Background: The mechanisms of tumor progression in mycosis fungoides (MF) and Sézary syndrome (SS) are poorly understood. Twist, a transcription factor, is thought to promote solid tumor progression by blocking p53 and inhibiting c-myc-induced apoptosis. Whether Twist expression is correlated to MF/SS stages remains unknown.

Methods: Twist, c-myc and p53 proteins in 68 MF/SS lesions across all T stages were examined by immunohistochemistry, and mRNA levels in peripheral blood CD4+ T-cells from SS patients were measured by QT-PCR.

Results: Positive staining for Twist was found in 12.5% (2/16) of T1 and 33.3% (7/21) of T2 early stage patches/plaques compared to 50.0% (9/18) of T3 tumors and 84.6% (11/13) of T4 erythroderma. Most T4 erythroderma were positive for Twist in dermal lymphocytes, with the strongest staining. Positive staining for c-myc was higher in T3/T4 lesions (29/31, 93.5%) than T1/T2 lesions (25/37, 67.6%, p<0.05), with strongest staining in T3 tumors. Aberrant p53 expression was more common in T3/T4 lesions (8/31; 25.8%) than in T1/T2 lesions (2/37, 5.4%, p<0.05). Twist mRNA was detected in all CD4+ T cells from SS patients but not in normal donors.

Conclusions: Increased Twist protein expression in advanced MF/SS lesions suggests that Twist expression may correlate with MF/SS stages.

Stem cell pathologies and neurological disease

Modern Pathology 25, 157 (February 2012). doi:10.1038/modpathol.2011.165

Authors: Dennis A Steindler, Michael S Okun & Björn Scheffler

The extent of retraction clefts correlates with lymphatic vessel density and VEGF-C expression and predicts nodal metastasis and poor prognosis in early-stage breast carcinoma

Modern Pathology 25, 163 (February 2012). doi:10.1038/modpathol.2011.138

Authors: Geza Acs, Gyorgy Paragh, Zsuzsa Rakosy, Christine Laronga & Paul J Zhang

Metaplastic breast carcinomas are enriched in markers of tumor-initiating cells and epithelial to mesenchymal transition

Modern Pathology 25, 178 (February 2012). doi:10.1038/modpathol.2011.167

Authors: Yanhong Zhang, Kathy A Toy & Celina G Kleer

Distinct patterns of promoter CpG island methylation of breast cancer subtypes are associated with stem cell phenotypes

Modern Pathology 25, 185 (February 2012). doi:10.1038/modpathol.2011.160

Authors: So Yeon Park, Hyeong Ju Kwon, Yoomi Choi, Hee Eun Lee, Sung-Won Kim, Jee Hyun Kim, In Ah Kim, Namhee Jung, Nam-Yun Cho & Gyeong Hoon Kang

From PTEN loss of expression to RICTOR role in smooth muscle differentiation: complex involvement of the mTOR pathway in leiomyosarcomas and pleomorphic sarcomas

Modern Pathology 25, 197 (February 2012). doi:10.1038/modpathol.2011.163

Authors: Laure Gibault, Céline Ferreira, Gaëlle Pérot, Anne Audebourg, Frédéric Chibon, Sarah Bonnin, Pauline Lagarde, Marie-Cécile Vacher-Lavenu, Philippe Terrier, Jean-Michel Coindre & Alain Aurias

Involvement of the PI3K/Akt pathway in myxoid/round cell liposarcoma

Modern Pathology 25, 212 (February 2012). doi:10.1038/modpathol.2011.148

Authors: Elizabeth G Demicco, Keila E Torres, Markus P Ghadimi, Chiara Colombo, Svetlana Bolshakov, Aviad Hoffman, Tingsheng Peng, Judith V M G Bovée, Wei-Lien Wang, Dina Lev & Alexander J Lazar

Histone deacetylase 1 and 2 in mesenchymal tumors

Modern Pathology 25, 222 (February 2012). doi:10.1038/modpathol.2011.157

Authors: Marina Pacheco & Torsten O Nielsen

N-terminal PAX8 polyclonal antibody shows cross-reactivity with N-terminal region of PAX5 and is responsible for reports of PAX8 positivity in malignant lymphomas

Modern Pathology 25, 231 (February 2012). doi:10.1038/modpathol.2011.162

Authors: Lucas Moretti, L Jeffrey Medeiros, Kranthi Kunkalla, Michelle D Williams, Rajesh R Singh & Francisco Vega

Therapy-related myeloid neoplasms following fludarabine, cyclophosphamide, and rituximab (FCR) treatment in patients with chronic lymphocytic leukemia/small lymphocytic lymphoma

Modern Pathology 25, 237 (February 2012). doi:10.1038/modpathol.2011.158

Authors: Yi Zhou, Guilin Tang, L Jeffrey Medeiros, Timothy J McDonnell, Michael J Keating, William G Wierda & Sa A Wang

Phenotypic complexity of T regulatory subsets in patients with B-chronic lymphocytic leukemia

Modern Pathology 25, 246 (February 2012). doi:10.1038/modpathol.2011.164

Authors: Angélique Biancotto, Pradeep K Dagur, John C Fuchs, Adrian Wiestner, C Bruce Bagwell & J Philip McCoy

A nuclear grading system is a strong predictor of survival in epitheloid diffuse malignant pleural mesothelioma

