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Cytokine Signaling in Tumor Progression

Cytokines are molecules that play critical roles in the regulation of a wide range of normal functions leading to cellular proliferation, differentiation and survival, as well as in specialized cellular functions enabling host resistance to pathogens. Cytokines released in response to infection, inflammation or immunity can also inhibit cancer development and progression. The predominant intracellular signaling pathway triggered by cytokines is the JAK-signal transducer and activator of transcription (STAT) pathway. Knockout mice and clinical human studies have provided evidence that JAK-STAT proteins regulate the immune system, and maintain immune tolerance and tumor surveillance. Moreover, aberrant activation of the JAK-STAT pathways plays an undeniable pathogenic role in several types of human cancers.

Cancer-linked gene uses ‘shortcut’ to trigger cell division

Living cells are one of the few materials that can replicate themselves, and this is crucial for tissue development and recovery from injury or illness. But making sure cell division only happens at the right time is essential; otherwise, unregulated replication can lead to problems like cancer.

Researchers at the University of California, Santa Cruz, are studying how cells know when and how to divide, and how genes known to be important in cancer influence these processes.

A new study published in The EMBO Journal finds that a gene affected in many cancers, known as E2F1, can cause cells to divide without having to abide by the normal rules of cell division. Instead of having to unpack the genetic material inside the cell, E2F1 takes a shortcut by binding directly to a small area of the DNA that remains tightly packaged inside the cell.

How Neuroscience Can Give Paralyzed People The Chance to Speak Again

A young adult man with closely cropped dark brown hair sits in a wheelchair in a dimly lit room, facing a computer screen on which a simple phrase is typed out: “How are you today?” Underneath the question on the screen, three dots appear—similar to the ones messaging apps use to signal that your conversation partner is composing a response—and flash with anticipation. One by one, new words materialize: “I am very good.”

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At first glance, this brief conversation doesn’t seem particularly special, but the man’s situation is anything but ordinary. On top of his head is a small box, about one inch square in size, connected to a circular portal in his skull about the size of a nickel. Protruding from the box is a thin black cable. The man, who goes by the nickname Pancho, is paralyzed and unable to speak, but a BCI records brain waves from the part of his cortex that is responsible for generating speech, the vocal motor cortex, and translates them into words on the computer screen.

Common MC1R Variants and Parkinson Disease Progression

This longitudinal cohort study used data from PPMI, including participants from the PD, genetic registry, and prodromal cohorts.29 Participants carrying known pathogenic variants in SNCA (n = 39), PRKN (n = 9), PINK1 (n = 1), PARK7 (n = 1), and VPS35 (n = 1), as well as those without evidence of dopamine deficiency (n = 66), were excluded. Using genomewide sequencing data generated by the PPMI Genetics Core (Illumina platform processed following Genomic Analysis ToolKit Best Practices), 809 participants with PD were classified as having sporadic (n = 383) or monogenic disease (n = 426) based on LRRK2 and GBA carrier status.29 The sporadic cohort served as the primary analysis group. Participants within each group were then stratified by MC1R loss-of-function carrier status (sporadic: 231 carriers and 152 noncarriers). Separately, 53 participants with prodromal PD enrolled for rapid eye movement sleep behavior disorder (clinical diagnosis by site investigator, with polysomnography where available) or hyposmia (University of Pennsylvania Smell Identification Test ≤15th age-and sex-adjusted percentile) with available genomewide sequencing data and without LRRK2 or GBA variants were stratified into carriers (n = 34; 21 with rapid eye movement sleep behavior disorder, 13 with hyposmia) and noncarriers (n = 19; 13 with rapid eye movement sleep behavior disorder and 6 with hyposmia).

MC1R loss-of-function variants were defined as coding variants with experimentally demonstrated reductions in MC1R function.5,6,16,20 Variants were further classified by penetrance: high-penetrance R variants substantially reduce MC1R function, while low-penetrance r variants reduce function to a lesser extent.5,6 MC1R loss-of-function carriers were further stratified by zygosity (heterozygosity [including compound heterozygosity] vs homozygosity), variant penetrance, and variant.

Data were collected by PPMI between July 7, 2010, and January 1, 2026, and last accessed via the PPMI portal on February 14, 2026. Informed consent was obtained from all PPMI participants at their respective enrollment sites as part of the PPMI study protocol.