Cellular injury if stalled in the G1 phase causes the majority of sporadic, (adult), cancers.
Tumor Evolution & Progression
Cancer Research Ideas - Tumor Evolution & Progression (Archived)
Cancer genomics has yielded a greater understanding of the mutations that occur within cancer cells and their roles in tumor initiation and progression. Concurrent with an increased understanding of cancer genomics, a greater appreciation has developed for the enormous heterogeneity of cancer cells that evolve within a tumor, the metabolic changes in both the cancer cell and immune cells in the microenvironment, and the roles of the non-cancer cellular and molecular components of the tumor microenvironment that both support and suppress tumor progression.
The submission period for Tumor Evolution & Progression ideas ended on July 1. However, we encourage you to sign up for regular e-mail updates about the National Cancer Moonshot Initiative at the Cancer Moonshot Milestones web page.
Cancer development involves independent genetic alterations of genes that regulate cell proliferation, differentiation, and survival. Chromosomal alteration is crucial to cancer progression. Thus, Targeting HERVs & cancer gene loci may be important
580,000 Americans die each year from cancer. The majority from metastatic cancer. We need to not write these patients off every year. Currently we are. We are leaving a half million Americans behind every year by excluding metastatic research.
Cancer progression is assumed to be driven by somatic Darwinian evolution and there is a myopic focus on mutations. However, non-Darwinian, Lamarckian-like mechanisms also play a role which offers a wealth of lever points for molecular intervention.
Replicated research studies suggest that cell phone radiation can impact tumor progression. Adequate data needs to be routinely gathered by clinicians on patients cell/Wi-Fi use. Patients need to be educated on reducing exposure to promote recovery.
Better prediction of breast cancer recurrence will help tailor patient care and improve overall health. A combination of genetic, metabolic, and microenviroment studies could yield a comprehensive panel of predictors.
Every dead cancer cell sends signals to its neighbor cells that makes them resilient to drugs. This is one reason why targeted therapy is inherently limited. This collective cell population level response could be a target for a new class of drugs.
All therapies seek to kill tumor cells. But killing is probabilistic. The inevitable surviving cancer cells are stressed to become cancer stem-cells. Therapy backfires in hidden ways. Targeting this cell response will improve existing therapies.
Arachidonic acid is a key mediator of inflammation, which plays a role in carcinogenesis. Prostaglandins and leukotriene blockade may decrease the risk of premalignant transformation, influence cell survival and modify radiation response.