Cancer tumor cells

HDAC inhibitors can also operate independent of p53. HDAC inhibitors are able to upregulate p21, a cyclin-dependent kinase. They can also target TOB-l,i< p27 P ," GADDTS. CYCLIN Bl, CYCLIN Dl, and CYCLIN A genes. Downregulation of genes such as can also be achieved by HDAC inhibitors. All of these contribute to cell cycle progression and apoptosis of the cancer/tumor cells. 

Oncogene A gene that transforms normal cells into cancerous tumor cells, especially... 

Cao T, Heng BC (2005) Differentiation therapy of cancer. Potential advantages over conventional therapeutic approaches targeting death of cancer/tumor cells. Med Hypotheses 65(6) 1202-1203... 

Recently, investigation of the possibility of synchronizing cancerous tumor cells is gaining momentum so that most likely all cells are in the same phase of the cycle. In case, such in ideal situation may be accomplished then ... 

Example. A plethora of malignant tumors of need much more asparagine (a nonessential amino acid) in comparison to normal cells therefore, if by any manner the plasma asparagine gets destroyed (enzymatically), the cancerous tumor cells in turn are selectively starved to death. 

It has been well-defined that the efficiency of anitneoplastic drugs may be characterized by their inherent log cell-kill index. In other words, the negative log of the fraction of the cancerous tumor cell population which essentially survives a single-course of treatment. 

Whereas epidermal growth factor (EGF) enhances the radiosensitivity of human squamous ceU carcinoma cells in vitro (197), addition of EGF to hormone-deprived MCE-7 breast cancer cells prior to irradiation results ia iacreased radioresistance (198). An anti-EGE-receptor monoclonal antibody blocks the abiUty of EGE to enhance growth and radioresistance. Tumor cells, the growth of which is stimulated by EGE, appear to be protected those where growth is iohibited are sensitized (198). 

A protein with the innocuous name p53 is one of the most frequently cited biological molecules in the Science Citation Index. The "p" in p53 stands for protein and "53" indicates a molecular mass of 53 kDa. The p53 protein plays a fundamental role in human cell growth and mutations in this protein are frequently associated with the formation of tumors. It is estimated that of the 6.5 million people diagnosed with one or another form of cancer each year about half have p53 mutations in their tumor cells and that the vast majority of these mutations are single point mutations. 

Clinical trials showed therapeutic efficacy in a broad spectrum of tumors these include SCLC, testicular tumors, sarcomas, breast cancer, renal cell cancer, pancreatic tumors and lymphomas. Ifosfamide is less myelosuppressive than cyclophosphamide but is more toxic to the bladder. Therefore it is recommended that ifosfamide is coadministered with the thiol compound mesna to avoid hemorrhagic cystitis and to reduce the risk of developing bladder cancer. Other side effects include neurotoxicity and myelosuppression. 

Antineoplastic agents that cannot be grouped under subheadings 1-9 include miltefosine which is an alkylphosphocholine that is used to treat skin metastasis of breast cancer, and crispantase which breaks down asparagine to aspartic acid and ammonia. It is active against tumor cells that lack the enzyme asparaginase, such as acute lymphoblastic leukemia cells. Side effects include irritation of the skin in the case of miltefosine and anaphylactic reactions in the case of crispantase. Another recent development is the proteasome inhibitor bortezomib which is used to treat multiple myeloma. 

A substantial amount of indirect evidence supports the contention that the induction of apoptosis in tumor cells is critical to successful therapy. Cancer therapy might therefore be viewed as an attempt to induce apoptosis in a population of cells that have undergone selection for apoptotic defects. If correct, this hypothesis would suggest why cancer therapy is in many cases unsuccessful. However, recent studies indicate that this fundamental problem can be circumvented. Progress in the identification of molecules key to the cell death pathways has led to a growing understanding of how apoptosis occurs [3]. It has become clear that pathways to apoptosis are numerous and often interconnected. A solution to the clinical problem of therapeutic resistance, then, may lie in the fact that there appears to be multiple ways that a cell death program can be implemented. 

Though DNA damage-based therapies havebeen in use for many years, it has remained unclear why such treatment often causes the selective death of tumor cells while sparing adjacent normal tissue. The genetic alterations that occur in cancers that alter the DNA damage reponse may explain why such therapy can be efficacious. 

Brown JM, Wouters BG (1999) Apoptosis, p53, and tumor cell sensitivity to anticancer agents. Cancer Res 59 1391-1399... 

Dead or live bacteria may be effective to stimulate inflammatory reactions of phagocytic cells against tumor cells. The best-characterized treatment is the use of Bacillus Calmette Guerin (BCG) in the case of bladder cancer where activation of the immune response is capable of controlling tumor growth. 

---