http://ift.tt/2suOZKL
Κυριακή 4 Ιουνίου 2017
Atypical presentation of sigmoid carcinoma
http://ift.tt/2suOZKL
Ethmoid malformation associated with pediatric nasal polyposis and allergic fungal sinusitis
http://ift.tt/2suDCCg
Primary extrahepatic bile duct neuroendocrine tumor with obstructive jaundice masquerading as a Klatskin tumor
http://ift.tt/2suDFhz
Early ovariectomy reveals the germline encoding of natural anti-A- and Tn-cross-reactive immunoglobulin M (IgM) arising from developmental O-GalNAc glycosylations. (Germline-encoded natural anti-A/Tn cross-reactive IgM)
Abstract
While native blood group A-like glycans have not been demonstrated in prokaryotic microorganisms as a source of human "natural" anti-A isoagglutinin production, and metazoan eukaryotic N-acetylgalactosamine O-glycosylation of serine or threonine residues (O-GalNAc-Ser/Thr-R) does not occur in bacteria, the O-GalNAc glycan-bearing ovarian glycolipids, discovered in C57BL/10 mice, are complementary to the syngeneic anti-A-reactive immunoglobulin M (IgM), which is not present in animals that have undergone ovariectomy prior to the onset of puberty. These mammalian ovarian glycolipids are complementary also to the anti-A/Tn cross-reactive Helix pomatia agglutinin (HPA), a molluscan defense protein, emerging from the coat proteins of fertilized eggs and reflecting the snail-intrinsic, reversible O-GalNAc glycosylations. The hexameric structure of this primitive invertebrate defense protein gives rise to speculation regarding an evolutionary relationship to the mammalian nonimmune, anti-A-reactive immunoglobulin M (IgM) molecule. Hypothetically, this molecule obtains its complementarity from the first step of protein glycosylations, initiated by GalNAc via reversible O-linkages to peptides displaying Ser/Thr motifs, whereas the subsequent transferase depletion completes germ cell maturation and cell renewal, associated with loss of glycosidic bonds and release of O-glycan-depleted proteins, such as complementary IgM revealing the structure of the volatilely expressed "lost" glycan carrier through germline Ser residues. Consequently, the evolutionary/developmental first glycosylations of proteins appear metabolically related or identical to that of the mucin-type, potentially "aberrant" monosaccharide GalNAcα1-O-Ser/Thr-R, also referred to as the Tn (T "nouvelle") antigen, and explain the anti-Tn cross-reactivity of human innate or "natural" anti-A-specific isoagglutinin and the pronounced occurrence of cross-reactive anti-Tn antibody in plasma from humans with histo-blood group O. In fact, A-allelic, phenotype-specific GalNAc glycosylation of plasma proteins does not occur in human blood group O, affecting anti-Tn antibody levels, which may function as a growth regulator that contributes to a potential survival advantage of this group in the overall risk of developing cancer when compared with non-O blood groups.
In mouse and man, the complementarity of the nonimmune anti-A/Tn cross-reactive IgM most likely occurs in a process of rapid glycosylations/deglycosylations, called "single cycle event", which causes the release of an antibody molecule that displays a predetermined breaking point through the hydroxyl (–OH) functional group of terminal serine/threonine residues. The germline encoded anti-Tn cross-reactivity of the anti-A-specific isoagglutinin and the pronounced occurrence of anti-Tn reactivity in plasma from humans with histo (blood) group O(H), could contribute to the potential, currently discussed survival advantage of this group in the overall risk of developing cancer when compared with non-O blood groups.
from Cancer via ola Kala on Inoreader http://ift.tt/2suhCHV
via IFTTT
Cervical cancer screening in a low-resource setting: a pilot study on an HPV-based screen-and-treat approach
Abstract
Cervical cancer (CC) is the leading cause of cancer-related death among women in sub-Saharan Africa, primarily because of limited access to effective screening and preventive treatment. Our aim was to assess the feasibility of a human papillomavirus (HPV)-based CC screen-and-treat approach in a low-resource context. We recruited 1012 women aged 30–49 years through a CC screening campaign conducted in the District Hospital of Dschang, Cameroon. Participants performed HPV self-sampling, which was tested for high-risk HPV (HR-HPV) DNA using the point-of-care Xpert HPV assay. All HPV-positive women were invited for visual inspection with acetic acid and Lugol's iodine (VIA/VILI) to exclude CC or enable triage. A cervical sample for histological analysis was also collected. Women positive for HPV 16/18/45 and for other HR-HPV with pathological VIA/VILI were selected to undergo treatment with thermocoagulation. The HPV prevalence in the study population was 18.5% (n = 187); of these cases, 20 (10.6%), 42 (22.3%) and 140 (74.9%) were positive for HPV16, HPV18/45 and other HR-HPV types, respectively. Overall, 107/185 (57.8%) VIA/VILI examinations were classified as pathological and 78 (42.2%) as normal. Women positive for HPV16/18/45 were 4.2 times more likely to harbor cervical intraepithelial neoplasia grade 2 or worse (CIN2+) than those with other HPV types. The specificity of HPV 16/18/45 genotypes for detection of high-grade lesions among HR-HPV positive women was higher than that of VIA/VILI in all age groups. The sensitivity and specificity of VIA/VILI in detecting CIN2+ among HPV positive women were 80% and 44%, respectively. Overall, 110/121 screen-positive women (90.9%) were eligible for, and were treated with, thermocoagulation. An HPV-based screen-and-treat approach is feasible in a low-resource context and may contribute to improving the effectiveness of CC prevention programs. Immediate thermocoagulation treatment for women who are HPV16- and/or HPV18/45-positive is a practical approach for the treatment of CIN2+. The combination of HPV-testing and VIA/VILI for CC screening might reduce overtreatment.