Modern Pathology 25, 260 (February 2012). doi:10.1038/modpathol.2011.146

Authors: Kyuichi Kadota, Kei Suzuki, Christos Colovos, Camelia S Sima, Valerie W Rusch, William D Travis & Prasad S Adusumilli

Mesotheliomas with crystalloid structures: report of nine cases, including one with oncocytic features

Modern Pathology 25, 272 (February 2012). doi:10.1038/modpathol.2011.159

Author: Nelson G Ordóñez

Loss of ARID1A expression is related to shorter progression-free survival and chemoresistance in ovarian clear cell carcinoma

Modern Pathology 25, 282 (February 2012). doi:10.1038/modpathol.2011.161

Authors: Atsuko Katagiri, Kentaro Nakayama, Mohammed Tanjimur Rahman, Munmun Rahman, Hiroshi Katagiri, Naomi Nakayama, Masako Ishikawa, Tomoka Ishibashi, Kouji Iida, Hiroshi Kobayashi, Yoshiro Otsuki, Satoru Nakayama & Kohji Miyazaki

Chemotherapy-related leiomyopathy: a suggested morphological explanation for the intestinal dysmotility affecting patients treated with anthracyclines

Modern Pathology 25, 289 (February 2012). doi:10.1038/modpathol.2011.115

Authors: Karmaine A Millington, Judy Mae Pascasio, Gregory E Halligan & Jean-Pierre de Chadarévian

Clinical and pathological analysis of colonic Crohn's disease, including a subgroup with ulcerative colitis-like features

Modern Pathology 25, 295 (February 2012). doi:10.1038/modpathol.2011.120

Authors: Genevieve Soucy, Helen H Wang, Francis A Farraye, Jason F Schmidt, Alton B Farris, Gregory Y Lauwers, Sandra R Cerda, Kleanthis G Dendrinos & Robert D Odze

Molecular heterogeneity of TFE3 activation in renal cell carcinomas

Modern Pathology 25, 308 (February 2012). doi:10.1038/modpathol.2011.169

Authors: Stephan Macher-Goeppinger, Wilfried Roth, Nina Wagener, Markus Hohenfellner, Roland Penzel, Axel Haferkamp, Peter Schirmacher & Sebastian Aulmann

Mutation of the genes encoding components of the TNFα-like (tumour necrosis factor α) pathway involved in signal transduction between the ectoderm and the mesenchyme during embryonic development causes hypohidrotic ectodermal dysplasia (HED), resulting from the abnormal differentiation of tooth buds, hair follicles and eccrine sweat glands. Two phenotypically indistinguishable forms of HED, X-linked recessive and autosomal (dominant or recessive), have been discerned in mice and humans.1 The X-linked form (OMIM #305100) is caused by mutations in the ED1 gene, which encodes two principal ectodysplasins. EDA-A1 is recognized by receptor EDA1R (ectodysplasin A1 receptor), causing the recruitment of an adaptor, EDARADD (EDA1R-associated death domain), which interacts with TRAF6 (tumour necrosis factor receptor-associated factor 6) leading to translocation of NFκB (nuclear factor κB) to the nucleus.2 Thus EDA-A1 ultimately activates NFκB to stimulate transcription of genes whose protein products are involved in the differentiation of skin appendages.1 In patients with HED, more than 100 different mutations in ED1, approximately 30 in EDA1R, and several in EDARADD have been reported (http://www.hgmd.cf.ac.uk). Studies conducted in mice have demonstrated that mutations in the tabby, downless or crinkled, genes, encoding the orthologues of EDA, EDAR1, and EDARADD, respectively, cause symptoms of HED.1 Furthermore, Naito et al.3 have shown that TRAF6–deficient mice also display symptoms of HED. To date, however, mutations in TRAF6, another component of the same signal transduction pathway, have not been reported in HED patients. In the present report is described the first mutation ever reported in TRAF6 in a female patient with symptoms typical of HED.

This review investigates the effectiveness of ablative and non-ablative Fractional Photothermolysis (FP) lasers for treating facial acne scars. 26 studies (13=ablative FP; 13=non-ablative FP) published between year-2003 to January 2011 were reviewed. Quantitative and qualitative data from each article were examined and analysed. 4 studies were split-face randomised controlled studies (RCTs). Whilst the data analysed where all clinically relevant and significant, there were some methodological differences between the studies. Outcomes included subjective and objective assessment of scar appearance, pre- and postoperative treatment, side effects and pain scores. A small number of studies used 3D Optical Profiling Imaging and histology for objective assessment. Even allowing for methodological variability, ablative FP seems to have an improvement range of 26-83% whereas non-ablative FP demonstrates an improvement range of 26-50%. Patients who undergo ablative FP laser experience erythema for 3-14 days and it resolves by 12 weeks, whereas patients who opt for the non-ablative FP laser experience erythema between 1-3 days and this resolves within a week. A higher proportion of patients (up to 92.3%) who undertake ablative FP experience post inflammatory hyperpigmentation (PIH) than those who have non-ablative FP (up to 13%). The maximum duration of PIH in ablative FP is up to 6 months whereas in non-ablative FP it lasts up to 1 week. Ablative FP and the procedure can be relatively uncomfortable in comparison to non-ablative FP. Ablative pain score range from 5.90-8.10 (scale 1-10) and the non-ablative FP pain score range from 3.90-5.66 (scale 1-10).