Cancer Research

Apoptosis is a genetically encoded cell death program and plays an important role in the regulation of both normal and malignant processes. Recently, many factors involved in the control of apoptosis have been isolated and characterized, and thereby studies on the molecular mechanism of the signaling pathway of apoptosis have made rapid progress

Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome. Despite its simplicity, recent progress has demonstrated that autophagy plays a wide variety of physiological and pathophysiological roles, which are sometimes complex. Autophagy consists of several sequential steps–sequestration, transport to lysosomes, degradation, and utilization of degradation products–and each step may exert different function. In this review, the process of autophagy is summarized, and the role of autophagy is discussed in a process-based manner.

Cancer biomarkers are substances indicate that tumor state, progression characteristics, and response to therapies. Most cancer biomarkers are transcription factors, cell surface receptors, or secreted proteins that are produced by either cancer cells or other cells in response to cancer.

Cancer Drug Targets are anticancer drugs targeted at molecular targets, which are highly targeted and have remarkable effects. Currently, there are many anticancer drugs targeted at molecular targets, including monoclonal antibodies (mabs) targeting antigens or receptors on the surface of tumor cells, inhibitors of cell signal transduction molecules, angiogenesis inhibitors, inhibitors targeting telomerase, and reversal agents targeting tumor resistance

Cancer immunology has been an area of investigation since the 1960s but it is within the last decade that we have seen its promise start to come to fruition. Indeed, tumor-induced immune-suppression is now recognized as a key factor in oncogenic progression and immune-based therapeutics are becoming first or second-line options in an increasing array of malignancies. In brief, cancer immunology studies the reaction of the host to the development and growth of the invading malignancy.

Cell metabolism is a general term for a series of ordered chemical reactions that occur in cells to support life. These processes allow organisms to grow and reproduce, maintain their structure, and respond to the environment. Metabolism is usually divided into two categories: catabolism, which breaks down large molecules for energy (such as cellular respiration); anabolism uses energy to synthesize components of cells, such as proteins and nucleic acids.

Oncoproteins play an important role in tumorigenic cell growth which are encoded by oncogenes. Some oncoproteins are accepted and used as tumor markers.There are many oncoproteins, such as EGFR, VEGFR, Ras protein, cyclin-dependent kinases.

There are many applications of signal transduction in the treatment of cancer. The main treatment methods are divided into three types: directly inducing the apoptosis of cancer cells by inhibiting the signal transduction of cancer cells; Inducing or inhibiting gene expression products to inhibit signal transduction in cancer cells; physical methods inhibit the signal transduction of cancer cells. Physical methods, such as radiation and photodynamics, destroy the surfactant molecular structure of the key substances in cancer cells, thereby impeding the transduction of signaling pathways.

Tumor suppressor genes were first identified by making cell hybrids between tumor and normal cells. On some occasions a chromosome from the normal cell reverted the transformed phenotype. Several familial cancers have been shown to be associated with the loss of function of a tumor suppressor gene. They include the retinoblastoma susceptibility gene (RB), Wilms’ tumors (WT1), neurofibromatosis type-1 (NF1), familial adenomatosis polyposis coli (FAP), von Hippel-Lindau syndrome (VHL), and those identified through loss of heterozygosity such as in colorectal carcinomas (called DCC for deleted in colon carcinoma) and P53 which was originally thought to be a proto-oncogene. However, the wild-type P53 protein suppresses the activity of mutant alleles of p53 which are the oncogenic forms of P53.