This study assesses the feasibility of a cervical cancer (CC) screen-and-treat 1-day approach including vaginal self-sampling and point-of-care HPV testing in a developing country. This approach may contribute to improving the effectiveness of CC prevention programs and decrease CC mortality in low-resource countries.
from Cancer via ola Kala on Inoreader http://ift.tt/2rV34DV
via IFTTT
Early ovariectomy reveals the germline encoding of natural anti-A- and Tn-cross-reactive immunoglobulin M (IgM) arising from developmental O-GalNAc glycosylations. (Germline-encoded natural anti-A/Tn cross-reactive IgM)
Abstract
While native blood group A-like glycans have not been demonstrated in prokaryotic microorganisms as a source of human "natural" anti-A isoagglutinin production, and metazoan eukaryotic N-acetylgalactosamine O-glycosylation of serine or threonine residues (O-GalNAc-Ser/Thr-R) does not occur in bacteria, the O-GalNAc glycan-bearing ovarian glycolipids, discovered in C57BL/10 mice, are complementary to the syngeneic anti-A-reactive immunoglobulin M (IgM), which is not present in animals that have undergone ovariectomy prior to the onset of puberty. These mammalian ovarian glycolipids are complementary also to the anti-A/Tn cross-reactive Helix pomatia agglutinin (HPA), a molluscan defense protein, emerging from the coat proteins of fertilized eggs and reflecting the snail-intrinsic, reversible O-GalNAc glycosylations. The hexameric structure of this primitive invertebrate defense protein gives rise to speculation regarding an evolutionary relationship to the mammalian nonimmune, anti-A-reactive immunoglobulin M (IgM) molecule. Hypothetically, this molecule obtains its complementarity from the first step of protein glycosylations, initiated by GalNAc via reversible O-linkages to peptides displaying Ser/Thr motifs, whereas the subsequent transferase depletion completes germ cell maturation and cell renewal, associated with loss of glycosidic bonds and release of O-glycan-depleted proteins, such as complementary IgM revealing the structure of the volatilely expressed "lost" glycan carrier through germline Ser residues. Consequently, the evolutionary/developmental first glycosylations of proteins appear metabolically related or identical to that of the mucin-type, potentially "aberrant" monosaccharide GalNAcα1-O-Ser/Thr-R, also referred to as the Tn (T "nouvelle") antigen, and explain the anti-Tn cross-reactivity of human innate or "natural" anti-A-specific isoagglutinin and the pronounced occurrence of cross-reactive anti-Tn antibody in plasma from humans with histo-blood group O. In fact, A-allelic, phenotype-specific GalNAc glycosylation of plasma proteins does not occur in human blood group O, affecting anti-Tn antibody levels, which may function as a growth regulator that contributes to a potential survival advantage of this group in the overall risk of developing cancer when compared with non-O blood groups.
In mouse and man, the complementarity of the nonimmune anti-A/Tn cross-reactive IgM most likely occurs in a process of rapid glycosylations/deglycosylations, called "single cycle event", which causes the release of an antibody molecule that displays a predetermined breaking point through the hydroxyl (–OH) functional group of terminal serine/threonine residues. The germline encoded anti-Tn cross-reactivity of the anti-A-specific isoagglutinin and the pronounced occurrence of anti-Tn reactivity in plasma from humans with histo (blood) group O(H), could contribute to the potential, currently discussed survival advantage of this group in the overall risk of developing cancer when compared with non-O blood groups.
