.12.- / Luciferases; EC 6.3.2.19 / TNFAIP3 protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Posttranslational regulation of Myc by promyelocytic leukemia zinc finger protein.

The promyelocytic leukemia zinc finger (PLZF) protein, a transcriptional repressor, induces cellular resistance to oncogenic transformation by diverse oncoproteins.

Two point mutants of PLZF that have lost the antioncogenic activity of the wild-type protein are oncogenic in chicken embryo fibroblasts; this activity is correlated with differential effects on Myc.

Wild-type PLZF represses Myc transcription without affecting total Myc protein levels and reduces the levels of phosphorylated Myc.

The PLZF mutants do not alter Myc transcription or protein expression but increase the levels of phosphorylated Myc.

Wild-type PLZF downregulates the MAPK pathway and activates Akt, resulting in reduced phosphorylation on serine 62 of Myc by Erk and on threonine 58 by glycogen synthase kinase 3beta.

We postulate that the 2 PLZF mutants are oncogenic, because they function as dominant negatives of wild-type PLZF, enhancing Myc phosphorylation and increasing Myc transcriptional and oncogenic activity.

COS Scholar Universe. author profiles.

Addgene Non-profit plasmid repository. clones/clone libraries - Get Article's Plasmids - Addgene (subscription/membership/fee required).

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Oncogene. 1998 Jul 23;17(3):313-25 [9690513.001]

[Cites] Mol Cell Biochem. 1998 May;182(1-2):135-41 [9609122.001]

[Cites] Virology. 1998 Sep 1;248(2):305-11 [9721239.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14950-5 [9843996.001]

[Cites] Oncogene. 2007 Jan 18;26(3):339-48 [16862184.001]

[Cites] PLoS Genet. 2007 Aug;3(8):e146 [17784791.001]

[Cites] Nat Cell Biol. 2008 Jul;10(7):788-801 [18568019.001]

[Cites] Mol Cell Biol. 1999 Jan;19(1):1-11 [9858526.001]

[Cites] Virology. 1999 Jan 20;253(2):193-207 [9918878.001]

[Cites] Oncogene. 1999 Jan 28;18(4):925-34 [10023668.001]

[Cites] Mol Cell. 1999 Feb;3(2):169-79 [10078200.001]

[Cites] Oncogene. 1999 May 13;18(19):3004-16 [10378696.001]

[Cites] Nucleic Acids Res. 1999 Oct 15;27(20):4106-13 [10497277.001]

[Cites] Bioorg Med Chem. 2006 Apr 15;14(8):2660-73 [16384710.001]

[Cites] J Biol Chem. 2000 Mar 3;275(9):6267-75 [10692423.001]

[Cites] Mol Cell Biol. 2000 Apr;20(7):2423-35 [10713166.001]

[Cites] Nat Genet. 2000 Jun;25(2):166-72 [10835630.001]

[Cites] Genes Dev. 2000 Oct 1;14(19):2501-14 [11018017.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3830-5 [11891322.001]

[Cites] Cell. 2002 May 3;109(3):321-34 [12015982.001]

[Cites] J Biol Chem. 2002 May 24;277(21):19229-35 [11904304.001]

[Cites] Oncogene. 2002 Oct 10;21(46):6983-91 [12370820.001]

[Cites] Dev Cell. 2002 Oct;3(4):499-510 [12408802.001]

[Cites] Mol Cell. 2002 Dec;10(6):1283-94 [12504005.001]

[Cites] Cancer Cell. 2003 Mar;3(3):219-31 [12676581.001]

[Cites] Am J Pathol. 2003 May;162(5):1603-10 [12707044.001]

[Cites] EMBO Rep. 2003 May;4(5):484-90 [12776737.001]

[Cites] Oncogene. 2003 Sep 18;22(40):6151-9 [13679853.001]

[Cites] Mol Cell Biol. 2003 Dec;23(24):9375-88 [14645547.001]

[Cites] J Biol Chem. 2003 Dec 19;278(51):51606-12 [14563837.001]

[Cites] Expert Rev Anticancer Ther. 2004 Apr;4(2):289-302 [15056059.001]

[Cites] Nat Genet. 2004 Jun;36(6):653-9 [15156143.001]

