Journal of Cancer Immunology

CD8+ cytotoxic T cells recognise and kill cancer cells that present immunogenic peptides bound to the cell surface major histocompatibility complex class I (MHC-I) molecules.

The protein tyrosine phosphatase SHP2, encoded by PTPN11, functions as a critical signal transduction regulator and interacts with key signaling molecules in both RAS/ERK and PD-1/PD-L1/ BTLA (B- and T-lymphocyte attenuator) pathways. Targeting SHP2 pharmacologically, therefore, may be a promising therapeutic strategy for many RAS-driven cancers.

Since the discovery of escaping mechanism of tumor from negative immune regulation, the paradigm of drug discovery for anti-cancer agents has been dramatically shifted to cancer immunotherapy (e.g., dendritic cell therapy, CAR-T cell therapy, or antibody therapy) by stimulating patient’s immune system to treat cancer. 

Polyploid cancer cells can arise de novo in tumors or they can be induced by therapeutics that inadvertently increase the rate of cytokinetic failure. These cells portend a poor outcome in many cancers because polyploid cancer cells can undergo error prone reductive cell divisions to yield aneuploid progeny. The immune system has evolved mechanisms by which it can specifically recognize and remove polyploid cancer cells, but these appear to be tampered with malignancy so that polyploid cells can persist and fuel the development of cancer cell clones that are resistant to therapeutics and have metastatic potential.

We review here the evidence for participation of mitochondrial autoimmunity in BC inception and progression and propose a new paradigm that may challenge the prevailing thinking in oncogenesis by suggesting that mitochondrial autoimmunity is a major contributor to breast carcinogenesis and probably to the inception and progression of other solid tumors. It has been shown that MNRR1 mediated mitochondrial-nuclear function promotes BC cell growth and migration and the development of metastasis and constitutes a proof of concept supporting the participation of mitochondrial autoimmunity in breast carcinogenesis. 

Tissues are composed of various types of interacting cells [1]. To understand the cellular organization and function in tissues, it is necessary to identify all of the different cell types and the locations of these different cell types within tissue structures. The transformative advances in experimental and computational methods will help us to build the complex map of the tissues and study how tissue organization influences the cell’s molecular state and interactions in healthy and diseased tissue.

Plant virus nanoparticles (PVNPs) are increasingly recognized and studied for use in biomedical applications. PVNPs include plant virions with self-assembled capsid protein coats (PC) that encapsulate the virus genome, and virus-like particles (VLPs), a capsid without the viral genome.

In 1989, researchers proposed an intricate strategy in the field of adoptive cell therapy (ACT). Using the T-cell receptor (TCR) as a template, they replaced the coding sequence for the Vα and Vβ chains with the antigen- recognition domains from an antibody (VH and VL chains).

Bladder cancer is one of the most common and expensive cancers in the United States, with an expected 81,400 new cases and 17,980 deaths in 2020 alone. The incidence is increased among white men and diagnoses often occur in the 7th decade of life.

“Women are not dying because of diseases we cannot treat. They are dying because societies have yet to make the decision that their lives are worth saving.”

Cell Death has long been considered to be an inevitable part of the life cycle of a cell and hence, considered a familiar consequence of cellular life.

The protein tyrosine phosphatase SHP2, encoded by PTPN11, functions as a critical signal transduction regulator and interacts with key signaling molecules in both RAS/ERK and PD-1/PD-L1/ BTLA (B- and T-lymphocyte attenuator) pathways. Targeting SHP2 pharmacologically, therefore, may be a promising therapeutic strategy for many RAS-driven cancers.

Tumor-induced immune suppression has been recognized as one of the major barriers for cancer immune therapies, including checkpoint inhibitors. Immunosuppressive mechanisms that tumors utilize to silence anti-tumor immune cells are numerous and differ between tumor types. 

Protein post-translational modifications play a vital role in various cellular events essential for maintaining cellular physiology and homeostasis. In cancer cells, aberrant post-translational modifications such as glycosylation, acetylation, and phosphorylation on proteins can result in the generation of antigenic peptide variants presented in complex with MHC molecules. These modified peptides add to the class of tumor-specific antigens and offer promising avenues for targeted anti- cancer therapies. In this review, we focus on the role of phosphorylated peptides (p-peptides) in cancer immunity.

The aromatase inhibitors (AIs) anastrozole, letrozole, and exemestane are often prescribed as endocrine therapy for patients with estrogen receptor–positive breast cancer. AIs are associated with musculoskeletal side effects such as bone loss, arthralgias, myalgias, and tenosynovitis. Notably, exemestane is a steroidal AI and both anastrozole and letrozole are non-steroidal AIs. 

Checkpoint inhibitors offer promise in treating muscle-invasive and metastatic bladder cancer, but the optimal timing of their administration—neoadjuvant or adjuvant—remains unclear. To determine the efficacy of combining checkpoint inhibition with standard cisplatin-based chemotherapy, we conducted a phase II trial of neoadjuvant anti-PD-1 (αPD-1) and anti-CTLA-4 (αCTLA-4), in combination with cisplatin-gemcitabine, for patients with muscle-invasive bladder cancer prior to radical cystectomy. 

The emergence of chimeric antigen receptor T cell (CAR-T cell) therapy has revolutionized cancer treatment, particularly for hematologic malignancies. This commentary discusses developments in CAR-T cell therapy, focusing on the molecular mechanisms governing T cell fate and differentiation. Transcriptional and epigenetic factors play a pivotal role in determining the specificity, effectiveness, and durability of CAR-T cell therapy.

The role of the microbiome in the development and treatment of genitourinary malignancies is just starting to be appreciated. Accumulating evidence suggests that the microbiome can modulate immunotherapy through signaling in the highly dynamic tumor microenvironment. Nevertheless, much is still unknown about the immuno-oncology-microbiome axis, especially in urologic oncology. The objective of this review is to synthesize our current understanding of the microbiome’s role in modulating and predicting immunotherapy response to genitourinary malignancies.