Introduction A pandemic coronavirus, SARS‐CoV‐2, causes COVID‐19, a potentially life‐threatening respiratory disease. Patients with cancer may have compromised immunity due to their malignancy and/or treatment, and may be at elevated risk of severe COVID‐19. Community transmission of COVID‐19 could overwhelm health care services, compromising delivery of cancer care. This interim consensus guidance provides advice for clinicians managing patients with cancer during the pandemic. Main recommendations During the COVID‐19 pandemic: In patients with cancer with fever and/or respiratory symptoms, consider causes in addition to COVID‐19, including other infections and therapy‐related pneumonitis. For suspected or confirmed COVID‐19, discuss temporary cessation of cancer therapy with a relevant specialist. Provide information on COVID‐19 for patients and carers. Adopt measures within cancer centres to reduce risk of nosocomial SARS‐CoV‐2 acquisition; support population‐wide social distancing; reduce demand on acute services; ensure adequate staffing; and provide culturally safe care. Measures should be equitable, transparent and proportionate to the COVID‐19 threat. Consider the risks and benefits of modifying cancer therapies due to COVID‐19. Communicate treatment modifications, and review once health service capacity allows. Consider potential impacts of COVID‐19 on the blood supply and availability of stem cell donors. Discuss and document goals of care, and involve palliative care services in contingency planning. Changes in management as a result of this statement This interim consensus guidance provides a framework for clinicians managing patients with cancer during the COVID‐19 pandemic. In view of the rapidly changing situation, clinicians must also monitor national, state, local and institutional policies, which will take precedence. Endorsed by Australasian Leukaemia and Lymphoma Group; Australasian Lung Cancer Trials Group; Australian and New Zealand Children's Haematology/Oncology Group; Australia and New Zealand Society of Palliative Medicine; Australasian Society for Infectious Diseases; Bone Marrow Transplantation Society of Australia and New Zealand; Cancer Council Australia; Cancer Nurses Society of Australia; Cancer Society of New Zealand; Clinical Oncology Society of Australia; Haematology Society of Australia and New Zealand; National Centre for Infections in Cancer; New Zealand Cancer Control Agency; New Zealand Society for Oncology; and Palliative Care Australia.

Background:The COVID-19 pandemic has disrupted cancer services globally. New Zealand has pursued an elimination strategy to COVID-19, reducing (but not eliminating) this disruption. Early in the pandemic, our national Cancer Control Agency ( Te Aho o Te Kahu ) began monitoring and reporting on service access to inform national and regional decision-making. In this manuscript we use high-quality, nationallevel data to describe changes in cancer registrations, diagnosis and treatment over the course of New Zealand's response to COVID-19. Methods: Data were sourced (2018-2020) from national collections, including cancer registrations, inpatient hospitalisations and outpatient events. Cancer registrations, diagnostic testing (gastrointestinal endoscopy), surgery (colorectal, lung and prostate surgeries), medical oncology access (first specialist appointments [FSAs] and intravenous chemotherapy attendances) and radiation oncology access (FSAs and megavoltage attendances) were extracted. Descriptive analyses of count data were performed, stratified by ethnicity (Indigenous M āori, Pacific Island, non-M āori/non-Pacific). Findings: Compared to 2018-2019, there was a 40% decline in cancer registrations during New Zealand's national shutdown in March-April 2020, increasing back to pre-shutdown levels over subsequent months. While there was a sharp decline in endoscopies, pre-shutdown volumes were achieved again by August. The impact on cancer surgery and medical oncology has been minimal, but there has been an 8% year-todate decrease in radiation therapy attendances. With the exception of lung cancer, there is no evidence that existing inequities in service access between ethnic groups have been exacerbated by COVID-19. Interpretation: The impact of COVID-19 on cancer care in New Zealand has been largely mitigated. The New Zealand experience may provide other agencies or organisations with a sense of the impact of the COVID-19 pandemic on cancer services within a country that has actively pursued elimination of COVID-19. Funding: Data were provided by New Zealand's Ministry of Health, and analyses completed by Te Aho o Te Kahu staff.

Surgically induced endometriosis in the mouse has been described as a model to investigate the effect of environmental pollutants on the growth of endometriotic implants. The objectives of this study were to evaluate a modified surgical procedure to induce endometriosis and validate the model by comparing the effects of estrogen, 4-chlorodiphenyl ether (4-CDE) as a possible estrogenic contaminant, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a contaminant with predominantly anti-estrogenic activities, on the growth of endometrial implants. Uterine strips (1.0 x 4.0 mm2) were autotransplanted to multiple sites in the abdomen of sexually mature female B6C3F1 mice (n = 33), which were randomly assigned to the following groups: intact control (n = 4); ovariectomized (OVX, n = 9); OVX and treated with 4-CDE (n = 6); OVX and treated with 17 beta-estradiol (E2, n = 9); and OVX and treated with E2 plus TCDD (n = 5). Endometrial implants survived warm ischemia regardless of implant site and appeared as small clear spherical or ovoid fluid-filled cysts. The diameter of the endometrial cysts in the OVX animals was significantly (p < 0.0001) smaller compared with the intact animals and OVX animals replaced with E2 or 4-CDE. In contrast, TCDD treatment inhibited the growth of endometrial cysts in the presence of estrogen. We conclude that autotransplantation of uterine slices to multiple abdominal sites results in formation of endometriotic cysts that are responsive to estrogen, and that environmental contaminants possess the potential to affect the survival and growth of endometrial cysts. Therefore, we concluded that the mouse endometriosis model described in this paper has applications to investigate the possible role of environmental pollutants in the development of endometriosis.

Surgically induced endometriosis in the mouse has been described as a model to investigate the effect of environmental pollutants on the growth of endometriotic implants. The objectives of this study were to evaluate a modified surgical procedure to induce endometriosis and validate the model by comparing the effects of estrogen, 4-chlorodiphenyl ether (4-CDE) as a possible estrogenic contaminant, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a contaminant with predominantly anti-estrogenic activities, on the growth of endometrial implants. Uterine strips (1.0 x 4.0 mm2) were autotransplanted to multiple sites in the abdomen of sexually mature female B6C3F1 mice (n = 33), which were randomly assigned to the following groups: intact control (n = 4); ovariectomized (OVX, n = 9); OVX and treated with 4-CDE (n = 6); OVX and treated with 17 beta-estradiol (E2, n = 9); and OVX and treated with E2 plus TCDD (n = 5). Endometrial implants survived warm ischemia regardless of implant site and appeared as small clear spherical or ovoid fluid-filled cysts. The diameter of the endometrial cysts in the OVX animals was significantly (p < 0.0001) smaller compared with the intact animals and OVX animals replaced with E2 or 4-CDE. In contrast, TCDD treatment inhibited the growth of endometrial cysts in the presence of estrogen. We conclude that autotransplantation of uterine slices to multiple abdominal sites results in formation of endometriotic cysts that are responsive to estrogen, and that environmental contaminants possess the potential to affect the survival and growth of endometrial cysts. Therefore, we concluded that the mouse endometriosis model described in this paper has applications to investigate the possible role of environmental pollutants in the development of endometriosis.