http://ift.tt/2suhCHV
Cervical cancer screening in a low-resource setting: a pilot study on an HPV-based screen-and-treat approach
Abstract
Cervical cancer (CC) is the leading cause of cancer-related death among women in sub-Saharan Africa, primarily because of limited access to effective screening and preventive treatment. Our aim was to assess the feasibility of a human papillomavirus (HPV)-based CC screen-and-treat approach in a low-resource context. We recruited 1012 women aged 30–49 years through a CC screening campaign conducted in the District Hospital of Dschang, Cameroon. Participants performed HPV self-sampling, which was tested for high-risk HPV (HR-HPV) DNA using the point-of-care Xpert HPV assay. All HPV-positive women were invited for visual inspection with acetic acid and Lugol's iodine (VIA/VILI) to exclude CC or enable triage. A cervical sample for histological analysis was also collected. Women positive for HPV 16/18/45 and for other HR-HPV with pathological VIA/VILI were selected to undergo treatment with thermocoagulation. The HPV prevalence in the study population was 18.5% (n = 187); of these cases, 20 (10.6%), 42 (22.3%) and 140 (74.9%) were positive for HPV16, HPV18/45 and other HR-HPV types, respectively. Overall, 107/185 (57.8%) VIA/VILI examinations were classified as pathological and 78 (42.2%) as normal. Women positive for HPV16/18/45 were 4.2 times more likely to harbor cervical intraepithelial neoplasia grade 2 or worse (CIN2+) than those with other HPV types. The specificity of HPV 16/18/45 genotypes for detection of high-grade lesions among HR-HPV positive women was higher than that of VIA/VILI in all age groups. The sensitivity and specificity of VIA/VILI in detecting CIN2+ among HPV positive women were 80% and 44%, respectively. Overall, 110/121 screen-positive women (90.9%) were eligible for, and were treated with, thermocoagulation. An HPV-based screen-and-treat approach is feasible in a low-resource context and may contribute to improving the effectiveness of CC prevention programs. Immediate thermocoagulation treatment for women who are HPV16- and/or HPV18/45-positive is a practical approach for the treatment of CIN2+. The combination of HPV-testing and VIA/VILI for CC screening might reduce overtreatment.
This study assesses the feasibility of a cervical cancer (CC) screen-and-treat 1-day approach including vaginal self-sampling and point-of-care HPV testing in a developing country. This approach may contribute to improving the effectiveness of CC prevention programs and decrease CC mortality in low-resource countries.
http://ift.tt/2rV34DV
B lymphocytes repress hepatic tumorigenesis but not development in Hras12V transgenic mice
Abstract
Increasing reports show non-inflammation underlying HCC, challenging our understanding of the roles of the immune system in hepatocarcinogenesis. By exploring a mouse model of hepatic tumor induced by hepatocyte-specific expression of the Hras12V oncogene without obvious inflammation, we found that the proportion of B cells, but not T cells, progressively and significantly decreased in 3, 5-month-old transgenic mice (Tg) compared with non-transgenic mice. Notably, the proportions of total and activated B and T cells all significantly decreased in 9-month-old Tg with multiple massive hepatic tumors. Together with the decreased B cell proportion, serum IgG1/2 also significantly decreased in 5, 9-month-old Tg. Interestingly, homozygous Tg showed significantly higher B cell proportion and IgG2 levels, accompanied by significantly lower incidences of liver nodules but not adenomas and carcinomas compared with heterozygous Tg. Treatment of Tg with PCI-32765, a potent Bruton's tyrosine kinase (BTK) inhibitor for suppressing B cell proliferation and activation, significantly decreased the B cell proportion and IgG2 levels, accompanied by a significantly higher incidence of liver nodules, but had no effects on adenoma and carcinoma. Treatment of Tg with insulin-like growth factor 1(IGF-1) significantly increased the B cell proportion and IgG2 levels, accompanied by a significantly lower incidence of liver nodules and carcinoma, but had no effects on adenoma. Conclusively, B cells and IgG2 may play important roles in suppressing hepatic tumorigenesis, but not development. In addition, hepatocyte-specific expression of the ras oncogene may play roles in suppressing B cells, while developed hepatic tumors suppress both B and T cells. This article is protected by copyright. All rights reserved.
