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Background: Epidermal Growth Factor Receptor (EGFR) molecular analysis is performed to assess the responsiveness to Tyrosine Kinase Inhibitors (TKIs) in patients with Non-Small Cell Lung Cancer (NSCLC). The existence of molecular intra-tumoral heterogeneity has been observed in lung cancers. The aim of the present study is to investigate if the percentage of mutated neoplastic cells within the tumor sample might influence the responsiveness to TKIs treatment., Material and Methods: A total of 931 cases of NSCLC were analyzed for EGFR mutational status (exon 18, 19, 20, 21) using Next Generation Sequencer. The percentage of mutated neoplastic cells was calculated after normalizing the percentage of mutated alleles obtained after next generation sequencer analysis with the percentage of neoplastic cells in each tumor., Results: Next generation sequencing revealed an EGFR mutation in 167 samples (17.9%), mainly deletions in exon 19. In 18 patients treated with TKIs and with available follow-up, there was a significant correlation between the percentage of mutated neoplastic cells and the clinical response (P = 0.017). Patients with a percentage of mutated neoplastic cells greater than 56%, have a statistical trend (P = 0.081) for higher Overall Survival (26.3 months) when compared to those with a rate of mutated neoplastic cells lower than 56% (8.2 months)., Conclusions: The percentage of EGFR-mutated neoplastic cells in the tumor is associated with response to TKIs. A "quantitative result" of EGFR mutational status might provide useful information in order to recognize those patients which might have the greatest benefit from TKIs.

Sarcoidosis is a systemic granulomatous disease of unknown aetiology. The breast is involved in less than 1% of cases. Breast can be either a primary or a secondary site of presentation. Breast sarcoidosis often mimics carcinomas at clinical examination. We report a case of breast sarcoidosis detected during screening mammography in a 57-year-old woman. The lesion presented as a 1.4 cm nodule located in the right breast. On histology, it was characterized by non-caseating giant cell granulomas. Differential diagnoses included idiopathic granulomatous mastitis, tuberculosis, fungal infection, cat-scratch disease and sarcoid-like reactions to cancer. Further clinical and laboratory investigations were consistent with a diagnosis of sarcoidosis. Specifically, serum levels of angiotensin-converting enzyme (ACE) were elevated and a CT scan showed small bilateral pulmonary nodules distributed along the pleura and bronchovascular bundles (perilymphatic pattern), as well as enlarged bilateral hilar and mediastinal lymph nodes. The patient received corticosteroid treatment, and is presently asymptomatic. Breast involvement by sarcoidosis, although rare, should be considered when dealing with granulomatous lesions of the breast.

Two N-terminal isoforms characterize the p63 protein: the transactivating isoform TAp63 and the amino-terminal truncated isoform DeltaNp63. Two further N-terminal isoforms lacking exon 4 (d4TAp63 and DeltaNp73L) have been reported. Purpose of the study was to investigate the molecular expression of N-terminal p63 isoforms in benign and malignant breast tissues. Eighteen randomly selected cases of invasive breast carcinoma (IBC) of luminal type, two cases of in situ duct carcinoma (DCIS/DIN), and 20 specimens of normal and benign breast tissues were studied. All cases were immunostained for p63. Reverse polymerase chain reaction and nested PCR were performed to evaluate p63 N-terminal expression patterns. These isoforms whenever present were validated by sequencing. All cases of normal breast, benign lesions, and the two cases of DCIS/DIN expressed DeltaNp63 and TAp63 isoforms only. The two variants lacking exon 4 (DeltaNp73L and d4TAp63) were not found. All invasive carcinomas expressed the DeltaNp63 and TAp63 isoforms as well as the two short isoforms lacking exon 4 which were found in 11 (d4TAp63) and four (DeltaNp73L) cases. The present cases of luminal-type IBC showed p63 isoforms together with short variants lacking exon 4. These isoforms were not observed in non-neoplastic breast tissue. Presence of p63 in invasive breast carcinomas of luminal type, as seen at molecular level, suggests caution to include p63 as a marker of basal-like carcinomas.

The discovery of HER2 gene amplification and protein overexpression in approximately 15-20% of breast cancers and access to the tailored humanized antibody, trastuzumab (Herceptin), have heralded a new era in breast cancer therapy. Trastuzumab combined with chemotherapy has caused marked tumor responses and increased overall survival in patients with metastatic breast cancer, and has also increased survival in the adjuvant setting after radical surgery. However, due to many causes, trastuzumab resistance usually occurs during treatment. In this event, possible options include the replacement of trastuzumab with lapatinib, the continuation of trastuzumab after disease progression with changed chemotherapy and the suspension of the use of targeted agents. New-generation tyrosine kinase inhibitors, which have a broader target, are now considered the key to treatment for breast cancer.

The authors report 4 cases of patients with AIDS and harbouring oral lesions of Kaposi's sarcoma. They describe the macroscopic appearance and clinical signs in relation to epidemic Kaposi's systemic ones. Because of the anamnestic or coexistence of oral mycosis (Candida), in every case the authors suppose that it may precede Kaposi's manifestations, with a very severe prognosis, correlated to progressive and deadly course of this illness.

Oral complications of cancer chemotherapy have been studied in a group of 50 adult patients. A number of 25 patients was treated by means of oral hygiene and prophylactic measures: drugs and topical agents, while the other group of 25 patients had not received stomatological prevention. The goal of the research has showed that prevention measures and elimination of existing or potential sources of infection reduce and minimize mucositis, infection etc.