Use of telehealth for psychosocial oncology: A mixed methods study about barriers to and opportunities with Latino patients from Latin America, Spain, and the United States.

OBJECTIVES: Telehealth for mental healthcare expanded rapidly with the COVID-19 pandemic's onset; however, global access disparities emerged. Telehealth challenges and opportunities for Latino cancer patients from different geographical regions must be explored. METHODS: A cross-sectional online survey (March-July 2021) of mental health providers, serving Latino cancer patients in Latin America, United States, and Spain, contained close-ended questions related to the use of telehealth during the pandemic and open-ended questions on recommending/not recommending telehealth. RESULTS: In a sample of 148 providers from 21 countries, 60.5% reported that at least some of their patients had difficulties with Internet speed and connectivity and lacked knowledge about using electronic devices (43.2%) or the Internet (45.4%). Lacking privacy at home (66.0%) and childcare (26.0%) were reported patient challenges. Internet connectivity or speed were issues for providers (43.2%) themselves. Improving patient reach was a reported telehealth benefit (64.2%). Geographical access (43.2%) and physical limitations (35.8%) were considerations in offering telehealth. Considerations for not recommending telehealth were patient age (24.3%) and lacking technological knowledge (29.1%). CONCLUSIONS: Telehealth for mental healthcare may improve patient access issues caused by geographical and transportation conditions and patient functionality. Findings provide insight into telehealth benefits and challenges in Latino patient populations. Future studies should examine patient access and use by region.

Exploiting oncogene-induced replicative stress for the selective killing of Myc-driven tumors.

Oncogene-induced replicative stress activates an Atr- and Chk1-dependent response, which has been proposed to be widespread in tumors. We explored whether the presence of replicative stress could be exploited for the selective elimination of cancer cells. To this end, we evaluated the impact of targeting the replicative stress-response on cancer development. In mice (Mus musculus), the reduced levels of Atr found on a mouse model of the Atr-Seckel syndrome completely prevented the development of Myc-induced lymphomas or pancreatic tumors, both of which showed abundant levels of replicative stress. Moreover, Chk1 inhibitors were highly effective in killing Myc-driven lymphomas. By contrast, pancreatic adenocarcinomas initiated by K-Ras(G12V) showed no detectable evidence of replicative stress and were nonresponsive to this therapy. Besides its impact on cancer, Myc overexpression aggravated the phenotypes of Atr-Seckel mice, revealing that oncogenes can modulate the severity of replicative stress-associated diseases.

A mouse model of ATR-Seckel shows embryonic replicative stress and accelerated aging.

Although DNA damage is considered a driving force for aging, the nature of the damage that arises endogenously remains unclear. Replicative stress, a source of endogenous DNA damage, is prevented primarily by the ATR kinase. We have developed a mouse model of Seckel syndrome characterized by a severe deficiency in ATR. Seckel mice show high levels of replicative stress during embryogenesis, when proliferation is widespread, but this is reduced to marginal amounts in postnatal life. In spite of this decrease, adult Seckel mice show accelerated aging, which is further aggravated in the absence of p53. Together, these results support a model whereby replicative stress, particularly in utero, contributes to the onset of aging in postnatal life, and this is balanced by the replicative stress-limiting role of the checkpoint proteins ATR and p53.