from Cancer via ola Kala on Inoreader http://ift.tt/2rV9t29
via IFTTT
A classifier integrating plasma biomarkers and radiological characteristics for distinguishing malignant from benign pulmonary nodules
Abstract
Lung cancer is primarily caused by cigarette smoking and the leading cancer killer in the USA and across the world. Early detection of lung cancer by low-dose CT (LDCT) can reduce the mortality. However, LDCT dramatically increases the number of indeterminate pulmonary nodules (PNs), leading to overdiagnosis. Having a definitive preoperative diagnosis of malignant PNs is clinically important. Using microarray and droplet digital PCR to directly profile plasma miRNA expressions of 135 patients with PNs, we identified 11 plasma miRNAs that displayed a significant difference between patients with malignant versus benign PNs. Using multivariate logistic regression analysis of the molecular results and clinical/radiological characteristics, we developed an integrated classifier comprising two miRNA biomarkers and one radiological characteristic for distinguishing malignant from benign PNs. The classifier had 89.9% sensitivity and 90.9% specificity, being significantly higher compared with the biomarkers or clinical/radiological characteristics alone (All P <0.05). The classifier was validated in two independent sets of patients. We have for the first time shown that the integration of plasma biomarkers and radiological characteristics could more accurately identify lung cancer among indeterminate PNs. Future use of the classifier could spare individuals with benign growths from the harmful diagnostic procedures, while allowing effective treatments to be immediately initiated for lung cancer, thereby reduces the mortality and cost. Nevertheless, further prospective validation of this classifier is warranted. This article is protected by copyright. All rights reserved.
from Cancer via ola Kala on Inoreader http://ift.tt/2suoq8a
via IFTTT
B lymphocytes repress hepatic tumorigenesis but not development in Hras12V transgenic mice
Abstract
Increasing reports show non-inflammation underlying HCC, challenging our understanding of the roles of the immune system in hepatocarcinogenesis. By exploring a mouse model of hepatic tumor induced by hepatocyte-specific expression of the Hras12V oncogene without obvious inflammation, we found that the proportion of B cells, but not T cells, progressively and significantly decreased in 3, 5-month-old transgenic mice (Tg) compared with non-transgenic mice. Notably, the proportions of total and activated B and T cells all significantly decreased in 9-month-old Tg with multiple massive hepatic tumors. Together with the decreased B cell proportion, serum IgG1/2 also significantly decreased in 5, 9-month-old Tg. Interestingly, homozygous Tg showed significantly higher B cell proportion and IgG2 levels, accompanied by significantly lower incidences of liver nodules but not adenomas and carcinomas compared with heterozygous Tg. Treatment of Tg with PCI-32765, a potent Bruton's tyrosine kinase (BTK) inhibitor for suppressing B cell proliferation and activation, significantly decreased the B cell proportion and IgG2 levels, accompanied by a significantly higher incidence of liver nodules, but had no effects on adenoma and carcinoma. Treatment of Tg with insulin-like growth factor 1(IGF-1) significantly increased the B cell proportion and IgG2 levels, accompanied by a significantly lower incidence of liver nodules and carcinoma, but had no effects on adenoma. Conclusively, B cells and IgG2 may play important roles in suppressing hepatic tumorigenesis, but not development. In addition, hepatocyte-specific expression of the ras oncogene may play roles in suppressing B cells, while developed hepatic tumors suppress both B and T cells. This article is protected by copyright. All rights reserved.
http://ift.tt/2rV9t29
A classifier integrating plasma biomarkers and radiological characteristics for distinguishing malignant from benign pulmonary nodules
Abstract
Lung cancer is primarily caused by cigarette smoking and the leading cancer killer in the USA and across the world. Early detection of lung cancer by low-dose CT (LDCT) can reduce the mortality. However, LDCT dramatically increases the number of indeterminate pulmonary nodules (PNs), leading to overdiagnosis. Having a definitive preoperative diagnosis of malignant PNs is clinically important. Using microarray and droplet digital PCR to directly profile plasma miRNA expressions of 135 patients with PNs, we identified 11 plasma miRNAs that displayed a significant difference between patients with malignant versus benign PNs. Using multivariate logistic regression analysis of the molecular results and clinical/radiological characteristics, we developed an integrated classifier comprising two miRNA biomarkers and one radiological characteristic for distinguishing malignant from benign PNs. The classifier had 89.9% sensitivity and 90.9% specificity, being significantly higher compared with the biomarkers or clinical/radiological characteristics alone (All P <0.05). The classifier was validated in two independent sets of patients. We have for the first time shown that the integration of plasma biomarkers and radiological characteristics could more accurately identify lung cancer among indeterminate PNs. Future use of the classifier could spare individuals with benign growths from the harmful diagnostic procedures, while allowing effective treatments to be immediately initiated for lung cancer, thereby reduces the mortality and cost. Nevertheless, further prospective validation of this classifier is warranted. This article is protected by copyright. All rights reserved.
