The traditional "germinal center" (GC) classification for DLBCL is overly simplistic. Molecular analysis reveals distinct subtypes within GC, such as "dark zone" and "light zone" signatures, which have different prognoses and responses to targeted therapies like polatuzumab.

A key clinical nuance in CLL is that not all prognostic markers are static. The IGHV mutation status remains unchanged, requiring a one-time test. However, chromosomal abnormalities like deletion 17p can evolve, necessitating re-evaluation at each relapse to guide subsequent therapy choices and adapt the treatment strategy.

When a sentinel lymph node biopsy is skipped, radiation oncologists lack crucial staging information. This can make them hesitant to recommend less-invasive partial breast radiation, even if a patient otherwise qualifies. They may instead recommend whole breast radiation to treat any potential, unconfirmed microscopic disease in the axilla.

Despite new therapies for follicular lymphoma (FL), bendamustine-rituximab (BR) will likely remain the community standard due to its simplicity. This may create a growing gap in treatment approaches between academic centers using novel agents and community practices favoring the familiar BR regimen.

When treating testicular DLBCL, administering systemic methotrexate for CNS prophylaxis before testicular radiation is crucial. Reversing the order can cause a severe skin reaction known as radiation recall, a critical and potentially dangerous complication.

For patients who previously received immunotherapy (IO), a recurrence more than 12 months after completing treatment makes re-challenging with an IO agent a reasonable option. The likelihood of benefit is lower if the recurrence is within 6-12 months and minimal if under 6 months.

CLL-associated immunosuppression dramatically increases the risk and aggressiveness of skin cancers. This risk is not mitigated by novel therapies, and in some cases, the secondary skin malignancy can become a greater threat to a patient's life than their underlying CLL.

The interpretation of ctDNA is context-dependent. Unlike in the adjuvant setting, in the neoadjuvant setting, remaining ctDNA positive post-treatment signifies that the current therapy has failed. These high-risk patients need a different therapeutic approach, not an extension of the ineffective one.

Recurrent non-melanoma skin cancers in patients on ruxolitinib may be attributable to its JAK1 inhibition. In such cases, a viable strategy is to switch the patient to a more JAK2-selective inhibitor, such as pacritinib or fedratinib, to potentially mitigate this specific side effect while maintaining disease control.