Invasive micropapillary carcinoma (IMPC) is a rare, distinct histological subtype of breast carcinoma. While micropapillary histological architecture is found in up to 2-8% of all breast cancers, pure micropapillary carcinoma is infrequent and comprises 0.9-2% of breast carcinomas. Invasive micropapillary carcinoma is emerging as an oncological and surgical challenge due to a plethora of characteristics that constitute this histological pattern -interestingly, both elusive and aggressive. We present the case of a woman presenting with IMPC, who was primarily treated with tumour and lymph node marking, followed by primary systemic therapy (PST), and consequent oncoplastic surgery with sentinel lymph node biopsy. Our case report outlines the importance of awareness of histological subtypes in breast cancer by focusing on a case report of IMPC. The breast surgeon must be aware of the lymphotropic behaviour of this subtype and the high prevalence of lymph node involvement in such patients, and therefore focus on rigorous axillary assessment. One must not forget that, despite having a more aggressive biological profile, IMPC has demonstrated no difference in survival when compared to other histological subtypes, and treatment should conform to international guidelines with an emphasis on nodal staging.

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Prostate cancer (PCa) has a distinct molecular signature, including characteristic chromosomal translocations, gene deletions and defective DNA damage repair mechanisms. One crucial pathway involved is homologous recombination deficiency (HRD) and it is found in almost 20% of metastatic castrate-resistant PCa (mCRPC). Inherited/germline mutations are associated with a hereditary predisposition to early PCa development and aggressive behavior. BRCA2, ATM and CHECK2 are the most frequently HRD-mutated genes. BRCA2-mutated tumors have unfavorable clinical and pathological characteristics, such as intraductal carcinoma. PARP inhibitors, due to the induction of synthetic lethality, have been therapeutically approved for mCRPC with HRD alterations. Mutations are detected in metastatic tissue, while a liquid biopsy is utilized during follow-up, recognizing acquired resistance mechanisms. The mismatch repair (MMR) pathway is another DNA repair mechanism implicated in carcinogenesis, although only 5% of metastatic PCa is affected. It is associated with aggressive disease. PD-1 inhibitors have been used in MMR-deficient tumors; thus, the MMR status should be tested in all metastatic PCa cases. A surrogate marker of defective DNA repair mechanisms is the tumor mutational burden. PDL-1 expression and intratumoral lymphocytes have ambivalent predictive value. Few experimental molecules have been so far proposed as potential biomarkers. Future research may further elucidate the role of DNA damage pathways in PCa, revealing new therapeutic targets and predictive biomarkers.