http://ift.tt/2suoq8a
Predispositions to Leukemia in Down Syndrome and Other Hereditary Disorders
Opinion statement
Leukemia is the most common pediatric cancer and accounts for approximately one third of childhood malignancies. There are germline genetic alterations that significantly increase the risk of developing hematopoietic malignancies in childhood. In this review, we describe a number of these hereditary disorders and their clinical features. These predispositions to cancer syndromes can be attributed to DNA repair/genetic instability, RAS pathway dysfunction, bone marrow failure, telomeropathies, immunodeficiencies, transcription factor abnormalities, pure familial leukemia, and aneuploidy. We focus especially on acute myeloid leukemia associated with Down syndrome, but also include other hereditary syndromes in this review. Recent advances in high-throughput genotyping technology have identified new genetic variations prone to human leukemia. Understanding of the mechanism of leukemia development in these hereditary syndromes allows us to gain insight into leukemogenesis in general and suggests therapeutic strategies based on these findings.
from Cancer via ola Kala on Inoreader http://ift.tt/2rAknqN
via IFTTT
Predispositions to Leukemia in Down Syndrome and Other Hereditary Disorders
Opinion statement
Leukemia is the most common pediatric cancer and accounts for approximately one third of childhood malignancies. There are germline genetic alterations that significantly increase the risk of developing hematopoietic malignancies in childhood. In this review, we describe a number of these hereditary disorders and their clinical features. These predispositions to cancer syndromes can be attributed to DNA repair/genetic instability, RAS pathway dysfunction, bone marrow failure, telomeropathies, immunodeficiencies, transcription factor abnormalities, pure familial leukemia, and aneuploidy. We focus especially on acute myeloid leukemia associated with Down syndrome, but also include other hereditary syndromes in this review. Recent advances in high-throughput genotyping technology have identified new genetic variations prone to human leukemia. Understanding of the mechanism of leukemia development in these hereditary syndromes allows us to gain insight into leukemogenesis in general and suggests therapeutic strategies based on these findings.
http://ift.tt/2rAknqN
Predispositions to Leukemia in Down Syndrome and Other Hereditary Disorders
Opinion statement
Leukemia is the most common pediatric cancer and accounts for approximately one third of childhood malignancies. There are germline genetic alterations that significantly increase the risk of developing hematopoietic malignancies in childhood. In this review, we describe a number of these hereditary disorders and their clinical features. These predispositions to cancer syndromes can be attributed to DNA repair/genetic instability, RAS pathway dysfunction, bone marrow failure, telomeropathies, immunodeficiencies, transcription factor abnormalities, pure familial leukemia, and aneuploidy. We focus especially on acute myeloid leukemia associated with Down syndrome, but also include other hereditary syndromes in this review. Recent advances in high-throughput genotyping technology have identified new genetic variations prone to human leukemia. Understanding of the mechanism of leukemia development in these hereditary syndromes allows us to gain insight into leukemogenesis in general and suggests therapeutic strategies based on these findings.
from Cancer via ola Kala on Inoreader http://ift.tt/2rAknqN
via IFTTT
Implications of the lysophosphatidic acid signaling axis in liver cancer
Publication date: Available online 4 June 2017
Source:Biochimica et Biophysica Acta (BBA) - Reviews on Cancer
Author(s): Chiara Lopane, Pasquale Agosti, Isabella Gigante, Carlo Sabba, Antonio Mazzocca
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death in western countries. The major risk factors for HCC are hepatitis C or B viruses, alcohol and metabolic disorders. The increasing risk of HCC in patients with metabolic disorders (i.e. obesity, diabetes and non-alcoholic steatohepatitis/NASH) regardless of the presence of liver cirrhosis is becoming relevant. Nevertheless, molecular mechanisms linking these risk factors to liver oncogenesis are unclear. This review focuses on the pathogenic role of the lysophosphatidic acid (LPA) pathway in HCC, highlighting the implications of this bioactive phospholipid in liver cancer biology and metabolism and as potential therapeutic target.
http://ift.tt/2rUsamk
CD5-negative mantle cell lymphoma shows a less aggressive outcome and variable SOX11 staining
Abstract
Mantle cell lymphoma (MCL) is an uncommon B-cell lymphoma that prototypically expresses CD5, but a small subset is CD5 negative. The clinical significance of CD5 negativity is not yet well-elucidated. This case series aims to contribute to the understanding of CD5-negative MCL by looking at specific markers and outcome in our cases with long-term follow-up. Eight cases of CD5-negative MCL were identified in the case files at the Massachusetts General Hospital from 1978 to 2016. Clinicopathological characteristics were evaluated, including immunohistochemical stains for cyclin D1, SOX11, Ki67, and p53. Patients initially presented with involvement of lymph nodes and spleen (n = 4), sinonasal or oral mucosa (n = 2), orbital soft tissue (n = 1), and salivary gland (n = 1). On histology, the cases all showed classic MCL morphology, with a monotonous population of medium-sized cells with irregular nuclear contours. The cases were positive by immunohistochemistry for cyclinD1 (8/8 cases), essentially negative for p53 staining (8/8 cases), and mostly positive for SOX11 (5/8 cases). All cases had a low Ki67 proliferation rate (<5%). Long-term clinical follow-up on five cases showed that four patients had a clinical course complicated by multiple relapses to the skin, soft tissue, liver, and bone marrow. Seven cases with available follow-up showed an average survival of 121 months (SD 86 months), with no detectable survival difference between the SOX11 positive and negative cases. CD5-negative MCL is an uncommon subtype of MCL that overall appears to have a better prognosis and longer overall survival than classic MCL, despite SOX11 expression. The cases also show little p53 expression and a low Ki67 proliferation index.
