Correction: Regulation of the DNA Damage Response and Gene Expression by the Dot1L Histone Methyltransferase and the 53Bp1 Tumour Suppressor.

[This corrects the article DOI: 10.1371/journal.pone.

High-affinity T cell receptor ImmTAC® bispecific efficiently redirects T cells to kill tumor cells expressing the cancer-testis antigen PRAME.

Background: PRAME (eferentially expressed ntigen in lanoma) is a cancer-testis antigen expressed in several tumor indications, representing an attractive anticancer target. However, its intracellular location limits targeting by traditional methods. PRAME peptides are presented on the surface of tumor cells by human leukocyte antigen (HLA) molecules, indicating that a T cell receptor (TCR)-based strategy that redirects T cells to kill PRAME tumors could be a novel immunotherapeutic option.

Therapeutic high affinity T cell receptor targeting a KRAS cancer neoantigen.

Neoantigens derived from somatic mutations are specific to cancer cells and are ideal targets for cancer immunotherapy. KRAS is the most frequently mutated oncogene and drives the pathogenesis of several cancers. Here we show the identification and development of an affinity-enhanced T cell receptor (TCR) that recognizes a peptide derived from the most common KRAS mutant, KRAS, presented in the context of HLA-A*11:01.

Understanding Texts with the Help of Experimentation: The Example of Cupellation in Arabic Scientific Literature.

The article aims to show how experimentation can help us understand historical texts, by focusing on the specific case of cupellation in Arabic scientific literature. It also provides new information about cupellation in the Arab-Muslim Middle Ages. The article consists of translations of three of the most detailed accounts of cupellation: Hamdānī's Kitāb al-jawharatayn al-'atīqatayn (first half of the fourth/tenth century), Maslama b.

A role for the p53 tumour suppressor in regulating the balance between homologous recombination and non-homologous end joining.

Loss of p53, a transcription factor activated by cellular stress, is a frequent event in cancer. The role of p53 in tumour suppression is largely attributed to cell fate decisions. Here, we provide evidence supporting a novel role for p53 in the regulation of DNA double-strand break (DSB) repair pathway choice.