Deposits of clastic carbonate-dominated (calciclastic) sedimentary slope systems in the rock record have been identified mostly as linearly-consistent carbonate apron deposits, even though most ancient clastic carbonate slope deposits fit the submarine fan systems better. Calciclastic submarine fans are consequently rarely described and are poorly understood. Subsequently, very little is known especially in mud-dominated calciclastic submarine fan systems. Presented in this study are a sedimentological core and petrographic characterisation of samples from eleven boreholes from the Lower Carboniferous of Bowland Basin (Northwest England) that reveals a >250 m thick calciturbidite complex deposited in a calciclastic submarine fan setting. Seven facies are recognised from core and thin section characterisation and are grouped into three carbonate turbidite sequences. They include: 1) Calciturbidites, comprising mostly of highto low-density, wavy-laminated bioclast-rich facies; 2) low-density densite mudstones which are characterised by planar laminated and unlaminated muddominated facies; and 3) Calcidebrites which are muddy or hyper-concentrated debrisflow deposits occurring as poorly-sorted, chaotic, mud-supported floatstones. These

Phd by thesis

MYC on the Path to Cancer

Nuclear factor of κB (NF-κB) is a sequence-specific transcription factor that is known to be involved in the inflammatory and innate immune responses. Although the importance of NF-κB in immunity is undisputed, recent evidence indicates that NF-κB and the signalling pathways that are involved in its activation are also important for tumour development. NF-κB should therefore receive as much attention from cancer researchers as it has already from immunologists.

NF-κB in cancer: from innocent bystander to major culprit

ENDF/B-VII.1 Nuclear Data for Science and Technology: Cross Sections, Covariances, Fission Product Yields and Decay Data

Monthly Notices is one of the three largest general primary astronomical research publications. It is an international journal, published by the Royal Astronomical Society. This article 1 describes its publication policy and practice.

Monthly Notices of the Royal Astronomical Society

Primary diffuse large B-cell lymphoma of the bone (PB-DLBCL) is a rare event and is a diagnosis by exclusion of secondary bone involvement. Here we review the literature regarding PB-DLBCL and give essentials for this diagnosis. Furthermore, we give an overview of potential precursors and discuss chronic recurrent multifocal osteomyelitis (CRMO) as a potential risk factor for PB-DLBCL development in the young. Primary Bone Diffuse Large B-cell Lymphoma (PB-DLBCL) Primary bone non-Hodgkin lymphoma, other than plasmocytic myeloma and solitary plasmacytoma of bone, is defined by the World Health Organization (WHO) as a neoplasm composed of malignant lymphoid cells, with one or more bone lesions; by definition, lymph node or other extranodal lesions are not involved [1]. Primary lymphoma of bone is rare and accounts for less than 2% of adult lymphomas [2] and approximatively for 7 % of malignant bone tumors. Between 70 and 80% of primary bone lymphomas are classified as diffuse large B-cell lymphoma (DLBCL), the rest are anaplastic large, mostly ALK-positive T-cell lymphomas [3–5]. These aggressive lymphomas have preference for the axial skeleton and long tubular bones. The most commonly affected bones are femur, ilium, vertebrae, and humerus. PB-DLBCL is exceedingly rare in the young and tends to occur at the age of 45 while the peak incidence is in the range of 75 to 79 years [6]. Main symptoms are pain, local tenderness, redness, swelling, and nerve compression (related to the tumor location). Pathological fractures occur in 10–20% of PB-DLBCL, and, therefore, this is the most frequent complication at presentation of primary bone lymphoma [7]. The standard treatment for all kinds of DLBCL is the R-CHOP (Rituximab immunotherapy, i.e., an anti CD20 monoclonal antibody), combined with cyclophosphamide, doxorubicin hydrochloride, vincristine, and prednisone), the total number of cycles and addition of radiation therapy depending on tumor bulk [8]. DLBCL is a neoplasm of diffusely arranged medium or large lymphoid B-cells with nuclei more than twice the size of normal lymphocytes nuclei featuring open chromatin [9]. These lymphomas are CD20 + (▶Figure 1 A–D), CD3-, CyclinD1-, CD138and have a high proliferation (KI-67) index generally above 50%. Traditionally, DLBCLs were further characterized by cytomorphology as centroblastic, immunoblastic, plasmoblastic, and anaplastic. The current WHO classification still lists these variants, however, has promoted the transciptomebased molecular subgrouping with the two major subtypes activated B-cell-like (ABC) and germinal-center B-cell-like (GCB); by immunohistochemistry, this subdivision can be approximately done using an algorithm proposed by Hans following the expression of CD10, Bcl-6, and MUM-1 [10]. More recently, multiplatform genetic analysis allowed the identification of five subtypes of DLBCL making a further step in the direction of precision medicine [11, 12]. PB-DLBCL has been found to be predominantly of the ABC type [13]. Regarding bone as primary DLBCL location, the clinical significance of multifocal bone involvement has been investigated, in comparison with unifocal primary and secondary bone lymphoma. Multifocal primary bone DLBCL is very rare and constitutes around 3–10% of cases in the largest reported series of primary bone lymphomas [14]. Findings of Wu et al. (2014) suggest a major similarity between multifocal primary bone and secondary involvement rather than with unifocal DLBCL of the bone [15]. On the other hand, in the study of Messina et al. (2014) prognosis of multifocal primary bone DLBCL is significantly better than bone involvement at advanced stages of systemic DLBCL [14]. The relationship between chronic inflammation and lymphoma development is well established for marginal B-cell lymphoma of the salivary gland and Sjögrens’ disease, of lacrimal gland and chlamydial dacryoadenitis, of gastric marginal B-cell lymphoma and chronic gastritis, e.g., due to H. pylori infection, and for gluten-sensitive enteropathy-associated intestinal T-cell lymphoma [9]. The relationship is far less clear, if at all existing for chronic inflammation of the bone and subsequent lymphoma development. We here list anecdotal observations suggesting such a relationship. ▪ Rheumatoid arthritis: Patients with rheumatoid arthritis (RA) are at a double risk of developing malignant lymphoma and studies and case series of RA-associated lymphomas indicate an increased proportion of diffuse large Bcell lymphomas (DLBCLs) in RA patients [16]. ▪ Implantation of cobalt-chromiummolybdenum alloy joint prosthesis: The coincidence of PB-DLBCL was described in a patient during a surgical revision of the loosened prosthesis. Debris in the periprosthetic membrane are antigenic and lead to chronic inflammation through macrophage activation [17]. The pathogenesis has also been correlated with the release of chromium and cobalt ions from the