http://ift.tt/2qQJqsz
Unusual presentation of right coronary artery fistula
Ahmed MSEK Abdelaty<br />May 12, 2017; 2017:bcr-2017-220424-bcr-2017-220424<br />other
http://ift.tt/2qUPzPE
Anisakiasis: a growing cause of abdominal pain!
Joana Carmo<br />May 11, 2017; 2017:bcr2016218857-bcr2016218857<br />case-report
http://ift.tt/2rq2UDj
Long-term stabilisation of myeloma with curcumin
Abbas Zaidi<br />Apr 16, 2017; 2017:bcr2016218148-bcr2016218148<br />case-report
http://ift.tt/2qUKQ0z
Azacitidine in adult patients with acute myeloid leukemia
Publication date: Available online 3 June 2017
Source:Critical Reviews in Oncology/Hematology
Author(s): Andre C. Schuh, Hartmut Döhner, Lisa Pleyer, John F. Seymour, Pierre Fenaux, Hervé Dombret
Azacitidine is recommended front-line treatment for older patients with acute myeloid leukemia (AML) who are not candidates for intensive treatment regimens, and was recently granted approval in the European Union for treatment of adult AML. Reviewed here is azacitidine experience in AML, including: mechanistic and pharmacokinetic data; safety and efficacy in controlled trials; treatment effects in AML subpopulations defined by disease characteristics; experience in unselected patients treated in the community setting; clinical outcomes relative to other approved AML therapies; and experience with azacitidine-based combination treatment regimens. Collectively, these data suggest that (a) azacitidine may prolong overall survival to a similar or greater extent than do other approved AML treatments, but with less toxicity, (b) azacitidine may be the preferred treatment option for older patients with unfavorable cytogenetics, and (c) experience and outcomes with azacitidine in the clinic are similar to those seen in clinical trials. Continued investigation of combination regimens on an azacitidine backbone is warranted.
from Cancer via ola Kala on Inoreader http://ift.tt/2qUMzmn
via IFTTT
Reviewing the current evidence supporting early B-cells as the cellular origin of Merkel Cell Carcinoma
Publication date: Available online 3 June 2017
Source:Critical Reviews in Oncology/Hematology
Author(s): C.M. Sauer, A.M. Haugg, E. Chteinberg, D. Rennspiess, V. Winnepenninckx, E.-J. Speel, J.C. Becker, A.K. Kurz, A. zur Hausen
Merkel cell carcinoma (MCC) is a highly malignant skin cancer characterized by early metastases and poor survival. Although MCC is a rare malignancy, its incidence is rapidly increasing in the U.S. and Europe. The discovery of the Merkel cell polyomavirus (MCPyV) has enormously impacted our understanding of its etiopathogenesis and biology. MCCs are characterized by trilinear differentiation, comprising the expression of neuroendocrine, epithelial and B-lymphoid lineage markers. To date, it is generally accepted that the initial assumption of MCC originating from Merkel cells (MCs) is unlikely. This is owed to their post-mitotic character, absence of MCPyV in MCs and discrepant protein expression pattern in comparison to MCC. Evidence from mouse models suggests that epidermal/dermal stem cells might be of cellular origin in MCC. The recently formulated hypothesis of MCC originating from early B-cells is based on morphology, the consistent expression of early B-cell lineage markers and the finding of clonal immunoglobulin chain rearrangement in MCC cells. In this review we elaborate on the cellular ancestry of MCC, the identification of which could pave the way for novel and more effective therapeutic regimens.
