PURPOSE This Provisional Clinical Opinion update presents a clinically pragmatic approach to hepatitis B virus (HBV) screening and management. PROVISIONAL CLINICAL OPINION All patients anticipating systemic anticancer therapy should be tested for HBV by 3 tests—hepatitis B surface antigen (HBsAg), hepatitis B core antibody (anti-HBc) total immunoglobulin (Ig) or IgG, and antibody to hepatitis B surface antigen—but anticancer therapy should not be delayed. Findings of chronic HBV (HBsAg-positive) or past HBV (HBsAg-negative and anti-HBc–positive) infection require HBV reactivation risk assessment. Patients with chronic HBV receiving any systemic anticancer therapy should receive antiviral prophylactic therapy through and for minimum 12 months following anticancer therapy. Hormonal therapy alone should not pose a substantial risk of HBV reactivation in patients with chronic HBV receiving hormonal therapy alone; these patients may follow noncancer HBV monitoring and treatment guidance. Coordination of care with a clinician experienced in HBV management is recommended for patients with chronic HBV to determine HBV monitoring and long-term antiviral therapy after completion of anticancer therapy. Patients with past HBV infection undergoing anticancer therapies associated with a high risk of HBV reactivation, such as anti-CD20 monoclonal antibodies or stem-cell transplantation, should receive antiviral prophylaxis during and for minimum 12 months after anticancer therapy completion, with individualized management thereafter. Careful monitoring may be an alternative if patients and providers can adhere to frequent, consistent follow-up so antiviral therapy may begin at the earliest sign of reactivation. Patients with past HBV undergoing other systemic anticancer therapies not clearly associated with a high risk of HBV reactivation should be monitored with HBsAg and alanine aminotransferase during cancer treatment; antiviral therapy should commence if HBV reactivation occurs. Additional information is available at www.asco.org/supportive-care-guidelines .
Abstract. The colocalization of integrins ot2/~ and ot3fl~ at intercellular contact sites of keratinocytes in culture and in epidermis suggests that these integrins may mediate intercellular adhesion (ICA). P1B5, an anti-u3fl~ rnAb previously reported to inhibit keratinocyte adhesion to epiligrin, was also found to induce ICA. Evidence that P1B5-induced ICA was mediated by a2/3~ and O/3/~1 was obtained using both ICA assays and assays with purified, mAb-immobilized integrins. Selective binding of ot2/3~-coated beads to epidermal cells or plate-bound O/3~31 was observed. This binding was inhibited by mAbs to integrin o~3, oL2, or fl, subunits and could be stimulated by PIB5. We also demonstrate a selective and inhibitable interaction between afffinity-purified integrins ot2/3~ and o~3/31. Finally, we show that expression of ot2/31 by CHO fibroblasts results in the acquisition of collagen and o~3/3~binding. Binding to both of these ligands is inhibited by P1H5, an anti-a2/3~ specific mAb. Results of these in vitro experiments suggest that integrins o~2/3~ and a3/3~ can interact and may do so to mediate ICA in vivo. Thus, c~3/31 mediates keratinocyte adhesion to epiligrin and plays a second role in ICA via {~2~1 9
PURPOSE Patients with cancer living in socioeconomically disadvantaged areas have worse cancer outcomes. The association between socioeconomic deprivation and outcomes among patients with cancer participating in clinical trials has not been systematically examined. METHODS We examined survival outcomes for patients enrolled in phase III and large phase II clinical trials for major cancers conducted by the SWOG Cancer Research Network from 1985 to 2012. Socioeconomic deprivation was measured using trial participants' residential zip codes linked to the Area Deprivation Index (ADI). Five-year overall survival, progression-free survival, and cancer-specific survival were examined using Cox regression frailty models, adjusting for age, sex, and race, and separately for insurance status, prognostic risk, and rural or urban residency. RESULTS We examined 41,109 patients from 55 trials comprising 24 cancer histology and stage-specific cohorts. Compared with trial participants in the most affluent areas (ADI, 0%-20%), trial participants from areas with the highest socioeconomic deprivation (ADI, 80%-100%) had worse overall (hazard ratio [HR] = 1.28, 95% CI, 1.20 to 1.37, P < .001), progression-free (HR = 1.20, 95% CI, 1.13 to 1.28, P < .001), and cancer-specific survival (HR = 1.27, 95% CI, 1.18 to 1.37, P < .001). The results were similar after adjusting for insurance status, prognostic risk, and rural or urban residency. There was a continuous increase in risk of all outcomes as the ADI quintile increased. CONCLUSION In patients with cancer with access to protocol-directed care in clinical trials, high area-level socioeconomic deprivation was associated with worse survival. Future research should examine whether the etiology of this residual disparity is related to reduced access to supportive care or postprotocol therapy and/or to differences in health status not reflected by protocol selection criteria.
Key Points Question Do rural and urban patients with cancer receiving similar care in clinical trials have similar outcomes? Findings In this comparative effectiveness study, 36 995 patients from all 50 states enrolled in 44 SWOG treatment trials from 1986 to 2012, composing 17 different cancer-specific analysis cohorts, were examined. Rural patients had statistically significantly worse survival in only 1 of the 17 analysis cohorts (those with adjuvant-stage, estrogen receptor–negative and progesterone receptor–negative breast cancer) irrespective of how rural residency was defined. Meaning Improving access to uniform treatment strategies such as those found in clinical trials may help resolve the disparity in cancer outcomes between rural and urban patients.
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