BBA - Reviews on Cancer (v.1704, #1)

Gastrins, cholecystokinins and gastrointestinal cancer by Ahmad Aly; Arthur Shulkes; Graham S Baldwin (1-10).
The gastrointestinal peptide hormones gastrin and cholecystokinin (CCK) are well known for their ability to stimulate gastric acid secretion and pancreatic enzyme secretion, respectively. The suggestion that gastrin and CCK might also promote the development of cancers of the gastrointestinal tract has been controversial, but an increasing body of evidence now supports the view that the amidated and non-amidated forms of gastrin act as growth factors via different receptors in different regions of the gut. For example, animal experiments indicate that amidated gastrins are involved in cellular differentiation and repair in the gastric mucosa, and synergise with Helicobacter pylori infection in the development of gastric carcinoma. In contrast, non-amidated gastrins stimulate colonic mucosal growth, accelerate the early steps in colorectal carcinoma formation, and are elevated in the tumour and circulation of patients with colorectal cancer. Although human pancreatic carcinomas express CCK-1 and CCK-2 receptors, the role of gastrins and CCK in pancreatic carcinogenesis is yet to be established. Further investigation of the possible role of the CCK-2 receptor in gastric and pancreatic neoplasia, and of the hypothesis that gastrin precursors act as autocrine growth factors in colorectal carcinoma, is warranted. However, therapies aimed at the gastrins must be targeted to the relevant gastrin/gastrin receptor combination.
Keywords: Colorectal cancer; Gastric cancer; Gastrin; Migration; Pancreatic cancer; Proliferation;

Vaccine and antibody-directed T cell tumour immunotherapy by Said Dermime; David E Gilham; David M Shaw; Emma J Davidson; El-Kahina Meziane; Anne Armstrong; Robert E Hawkins; Peter L Stern (11-35).
Clearer evidence for immune surveillance in malignancy and the identification of many new tumour-associated antigens (TAAs) have driven novel vaccine and antibody-targeted responses for therapy in cancer. The exploitation of active immunisation may be particularly favourable for TAA where tolerance is incomplete but passive immunisation may offer an additional strategy where the immune repertoire is affected by either tolerance or immune suppression. This review will consider how to utilise both active and passive types of therapy delivered by T cells in the context of the failure of tumour-specific immunity by presenting cancer patients. This article will outline the progress, problems and prospects of several different vaccine and antibody-targeted approaches for immunotherapy of cancer where proof of principle pre-clinical studies have been or will soon be translated into the clinic. Two examples of vaccination-based therapies where both T cell- and antibody-mediated anti-tumour responses are likely to be relevant and two examples of oncofoetal antigen-specific antibody-directed T cell therapies are described in the following sections: (1) therapeutic vaccination against human papillomavirus (HPV) antigens in cervical neoplasia; (2) B cell lymphoma vaccines including against immunoglobulin idiotype; (3) oncofoetal antigens as tumour targets for redirecting T cells with antibody strategies.
Keywords: Vaccine; Antibody targeting; immunotherapy; Human papillomavirus; Idiotype; B lymphoma; Cervical cancer; Oncofoetal antigens; Chimeric immune receptor;

Do human RNA helicases have a role in cancer? by Mohamed Abdelhaleem (37-46).
Human RNA helicases (HRH) represent a large family of enzymes that play important roles in RNA processing. The biochemical characteristics and biological functions of the majority of HRH are still to be determined. However, there are examples of dysregulation of HRH expression in various types of cancer. In addition, some HRH have been shown to be involved in the regulation of, or the molecular interaction with, molecules implicated in cancer. Other helicases take part in fusion transcripts resulting from cancer-associated chromosomal translocation. These findings raise the question of whether HRH can contribute to cancer development/progression. In this review, I summarize the cancer-related features of HRH.
Keywords: RNA helicase; Cancer; RNA metabolism; Transcription; Splicing; Translation; DDX and DHX;