from Cancer via ola Kala on Inoreader http://ift.tt/2rpK5QE
via IFTTT
ETV6 and ETV7: siblings in hematopoiesis and its disruption in disease
Publication date: Available online 3 June 2017
Source:Critical Reviews in Oncology/Hematology
Author(s): Parisa Rasighaemi, Alister C. Ward
ETV6 (TEL1) and ETV7 (TEL2) are closely-related members of the ETS family of transcriptional regulators. Both ETV6 and ETV7 have been demonstrated to play key roles in hematopoiesis, particularly with regard to maintenance of hematopoietic stem cells and control of lineage-specific differentiation, with evidence of functional interactions between both proteins. ETV6 has been strongly implicated in the molecular etiology of a number of hematopoietic diseases, including as a tumor suppressor, an oncogenic fusion partner, and an important regulator of thrombopoiesis, but recent evidence has also identified ETV7 as a potential oncogene in certain malignancies. This review provides an overview of ETV6 and ETV7 and their contribution to both normal and disrupted hematopoiesis. It also highlights the key clinical implications of the growing knowledge base regarding ETV6 abnormalities with respect to prognosis and treatment.
from Cancer via ola Kala on Inoreader http://ift.tt/2qULHyp
via IFTTT
Azacitidine in adult patients with acute myeloid leukemia
Publication date: Available online 3 June 2017
Source:Critical Reviews in Oncology/Hematology
Author(s): Andre C. Schuh, Hartmut Döhner, Lisa Pleyer, John F. Seymour, Pierre Fenaux, Hervé Dombret
Azacitidine is recommended front-line treatment for older patients with acute myeloid leukemia (AML) who are not candidates for intensive treatment regimens, and was recently granted approval in the European Union for treatment of adult AML. Reviewed here is azacitidine experience in AML, including: mechanistic and pharmacokinetic data; safety and efficacy in controlled trials; treatment effects in AML subpopulations defined by disease characteristics; experience in unselected patients treated in the community setting; clinical outcomes relative to other approved AML therapies; and experience with azacitidine-based combination treatment regimens. Collectively, these data suggest that (a) azacitidine may prolong overall survival to a similar or greater extent than do other approved AML treatments, but with less toxicity, (b) azacitidine may be the preferred treatment option for older patients with unfavorable cytogenetics, and (c) experience and outcomes with azacitidine in the clinic are similar to those seen in clinical trials. Continued investigation of combination regimens on an azacitidine backbone is warranted.
http://ift.tt/2qUMzmn
Reviewing the current evidence supporting early B-cells as the cellular origin of Merkel Cell Carcinoma
Publication date: Available online 3 June 2017
Source:Critical Reviews in Oncology/Hematology
Author(s): C.M. Sauer, A.M. Haugg, E. Chteinberg, D. Rennspiess, V. Winnepenninckx, E.-J. Speel, J.C. Becker, A.K. Kurz, A. zur Hausen
Merkel cell carcinoma (MCC) is a highly malignant skin cancer characterized by early metastases and poor survival. Although MCC is a rare malignancy, its incidence is rapidly increasing in the U.S. and Europe. The discovery of the Merkel cell polyomavirus (MCPyV) has enormously impacted our understanding of its etiopathogenesis and biology. MCCs are characterized by trilinear differentiation, comprising the expression of neuroendocrine, epithelial and B-lymphoid lineage markers. To date, it is generally accepted that the initial assumption of MCC originating from Merkel cells (MCs) is unlikely. This is owed to their post-mitotic character, absence of MCPyV in MCs and discrepant protein expression pattern in comparison to MCC. Evidence from mouse models suggests that epidermal/dermal stem cells might be of cellular origin in MCC. The recently formulated hypothesis of MCC originating from early B-cells is based on morphology, the consistent expression of early B-cell lineage markers and the finding of clonal immunoglobulin chain rearrangement in MCC cells. In this review we elaborate on the cellular ancestry of MCC, the identification of which could pave the way for novel and more effective therapeutic regimens.
http://ift.tt/2rpK5QE
ETV6 and ETV7: siblings in hematopoiesis and its disruption in disease
Publication date: Available online 3 June 2017
Source:Critical Reviews in Oncology/Hematology
Author(s): Parisa Rasighaemi, Alister C. Ward
ETV6 (TEL1) and ETV7 (TEL2) are closely-related members of the ETS family of transcriptional regulators. Both ETV6 and ETV7 have been demonstrated to play key roles in hematopoiesis, particularly with regard to maintenance of hematopoietic stem cells and control of lineage-specific differentiation, with evidence of functional interactions between both proteins. ETV6 has been strongly implicated in the molecular etiology of a number of hematopoietic diseases, including as a tumor suppressor, an oncogenic fusion partner, and an important regulator of thrombopoiesis, but recent evidence has also identified ETV7 as a potential oncogene in certain malignancies. This review provides an overview of ETV6 and ETV7 and their contribution to both normal and disrupted hematopoiesis. It also highlights the key clinical implications of the growing knowledge base regarding ETV6 abnormalities with respect to prognosis and treatment.
http://ift.tt/2qULHyp
Kinesiology taping as an adjunct for pain management in cancer?
