Identification of tyrosine kinase, HCK, and tumor suppressor, BIN1, as potential mediators of AHI-1 oncogene in primary and transformed CTCL cells

Kennah, Erin; Ringrose, Ashley; Zhou, Liang; Esmailzadeh, Sharmin; Qian, Hong; Su, Mingwan; Zhou, Youwen; Jiang, Xiaoyan

doi:10.1182/blood-2008-08-174037

Cited by 32 publications

(36 citation statements)

References 49 publications

(78 reference statements)

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“…The purification of Sézary cells from Sézary patients (n 5 9) and benign control CD4 T cells from healthy donors (n 5 8) was performed as previously described. [24][25][26][27] Total cellular RNA was extracted using the RNeasy Mini Kit (Qiagen, Mississauga, ON, Canada) according to the manufacturer's instructions. RNA was reverse transcribed using random primers and SuperScript III reverse transcriptase (Invitrogen).…”

Section: Patientsmentioning

confidence: 99%

Elucidating the role of interleukin-17F in cutaneous T-cell lymphoma

Krejsgaard

Litvinov

Wei

et al. 2013

Blood

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100

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Section: Patientsmentioning

confidence: 99%

Elucidating the role of interleukin-17F in cutaneous T-cell lymphoma

Krejsgaard

Litvinov

Wei

et al. 2013

Blood

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100

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“…Cyclin upregulation, including cyclinD1, and loss of RB1 have also been described [94]. As gene-expression profiling and nextgeneration sequencing technologies are used, additional pathogenic pathways, including those involving transcription factors regulating T-cell differentiation [35,36], c-MYC [95,96], RAS/RAF/MEK signaling [97], among others [90,98], may be identified in subsets of CTCL.…”

Section: Immunopathogenesismentioning

confidence: 99%

Cutaneous T‐cell lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Wilcox

2011

American J Hematol

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Disease overview: Cutaneous T‐cell lymphomas are a heterogenous group of T‐cell lymphoproliferative disorders involving the skin, the majority of which may be classified as Mycosis fungoides (MF) or Sézary syndrome (SS).Diagnosis: The diagnosis of MF or SS requires the integration of clinical and histopathologic data.Risk‐adapted therapy: Tumor, node, metastasis, and blood (TNMB) staging remains the most important prognostic factor in MF/SS and forms the basis for a “risk‐adapted,” multidisciplinary approach to treatment. For patients with disease limited to the skin, expectant management or skin‐directed therapies is preferred, as both disease‐specific and overall survival for these patients is favorable. In contrast, patients with advanced‐stage disease with significant nodal, visceral, or blood involvement are generally approached with biologic‐response modifiers, denileukin diftitox, and histone deacetylase inhibitors before escalating therapy to include systemic, single‐agent chemotherapy. Multiagent chemotherapy may be used for those patients with extensive visceral involvement requiring rapid disease control. In highly‐selected patients with disease refractory to standard treatments, allogeneic stem‐cell transplantation may be considered. Am. J. Hematol., 2011. © 2011 Wiley‐Liss, Inc.

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“…31 This inhibition may be mediated by physical associations between BIN1 and MYC or the RAS-specific guanine nucleotide exchange factors SOS-1 and SOS-2, which may function to inhibit MYC-induced gene activation and limit invasiveness of RAS-dependent cancers, respectively. [32][33][34][35] Furthermore, Bin1 mutant mice are cancer prone, and Bin1 deficiency has also been shown to play an important role in the ability of cancer cells to avoid detection and destruction by the immune system. 36,37 Interestingly, loss of BIN1 expression without genetic mutation has been observed in several human cancers, suggesting the mechanism of inactivation may primarily be epigenetic.…”

Section: -21mentioning

confidence: 99%