Innovation and Design in the Age of Artificial Intelligence

At the heart of any innovation process lies a fundamental practice: the way people create ideas and solve problems. This \u201cdecision making\u201d side of innovation is what scholars and practitioners refer to as \u201cdesign.\u201d Decisions in innovation processes have so far been taken by humans. What happens when they can be substituted by machines? Artificial Intelligence (AI) brings data and algorithms to the core of the innovation processes. What are the implications of this diffusion of AI for our understanding of design and innovation? Is AI just another digital technology that, akin to many others, will not significantly question what we know about design? Or will it create transformations in design that current theoretical frameworks cannot capture?. This paper proposes a framework for understanding the design and innovation in the age of AI. We discuss the implications for design and innovation theory. Specifically, we observe that, as creative problem-solving is significantly conducted by algorithms, human design increasingly becomes an activity of sensemaking, that is, understanding which problems should or could be addressed. This shift in focus calls for the new theories and brings design closer to leadership, which is, inherently, an activity of sensemaking. Our insights are derived from and illustrated with two cases at the frontier of AI\u2014Netflix and Airbnb (complemented with analyses of Microsoft and Tesla)\u2014which point to two directions for the evolution of design and innovation in firms. First, AI enables an organization to overcome many past limitations of human-intensive design processes, by improving the scalability of the process, broadening its scope across traditional boundaries, and enhancing its ability to learn and adapt on the fly. Second, and maybe more surprising, while removing these limitations, AI also appears to deeply enact several popular design principles. AI thus reinforces the principles of Design Thinking, namely: being people-centered, abductive, and iterative. In fact, AI enables the creation of solutions that are more highly user centered than human-based approaches (i.e., to an extreme level of granularity, designed for every single person); that are potentially more creative; and that are continuously updated through learning iterations across the entire product life cycle. In sum, while AI does not undermine the basic principles of design, it profoundly changes the practice of design. Problem-solving tasks, traditionally carried out by designers, are now automated into learning loops that operate without limitations of volume and speed. The algorithms embedded in these loops think in a radically different way than a designer who handles the complex problems holistically with a systemic perspective. Algorithms instead handle complexity through very simple tasks, which are iterated continuously. This paper discusses the implications of these insights for design and innovation management scholars and practitioners

When hardware matters: innovation strategies to integrate digital technologies in physical products

Notwithstanding AI adoption has been leading to critical jumps in the productivity of platform-based firms like Amazon, Netflix, Uber, or Airbnb, traditional manufacturing firms are often not capable to fully benefit from AI adoption. One of the reasons for this failure is that those firms’ value propositions are highly based on hardware, which clashes with AI. Contrary to AI, hardware suffers from low scalability and low adaptability inertias. In this paper, we investigate strategies to mitigate those inertias by adopting a multiple-case study methodology, drawing on the instances of four companies that innovatively redesign hardware to relax the constraints that the presence of hardware imposes on AI. This analysis identifies two strategic initiatives that can be undertaken by firms, which are the Minimum Valuable Hardware and the Anticipation strategies

Lung metastasis from TTF-1 positive sigmoid adenocarcinoma. pitfalls and management.

The lung is a frequent site of metastatic involvement, and in many cases the differential diagnosis between a metastasis and a primary carcinoma is a substantial question. TTF-1 is considered as a reliable marker for differential diagnosis in distinguishing primary lung carcinoma and metastasis, especially when dealing with an adenocarcinoma or a large-cell carcinoma. It was generally thought that adenocarcinomas arising in the gastrointestinal tract do not express TTF-1. Recently, it has been reported that a small percentage (1.8%-5.8%) of intestinal adenocarcinoma TTF-1 positive show differences in sensitivity/specificity depending on the antibody clones. We report a case of lung localization of a TTF-1 positive adenocarcinoma in a patient with a history of colon adenocarcinoma. Based on the current results and previous reports, we propose the following criteria for diagnosing lung metastasis from TTF-1 positive intestinal adenocarcinoma. 1) Clinical features and anamnestic history are diagnostic milestones, and provide very important information as a prognostic parameter of primary carcinoma and the time interval between the two localizations (primary and metastasis). 2) The histologic features are compatible with an enteric differentiation. 3) TTF-1 must be tested in the primary carcinoma. 4) In lung lesions, in association with TTF-1, it could be useful to test other immunohistochemical markers such as CDX-2 and NapsinA. 5) Testing other immunohistochemical or molecular markers in either lesion is not very useful. Heterogeneity between primary and metastatic lesions has been reported in the literature. Application of the above-mentioned criteria would simplify diagnosis of lung metastases from TTF-1 positive intestinal adenocarcinoma

