The biology of cancer testis antigens: Putative function, regulation and therapeutic potential

Fratta, Elisabetta; Coral, Sandra; Covre, Alessia; Parisi, Giulia; Colizzi, Francesca; Danielli, Riccardo; Nicolay, Hugues J. M.; Sigalotti, Luca; Maio, Michele

doi:10.1016/j.molonc.2011.02.001

Cited by 285 publications

(290 citation statements)

References 175 publications

Supporting

Mentioning

278

Contrasting

Unclassified

Order By: Relevance

“…Many genes that are silent in healthy somatic tissue are specifically activated during the spermatogenic program, providing functions that modulate cellular morphologic changes and meiosis. These genes are known as cancer/testis (CT) genes (or cancer germline genes) when they become aberrantly activated in cancerous tissue (11)(12)(13). The proteins encoded by these genes have garnered interest in the field of clinical oncology as they can potentially serve as targets for immune therapies and expression of CT genes can be applied to patient stratification (for examples, see refs.…”

Section: Activation Of Meiotic Functions In Cancer Cellsmentioning

confidence: 99%

Meiosis-like Functions in Oncogenesis: A New View of Cancer

McFarlane

Wakeman

2017

Cancer Research

View full text Add to dashboard Cite

Cancer cells have many abnormal characteristics enabling tumors to grow, spread, and avoid immunologic and therapeutic destruction. Central to this is the innate ability of populations of cancer cells to rapidly evolve. One feature of many cancers is that they activate genes that are normally associated with distinct developmental states, including germ cell–specific genes. This has historically led to the proposal that tumors take on embryonal characteristics, the so called embryonal theory of cancer. However, one group of germline genes, not directly associated with embryonic somatic tissue genesis, is the one that encodes the specific factors to drive the unique reductional chromosome segregation of meiosis I, which also results in chromosomal exchanges. Here, we propose that meiosis I–specific modulators of reductional segregation can contribute to oncogenic chromosome dynamics and that the embryonal theory for cancer cell growth/proliferation is overly simplistic, as meiotic factors are not a feature of most embryonic tissue development. We postulate that some meiotic chromosome-regulatory functions contribute to a soma-to-germline model for cancer, in which activation of germline (including meiosis) functions drive oncogenesis, and we extend this to propose that meiotic factors could be powerful sources of targets for therapeutics and biomonitoring in oncology. Cancer Res; 77(21); 5712–6. ©2017 AACR.

show abstract

Section: Activation Of Meiotic Functions In Cancer Cellsmentioning

confidence: 99%

Meiosis-like Functions in Oncogenesis: A New View of Cancer

McFarlane

Wakeman

2017

Cancer Research

View full text Add to dashboard Cite

show abstract

“…Another important factor for the successful immunotherapy response is the expression of tumor-associated antigens [100]. Along this line, it has been shown that the expression of high molecular weight-melanoma associated antigen (HMW-MAA) is regulated by DNA methylation as its expression correlates with promoter methylation.…”

Section: Epigenetic Alterations and Immunotherapymentioning

confidence: 99%

Epigenetics in Melanoma Development and Drug Resistance

Hammerlindl¹,

Schaider²

2018

Human Skin Cancers - Pathways, Mechanisms, Targets and Treatments

View full text Add to dashboard Cite

Melanomas, which originate from melanocytic cells, mainly develop in the skin but can also arise at other body sites. The disease accounts for approximately 90% of deaths related to cutaneous tumors with late stage metastatic melanoma having a very poor prognosis of 6-9 month median survival for untreated patients. Research in the last decades resulted in ground-breaking discoveries of melanoma genetics and biology. High frequency mutations in genes like BRAF, NRAS and KIT, which lead to hyper-activation of the MAPK signaling pathway, drive melanoma progression. Targeting the MAPK signaling pathway has successfully been translated into effective therapies that significantly improve patient survival. Despite the unquestionable importance of such genetic events, the involvement of epigenetic alterations for melanoma development, and resistance to aforementioned therapies is becoming increasingly apparent. In this chapter, epigenetic alterations commonly found in melanoma are introduced, with a focus on histone and DNA modifications and their relevance for melanoma development, progression and therapy response. Detailed knowledge about this emerging aspect of melanoma research will help to understand the plastic nature of melanoma and set the foundation for novel treatment strategies that target aberrant gene regulation on genetic and epigenetic levels.

show abstract

“…[18][19][20] Of note, TAAs can be (1) viral, in the case of virus-induced tumors (e.g., the E6 and E7 proteins of human papillomavirus type 16, HPV-16, which is associated with cervical and oropharyngeal carcinoma); (2) unique, when they reflect a genetic alteration that is proper of a single cancer cell and its progeny (e.g., the B-cell receptor expressed by some form of lymphoma); (3) tumor-specific, when they are not expressed by normal cells but are found in different neoplasms of the same type (e.g., the BCR-ABL fusion protein, which is expressed by a vast majority of chronic lymphocytic leukemia); (4) shared, when they are expressed by malignant cells as well as by non-transformed cells of some type. [18][19][20]34 Shared TAAs include oncofetal antigens, which are expressed only during embryonic development, as well as cancer-testis antigens, whose normal expression is restricted to male germ cells in the testis 20,[35][36][37][38] Several immunotherapeutic interventions have been developed throughout the past decade to harness TAAs for eliciting tumor-specific adaptive immune responses of therapeutic value. [39][40][41] One of such approaches relies on the administration of purified or recombinant TAAs (or peptides thereof) in the presence of adequate immunostimulatory molecules (so-called adjuvants).…”

Section: Introductionmentioning

confidence: 99%