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Biology subjects

Samuel, P.

Publications and source records attributed to Samuel, P..

2 recordsLinked to original sources

HIF-1 regulated TPM3 links hypoxia to motility and invasion beyond the hypoxic fraction in triple-negative breast cancer

Hypoxia is a defining feature of triple-negative breast cancer (TNBC), driving invasion, metastasis, and therapy resistance. Understanding the molecular effectors of hypoxia is essential to identify new therapeutic targets. Here, we investigated tropomyosin 3 (TPM3), an actin-binding protein that regulates filament stability. TPM3 is significantly upregulated in breast cancer, including in TNBC, where elevated levels correlate with poor overall survival. Using validated hypoxia signatures and TNBC cell models, we show that TPM3 is induced in physiologically relevant hypoxic conditions in a HIF-1-dependent manner. Both mRNA and protein levels of TPM3 increased in response to hypoxia, and TPM3 colocalised with F-actin, supporting cytoskeletal organisation. Functional assays demonstrated that depletion or inhibition of TPM3 impaired cell morphology, motility, and invasion in hypoxic TNBC cells, while not affecting viability. Notably, TPM3 inhibition synergised with Paclitaxel and Doxorubicin, enhancing therapeutic efficacy. In addition, TPM3 was incorporated into extracellular vesicles (EVs), with hypoxia increasing EV-mediated transfer of TPM3 to normoxic cells and promoting their motility. These findings establish TPM3 as a hypoxia-inducible, HIF-1-regulated effector of cytoskeletal dynamics and intercellular communication, underscoring its potential as a therapeutic target to limit TNBC aggressiveness and improve treatment outcomes.

cancer biology↗

Heterogeneous susceptibility to rotavirus infection and gastroenteritis in two birth cohort studies: parameter estimation and epidemiological implications

Variation in susceptibility is a known contributor to bias in studies estimating immune protection acquired from vaccination or natural infection. However, difficulty measuring this heterogeneity hinders assessment of its influence on estimates. Cohort studies, randomized trials, and post-licensure studies have reported reduced natural and vaccine-derived protection against rotavirus gastroenteritis in low- and middle-income countries (LMICs). We sought to understand differences in susceptibility among children enrolled in two birth-cohort studies of rotavirus in LMICs, and to explore the implications for estimation of immune protection. We re-analyzed data from studies conducted in Mexico City, Mexico and Vellore, India. Cumulatively, 573 unvaccinated children experienced 1418 rotavirus infections and 371 episodes of rotavirus gastroenteritis (RVGE) over 17,636 child-months. We developed a model characterizing susceptibility to rotavirus infection and RVGE among children, accounting for aspects of the natural history of rotavirus and differences in transmission rates between settings, and tested whether modelgenerated susceptibility measurements were associated with demographic and anthropometric factors. We identified greater variation in susceptibility to rotavirus infection and RVGE in Vellore than in Mexico City. In both cohorts, susceptibility to rotavirus infection and RVGE were associated with male sex, lower birth weight, lower maternal education, and having fewer siblings; within Vellore, susceptibility was also associated with lower socioeconomic status. Children who were more susceptible to rotavirus also experienced higher rates of diarrhea due to other causes. Simulations suggest that discrepant estimates of naturally-acquired immunity against RVGE can be attributed, in part, to between-setting differences in transmission intensity and susceptibility of children. We found that more children in Vellore than in Mexico City belong to a high-risk group for rotavirus infection and RVGE, and demonstrate that bias owing to differences in rotavirus transmission intensity and population susceptibility may hinder comparison of estimated immune protection against RVGE.\n\nAuthor summaryDifferences in susceptibility can help explain why some individuals, and not others, acquire infection and exhibit symptoms when exposed to infectious disease agents. However, it is difficult to distinguish between differences in susceptibility versus exposure in epidemiological studies. We developed a modeling approach to distinguish transmission intensity and susceptibility in data from cohort studies of rotavirus infection among children in Mexico City, Mexico, and Vellore, India, and evaluated how these factors may have contributed to differences in estimates of naturally-acquired immune protection between the studies. We found that more children were at \"high risk\" of acquiring rotavirus infection, and of experiencing gastroenteritis when infected, in Vellore versus Mexico City. The probability of belonging to this high-risk stratum was associated with recognized risk factors such as lower socioeconomic status, lower birth weight, and risk of diarrhea due to other causes. We also found the risk for rotavirus infections to cause symptoms declined with age, and was independent of acquired immunity. Together, these findings can account for estimates of lower protective efficacy of acquired immunity against rotavirus gastroenteritis in high-incidence settings, which mirrors estimates of reduced effectiveness of live oral rotavirus vaccines in low- and middle-income countries.

epidemiology↗