and Linda R. Dietel Philanthropic Fund at the Northern Piedmont Community Foundation, Tamkin Foundation, Jennifer Jones-Simon Foundation, Capital Venetoclax cell line Group Companies Charitable Foundation, Robson Family, and Northstar Fund. The project described was supported by grant numbers RR12169, RR13642, and RR00865 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH);

its contents are solely the responsibility of the authors and do not necessarily represent the official views of NCR or NIH. “
“(Neuron 48, 123–137; October 5, 2005) In the original paper, the middle initial was missing from Dr. Susan L. Patterson’s name in the author list. The author list is correct as shown here. “
“(Neuron 68, Smoothened inhibitor 948–963; December 8, 2010) The original publication omitted one affiliation for Dr. M. Petrovic: Institute of Medical Physiology, School of Medicine, University of Belgrade, 11000 Belgrade, Serbia. This affiliation has been added to the article online. “
“(Neuron 69, 423–435; February 10, 2011) The strains published by Menalled et al. (2003) and Lin et al. (2001) are known by alternative titles in the literature, either CAG140 or HdhQ140 for the Menalled et al. (2003) strain and either CAG150 or HdhQ150 for Lin et al. (2001). In preparing the manuscript, the strains were listed in the text and Table

1 as HdhQ140 and HdhQ150, respectively, but were referred to as CAG140 and CAG150, respectively, in Figure 1, a nomenclature error which was missed prior to publication. For the sake of consistency with the text, Figure 1 has been revised to name the strains first CYTH4 described by Menalled et al. (2003) and Lin et al. (2001) as HdhQ140 and HdhQ150, respectively. The corrected figure is included here and in the article available online. “
“Hanahan and Weinberg revisited and updated the hallmarks of cancer in 2011 based on the conceptual progress

of cancer in the last decade [1]. Two emerging hallmarks combined with previous six biological capabilities are widely accepted and acknowledged. They constitute the current eight hallmarks of cancer development and progression. These include: (1) stimulation of continuous proliferative signalling, (2) evasion of growth suppressors, (3) resistance to cell death, (4) potential of limitless replication, (5) induction of angiogenesis, (6) activation of invasion and metastasis, (7) deregulation of cellular energetics and (8) insensitivity of immune destruction [1] and [2]. A variety of stimulations and signals associated with tumour development are involved in one step or multiple steps of the eight hallmarks or other unapprehend processes to some extent. Tumorigenesis is a multistep and complicated process which is controlled by a cross-connected biological network. Tumour mass is not an independent entity only consisting of proliferative cancer cells.