[Cites] Oncogene. 2004 Jun 3;23(26):4567-76 [15077196.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):9085-90 [15150404.001]

[Cites] Oncogene. 2004 Sep 30;23(45):7561-70 [15334066.001]

[Cites] Nature. 1981 Apr 9;290(5806):475-80 [6261142.001]

[Cites] Cell. 1983 Oct;34(3):789-98 [6313208.001]

[Cites] Cell. 1983 Dec;35(3 Pt 2):603-10 [6606489.001]

[Cites] Nature. 1983 Dec 22-1984 Jan 4;306(5945):799-803 [6419123.001]

[Cites] Nature. 1984 Mar 15-21;308(5956):286-8 [6700731.001]

[Cites] Mol Cell Biol. 1984 Jun;4(6):1172-4 [6330534.001]

[Cites] Proc Natl Acad Sci U S A. 1985 Apr;82(7):1984-8 [3856876.001]

[Cites] Nucleic Acids Res. 1985 Mar 25;13(6):2141-52 [3923436.001]

[Cites] Science. 1986 Jul 25;233(4762):461-4 [3014659.001]

[Cites] Proc Natl Acad Sci U S A. 1986 Aug;83(15):5414-8 [3526329.001]

[Cites] Mol Cell Biol. 1987 Dec;7(12):4513-21 [3325826.001]

[Cites] J Biol Chem. 1990 Jan 5;265(1):396-400 [1688432.001]

[Cites] J Biol Chem. 1991 Dec 15;266(35):23521-4 [1748630.001]

[Cites] Cell. 1992 Apr 3;69(1):119-28 [1555236.001]

[Cites] EMBO J. 1993 Mar;12(3):1161-7 [8384553.001]

[Cites] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3216-20 [8386367.001]

[Cites] J Clin Invest. 1993 May;91(5):2260-7 [8387545.001]

[Cites] Gene. 1993 Jun 30;128(2):269-72 [8514192.001]

[Cites] Proc Natl Acad Sci U S A. 1995 Mar 14;92(6):2249-53 [7892256.001]

[Cites] J Neurosci. 1995 Jul;15(7 Pt 1):4927-42 [7623123.001]

[Cites] Nature. 1995 Dec 21-28;378(6559):785-9 [8524413.001]

[Cites] Proc Natl Acad Sci U S A. 1996 Jul 23;93(15):7522-7 [8755507.001]

[Cites] FEBS Lett. 1996 Dec 16;399(3):333-8 [8985174.001]

[Cites] Oncogene. 1997 Mar 6;14(9):1067-74 [9070655.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Aug 19;94(17):9028-33 [9256429.001]

[Cites] J Biol Chem. 1997 Sep 5;272(36):22447-55 [9278395.001]

[Cites] Mol Cell Biol. 1998 Sep;18(9):5533-45 [9710637.001]

(PMID = 19444914.001).

[ISSN] 1097-0215

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P01 CA078045-07; United States / NCI NIH HHS / CA / R01 CA078230-07; United States / NCI NIH HHS / CA / CA078045-09; United States / NCI NIH HHS / CA / CA078230-07; United States / NCI NIH HHS / CA / R01 CA078230; United States / NCI NIH HHS / CA / R01 CA078230-10; United States / NCI NIH HHS / CA / CA078230-09; United States / NCI NIH HHS / CA / P01 CA078045-10; United States / NCI NIH HHS / CA / R01 CA078230-08; United States / NCI NIH HHS / CA / CA078230-08; United States / NCI NIH HHS / CA / CA078045-07; United States / NCI NIH HHS / CA / P01 CA078045; United States / NCI NIH HHS / CA / CA078045-10; United States / NCI NIH HHS / CA / R01 CA078230-09; United States / NCI NIH HHS / CA / CA078230-10; United States / NCI NIH HHS / CA / P01 CA078045-08; United States / NCI NIH HHS / CA / CA078045-08; United States / NCI NIH HHS / CA / P01 CA078045-09

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Kruppel-Like Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 147855-37-6 / ZBTB16 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases

[Other-IDs] NLM/ NIHMS115924; NLM/ PMC2721905

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Diagnosis and monitoring of PML-RARalpha-positive acute promyelocytic leukemia by quantitative RT-PCR.

