“We are massively outnumbered,” said Jeremy K. Nicholson, chairman of biological chemistry and head of the department of surgery and cancer at Imperial College London. Altogether, he said, 99 percent of the functional genes in the body are microbial.

In Orlando, he and other researchers described how genes in this microbiome — exchanging messages with genes inside human cells — may be involved with cancers of the colon, stomach, esophagus and other organs.

These shifts in perspective, occurring throughout cellular biology, can seem as dizzying as what happened in cosmology with the discovery that dark matter and dark energy make up most of the universe: Background suddenly becomes foreground and issues once thought settled are up in the air. In cosmology the Big Bang theory emerged from the confusion in a stronger but more convoluted form. The same may be happening with the science of cancer.

Exotic Players

According to the central dogma of molecular biology, information encoded in the DNA of the genome is copied by messenger RNA and then carried to subcellular structures called ribosomes, where the instructions are used to assemble proteins. Lurking behind the scenes, snippets called microRNAs once seemed like little more than molecular noise. But they have been appearing with increasing prominence in theories about cancer.

By binding to a gene’s messenger RNA, microRNA can prevent the instructions from reaching their target — essentially silencing the gene — and may also modulate the signal in other ways. One presentation after another at the Orlando meeting explored how microRNAs are involved in the fine-tuning that distinguishes a healthy cell from a malignant one.

Ratcheting the complexity a notch higher, Dr. Pandolfi, the Harvard Medical School researcher, laid out an elaborate theory involving microRNAs and pseudogenes. For every pseudogene there is a regular, protein-encoding gene. (Both are believed to be derived from a common ancestral gene, the pseudogene shunted aside in the evolutionary past when it became dysfunctional.) While normal genes express their will by sending signals of messenger RNA, the damaged pseudogenes either are mute or speak in gibberish.

Or so it was generally believed. Little is wasted by evolution, and Dr. Pandolfi hypothesizes that RNA signals from both genes and pseudogenes interact through a language involving microRNAs. (These signals are called ceRNAs, pronounced “sernas,” meaning “competing endogenous RNAs.”)