Right-sided rhabdoid colorectal tumors might be related to the serrated pathway

BACKGROUND: Rhabdoid colorectal tumor (RCT) is a rare, highly aggressive neoplasm recurrent in elderly patients, commonly at the caecum. The molecular mechanisms underlying RCT pathogenesis remain poorly elucidated. The differential diagnosis is with the malignant rhabdoid tumors of infancy characterized by genetic inactivation of SMARCB1 (INI1) or deletions of chromosome 22q12 locus. MATERIALS AND METHODS: To shed light on RCT pathogenesis, we investigated genetic and epigenetic alterations in two cases of pure and composite RCT and compared them with the profiles of matched adenomas and normal mucosa. Immunohistochemical analysis, FISH, methylation specific PCR and DNA sequencing analysis were performed on paraffin-embedded tissues. RESULTS: Loss of epithelial markers, (CK20, CDX2 and E-cadherin) and intense vimentin expression was observed in RCTs but neither in the normal mucosa or adenomas. INI1 expression was detected in normal mucosa, adenomas and retained in pure RCT, while it was undetected in composite RCT. Rearrangement of the 22q12 locus was found only in pure RCT. The APC/\u3b2-catenin pathway was not altered, while MLH1 immunostaining was negative in RCTs and positive in adenomas and normal mucosa. These expression profiles were associated with V600E BRAF mutation, a progressive accumulation of promoter methylation at specific CIMP loci and additional genes from the normal mucosa to tubular adenoma and RCT. CONCLUSIONS: Right-sided RCT could be characterized by epigenetic events and molecular features likely similar to those occurring in the serrated pathway and associated with epithelial-mesenchymal transition. These extremely rare tumors may benefit from the use of new biological molecules specific for colorectal carcinoma

The chromatin remodelling component SMARCB1/INI1 influences the metastatic behavior of colorectal cancer through a gene signature mapping to chromosome 22

BACKGROUND:INI1 (Integrase interactor 1), also known as SMARCB1, is the most studied subunit of chromatin remodelling complexes. Its role in colorectal tumorigenesis is not known.METHODS:We examined SMARCB1/INI1 protein expression in 134 cases of colorectal cancer (CRC) and 60 matched normal mucosa by using tissue microarrays and western blot and categorized the results according to mismatch repair status (MMR), CpG island methylator phenotype, biomarkers of tumor differentiation CDX2, CK20, vimentin and p53. We validated results in two independent data sets and in cultured CRC cell lines.RESULTS:Herein, we show that negative SMARCB1/INI1 expression (11% of CRCs) associates with loss of CDX2, poor differentiation, liver metastasis and shorter patients' survival regardless of the MMR status or tumor stage. Unexpectedly, even CRCs displaying diffuse nuclear INI1 staining (33%) show an adverse prognosis and vimentin over-expression, in comparison with the low expressing group (56%). The negative association of SMARCB1/INI1-lack of expression with a metastatic behavior is enhanced by the TP53 status. By interrogating global gene expression from two independent cohorts of 226 and 146 patients, we confirm the prognostic results and identify a gene signature characterized by SMARCB1/INI1 deregulation. Notably, the top genes of the signature (BCR, COMT, MIF) map on the long arm of chromosome 22 and are closely associated with SMARCB1/INI1.CONCLUSION:Our findings suggest that SMARCB1/INI1-dysregulation and genetic hot-spots on the long arm of chromosome 22 might play an important role in the CRC metastatic behavior and be clinically relevant as novel biomarkers