The last 15 yr have produced dramatic improvements in the survival rate of patients with acute promyelocytic leukemia (APL).

These improvements have been due mainly to the introduction of targeted therapies and improved methods for diagnosing and monitoring this disease.

The underlying molecular lesion in APL involves a t(15:17) translocation which leads to the generation of PML-RARalpha fusion transcripts and proteins.

The PML-RARalpha fusion transcripts have been shown to be useful markers for establishing the diagnosis and for monitoring the response to treatment.

This manuscript describes the application of QZyme reverse-transcription polymerase chain reaction (RT-PCR) to the quantification of PML-RARalpha transcripts as a marker of APL.

The approach is well suited to monitoring minimal residual disease (MRD) in patients with APL, as a result of its ability to detect low numbers of transcripts and accurately measure differences in concentration over a broad dynamic range.

Further, its capacity for duplex analysis has multiple advantages for analysis of clinical specimens.

Protocols for duplex, single-tube QZyme RT-PCR assays, which allow simultaneous quantification of PML-RARalpha fusion transcripts (either L-type and V-type, or S-type) and the internal control BCR transcript, are provided.

These protocols can be used for analyzing patient RNA specimens and are suitable for clinical trial monitoring.

For this type of work, it is recommended that investigators validate the assays to ensure reproducible, accurate, and specific results on the equipment in their own laboratories.

[MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Transcription, Genetic

[MeSH-minor] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Humans. Monitoring, Physiologic / methods. RNA, Neoplasm / genetics. Translocation, Genetic

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16502582.001).

[ISSN] 1543-1894

[Journal-full-title] Methods in molecular medicine

[ISO-abbreviation] Methods Mol. Med.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cryptic PML-RARα positive acute promyelocytic leukemia with unusual morphology and cytogenetics.

Acute Promyelocytic Leukemia (APL) is different from other forms of acute myeloid leukemia (AML), to the reason being the potential devastating coagulopathy and the sensitivity to all-trans retinoic acid (ATRA) and arsenic trioxide (As 2 O 3 ).

We hereby present a case of APL, morphologically distinct from the hypergranular APL; however, the flow cytometry revealed a characteristic phenotype showing dim CD45, bright CD13, bright CD33 and dim CD117 positivity.

Conventional cytogenetics revealed a distinct karyotype of a male with translocation t(4;15)(q34.2:q26.3).

However, interphase fluorescence-in-situ hybridization (FISH) revealed PML/RARA fusion signal on chromosome 15 in 90% cells.

[MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / pathology. Leukocytes / cytology

Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 21045428.001).

[ISSN] 0974-5130

[Journal-full-title] Indian journal of pathology & microbiology

[ISO-abbreviation] Indian J Pathol Microbiol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] India

[Chemical-registry-number] 0 / Antigens, CD; 0 / HLA Antigens; 0 / Nuclear Proteins; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor alpha; 143220-95-5 / PML protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Detection of the STAT5B-RARA fusion transcript in acute promyelocytic leukemia with the normal chromosome 17 on G-banding.

Acute promyelocytic leukemia (APL) is characterized by chromosomal rearrangements of 17q21, leading to fusion of the gene-encoding retinoic acid receptor alpha (RARA) with a number of alternative partner genes.

We report a rare case of APL with STAT5B-RARA fusion transcript and the normal chromosome 17 on G-banding.

Administration of all trans-retinoic acid improved disseminated intravascular coagulation without decrease of the leukemia cells in his peripheral blood and bone marrow.

The molecular mechanism of fusion between STAT5B and RARA by chromosomal rearrangement is discussed based on the data from genome database.

Clinical characteristics of APL with STAT5B-RARA are also discussed.

[MeSH-major] Chromosomes, Human, Pair 17 / genetics. Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / analysis. Oncogene Proteins, Fusion / genetics. STAT5 Transcription Factor / analysis. STAT5 Transcription Factor / genetics. Transcription, Genetic / genetics

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Eur J Haematol. 2009 Nov;83(5):499-501 [19624718.001]

(PMID = 18221386.001).

[ISSN] 1600-0609

[Journal-full-title] European journal of haematology

[ISO-abbreviation] Eur. J. Haematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Denmark

[Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / STAT5 Transcription Factor; 0 / STAT5-RARalpha protein, human