/pdf/diffuse-large-b-cell-lymphoma-in-and-of-the-bone-forms-and-40lt0yl9yw.pdf

Diffuse large B-cell lymphoma in and of the bone. Forms and potential precursors

The Hodgkin cell line U-HO1 was established from a malignant pleural effusion of a 23-yr-old male patient during the end stage of refractory nodular sclerosing classical Hodgkin lymphoma (cHL). Since its establishment in 2005, U-HO1 has maintained stable characteristics in vitro and has a doubling time of about 4 days under standard culture conditions. U-HO1 forms typical Reed/Sternberg cells in suspension, is EBV negative, lacks HLA-ABC- but expresses HLA-D- proteins/CD74 and surface exposes CD15 together with CD30 in the absence of CD19 and CD20. Karyotype analysis of U-HO1 revealed a hyperdiploid karyotype with multiple clonal aberrations. Most significant is an elongated chromosome 2, der(2)t(2;10)(q35;q16.1)add(2)(p13). CGH analysis revealed the following imbalances: ish cgh dim(1)(p13p31)(p12q21), enh(2)(p13p23), dim(4)(q31.3qter), enh(6)(q22q27), enh(12), enh(18),enh(20)(q13.1pter). FISH analysis showed about six-fold amplification of REL and BCL-11A, thus, U-HO1 is prototypical for cHL in every aspect tested so far. Compared to other HL cell lines, U-HO1 proved far less genetically aberrant suggesting that U-HO1’s imbalances suffice to cause the full-blown phenotype of primary refractory cHL.

/pdf/u-ho1-a-new-cell-line-derived-from-a-primary-refractory-3pvcpqbkt9.pdf

[U-HO1. A new cell line derived from a primary refractory classical Hodgkin lymphoma].

Eine 26-jahige Patientin berichtete uber eine druckdolente Schwellung im Bereich der Rima ani. Intraoperativ stellte sich ein prasakral lokalisierter Tumor dar. Histologisch zeigte sich ein gut umschriebener biphanotypischer Tumor mit sowohl papillar konfigurierten myxoiden als auch zellarmen sklerosierenden Anteilen. Der vorliegende Fall eines myxopapillaren Ependymoms zeigt die Schwierigkeiten bei der Differenzierung zwischen myxoid konfigurierten Tumoren im Bereich des Os sacrum.

Presacral lesion at the rima ani

Brownian Shape Dynamics in Fission

Die chronische myeloische Leukamie (CML) wird diagnostisch uber die reziproke Translokation t(9;22)(q34;q11) definiert. Diese Aberration kann u. a. uber eine BCR-ABL-FISH (Fluoreszenz-in-situ-Hybridisierung) nachgewiesen werden. Dieser Artikel prasentiert eine vergleichende Untersuchung verschiedener kommerzieller FISH-Sondensatze zum Nachweis der BCR-ABL-Fusion und unterschiedlicher FISH-Protokolle zur Optimierung dieser Technik an formalinfixierten, paraffineingebetteten Knochenmarkstanzen.

Peter Möller

Papers

Diffuse large B-cell lymphoma in and of the bone. Forms and potential precursors

[U-HO1. A new cell line derived from a primary refractory classical Hodgkin lymphoma].

Presacral lesion at the rima ani

Brownian Shape Dynamics in Fission

[Detection of the BCR-ABL fusion: Comparative analysis of six commercially available FISH fusion probes].