Gourav Banerjee<br />Jul 14, 2016; 2016:bcr2016216439-bcr2016216439<br />case-report
http://ift.tt/2rTkCAo
Locally advanced adenocarcinoma of the rectum presenting with necrotising fasciitis of the perineum: successful management with early aggressive surgery and multimodal therapy
Luís Ferreira
Dec 16, 2015; 2015:bcr2015213245-bcr2015213245
case-report
http://ift.tt/2st1hmS
Surviving stroke in an Ebola Treatment Centre
Paul Dhillon<br />Oct 29, 2015; 2015:bcr2015211062-bcr2015211062<br />case-report
http://ift.tt/2rTbImx
Open removal of a retained retrohepatic inferior vena cava filter with a residual primary neuroectodermal renal tumoral thrombus
Carlos A Hinojosa<br />Oct 29, 2015; 2015:bcr2015212190-bcr2015212190<br />case-report
http://ift.tt/2ssvWAF
Freeman-Sheldon syndrome in a 29-year-old woman presenting with rare and previously undescribed features
Robert L Chamberlain<br />Oct 22, 2015; 2015:bcr2015212607-bcr2015212607<br />case-report
http://ift.tt/2rTkAbK
Serotonin syndrome in a breast-fed neonate
Rachel Morris<br />May 6, 2015; 2015:bcr2015209418-bcr2015209418<br />case-report
http://ift.tt/2sspiKL
Takotsubo cardiomyopathy case series: typical, atypical and recurrence
Jakub Lagan<br />Mar 5, 2015; 2015:bcr2014208741-bcr2014208741<br />case-report
http://ift.tt/2rTx6Io
Three-dimensional spectral domain optical coherence tomography in vitreomacular traction
Sandeep Saxena<br />Jun 17, 2014; 2014:bcr2013202065-bcr2013202065<br />case-report
http://ift.tt/2ssv5zM
Primary gut aspergillosis in a patient with acute myeloid leukaemia: the importance of early suspicion and definitive treatment
Elizabeth Li<br />Mar 18, 2014; 2014:bcr2013202316-bcr2013202316<br />case-report
http://ift.tt/2rTdFze
Two rare manifestations of Q fever: splenic and hepatic abscesses and cerebral venous thrombosis, with literature review ma non troppo
Manuel Mendes Gomes<br />Feb 5, 2014; 2014:bcr2013202843-bcr2013202843<br />case-report
http://ift.tt/2ssHdRi
Lemierre syndrome: more than just a sore throat
Christine Azzopardi<br />Nov 28, 2013; 2013:bcr2013201868-bcr2013201868<br />case-report
http://ift.tt/2rTlaGl
Postcaesarean open-heart surgery for Streptococcus sanguinis infective endocarditis
Kiattisak Kongwattanakul<br />Nov 14, 2013; 2013:bcr2013010103-bcr2013010103<br />case-report
http://ift.tt/2sskepz
Partial priapism
Peter Hoyerup<br />Aug 9, 2013; 2013:bcr2013200031-bcr2013200031<br />case-report
http://ift.tt/2rTbf3U
Complication of etanercept treatment for rheumatoid arthritis - purulent pericarditis caused by a commensal organism
Gemma K Taylor<br />May 8, 2012; 2012:bcr0120125644-bcr0120125644<br />case-report
http://ift.tt/2ssGYWu
[Adolescents and young adults with acute lymphoblastic leukemia. A specific management].
Related Articles |
[Adolescents and young adults with acute lymphoblastic leukemia. A specific management].
Bull Cancer. 2017 May 30;:
Authors: Boissel N, Ducassou S
Abstract
The acute lymphoblastic leukemia (ALL) is one of the first cancer for which emerged the particularity of the adolescent and young adult population. After decades of poorly concerted approaches, adult and pediatric haematologists found out that adolescents treated according to pediatric approaches had a better outcome than those treated in adult protocols. Therefore, pediatric-inspired therapies have been successfully implemented in the young adult population, leading to decreased criteria for allogeneic stem cell transplantation. More recently, a high prevalence of Philadelphia-like ALL has been identified in the AYA population, which opens the door to the combination of target therapy similar to Philadelphia-positive ALL. AYA patients require specific care programs including fertility counselling, adhesion evaluation, and long-term survivor follow-up. They are to be optimally treated by multidisciplinary teams, exploring their personal needs and determining the best management of the "whole patient".
PMID: 28576259 [PubMed - as supplied by publisher]
from Cancer via ola Kala on Inoreader http://ift.tt/2rFm74a
via IFTTT