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This clinical trial is studying nonsquamous non-small cell lung cancer (NSCLC). This clinical trial uses an experimental drug called sigvotatug vedotin, which is a type of antibody drug conjugate or ADC. ADCs are designed to stick to cancer cells and kill them. This clinical trial also uses a drug called docetaxel. Docetaxel is an anticancer drug that has been approved to treat non-small cell lung cancer. It is usually given to patients who previously received another anticancer treatment. In this study, one group of participants will get sigvotatug vedotin on Days 1 and 15 during each 28-day-cycle. A second group of participants will get docetaxel on Day 1 during each 21-day cycle. This study is being done to see if sigvotatug vedotin works better than docetaxel to treat participants with NSCLC. This study will also test what side effects happen when participants take these drugs. A side effect is anything a drug does to the body besides treating the disease.

A recent clinical trial found that after 36 months, patients taking tebentafusp had a median survival of 21.6 months, compared to 16.9 months for those in the control group. Since recruitment for tebentafusp in metastatic uveal melanoma (mUM) has ended, a new trial is starting to test whether adding IL-2 can help overcome resistance to tebentafusp and improve its effectiveness. This study aims to answer: Can combining tebentafusp with IL-2 improve tumor response and overall survival? What are the benefits and side effects of this combination therapy? All participants will receive both IL-2 and tebentafusp in a 28-day treatment cycle. The dosing schedule is as follows: Cycle1 Day1-3 IL-2, Day4 Tebentafusp, Day 10 IL-2, Day 11 Tebentafusp, Day 17 IL-2, Day 18 Tebentafusp, Day 24 IL-2, Day 25 Tebentafusp. Cycle 2 & thereafter: Day 1 IL-2, Day 2 Tebentafusp, Day 8 IL-2, Day 9 Tebentafusp, Day 15 IL-2, Day 16 Tebentafusp, Day 22 IL-2, Day 23 Tebentafusp.

This study aims to investigate immune reactions that can be involved in atopic dermatitis (eczema). It will do this by examining the composition and differences in the microorganisms, gene expression (regulated processes that allow a cell to respond to its changing environment) and lipids/metabolites (small proteins, sugars or fats produced by cells) of people with eczema vs. people without. This will potentially support more personalised and effective treatments for people with eczema and ultimately improve patient care.